Documenti di Didattica
Documenti di Professioni
Documenti di Cultura
1 Introduction 1-2
2 Aims And Objectives 3-3
3 Review of Literature 4-100
A. Historical Review 4-7
B. Previous Work Done 8-9
C. Disease Review 10-58
D. Drug Review 59-100
4 Materials And Methods 101-109
5 Observations And Results 110-144
6 Discussion 145-163
7 Conclusion 164-164
8 Summary 165-166
9 Annexure 167-186
A. Abbrivations 167-168
B. References 169-173
C. Bibliograpy 174-176
D. Consent Form 177-177
E. Case Record Form 178-183
F. Master Charts 184-186
0
INTRODUCTION
1
Therefore, there is lack of concern about „Dincharya and
Rutucharya‟. Irregular times of taking meal i.e. Adhyashan, Samashan,
Atitkal bhojan, Vishamashan and Ati Katu-Amla- Lavan rasa sevan like
Vada-pav, missal, Noodles and road side food items, increased alcohol
consumption, increased krodha due to stress full life, all these are
responsible for vitiation of Pitta Dosha by causing increased Dravta,
Tikshanata, Sarta Guna of Samyaka Pitta. Hence, most of the population
suffers from Agnimandya, Aruchi, Fatigue, and Nervousness which are the
common symptoms of any Pittaj Vyadhi.
In Ayurveda, „Kamala‟ vyadhi is known from Ancient times i.e. Right
from vedik kala. Aacharyas of Bruhatrayi i.e. Charaka, Sushruta and
Vagbhata had explained‟ Kamala‟ as „Pravardhaman avastha‟ or „updrava
of Pandu vyadhi‟. Also at the same time „Kamala‟ is explained as
„Swatantra vyadhi‟.
The liver plays major role in the maintenance of metabolic
Homeostasis. The development of clinically important liver disease is
accompanied by diverse manifestation of disordered metabolism. Jaundice
is a Hallmark symptom of liver disease and the most reliable marker of
severity.
In the present study, selection of Vasadi kwath from
Ashtanghrudayam is done on the basis of the fact that these ayurvedic
herbs act on the root of disease i.e on Vitiated pitta dosha by their
Madhur-Tikta rasa, sheeta virya and are Mrudu virechana, Rakta
prasadana, saraka and thus Pitta shamaka. Pathya –apathya also plays an
important role since they regulate Aahara- vihara and dincharya. Also,
this herbal preparation is cost effective,as per socio-economical status of
the patient.
2
AIMS AND OBJECTIVES
AIMS:
OBJECTIVES:
3
REVIEW OF LITERATURE
1. RUGVEDA:
In Rugveda, in one of its hymn referring to the submission to
remove Hariman, mentioned prayer of Surya (God sun) i.e. to remove
yellowish pigmentation and make the complexion normal. So, word
“Hariman” refers to kamala in Rugveda. In Puranas, word Harima is used
as synonym of kamala which depicts greenish discoloration of body.
AlÉÑxÉÑrÉïprÉÑSiÉÉÇ.............................WûËUqÉÉ cÉ iÉå
2. ATHARVAVEDA:
Atharvaveda is the most important and authentic source of
Ayurveda. Ayurveda is the upaveda of Atharvaveda.In Atharvaveda, the
4
word “Harima” refers to Kamala – It is so because all the body becomes
Haridravarna in Kamala Vyadhi.
(Ref. – Atharvaveda 1.22-1)
* Sutrasthana:
Kamala as swatantra Vyadhi (Ad. No. 19)
* Chikitsasthana
Kamala as Pravardhamana avastha of Pandu Vyadhi in
Chikitsasthana(Ad.No-16)
Nidanas, Lakshanas,Prakaras,Samprapti of Kamala.
Under Chikitsa, he explained mrudu virechana and shaman
chikitsa with various kalpas.
Charaka described that kamala becomes Kumbhakamala if it is
not treated properly.
5
In the same context description of liver and spleen is found.
„Kamala‟, „Panaki‟, „Kumbhavhaya‟, „Lagharaka‟, „Alasakhya‟ are
synonyms given by Sushrutacharya.
Lakshanas & chikitsa are also explained in Ad No. 44. Sushruta
commentator Dalhanacharya explained that, Kamala can occur.
a) Amante- Due to Ama
b) Pandu Rogante- At the end of Pandu Vyadhi
c) Anya Rogante- At the end of other Vyadhi
Explaination about Raktavaha srotodushti and its chikitsa also
mentioned there.
In Nidansthana: Ad No. 13
“Lodhra” word is used for Kamala. He stated that Kamala can
appear at the end of Pandu Vyadhi and Kamala can also appear as a
swatantra vyadhi.
He explained that if Kamala is not treated properly, it turns into
Kumbhakamla. Even if not treated, then turns into Lodhar, Halimaka.
6. BHAVAPRAKASHA (1600AD):
In Bhavaprakasha Madhyam khanda, description of Kamala along
with Pandu is found.
6
7. HARITA SAMHITA (1400 AD):
He has described 8 types of Pandu, in which 2 types of Kamala and
Halimaka are mentioned.
C. ADHUNIKA KALA:
In this period of 18th century which is called as Adhunikakala, many
authors have compiled materials from classical texts.
Numbers of researches have been carried out on liver disorders and
their management.
7
PREVIOUS WORK DONE:
8
12. A clinical study of Yogaraj rasayana in the patients of kamala
with spl. Ref. to hepatocellular jaundice. Mishra s.n- state ayurvedic
college, Lucknow.
13. Role of Kutaki yoga in the management ofkamala with spl.
Ref. to hepatocellular jaundice. Mahanty P. -Gopa bandhu ayurved
mahavidyalaya, Puri.
14. Effect of indigenous drug kutaki on jaundice- Pandey A.N,
BHU, Varanasi.
15. Clinical & conceptual studies on kamala roga & its treatment
with berberis aristate-adhikari b.m.das,university of Calcutta-1
9
DISEASE REVIEW:
Paribhasha:
The term Kamala can be defined as:
AjÉ MüÉqÉsÉåÌiÉ MüÉqÉzÉoS ArÉqÉç xÉÉkÉÉUhÉ zÉoS
RACHANA SHARIR
YAKRITA SHARIRA
10
VYUTPATTI :-
The term yakrit is formed from the root kru by prefixing
yamupasarg and suffixing tuk pratyaya.
NIRUKTI:
Yam iti samyayam karoti, yaman iti niyamanam karoti iti kruth i.e.
samyayam karoti iti yakrit, implies one which controls. [1]
SYNONYMS OF YAKRITA:
Pinda (Su.U.6/14)
Prakasha (Visheshana) (Su.Ni.2/11)
Kaleyam
UTAPATTI OF YAKRUTA:
Yakruta is a Matrija Avayava. According to Ayurvedic embryological
consideration given by Sushruta (Su.Sha.4/25) [9] and Vagbhatta, Yakrut
isderived from the Accha portion of the fetal blood [1]. According to
modernEmbryology, the liver developes from hollow endodermal bud from
theForegutduring 3rd week of pregnancy, Hence the structure is soft,
wellorganized and secretary in nature.
Yakruta is formed from the Rakta dhatu from the beginning and also
it is mulasthana of Raktavaha strotasa. (Su.Sha.4/25)[9]
STHANA OF YAKRUTA:
11
RAKTAVAHA SROTAS AND RAKTADHARA KALA:
Since Formation of Rakta dhatu occurs in Yakruta by means of
RanjakaPitta. (Su.Su.21/10)[3] Yakrit is a Mulasthana of Raktavaha
srotasa (Su.Sha. 9/12[5], Cha.Vi.5/8 [4]. Yakruta is a site of Raktadhara
Kala. (Su.Sha.4/10-17)[7] Formation of Raktadhatu is done by
Raktadhara Kala.
CONCEPT OF RAKTOTAPATTI:
Rakta Dhatu is stated to be formed from ras dhatu through Dhatu
parinaman krama. (Cha.chi.15/16).
Three factors which participate in the formation of raktdhatu are
1. Rasagni
2. Raktagni
3. Ranjak pitta
Rasagni, Raktagni are the Dhatvagnis, which are specific in function
and are helpful in the formation of the respective Dhatus.Ranjak pitta is
located in Yakruta, Pleeha and Amashya (As.Hr.Su12)(Su.Su.21).
It has been stated that production of the Rakta dhatu takes place in
Raktavaha srotasa and the moola sthana of them is Yakrit and Pleeha
(Cha.Vi.5/8) [4]. Both Yakrit and Pleeha are also the sites of Ranjak pitta
and store houses of Rakta dhatu. As Kamla is a Rakta pradoshaj vikara,
Yakrita and pleeha are also involved in pathogenesis.
12
RELATION BETWEEN TRIDOSHA & YAKRITA:
Actually, all 3 doshas are related to Yakrit but the original & basic
pitta dhatu is formed in Yakruta. (Su.Su.21/7)[1]
It is primary place of Ranjaka Pitta. This Ranjaka pitta is a creator
of Rakta Dhatu from Rasa dhatu. (Su.Su.21/10)[3]
13
In Ayurvedic texts, various etiological factors of Kamala have been
mentioned by different aacharyas. They can be effectively assembled as
below:
1) Nij Hetu:
14
Manasa Hetu: Kama, krodha, chinta, bhaya, shoka, irsha
15
B. PURVARUPA :-
Purvaroopa marks the Sthanasanshraya awastha of dosha. These
are the prodromal symptoms that occur in rudimentary form before
complete manifestation of disease. This means that causative factor
(guna vishesha) of the dosha is not clear as yet. So some of the signs
occur fully or with a lesser intensity at this stage which is known as
purvarupa (Premonitory symptoms) of the disease.
Specific prodromal symptoms for Kamla have not been mentioned
either in Brihatrayi or Laghutrayi. But Aachrya Charaka and Sushruta
included general purvaroopas of Pandu as of Kamala (Su.u.44/6).
C. ROOPA :-
Roopa of the Vyadhi are Vyakta Lakshanas of the Vyadhi. They
exhibit 5th stage of kriyakala that is Vyaktavastha. They are specific
identification of vyadhi. The clear manifestation of the prodromal is called
as Roopa. In kamala, there are- Haridra varna of mala, mutra, netra,
anana and twaka.
16
The roopa gives us an important information for vyadhiviniscchaya
(Diagnosis), vyadhiawastha (Stage of disease), vyadhivyavaccheda
(differential Diagnosis), Vyadhiupashama (Prognosis) and Chikitsa
(treatment of the disease).
These Roopa of Kamala can be summarized in tabular form as
follows_
Tabular presentation of various Roopani :-
Haridra Netra + _ + + + +
Haridra Twak + _ + + + +
Haridra Anana + _ + + + +
Haridra Nakha + _ + + + +
Rakta-Pitashakruta + _ + + + +
Rakta-PitaMutra + _ + + + +
Bhekvarna + _ + + + +
Hatendriya + _ + + + +
Daha + _ + + + +
Avipaka + _ + + + +
Dourbalya + + _ + + +
Sadana + + _ + + +
Aruchi + _ _ + + +
Trishna - - + - - -
Tandra _ + _ _ _ _
Karshyata _ + _ _ _ _
Balakshaya _ + _ _ _ _
Bhrama _ + _ _ _ _
17
SHAKHASHRIT KAMLA LAKSHANAS: Found only in Charaka samhita and
Ashtang Hridaya. They are_
Dhatu :-
Rasagata
Twaka-Haridrata, Bhek Varna, Trushna, Aruchi
Raktagata
Netra, Nakha Haridratwam
Mamsagata
Daha, Daurbalya, Bala kshaya, Sadan, Twak Haridratwa
Mala :-
Haridra Mala
Haridra Mutra
18
Indriyas :-
Hatendriya( Blunting of senses)
Tandra
Agni:-
Avipaka
Aruchi
CLASSIFICATION OF KAMALA:
The classification of the Kamla is described by different Acharyas as
follows:-
Koshthashrit
1 + + + + +
kamala
Shakhashrit
2 + + + + +
Kamala
3 Kumbhakamala + + + + + +
4 Halimaka + + + + + +
5 Lagharaka +
6 Panaki +
7 Alasakhya +
19
Samprapti:
ÌlÉuÉ×̨ÉUÉqÉrÉxrÉxÉÉæ xÉÇmÉëÉÎmiÉeÉÉïÌiÉUÉaÉÌiÉ: ||
(A.WØû.ÌlÉ.1/8)
(cÉ,ÍcÉ.16/34)
1) BAHUPITTAKAMALA: -
When Pandu rogi consume more pittaprakopaka ahara, his pitta get
aggrevated, goes with blood and it vitiates the Rakta & Mamsa dhatu.
20
DESCRIPTION: -
While considering the samprapti of Panduvyadhi, it is clear that, in
Panduvyadhi, pittadominant vatadi tridosha vitiates the Raktadi dhatu and
produce looseness, heaviness of the body.
As a result of this Dosha- Dushya- Pradushana, prakrut bhavas of
Rasa dhatu like Bala, Varna, and Sneha are abolished. So there is no
prakrut utappatti of next raktadi dhatus. So, body bocomes „Nissar‟,
„Alpamedska”.
At this stage, consumption of more pittaprokopak ahara by
pandurogi, leads to less production of sarbhuta Rakta dhatu due to
Dhatvagnimandya& more production of malaswaroopa pitta due afflicted
dhatu parinaman krama. This excess malaswaroopa pitta spreads all over
the body & produce lakshanas like :- Netrapitata, Twaka- Nakha-Mukha
pitata, Rakta pitata of Mala- Mutra, Bhekavarna, Hatendriya, Aruchi,
Avipaka, Daha ,Daurbaly etc.
21
WAY OF VITIATED PITTA DOSHA IN BAHUPITTAKAMALA:-
YAKRUT
Yakrutta
2) RUDHAPATHAKAMALA :-
22
The causative factors explained for Shakhashrita Kamala are
Ruksha, sheeta, guru, madhur dravya sevana, Ativyayama
andVeganigraha. These etiological factors aggrevate Vata doshaa by
ruksha, sheeta guna and ativyayama, veganigrahawhereas Guru,
madhura rasa and sheeta guna aggrevates Kapha dosha, resulting in
Srotorodha.
23
WAY OF VITIATED PITTADOSHA IN RUDHAPATHA KAMALA:
Hetusevana
Vataprakopa Kaphaprakopa
24
UPASHAYA – ANUPASHAYA:
Aushadhi, Anna and Vihara which relieves the symptoms of vyadhi
are called asUpashaya and also called as Satmya. [19,20]
The opposite of upashaya, means the factors that aggrevate the
symptoms of vyadhi are called as Anupashaya.
Upashaya in Kamala:-
Aushadhi: Madhura rasa, sheeta virya, madhura
Vipaki, Pittashodhaka, Tikta and kashaya
rasa
Aahara: Madhura, sheeta aahara, Godhum, Shali
Vihara: Vishrama
Anupshaya: Masha, madya, ajamamsa, tiltailam
UPADRAVA:-
Upadrava is the occurrence of separate disease as a complication in
the wake of a primary disease. It can occure during or immediately after
the course of the disease.
In classical texts, specific upadrava of Bahupitta kamala are not
explained under separate heading, but „Kumbha Kamala‟ which occure in
the late stage due to neglection of disease, is described as Updrava in
Charka, Sushruta and Vagbhata.[22]
Charaka:-
Due to long standing kamala there is Saptadhatukarshan,
Rukshana, Krishna-peeta-mutrata, Sarvanga shotha called
Kumbhakamala, which is a Kruchhasadhya awastha. [21]
Sushruta:-
Shotha, Parvabheda
25
Halimaka:-
It is due tovata-pitta predominance. The varna of rugna will be
harita or neela. Jwara, Aruchi, bhrama, loss of natural desire of
intercourse are associated symptoms. [23]
According to Dalhana, in Kumbhakamal, when there is Harita, Pita,
Neelavarna to the body then that awastha is called as „Halimaka‟.
Panaki:-
It is characterised by Santap, atisara, yellowishness of all body.
[24]
VYADHIVYAVACCHEDA OF BAHUPITTAKAMALA:-
Bahupittakamala can be differentiated with Pittaja Pandu,
Haridrameha, Sannipataka jwara, Pittaja Gulma, Pittaja Apasmara,
Pittavrutta Apaana.
26
Chikitsa:-
Chikitsa siddhanta of Bahupittakamala is- “Kamali tu virechane”
which includes mainly-
Shodhana (Purificatory theory)- Sneha virechana
Samshamana (Palliative treatment)-Kapha pitta harnam chikitsa
27
This Tikta rasa improves digestion and liver function and thus
causes pitta, kapha and kleda shodhana in bahupitta kamala. The function
of virechana is not limited to mahastrotas but can reach all over the body
and it removes vitiated pitta dosha.
SAMSHAMAN CHIKITSA:-
After dosha shodhana by Virechna karma, it is also necessary to
give shaman chikista with respect to Dosha, Dushya, Bala, Kala, Prakriti,
Vaya. The shaman aushadhi of Pachana, Deepana guna in the form of
single or compound drugs can be given.
Owing tothis line of concept, in Ashtanga Hridayam, Acharya
Vgbhata, has advised oral administration of Vasadi kwath along with
madhu (As. Hr.Chi.16) .This is shaman in the form of Pittahara, Yakruta
uttejana, Deepana, Rechana, Jwarhara, Rakta shodhana, Rasyana dravya.
On this reference, an attempt was made to put forward the results of this
remedy.
PATHYAPATHYA:
According to Charaka, the diet which is beneficial for srotasa and
oris favourite to mana is called as Pathya.(Cha.su.25/45). Pathya means
which is compatible to the body. The opposite of Pathya, means not
favorite or liking to particular srotasa and or mana is Apathya. Apathya is
harmful to vital elements of the body also.
Nidana parivarjana is first line of treatment of any disease which
can be aopted by Pathyakara aahra-vihara.Yogaratnakar&Bhaishjya
Ratnawali described detail Pathy-apathya aahra-vihar in kamala Vyadhi.
28
PATHYA VIHARA:-Virechana, Vishrama
HALIMAKA CHIKITSA:-
According to Chrakac aacharya, Mahisham ghrita with guduchi
swarasaNishottara churna with Aamalaki swarasa, Madhura rasatmaka
aahara, Drakshaleha, Yapana basti, Ksheer basti, Anuvasan basti.
29
MODERN LITERATURE REVIEW
INTRODUCTION:-
Liver is the largest gland of the body. It is an organ having dual
functions- secretory and excretory functions. It occupies a substantial
portion of upper abdominal cavity.
LOCATION:-
Liver is located in the upper and the right quadrants of abdominal
cavity that is right hypochondrium and epigastrium, immediately beneath
the diaphragm.
WEIGHT:-
Liver weighs about 5% of the body weight in infancy and it
decreases approximately to 2% in adulthood. It weighs 1.4 to 1.6 kg in
males and 1.2 to1.4 kg in females.
COLOUR:-
The colour of liver is reddish brown normally but can vary according to fat
content.
SHAPE:-
Liver is a wedge shaped organ.The narrow end of the wedge lies
towards theleft hypochondrium and anterior edge points antero-inferiorly.
TEXTURE:-
Normal structure of the liver is soft to firm, depending upon volume
of the blood and fat it contains.
LOBES OF LIVER:-
There are 2 main anatomical lobes-right and left. The right being
six times thesize of left and largest in the volume. The right lobe has
quadratelobe on its inferior surface and a caudate lobe on posterior
surface. The right and the left lobes are separated by anteriorly by a fold
of peritoneum called falciforligament, inferiorly by fissure of
ligamentum teres, and posteriorly byfissure of ligamentum
venosum.The porta hepatis is a region on the inferior surface of theright
30
lobe where blood vessels, lymphatics, and common hepatic duct form
theHilum of the Liver.Liver is made up of many lobes called hepatic
lobes.A firm smooth layer ofconnective tissue called Glissons capsule
encloses the liver.
Hepatic lobules-
This is the structural & functional unit of liver. There are about
50,000 to1,00,000 lobules in the liver. The lobule is a honey comb like
structure & it is made up of liver cells called hepatocytes.
SURFACES OF LIVER:-
1. Superior
2. Inferior
3. Anterior
4. Posterior
5. Right
Of these, superior, anterior and right surface are continuous and no
definable border can separate them.
Superior surface: - It is the largest one and lies immediately below the
diaphragm.
Anterior surface- It is triangular and convex surface, covered by
peritoneum except at the attachment of falciform ligament.
Right surface- It is covered by peritoneum and lies adjacent to the right
dome of diaphragm.
Posterior surface- It is convexwide onright but narrow at left. It is
attached to diaphragm by loose connective tissue, forming triangular
„Bare area‟. The inferior vena cava lies at the medial end of „bare area‟.
Inferior surface- It is bounded by inferior edge of liver marked near the
midline by shrap fissure which contains Ligamentum teres. Gall bladder
usually lies in the shallow fossa.
BORDERS OF LIVER:-
Superiorborder: - It seperates anterior surface from inferior surface.
Inferior border- It is sharp.
31
Histology:
In section through the liver, the substance of the organ appears to
be made up of hexagonal areas that constitute hepatic lobules each being
about 1 mm in diameter.In transverse section each lobule appears to be
made up of cord of liver cells that bare separated by sinusoids. However
the cells are really in the form of plates that branch and anastomose with
one another to form a network space.
Along the periphery of each lobule ther are angular intervals filled
by connective tissue
These are called portal canals.Each canal consists of
1. A branch of portal vein
2. A branch of hepatic artery
3. An inter lobular bile duct from posterior to anterior
respectively.
32
These three structures collectively form a portal triad, blood form
the branch of hepatic artery enters the sinusoids at the periphery of the
lobule and passes towards its center.
Here the sinusoids open into a cental vein which occupies the centre
of the lobule.The vessel in a portal triad usually give branches to the parts
of three adjoining lobules.
Portal lobule:
A polygonal territory centered on aportal triad its boundry line
passing through adjacent central veins.It consists of adjoining parts of 3
hepatic lobules.Bile from which drains into bile ductile in the portal canal
at the meeting place ofthree hepatic lobule.
Portal acinus:
This unit is centered on a pre- terminal branch of a hepatic arteriole
and includes the parenchyma served by this vessel bounded by the
territories of the other portal acini and by two adjacent cental
veins.Several phenomenon e.g. Zones of anoxic damage,glycogen.
33
3 minor fissures: - Umbillical fissure
-Venous fissure
- Fissure of Gans
34
4) Liver stores glycogen, fats, Vitamin A, B12, D, E, K, and minerals
like Iron and the Copper.
5) Bile is secreted by the liver which contains bile salts, bile pigments,
cholesterol, and lecithin. This bile is used to break down and digest
fatty acids.
6) Blood coagulation: Liver synthesizes–Fibrinogen (factor I)
prothrombin, and factor V, VII, IX, X, XI and XII.
The billiary system collects bile from liver and stores it in the gall
bladder. The gall bladder transmits it to the second part of the duodenum.
This billiary system comprises of – Riht and Left hepatic ducts
-Common hepatic duct
-gall bladder
-Cystic duct
- Bile duct
Hepatic Ducts:
Right and left hepatic ducts emerge at the porta hepatis from the
right and left lobes of liver.
Common hepatic duct:-By the union of right and left hepatic ducts near
the right end of the porta hepatis, common hepatic duct is formed.
Bile duct:-This common hepatic duct runs downwords for about 3 cms
and is joined on its right side at an acute angle by cystic duct to form the
bile duct.
Cystic duct:-it is 3-4 cm long begins at the neck of the gall bladder. It is
8 cm long and has a diameter of about 6 mm.
35
Near the middle of the left side of the second part of the duodenum,
it comes in contact with the pancreatic duct and accompanies it through
the wall of the duodenum, within the wall of the duodenum. Both the two
ducts usually unite to form Hepato pancreatic ampullaof vater.
PROPERTIES OF BILE-
volume- 800 to 1200ml/day.
Reaction- alkaline
Colour- golden yellow/green.
PH- 8 to 8.6
Specific gravity- 1.010 to 1.011.
36
COMPOSITION OF BILE:-
Water- 97.6%
Solids- 2.45% (organic and inorganic substance)
STORAGE OF BILE-
The bile is primarily stored in gall bladder,it undergoes many
changesboth in quality & quantity such as volume & PH decrease; organic
substances concentration, sp.gravity increase.
SECRETION OF BILE-
Bile is secreted by hepatocytes.Hepatocytes→canaliculi→small duct
& hepatic duct→common hepatic duct from here bile is diverted either
directly into the intestine or into the gall bladder. Sodium bicarbonate &
water are added to bile when it passes through the duct.
BILE SALTS-
Bilesalts are the sodium & potassium salt of bile acid,which are
conjugated with glycine or taurine. These bile salts are formed from bile
acids- Primary bile acid in human-1. cholic acid and 2.Chenodeoxycholic
acid, which are formed in liver and enter intestine through bile. These
primary bile acids are converted into secondary bile acids as a result of
bacterial action in the intestine.
37
BILE PIGMENTS: -
Bile pigments are formed during the breakdown of haemoglobin,
which is released from the destroyed RBC‟s in the reticuloendothelial
system. Bile pigments are the excretory products in bile. Bilirubin &
biliverdin are two bile pigments and bilirubin is the major bile pigments
in human beings.
NORMAL BILIRUBIN METABOLISM:
In a normal healthy individual, about 250mg of bilirubin is
produced per day.The metabolism can be described under 4 stages-
38
then it is bound to albumin irreversibly and is termed as delta-bilirubin or
biliprotein. This irreversible conjugated delta bilirubin is not excreted from
the kidneys and remains detectable in serum for long time after recovery
from disease.
Conjugated Bilirubin is rapidly excreted into bile canaliculi and then
passes into the bile.
3) Intestinal phase: The conjugated Bilirubin which is excreted through
bile canaloculi reaches to the intestinal lumen where it is converted into
stercobilinoen followed by either direct excretion in stool as
stercobilinogen and urobilinoen by intestinal bacteria which imparts
normal colour to stools and urine respectively. About 70% of this is
reabsorbedin the colon and brought back to liver and re-excreted (entero
–hepatic circulation). Unabsorbed stercobilinoen ives brown colour to the
faeces.
JAUNDICE
39
Jaundice or Icterus can be defined as yellowish dicolouration of tissue
(skin, mucous membrane and sclera) resulted due toincreased bilirubin
level in the blood.Scleral icterus is seen when bilirubin level exceeds
from2.5 to 3 mg/dl.
Pathophysiology of Jaundice:-
Both unconjugated bilirubin and bilirubin glucuronides may
accumulate systemically and deposit in tissues, giving rise to the yellow
discoloration of jaundice. This is particularly evident in the yellowing of
the sclerae (icterus).
In the normal adult, serum bilirubin levels vary between 0.3 and 1.2
mg/dl and the rate of systemic bilirubin production is equal to the rates of
hepatic uptake, conjugation, and biliary excretion.
Jaundice occurs when the equilibrium between bilirubin production
and excretion is disturbed by one or more of the following mechanisms:
a. Excessive production of bilirubin
b. Reduced heapatocellular uptake
c. Impaired conjugation
d. Decreased hepatocellular excretion and
e. Impaired bile flow (Both intra and Extra Hepatic).
The first three mechanisms produce unconjugatedhyper
bilirubinemia, and the latter two produce predominantly conjugated
hyper bilirubinemia. More than one mechanism may operate to produce
jaundice, especially in hepatitis, which may produce unconjugated and
conjugated hyper bilirubinemia.
Prevalence
Jaundice is prevalent more in underdeveloped and developing
countries. But it is also seen in developed countries.
Epidemiological Factors
The etiology of jaundice is complex and includes multiple causes:
1. Age:
Jaundice can occur at any age.
40
2. Sex:
Jaundice is seen both in males as well as females. Sexual
promiscuity is one factor contributes to the jaundice.
3. Genetic factor:
Thallessemia major, Gillbert's syndrome, criggler-Najjar syndrome-I
& II. (Rh - incompatibility) Also Wilson's disease is preceded by family
history.
4. Socioeconomic Status:
Jaundice is mostly seen inlower socioeconomic groups. It is mostly
due to poor quality of drinking water.
5. Eating habits:
Eating and drinking habits are important. Because eating and
drinking contaminated food constitutes jaundice.
6. Blood transfusions:
Infective blood transfusion can cause hepatitis B.
7. Drugs:
Drugs like Rifampicin, INH, propranolol, probenecid for long
term lead to jaundice.
8. Alcohol:
Long term alcohol abuse may constitute jaundice which may be
acute.
TYPES OF JAUNDICE: -3 TYPES.
Prehepatic / Hemolytic jaundice
Hepatic / Hepatocellular jaundice.
Post-hepatic / Obstructive jaundice.
41
Hemolytic jaundice: -
Excessive destruction of RBSs resulting in increasedblood level of
free(unconjugated) bilirubin.
The excretory function of the liver is normal but the quantity of
bilirubin is increased enormously. The liver cells can notexcrete that much
excess bilirubin rapidly. Unconjugated bilirubin is insoluble inwater & is
not excreted in urine. So it accumulates in the blood resulting in
jaundice.Formationof urobilinogen also increases resulting in the excretion
of more amount of urobilinoen in urine.Excess un-conjugated (mainly)
bilirubin due to excess red cells breakdown. Icterus is mild and has lemon
hue.
Classical Triad
i) Jaundice
ii) Splenomegaly
iii) Anaemia
Tests done are
i) Peripheral
ii) Reticulocytosis.
iii) Bone marrow - erythroid hyperplasia
Above tests suggests increase RBC destruction.
CAUSES: -
Any conditionthat causes hemolyticanemia can lead to hemolytic jaundice.
Renal disorder, Hypersplenism and Auto immune diseases.
Burn
Infections such as- malaria,babesiosis,
Haemoglobin abnormalities-such as sickle cell anaemia or
thalassemia, spur cell anaemia.
Drug or chemical substances causing red cell damage.
Drugs –Rifampicin, Probenecid, Ribavirin.
Inherited conditions- Crigler-najjar types 1 & 2. Gilbert‟s
syndrome.
42
HEPATOCELLULAR / HEPATIC / CHOLESTATIC JAUNDICE: -
Hepaticjaundice occures due to damage of hepatic cells.As a result
of this damage, the conjugated bilirubin from liver cannot be excreted &
it returns to blood.
CAUSES:-Causes may be
a) Injury
b) Destruction
c) Dysfunction
a) Infections:
1) Weil's disease
2) Septicemia
3) Typhoid, malaria.
b) Toxic:
i. Drugs : Rifampicin, INH halothane, chloroform, propranolol,
probenecid.
ii. Chemicals : DDT
iii. Metals : Arsenic, mercury, gold, bismuth
iv. X-ray radiation
c) Cirrhosis of liver.
d) Starvation
Alcoholic hepatitis
Inherited conditions- 1) Dubin-johnson syndrome
2) Rotor‟s syndrome.
Viral hepatitis A B C D & E.
Epstein barr virus.
43
EXTRAHEPATIC / POSTHEPATIC / OBSTRUCTIVE JAUNDICE: -
Post hepatic type of jaundice occure because of the obstruction of
bile flow at any level of the biliary system. The bile cannot be excreted
into small intestine. So,bile salts and bile pigments enter the
circulation.Therefore, blood contains more amount of conjugated
bilirubinemia.There may be biliary colic and pain at right hypochondrium.
Jaundice may be dark yellow or greenish yellow. Faeces are clay coloured.
Alkaline phosphatase is raised.
Causes:-
a) Extra Hepatic:
i. Inflammatory: stone, stricture, parasites, acute cholangitis.
ii. Neoplasm: Carcinoma of head of the pancreas, tumours of
bile duct or gall bladder.
Malignant Benign
Cholangiocarcinoma -Choledocholithiasis
Gall bladder cancer -Post operative biliary
Ampullary cancer -Chronic pancreatitis
Malignant involvement of the hepatis lymph node – Ascariasis
b) Intrahepatic:
i. Cholestatic phase of infective hepatitis, infiltrating diseases
like amyloid, lymphoma causing cholestasis.
ii. Drugs: steroids, chlorpromazine, tolbutamide, ethanol
intoxication, carbon tetrachloride, phosphorus.
iii. Pregnancy.
44
Any change in appetite, taste, weight and bowel habits
Recent travel history
Duration of jaundice
Exposure to possibly contaminated food
Any history of blood transfusions, IV injections, tattooing,
unprotected sexual activity
Exposure to possibly contaminated food
Occupational exposure to hepatotoxins or chemicals
Detailed drug history, i.e. taken in the past or are being taken.
History of taking herbal or indigenous medicine
History of alcohol intake
History of pregnancy
History of epistaxis, haematemesis or bleeding tendency
Family history for congenital hyperbilirubinaemia, i.e. Gilbert‟s,
Criggler Najjar and Dubin-Johnson and Rotor syndromes
Presence of any accompanying symptoms such as arthralgias,
myalgias, weight loss, fever, pain in abdomen, pruritus and change
in colour of stool or urine
Symptoms of encephalopathy, i.e. mental features
Clinical Presentations:-
The clinical presentation of a case with jaundice varies according to
the cause.
1. Patients with hepatitis present with fever, abdominal pain, jaundice,
tender hepatomegaly, anorexia, distaste to food and smoking.
2. A patient with haemolytic jaundice usually complains of insidious
onset and long duration of jaundice with dark coloured urine and
stools.
3. Patients with obstructive jaundice present with seviour abdominal
pain in right upper quadrant and respiratory arrest on inspiration
(murphys traid) suggestive of Cholecystitis or rarely ascending
cholangitis.
4. Carcinoma of the pancreas produces painless progressive jaundice
with palpable gall bladder.
5. Patient with cirrhosis of liver present with features ofportal
hypertension (ascites, haematemesis, malaena, splenomegaly) and
jaundice develops during decompensation of liver disease, i.e.
hepatic encephalopathy (mental features will be present)
6. In benign intrahepaticcholestaticjaundice of pregnancy-Jaundice
may present during each pregnancy.
7. A young patient with recurrent jaundice of long duration usually
suffers from congenital hyperbilirubinaemia.
46
Systemic Examination Of jaundice patients:-
Abdominal Examination for
Hepatomegaly, e.g. note, size, shape, surface, movement with
respiration, consistency and whether pulsatile or not. Elicit
tenderness
Splenomegaly-define its characteristics
Ascitis, elicit all the signs for detection of fluid
Prominent venous collaterals or veins must be looked for.
Determine the flow of blood
Look at the hernial sites
Look for scratch marks.
HEPATITIS:-
Hepatitis implies injury to liver characterized by presence of
inflammatory cells in the tissue of organ.It is divided into two main types
depending on the cause.
1. Viral
2. Non viral (Alcohol/Drug induced)
1. VIRAL HEPATITIS:-
Viral hepatitis defined as infection of the liver caused by any of
A,B,C,D,E & G viruses. Many other viruses may be implicated in hepatitis
such as- Cytomegalo-virus, Epstein -barr virus, Yellow fever virus and
Rubella virus and virus of Herpes simplex, varicella and adeno viruses
47
can also cause severe hepatitis in immune-compromised individuals, but
are rare .
Hepatitis-A:-
It is formerly known as “Infectious hepatitis”or”Epidemic hepatitis”.
It is an acute infection caused by Hepatitis –A virus.
Host factors:-
Age: - More frequent among children than in adult, however people from
all ages
may be infected if susceptible.
Sex: - Both sexes.
Immunity:- probably lasts for life after attack
Environmental factors: - Period of heavy rainfall, water borne & food-
borne epidemics.
Mode of transmission: -Faecal-oral route, parenteral route, sexual
transmission.
Incubation period: -10-50 Days(usually 25-30days).
Clinical symptoms:-Nausea, vommitig, anorexia & mild fever.
Diagnosis-Test for abnormal liver function such as- serum
alanineaminotransferase (ALT) & bilirubin
-ELISA for measuring HAV antibodies.
-Anti-HAV appear in the IgM fraction during the acute phase.
-HAV particles or specific viral antigen in the faeces, bile & blood.
48
Epidemioloical factors:-
Causative agent: - The hepatitis “A‟ virus is an enterovirus (type-72)
of the picornaviri dae family .It multiplies only in hepatocytes. The faecal
shedding of the virus is at its highest during the later part of the
incubation period & early acute phase of illness.
Resistance -The virus is fairly resistant to heat & chemicals. It has been
shown to survive more than 10 weeks in well water.
Reservoir of infection -The human cases are the only reservior of
infection.
Period of infectivity -The risk of transmissitting HAV is greatest from 2
weeks beforeto 1 weekafter the onset of Jaundice.
Infective Material- Mainly human faeces, blood, serum & other fluids
are infectiveduring thebrief stage of Viraemia.
Viral excretion-In the faeces for about 2 weeks before the onset of
jaundice & forupto 2 weeks thereafter.
igM AntiHAV-Indictes acute infection
IgG Anti HAV-Indicates chronic infection
Prevention:-
Control of reservoir is difficult because faecal shedding of the virus
is at itsheight during the incubation period. The occurrence of large
number of subclinicalcases is due to absence of specific treatment and low
socio-economic profile.
Control of transmission-
-Personal& community hygiene,
-Proper autoclaving of syringes, needles & other equipment.
49
endemic areas, close personal contacts ofpatients with HAV, for control of
outbreaks in institutions.
Vaccines:- 4 inactivated hepatitis-A vaccines,given parenterally as a 2
dose series 6 to18 months apart.A combination vaccine containing
inactivated hepatitis-A andrecombinant hepatitis-B vaccines has been
licensed since 1996 for used in childrenaged 1 year or older in several
countries.
The combination vaccine is given as a 3 doses, using a 0, 1, 6 month
schedule.
Host factors-
Age- Acute hepatitis-B occurs in approximately 1% ofperinatal, 10% of
earlychildhood& 30% of late HBV infection. High risk group-recipients of
bloodtransfusion, health careand laboratory personnel, homosexuals,
prostitutes, percutaneous drug abuse, infants of HBV carrier mother and
parents who are immunocompromised.
-Humoral & cellular responses-HBV has3distinct antigens-
surface antigen/Australia antigen(HBsAg)
Core antigen(HBcAg)
e- antigen( HBeAg)
Mode of transmission: - parenteral route, perinatal transmission,
sexual transmission, other route- horizontaltransmission- child to child.
Incubation period: - 50 to 180 days.
Clinical picture: -Chronic liver diseaseprogress to primary liver cancer.
50
Epidemiological determinant-
51
Prevention: –
Hepatitis-B vaccine -Plasma derived vaccine-this is based
on the surfaceantigen (HBsAg) 1ml dose contains 20 micrograms of
hepatitis surface antigen.
RDNA-YEAST derived vaccine -in USA 1987, the recombinant DNA
vaccine elaborated from cultures ofyeast cloned with HBsAg s-gene.
Dose: - Adult - 10 to 20 micrograms initially & again at 1 & 6
month.
Children -half of the adult dose & the same time interval.
Site: - Deltoid muscle is preferred for injection i/m.
Hepatitis-B Immunoglobulin (HBIG) - Used for those acutely exposed
to HBsAg-positive blood, given as soon as possible after an accidental
inoculation (within 6hrs to 48 hrs).
Dose: -0.05 to 0.07 ml/kg body weight.
2 doses should be given 30 days apart.
Passive active immunization the simultaneous administration of
HBIG and
Hepatitis-B vaccine is more efficacious than HBIG alone.
HEPATITIS-C:-
HCV was identified in 1989, has been shown to be the major Cause of
parenterally transmitted non-A, non-B (PT-NANB) hepatitis.
-In India, HCV antibodies have been found in 2% of voluntary
blooddonars.
- The voluntary blood donars have a very high prevalence of
HCV infectionespecially in the developing world.
-HCV is a single stranded RNA virus with properties similar to
those Offlavivirus.
IgM Anti-HBc-Indicates acute infection
IgG Anti-HBc-chronic infection
Anti HCv-Acute infection by HCV
HCV-RNA-active replication
52
-It bears no genomic resemblance to hepatitis B to D.
Mode of transmission: -
- Intravenous drug user who share needles
- Transfusion of contaminated blood or blood products.
- Circumcision, tattooing & scarification with contaminated
instruments.
Incubation period: - 6-7weeks
HEPATITIS-D:-
The etiologic agent of delta hepatitis-HDV, causes infection only in
presence of HBV.
Anti-HDV-Acute infection
HDV-RNA-active replication
53
Incubation period-
It varies from 2-12 weeks.
2 epidemiological pattern of HDV infection have been identified:-
1. In Non-endemic areas, HDV infection is confined to personsexposed
frequently to blood, drug addicts & haemophilias.
2. HDV infection is endemic among person with hepatitis-B and most of
the infections are transmitted by intimate contact.
Prevention-
Vaccinating HBV susceptible persons with Hepatitis-B vaccine.
HEPATITIS-E:-
HEV is essentially water born disease. HEV was discovered in 1980.
Formerly termedas enterically transmitted hepatitis non-A, non-B
(HNANB)
HEV is a 29-nm to 32-nm RNA virus, self limiting, acute viral
hepatitis, appears lasting for a period of several weeks, which is
followed by recovery.
Formerly termed enterically transmitted hepatitis non-A, non-B
(HNANB).
HEV is a 29-nm to 32-nm RNA virus, self limitingacute viral
hepatitis appears lasting for a period of several weeks, which is
followed by recovery.
Incubation period -2-9 weeks
54
Diagnosis: -
It can be diagnosed by the level of anti-HEV antibodies in the
serum.Anti HEV IgM antibodies have been determined in the blood
sample.
Prevention:-
To take the usual elementary food and hygiene precaution.
HEPATITIS-G
HGV was discovered recently in 1996, the prevalence of this
infection is still not known.
55
Inflammatory cytokines (TNF-alpha, IL-6,IL-8)are thought to be
essential in the initiation and perpetuation of the liver injury by inducing
apaoptosis and necrosis.
Alcoholic Cirhossis:-
It is a late stage of ALD marked by inflammation, fibrosis and
damaged membranes preventing detoxification of chemicals in the body,
ending in scarring and necrosis. Between 10% and 20% of heavy drinkers
will develops cirrhosis of liver.
Symptoms include jaundice, liver enlargement, pain and
tenderness from the structural changes in the damaged liver architecture.
Late complications of cirrhosis or liver failure include portal
hypertension, coagulation disorder, ascites, and other complication
including hepatic encephalopathy and hepatorenal syndrome.
Cirrhosis can also results from other causes than alcohol abuse,
such as viral hepatitis and heavy exposure toxins other than alcohol.
Fatty change and alcohol hepatitis with abstinence can be
reversible.The later stage of fibrosis and cirrhosis tends to be irreversible,
but can usually be contained with abstinenece for long periods of time.
Treatment:
Abstinenece from alcohol intake and nutritional modification form
the backbone of the treatment.Symptomatic treatment can include
corticosteroid for severe cases,anticytokines,propylthiouracil to modify
metabolism and colchicine to inhibit hepatic fibrosis.When all else fails
and the liver is severly damaged,the only alternative is liver transplant.
INVESTIGATIONS
LFTs are useful in evaluation and management of patients with liver
dysfunction and used to-
1. Detect presence of liver disease.
2. Distinguish among different type of liver disorders.
56
3. Guage the extension of known liver damage.
4. Follow the response to treatment.
Classification of LFTs:
Based on detoxification and Excretory functions:
a) Sr.bilirubin-Direct,Indirect
b) Urine-BS,BP,Urobilinogen
c) Blood Ammonia
d) Sr.Enzymes
57
Blood coagulation tests:
The coagulation of blood depends upon the several compounds.The
factors usually affected by liver damage are Fibrinogen,Prothrombin,and
factors V,VII,IXand X.It can be used as a prognostic test in acute and
chronic hepatic damage.In acute condition the coagulation defect is due
to diminished formation of factors .
Enzyme study:
Serum Alkaline Phosphatase:
The enzyme which is hydrolized in an alkaline medium is known as
alkaline phosphatase.The alkaline phosphatase originates in the liver and
is localised in the hepatocytes.
Normal values are 21-85IU.It is slightly increased in liver cell
damage.
Serum Transaminase:
The transaminase is found in the mitochondrial cells,being essential
for the metabolic activity.Acute injury to hepatic cells release
transaminase that rise its level in blood.Significant elevations are noted in
early stages of Viral Hepatitis even prior to any evidence of jaundice.
SGOT: Serum Glutamic Oxalo Acetic Transaminse
It is present in large quantity in heart, Liver and muscles.The
normal value is 5to 17 IU.
SGPT: Serum Glutamic Pyurvic Transaminase
Since the content of this enzyme in liver is higher than in any other
oragn,the SGPT test provides a useful and the specific index of the acute
liver damage.The normal SGPT value is 35 u or 4to 13IU.But with acute
liver cell injurythe increase in the SGPT value may nbe for more than that
of the SGOT.
For viral hepatitis –
A battery of serological tests used.
58
DRUG REVIEW
VASA
Classical Categarization:-
Charaka : Tikta skandha – Bitter tasting groups of herbs
Vagbhata : Durvadi Gana
Synonyms : -
Sanskrit : Vasak, Vasika, Simhasya, Vajidant, Vrush Aatrushak, Simhi,
Bhishagmata, Tamruka, Simhaparni.
Hindi : Adosa, Arusha, Rus, Bansa, Adusa
Marathi : Adulsa, Adusa
59
Distribution: - Found Through out India, Usually grown on beside
compounds includes Shri Lanka, Nepal, Bangladesh, India, Pakistan,
Indonesia.
External Features:-
Shrub of 1-3 meters height Perennial
Leaf 8-10 cm long, Blackish Green soft and long like a Spear.
Flowers - Inflorescence looks like lion’s jaw.
Fruit - In 2cm long legume, fruits are pubescent & are with club-
shaped Capsules.
Bio-energetics:
Rasa - Tikta Kashaya
Virya - Sheeta
Vipaka - Katu
Guna - Laghu, Ruksha
Doshaghnata – Kapha – Pittaghnam, Vatakara.
60
Parts Used: -Leaf, Root, Flower, and Whole Plant
Udakvaha srotasa:-
It is useful in increased thirst especially kaphaj & pittaj type, due to
its tikta rasa & sheeta virya it acts as Trishna – shaman.
61
Mamsa – Medovaha srotes:
Kushtha: Useful in skin disorders Reduces Kandu, Daha because
of its Swedajanan & Kushthaghnam actions.
ExternalUses: Its leaves are made into paste and applied to relieve
inflammation, pain, Rheumatoid arthritis, worm infested wounds and skin
disorders.
REFERENCES:-
62
uÉxÉMüÉå uÉÉiÉM×üixuÉrÉï: xÉTüÌmɨÉÉxÉ lÉÉzÉlÉ: |
AMRUTA
Family: Meinispermaceae
63
Classical categorization:
Charka: Vayasthapana, Daha prashamana, Trishna nigrahana,
Triptighna, Stanyashodhana.
Sushruta: Guduchyadi, Patoladi, Kakolyadi, Vallipanchamool,
Aragvadhadi
Bhavpraksha: Guduchyadi varga.
Synonyms:
Sanskrit: Chakra lakshana, Madhuparni, Cchinnaruha, Kundalin,
Cchina, AmrutvalliAmruta, Chakrangi
Hindi: Giloy, Gulvel, Gurach
Marathi: Guduchi, Gulvel
External features:
It is a perenial small creeper, mainly found on Mango, Nimba trees
going in a spiral manner.
Chemical Composition:
Guduchi is highly rich in Anti-oxidants. It has wound healing
property, Antipyretic and Anti-viral properties.
64
Alkaloids: Berberine, choline, Mangoflorine, Tinosporin,
Palmetine.
Glyocosides: 18- Norclerodane glucoside, Tinocordiside,
cordioside, cordifolio
Streoids: B sitosteral, Delta – sitosteral 20/3
hydroyecdysone.
Nutritional compostion: Calcium, Phosphorus, Iron, copper, zinc,
Manganese.
Bio – Energetics:
65
Guduchi Aampachan & Agnideepan due to Tikta Rasa therefore
balances niram pitta & causes absorption of saam pitta. Reduces kapha
vibandha.
b) In Kamala-Yakrit Vikara :
Guduchi reduces inflammation of liver by purgation of vitiated &
vimargag Pitta dosha. Yakrit-Uttejana occurs by its Tikta Rasa. Due to
Tikta Rasa Vitiated Ranjak Pitta becomes normal and stimulates normal
circulation of Rasa & Rakta Dhatu. Therefore, Guduchi is said to be a Best
Hepatoprotective drug.
66
Matra (Dose): Kwath (Decoction) 40-80 ml.
Stem powder –churna – 1 -3 gm
REFERENCES: -
SÉåwÉMÑü¸M×üÍqÉcNûÉÌSïSÉWû uÉÉiÉÉxÉëmÉÉhQÒûiÉÉ: |
̧ÉSÉåwÉSlÉå xuÉÉSÒ mÉjrÉï cɤÉÑirÉÇ SÏmÉlÉÇ sÉbÉÑ| oÉrÉxÉ: xjÉÉmÉlÉÇ qÉåkrÉqÉqÉ×iÉÉzÉÉMüqÉç EcrÉiÉå ||11|| (Mæü. ÌlÉ.)
67
NIMBA
Classical Categorization:
Synonyms:
68
Utapttisthana (Habitat):
It occurs all over in India, especially in dry places of west & north
India.
External Features:
It is thick widely spread shadowing tree with height approximately
40-50 feet.
Leaves: At the end of small sub branches, there are 8-15 inch
long leaves. Leaflets are 14-14 in muber, opposite,
curved and bhalakar
Chemical Composition:
The bark and stem contains the bitter alkaloid priniciple Morgosine.
It also contains Nimbidin (0.5%), nimbin (0.03%), Nimbinin, Nimbasterol
and Volatile Oil. It also contains 6% Tannin.
The Neem oil contains all above priniciples with oleic acid, Linoleic
acid, palmitic acid, stearic acid and lignoceric acid.
69
Bio-Enegetics:
Rasa: Tikta, Katu, Kashaya
Virya: Sheeta
Vipaka: Katu
Guna: Laghu – Ruksha
Action on Dhatu: It purifies Rakta Dhatu by its tikta Rasa and sheeta
Virya & Reduces Kleda & kandu in skin disorders. Due to Tikta Rasa-
Laghu Ruksha Guna it Purifies kapha-Pitta Dushta Stanya.
Annavaha srotasa:
Rochan, Grahi, Krimghna, Yakrit uttejana therefore useful in Aruchi,
Chhardi, Grahani, Krimi, Atisara, and Yakrita, Vikara, Kamala.
It is a best drug for urdhwaga Amalpitta and Kapha-Pittaj Charadi
due to its tikta Rasa & Ruksha guna. Also, it is very useful in kaphaj krimi
& Raktaj Krimi due to its tikta rasa.
Aruchi – Being tikta Rasa – Vishad guna balances vitiated Kapha
kleda and mala of Jivhasthana. Therefore, Rochan function occurs. In
arsha & vimbandha- Nimboli is useful for Vatanuloman.
70
Udaka vaha Srotas: –
Trishna: Pittaj and Jwaraj trishna shamak. AlsoNimba siddhajala is
useful in Prameha to quench thirst.
Rasa: Raktavaha Srotas
Jwara: Aamjwara, Pittaj and Kaphaj Jwara.
Daha: Being Tikta and sheeta, Nimba is best Dahashamaka.
Kamal-Pandu-Raktapitta:
Nimba Balances vitiated Pitta, raktagata and Yakritastha pitta due
to its Tikta Rasa. Therefore, useful in Kamala & Raktapitta.
Firang- Updansh: Nimba works as anti-toxin.
Mamsa-Medovaha Srotas:
Useful in Pittaj and kaphaj kushtha namely Arunshi, Pama, Kandu,
Vicharchika, Eczema.
Prameha: Balances vitiated drava kapha, Kleda, & Reduces
Bahumutrata Symptoms.
Matra (Dose):
Churna -1-3gm
Swarasa (Leaves Juice) -10-20 ml c honey
Oil (Nimb tail) – 5-10 drops
REFERENCES:-
A¬SrÉ: ´ÉqÉiÉ×OèMüÉxÉeuÉUÉÂÍcÉM×üÍqÉmÉëMüiÉç |
71
KUTKI
Classical Categorizaion –
Classical Name:-
Sanskrit: Katuka, Tikta, Katurohini, Shakuladani,
Kandaruha, Matsya Shakala, Chakrangi,
Krushnabheda, Katvi, Katumbhara.
72
Hindi: Kutki, Katuka
English: Picrorrhiza, Hellebare, Picroliv
Marathi: Kali Katuki, Bala Kadu.
Varieties:-
73
Actions and Uses:-
74
Kalpa (formulations) - Aarogyavardhini Vati, Tiktadighrita, Tiktadi
Kwath
REFERENCES:-
MüOÒûMüÉ ÌmɨÉÎeĘ́ɣüÉ MüOÒû: zÉÏiÉxÉëSÉWûÎeÉiÉç |
MüOÒûMüÉÅÌiÉMüOÒûÎxiÉ£üÉ zÉÏiÉÌmɨÉÉxÉëSÉåwÉÉÎeÉiÉç |
BHUNIMBA
75
Bhunimb / Kirata Tikta-
The word meaning of Kirata Tikta is – Utterly bitter. It is a very
famous ayurvedic herb used in treatment of Infectious and Inflamatery
conditions like fever, skin diseases, kamala etc.
Family: Gentianaceae
Classical Categorization:
Classical Names: -
Sanskrit: Kirat, Bhunimb, Kiratak, Naditikta,
Jwarantaka, Katutikta, Nidrari, Ramsevaka.
Marathi: Kadechiraita, Kirait, Chirait
Hindi: Chirayata
English: Chitretta
76
Distribution: - Found in temperate Himalayas between kashmir and
Bhutan at 1200-1500 meter altitude.
Bio- energetic:-
Rasa: Tikta
Virya: Sheeta
Vpaka: Katu
Guna: Laghu, Rooksha
Effect on Tridosha: -
77
It is useful in relieving burning sensation. i.e. Dahahara. It is widely
used in the treatment of liver disorders. It reduces inflammation of liver
and spleen also.
Pranavaha Srotasa (Respiratoy System): -
Being Pittakaphaghna, it is useful in Pittakaphaj Kasa and Shwasa.
Mamsavaha Srotas: -
It is useful in Pittakaphaj, Kushtha, because it reduces Keda &
Kapha and thus Kandu, Daha, Kleda symptoms are deoreased.
It is used as a “Tiktapaushtika” being Agnidecpana, General Debility
fellowed by Jwara is easily relieved by Bhunimb.
REFERENCES:-
ÌMüUÉiÉ: xÉÉUMüÉå ¤É: zÉÏiÉsÉ: ÌiÉ£üMüÉå sÉbÉÑ: |
(MæürÉSåuÉ ÌlÉbÉhOÒû)
Triphala: -
Triphala is combination of Haritaki, Bibhitaki and Aamalaki. Triphala is
Kapha-pitta shamak, Dipan, Chakshusya, Meha, Kushta, Vishama jwara
nashak.
78
“mÉjrÉÉÌoÉpÉÏiÉkÉɧÉÏhÉÉÇ TüsÉæÈ xrÉÉÎi§ÉTüsÉÉ xÉqÉæÈ |
pÉÉ. mÉë.
xÉÑ. xÉÔ. 38
79
HARITAKI
Classical categorization:
Acharya Charaka: Prajasthapana, Jwaraghna, Kasaghna, Kusthaghna
Arshaghna
Acharya Sushruta: Triphala, Amalakyadi, Parushakadi
Classical Names:
Sanskrit: Shiva, Haimamati, Rohini, Kayastha, Shreyasi,
Chedanika, Abhaya, Pathya, Haritaki, Pachani
Hindi: Harad
English: Chebulic myrobalan
Bio-energetics: -
Rasa: Pancharasa (Lavana Varjita), Kashayapradhana
Virya: Ushna
Vipaka: Madhura
Guna: Laghu, Ruksh
Doshaghnata: Tridosha Shamaka (Vishesha Vatashamaka)
80
Chemical Composition:
Fruit contains tannin up to 30%, chebulinic acid; and it also
contains Gallic acid, resin etc, and some purgative of the nature of
anthraguinone. It contains tannic acid 45%, rich Gallic acid, mucilaginous
and colouring matter; its content chebulinic acid disintegrates into tannic
and Gallic acids on boiling in water.
Internal Uses: -
81
Majjavaha srotasa (Nervous system): -
Useful in weakness of nerves and brain as well as in vata disorders
and diminished vision.
Reproductive system: -
Useful in Shukrameha, Leucorrhoea and acts as an Uterine tonic.
Urinary system: -
Useful in Dysuria, Retention of Urine, Calculus and Kaphaj Prameha.
Skin: -
Useful in Erysipelas and other Skin disorders.Haritaki preventes
accumulation of pus in skin diseases.
Temprature: -
Useful in Typhoid fever and also chronic fever.
Restorative effect: -
Haritaki acts as a rejuvenator, but to produce rasayan effects, it
needs various supportive herbs in different seasons.This concept had
been explained by Bhavaprakashakara as Rutu haritaki.
Varsha - Saindhav
Sharad - Sugar
Hemant - Sunthi
Shishir - Pippali
Vasant - Honey
Greeshma - Guda.
82
Rogaghnata: -
It is useful in Prameha, Shwasa, Kasa, Grahani, Shopha, Kustha,
Udararoga, Hridroga etc. According to Bhavaprakasha it is effective in
Vibanda, Krimi, Trishna, Hikka, Kandu, Vedana, Yakritroga, Mutraroga
and Santarpanajanya Vikara.
Formulations:-
Srotogamitva: -
Dosha -Tridoshanashak
Dhatu -Ras, Majja, Rakta, Mamsa, Meda, Asti, Shukra.
Mala -Purisha, Mutra.
References: -
“WûËUiÉMüÐ mÉjrÉÉlÉÉÇ ´ÉãwPû: ||”
cÉ. xÉÔ. 25
pÉÉ. MÉë
pÉÉ. mÉë
qÉåWûMÑüwPûuÉëhÉcNûÌSïzÉÉåwÉuÉÉiÉÉxÉëM×cNíûÎeÉiÉç ||
kÉ. ÌlÉ.
83
BIBHITAKA
Classical categorization:
Acharya Charaka: Jwarahara, Virechanopaga
Acharya Sushruta: Triphala, Mustadi
Classical Names:
Sanskrit: Karshaphala, Aksha, Kalidrum, Bibhitaka,
Kalivruksha,
Telpushpak, Bhootawas, Romaharsha, Kalind.
Hindi: Bheda
English: Romaharsha, Kalind Belliric myrobalan
Bio-energetics:
Rasa: Kashaya
Virya: Ushna
Vipaka: Madhura
Guna: Ruksha, Laghu
Doshaghnata: Tridosha shamaka (Vishesha Kapha shamaka)
84
Parts used: Fruit
Chemical Composition:
The fruit contain gallo-tannic acid, colouring matter and resin.
Seeds yield greenish yellow oil.
Pharmacological Actions:
Astringent, Expectorant, Tonic and Laxative.
85
Reproductive system: -
The pulp is an Aphrodisiac. Used in Impotency and Libido.
Satmikaran: -
Rasa, Rakta, Mamsa and Meda gami, Dhatuvrardhak because of its
madhur vipak.
Rogaghnata:
It is useful in Kasa, Krimi, Ashmari, and Swarabhanga. The ripe fruit
is Laxative. Fruits are also effective in Bronchitis, Sore throat,
Inflammation, Asthma and Liver Diseases.
Formulations: -
Bibhitaka taila, Triphala churna, Phalatrikadi kwath, Lavangadi vati,
Bibhitaki sura.
Srotogamitva: -
Dosha -Tridosha
Dhatu -Majja, Rakta, Shukra, Rasa, Mamsa, gami.
Mala -Purisha, hair tonic
Organs -Eyes, Respiratory system.
Reference: -
“ÌoÉÍpÉiÉMÇü xuÉÉSÒmÉÉMÇü MüwÉÉrÉÇ MüTüÌmɨÉlÉÑiÉç |
pÉÉ.mÉë.
86
AMALAKI
Classical categorization:
Classical Name:
Sanskrit: Amalaki, Dhatri, Gayatri, Shriphala, Vrushya,
Tishyaphala, Amruta, Kayastha, Pancharasa.
Hindi: Amla
English: Emblica myrobalan
87
Bio-energetics:
Rasa: Pancharasa (Lavana Varjita), Amla Pradhana
Virya: Sheeta
Vipaka: Madhura
Guna: Laghu, Ruksha, Sheeta
Doshaghnata: Tridosha shamaka
Chemical Composition: -
It contains Gallic acid, tannic acid, Sugars, Albumin, Cellulose and
Minerals. It is rich source of Vitamin C.
Other contents are as follows (per 100gms of fruit):
Moisture: 81.20 mg
Protein: 0.5mg
Fat: 0.1mg
Minerals: 0.7 mg
Phosphorus: 0.02 mg
Iron: 1.2 mg
Nicotinic acid: 0.2 mg.
Pharmacological Actions:
Fresh fruit is diuretic and laxative. Fruit is also carminative.
88
Internal uses: -
Annavaha srotasa (Digestive system): -
It improves taste and Appetite, Curative, Antacid. It acts in loss of
taste, loss of Appetite, Anorexia, Constipation, Liver Disorders, Acid Peptic
Diseases, Eructations, Ascites and Piles through its properties of
digestion, laxation and rasayan.
Skin: -
Useful in Skin disease and erysipelas.
Temperature: -
Antipyretic, Refrigerant. Useful in Chronic fever, Thirst, burning
sensation etc.
89
Formulations: -Chavanprash, Bramharasayan, Dhatriloha, Amrutprash,
Amalaki rasayan.
Srotogamitva: -
Dosha: Pitta– nashak,
Kapha– nashak,
Vata – nashak
Dhatus: Rakta -Haemorrhagic disease, Jaundice.
Meda -Prameha
Shukra -Aphrodisiac
All Dhatus -Rasayan especially muscle
Mala: Purisha – laxative
Organs: Eyes, spleen, Liver, Lungs.
References: -
“WûUÏiÉMüÐ xÉqÉÇ kÉɧÉÏTüsÉÇ ÌMüliÉÑ ÌuÉzÉåwÉiÉÈ |
pÉÉ.mÉë.
xÉÑ. xÉÔ. 46
90
DARUHARIDRA
Classical categorization:
Arshaghna, Kandughna, Lekhaniya, Haridradi, Mustadi, Laksadi (S)
Kula: Daruharidra kula
Family: Berberidae (from Berberys = Arabic name)
91
Botonical Description:
Evergreen shrub having height 1.25 to 3 mtrs. The leaves are
strong with fine shorled venation, straight, but with dentate or corrugated
margins. Inflorescence 5 to 8 cms long, with large yellow coloured
flowers. The fruits are bluish purple and small (called zarishka in yunani).
Flowers bloom in spring and fruits in winter. The stem is ash
coloured from outside but is dark yellow coloured inside. Rasanjana
(rasot) is prepared from the chemical or juice of the chitra variety of
daruharida types. There are 12/13 types, the important ones being
Berberis aristata, Berberis chitra, and Berberis lycium.
Bio- energetic:
Rasa: Tikta Kashaya
Virya: Ushna
Vipaka: Katu
Guna: Laghu, ruksha
External Uses:
92
eyelids. The fluid can also be applied in the ears in earache or ear
discharge.
In diseases of the mouth and throat, rasanjana is used for gargling.
Rasanjana can be used to wash wounds or its paste can be applied on
ulcers. Chancroid ulcers, goitre, fistula, crysielas and other diseases are
treated by the application of the paste. Vaginal discharges are treated by
the vaginal douche prepared from berberis. Peripheral diseases are
treated by the application of rasanjana on perianal wounds.
Internal Uses:
Reproductive System:
Useful in uterine inflammations and vaginal discharges.
93
Skin:
Diaphoretic, useful in diseases of the skin like pruritus, boils etc.
Daruharidra decoction is useful in cleansing wounds. Rasanjana + honey
is used extemally in puerperal diseases. It is specially useful in ulcer. The
decoction is used for gargling in stomatitis.
Temperature:
Febrifuge and Diaphoretic and is a prophylactic treatment for
typhoid. Hence it is useful in common fever and also in chronic fever. It
causes sweating, is antipyretic and is useful in recurrent malaria. When
malarial parasites hide in the liver, quinine is not effective but
Daruharidra is very effective.
Satmikaran:
It is bitter and strengthening, hence useful in general debility.
Adulteration:
Daruharidra is adulterated with shoots of plants like samudrashosha
after boiling them in decoction of turmeric. The shoots of real daruharidra
are elastic and do not lose their yellow colour even after boiling.
Formulations:
Darvyadikwath, Daryadileha, Darvyaditaila
Dosage: Juice of root: 10 to 20 ml
Decoction: 50 to 100 ml
Rasanjana: ¼ to ½ gm.
Fruit: 1 gm.
In malaria (total) 5 to 10 mg as a stimulant for heart but larger
dose can lead to cardiac depression.
94
Rasanjanasuddhi:
Srotogamitva:
References: -
(kÉ.ÌlÉ.)
(pÉÉ.mÉë.)
95
MADHU
96
Types of Honey:
Acharya Sushruta and Acharya Charaka has described various types
of Honey.
“qÉÉ̤ÉMÇü pÉëÉqÉUǤÉÉæSìÇ mÉÉæ̨ÉMÇü qÉkÉÑeÉÉiÉrÉ:|
cÉ.xÉÔ. 27/243
xÉÑ.xÉÔ. 45/133
1. Makshik 2. Bhramar
3. Kshaudra 4. Pautik
5. Chatra 6. Aardhya
7. Daal 8. Auddalak
Properties of Honey:
Rasa: -Madhur, Kashaya
Guna: -Ruksha, Guru
Veerya: -Sheet
Vipak: -Madhur
Satmikaran: -Tridosha shamak.
97
Action on Doshas:
Madhu acts on all the doshas. It acts on Kapha Dosha through its
Kashaya Rasa, Ruksha, Guru guna and pacifies Vata-pitta by its viscocity,
sweet astringent properties. (According to Vagbhata Honey increases
Vata).
Dhatu-gamitva:
It acts on Meda, Shukra, Majja (Beneficial to Eye, Improves
intellect).
Guna karma:
By Acharya Charaka -
“uÉÉiÉsÉÇ aÉÑà vÉÏiÉÇ cÉ UYiÉÌmÉ¨É MüTüÉmÉWqÉç|
cÉ.xÉÑ. 27/245
Externally:
Locally when it is applied to mucous membrane it causes
stimulation of mucous membranes.
Internally:
Increases the Agni, used in Constipation, Indigestion, Abdominal
distention and Thirst. It improves complexion and voice, increase softness
of the Skin, Cardiac tonic, Aphrodisiac, Reunion of the bones, removes
vitiated doshas, improves wound healing, promote mental health.
Action on Diseases:
Diabetes, Hiccups, Asthma, Cough, Diarrhoea, Vomiting, Excessive
thirst, Helminthiasis, Toxins, Dermatosis, Jaundice, Haemmorhoids,
Abdominal distention, diseases of the Throat, Uneasiness, Intoxication,
Burning sensation, Constipation.
98
By Vagbhatacharya:
A.xÉÇ.xÉÔ.
Yogvahi Madhu:
“iɱÑYiÉÇÌuÉÌuÉkÉærÉÉæaÉæÌlÉWlrÉÉSÉqÉrÉÉlÉç oÉWÔlÉç |
xÉÑ.A. 45/142
mÉcrÉqÉÉlÉÇ rÉjÉæiÉlqÉkÉÑeÉsÉiÉæsÉÉerÉxÉÔiÉsÉÉåWÉÌS: |”
pÉÉ.mÉë. 6/230
99
Dextrose – 23 – 36%
Gulcose – 30 – 44
Dextrine – 0.7%
Ash – 0.1 – 7
References:
“iÉssÉbÉÑiuÉÉiÉç MüTüblÉ mÉæÎcNsrÉÉlqÉÉkÉÑrÉÉïiÉç|
MüwÉÉrÉpÉÉuÉÉŠ uÉÉiÉÌmɨÉblÉqÉç
xÉÑ.xÉÔ.45/141
cÉ.xÉÔ.27/4
100
MATERIALS AND METHODS
Materials:
Patients: The patients were selected from indoor and outdoor patients of
our hospital.
Drugs:
Trial Group: - Vasadi kwath with Madhu
A. Conceptual Study:
All sorts of references have been collected and compiled from
ayurvedic and modern texts, classes, commentaries, dissertations and
journals etc.
Mode of Action:
Vasadi kwath is pitta shamak, yakrut prabhavkar, Ruchikar, Deepan
and ampachan because of it‟s tikta, madhur and kashay rasa and sheeta
virya and katu, madhur vipaka.
Darvi Kwath is also pitta shamak and yakrut prabhavkar.
uÉÉxÉÉÌS YuÉÉjÉ
SÉuÉÏï YuÉÉjÉ
101
B. Pharmaceutical Study:
Preparation of the Kwatha:
Both the Kwathas were prepared according to Kwath vidhi told in
Sharangdharsamhita.
mÉÉlÉÏrÉwÉÉåQûwÉaÉÑhÉÇ ¤ÉÑhhÉåSìurÉmÉsÉÇͤÉmÉåiÉç|
qÉ×imÉɧÉåYuÉÉjÉrÉåSè aÉëɽqÉ·ÉzÉÉuÉzÉÉåÌwÉiÉqÉç ||
(zÉÉ.qÉ.ZÉÇ.2/1)
102
standardization of all this content was done by following parameters as
per API guidelines. Authentication and Standerdization certificates are
attached.
1. Pharmacognostic method
a. Organoleptic study
b. Foreign matter
c. Microscopic and macroscopic study
2. Physiochemical method
a. Moisture percentage
b. TLC (Thin layer chromatography)
Methodology:
This was randomized, single blind control clinical trial. Thorough
history and the complaints of the patients were taken in their
chronological order.
Each and every patient was carefully examined clinically for general
and systemic examination. Full explanation about the trial was given top
the each patient and informed written consent of each and every patient
was taken before the commencement of treatment, after that total 60
patients were selected for present clinical trial on the basis of clinical
diagnosis.
Total 60 patients of Bahupitta Kamala were randomly selected and
equally divided into two groups.
1) Trial Group: In this group, 30 patients of Bahupitta Kamala were
given 40 ml Vasadi kwath with 5ml honey for maximum of 60 days.
2) Control Group:
In this group, 30 patients of Bahupitta Kamala were given 60 ml
Daruharidra kwath with 5ml Madhu for maximum of 60 days.
103
STUDY DESIGN: -
Randomised Control Study
Screening of the patients for inclusion (counseling, informed concent)
Initial Assessment of patients (Dietary & Behavioral advice is given)
Group allocation by Randomizaton
104
SAMPLE SIZE CALCULATION:
η = t2 x P (1-P)/e2
Determination of sample size
η - Required sample size
t - Confidence level at95 %(Standard value of 1.96)
e – Margin of error at 5 % (Standard value of 0.5)
P- Estimated prevalence of Bahupitta Kamalain selected patients95
% (Standard value of 0.95)
η = t2 x P (1-P)/e2
= [(1.96)2 x 0.95 (1-0.950)]/ (0.05)2
= [3.84 x 0.95 x 0.05] / 0.025
= 0.1475 / 0.025
= 59.00 ≈ 60
= Approximately 60 Patients
i. e. Sample size: Total 60 Patients (30 in each group)
D.CLINICAL STUDY
Administration details:
Group A Group B
No. of patients 30 30
Treatment Darvi Kwath Vasadi kwath
Dose (Matra) 60 ml O.D 40 ml B.D
Kala Abhaktakala MadhyaBhakta
(Pratah kala)
Kalpana /Vidhi Kwath vidhi Kwath vidhi
Route Oral Oral
Duration 45 Days 45 Days
Pathya Madhur rasa adhar, Ikshu Madhur rasa adhar, Ikshu
rasa, Wheat, Green Dal rasa, Wheat, Green Dal
105
Criteria for Assessment
a. Inclusion Criteria
I. Patient willing for clinical trial.
II. Either sex
III. Occupation no barrier
IV. Religion-no barrier
V. Age between 18 to 60 yrs
VI. Having lakshanas of Bahupittakamala
VII. Hyperbillirubinemia having raised sr.billirubin (more
than 3mg/dl)
a. Exclusion Criteria
I. Patient not willing for clinical trial
II. Age less than 18 years and more than 60 years
III. Pregnant women and lactating mothers
IV. Obstructive jaundice
V. Sr. billirubin more than 10 mg per dl.
VI. Diebetes mellitus
VII. Liver cancer
VIII. Haemolytical Jaundice
IX. Patients of Hepatic Encephalopathy, Ascitis.
X. Patients having other systematic disorders like
Hypertention, Renal failure, Internal Bleeding
Diagnostic Criteria
106
The patients having above lakshanas predominantly along with
some lakshanas from subjective and objective criteria will be selected for
clinical study.
107
Normal 0
Up to 10 % reduced appetite 1
4. Agnimandya
Up to 50 % reduced appetite 2
Complete loss of appetite 3
Absent 0
Daha (Burning Occasionally 1
5.
Sensation) Occurs at particular time 2
Occur everytime 3
Absent 0
Daurbalya Mild 1
6.
(Weakness) Moderate 2
Severe 3
Normal 0
Less desire to eat with
1
nausea
7. Hrullas
Less desire to eat with severe
2
nausea
Vomitting 3
Sr. Billurubin 1 mg/dl 0
Sr. Billurubin > 2 mg/dl 1
8. Sr. Billurubin
Sr. Billurubin > 3 mg/dl 2
Sr. Billurubin > 6 mg/dl 3
108
Informed Consent
Patient fulfilling criteria for selection will be under the study after
receiving their written consent.
Pathypathya
It was explained to every patient, especially madhur rasa ahar,
Milka, Ikshu rasa (Laghu, Snigdha, Deepan, Pachan ahar).
109
OBSERVATION AND RESULTS
Group No of Patients
Control Group (A) 30
Trial Group (B) 30
Total 60
Distribution
Control Group
(A) Trial Group (B)
50% 50%
B) Age
Table 5.2 Shows Age wise distribution in both groups
Sr. No of Patients Total
No. Age (yrs) Group Group
A B
1 18 to 31 7 11 18
2 32 to 46 17 15 32
3 47 to 60 6 4 10
4 Total 30 30 60
110
Figure 5.2 Shows Age wise distributions in both groups
Age (yrs)
Group A Group B
17
15
11
7
6
4
18 to 31 32 to 46 47 to 60
C) Gender
Table 5.3 Shows Gender wise distribution in both groups
Sr. No of Patients Total
No. Gender Group Group
A B
1 Female 15 18 33
2 Male 15 12 27
3 Total 30 30 60
Gender
Female Male
18
15 15
12
Group A Group B
111
D) Occupation
Table 5.4 Shows Occupation wise distribution in both groups
Sr. No of Patients Total
No. Occupation Group Group
A B
1 Business Man 4 0 4
2 Business 2
0 2
Women
3 Driver 0 1 1
4 Farmer 3 2 5
5 House wife 9 7 16
6 Labour 4 6 10
7 Service 6 6 12
8 Student 4 6 10
9 Total 30 30 60
Occupation
Group A Group B
9
6 6 6 6
4 4 4
2 2
0 0 0
112
E) Prakruti
Table 5.5 Shows Prakruti wise distribution in both groups
Sr. No of Patients Total
No. Prakruti Group Group
A B
1 KP 0 2 2
2 KV 0 0 0
3 PK 8 8 16
4 PV 9 9 18
5 VK 4 6 10
6 VP 9 5 14
7 Total 30 30 60
Prakruti
Group A Group B
9 9 9
8 8
0 0 0
KP KV PK PV VK VP
113
F) Addiction
Table 5.6 Shows Addiction wise distribution in both groups
Sr. No of Patients Total
No. Addiction Group Group
A B
1 No 18 21 39
2 Tea 3 2 5
3 Tea + Alcohol 0 4 4
4 Tea + Tobacco 2 3 5
5 Tea + Tobacco + Alcohol 2 0 2
6 Tobacco + Alcohol 1 0 1
7 Tobacco +Gutkha + Alcohol 1 0 1
8 Tobacco + Gutkha 3 0 3
9 Total 30 30 60
Addiction
21 Group A Group B
18
4
3 3 3
2 2 2
1 1
0 0 0 0 0
114
G) Religion
Table 5.7 Shows Religion wise distribution in both groups
Sr. No of Patients Total
No. Religion Group Group
A B
1 Hindu 24 28 52
2 Muslim 6 2 8
3 Other 0 0 0
4 Total 30 30 60
28 Religion
24 Group A Group B
2
0 0
H) Diet
Table 5.8 Shows Diet wise distribution in both groups
Sr. No of Patients Total
No. Diet Group Group
A B
1 Mixed 18 16 34
2 Veg 12 14 26
3 Total 30 30 60
115
Figure 5.8 Shows Diet wise distributions in both groups
Diet
Mixed Veg
18
16
14
12
Group A Group B
I) Agni
Table 5.9 Shows Agni wise distribution in both groups
Sr. No of Patients Total
No. Agni Group Group
A B
1 Manda 7 3 10
2 Tikshna 15 17 32
3 Vishama 8 10 18
4 Total 30 30 60
Agni
Group A Group B
17
15
10
8
7
116
J) Koshtha
Table 5.10 Shows Koshtha wise distribution in both groups
Koshtha
Group A Group B
18
16
10
9
117
5.2. Changes in symptoms before and after treatment
Haridra Netra
Grade 3 Grade 2 Grade 1 Grade 0
21
20
16
15
14
13
9
8
2 2
0 0 0 0 0 0
BT AT BT AT
Group A Group B
118
B) Changes in Pita Mutrata (BT and AT) in Group A and Group B
Table 5.12 Shows Changes in Pita Mutrata in Group A and Group B
No. of Patients of Grade
Grade Group A Group B
BT AT BT AT
Grade 3 19 0 20 0
Grade 2 11 3 10 0
Grade 1 0 15 0 11
Grade 0 0 12 0 19
Total 30 30 30 30
Pita Mutrata
Grade 3 Grade 2 Grade 1 Grade 0
20
19 19
15
12
11 11
10
0 0 0 0 0 0 0
BT AT BT AT
Group A Group B
119
C) Changes in Purisha Pitata (BT and AT) in Group A and Group B
Table 5.13 Shows Changes in Purisha Pitata in Group A and Group B
No. of Patients of Grade
Grade Group A Group B
BT AT BT AT
Grade 3 19 0 20 0
Grade 2 11 7 10 3
Grade 1 0 21 0 16
Grade 0 0 2 0 11
Total 30 30 30 30
Purisha Pitata
Grade 3 Grade 2 Grade 1 Grade 0
21
20
19
16
11 11
10
3
2
0 0 0 0 0 0
BT AT BT AT
Group A Group B
120
D) Changes in Aruchi (BT and AT) in Group A and Group B
Table 5.14 Shows Changes in Aruchi in Group A and Group B
No. of Patients of Grade
Grade Group A Group B
BT AT BT AT
Grade 3 15 0 18 0
Grade 2 13 0 12 0
Grade 1 2 11 0 4
Grade 0 0 19 0 26
Total 30 30 30 30
Aruchi
Grade 3 Grade 2 Grade 1 Grade 0
26
19
18
15
13
12
11
4
2
0 0 0 0 0 0 0
BT AT BT AT
Group A Group B
121
E) Changes in Avipaka (BT and AT) in Group A and Group B
Table 5.15 Shows Changes in Avipaka in Group A and Group B
No. of Patients of Grade
Grade Group A Group B
BT AT BT AT
Grade 3 15 0 19 0
Grade 2 13 0 10 0
Grade 1 2 10 1 4
Grade 0 0 20 0 26
Total 30 30 30 30
Avipaka
Grade 3 Grade 2 Grade 1 Grade 0
26
20
19
15
13
10 10
4
2
1
0 0 0 0 0 0
BT AT BT AT
Group A Group B
122
F) Changes in Sadana (BT and AT) in Group A and Group B
Table 5.16 Shows Changes in Sadana in Group A and Group B
No. of Patients of Grade
Grade Group A Group B
BT AT BT AT
Grade 3 0 0 2 0
Grade 2 23 0 24 0
Grade 1 7 29 4 5
Grade 0 0 1 0 25
Total 30 30 30 30
Sadana
Grade 3 Grade 2 Grade 1 Grade 0
29
25
24
23
7
5
4
2
1
0 0 0 0 0 0 0
BT AT BT AT
Group A Group B
123
G) Changes in Daha (BT and AT) in Group A and Group B
Table 5.17 Shows Changes in Daha in Group A and Group B
Daha
Grade 3 Grade 2 Grade 1 Grade 0
26
20
16
15
14
10
9
6
4
0 0 0 0 0 0 0
BT AT BT AT
Group A Group B
124
H) Changes in Daurbalya (BT and AT) in Group A and Group B
Table 5.18 Shows Changes in Daurbalya in Group A and Group B
Daurbalya
Grade 3 Grade 2 Grade 1 Grade 0
25
23
22
17
8
7 7
6
5
0 0 0 0 0 0 0
BT AT BT AT
Group A Group B
125
I) Changes in Hrullas (BT and AT) in Group A and Group B
Table 5.19 Shows Changes in Hrullas in Group A and Group B
No. of Patients of Grade
Grade Group A Group B
BT AT BT AT
Grade 3 8 0 11 0
Grade 2 17 0 15 0
Grade 1 5 13 2 6
Grade 0 0 17 2 24
Total 30 30 30 30
Hrullas
Grade 3 Grade 2 Grade 1 Grade 0
24
17 17
15
13
11
8
6
5
2 2
0 0 0 0 0
BT AT BT AT
Group A Group B
126
5.3. Changes in Objective parameters before and after treatment
5.3.1. Decrease in Objective parameters before and after
treatment
Table 5.20 Shows decrease in objective parameters BT and AT
Sr. Sr. Billirubin Bile-Salt/Pigments
No. A B A B
1 3.7 6.1 3 3
2 4.9 8 2 2
3 6 4.4 2 2
4 8.1 5.9 1 2
5 4.2 6.8 2 2
6 4.7 7.7 1 3
7 4.5 5.3 3 2
8 4 7.1 2 2
9 5.5 7.1 1 2
10 4.9 2.3 1 2
11 3.1 4.8 2 2
12 4.8 6.5 2 2
13 3.3 3.5 2 3
14 4.5 6.7 2 2
15 3.3 6.7 1 2
16 3.4 6.8 2 2
17 2.3 6.6 2 3
18 4.6 6.6 2 2
19 4.9 6.1 2 2
20 4.4 5.3 2 2
21 4.9 5.8 2 3
22 6.4 5.2 2 2
23 3.8 6 2 2
24 4.4 6.7 2 3
25 4 3.2 2 3
26 4.8 5.4 3 3
27 2.9 6.2 2 3
28 3.5 3.1 1 2
29 3.8 4.8 1 3
30 4.8 3.8 2 2
Avg. 4.41 5.68 1.87 2.33
It was observed that all objective parameters were decreased more
in Group B than in Group A. (Table 5.20)
127
5.3.2. Average decrease in Objective parameters before and after
treatment
Table 5.21 shows average decrease in objective parameters Group A and
Group B
Sr. Parameter Average Decrease
No. Group A Group B
1 Sr. Billirubin 4.41 5.68
2 Bile-Salt/Pigments 1.87 2.33
Table 5.20 shows average decrease in objective parameters Group A and
Group B
5.68
4.41
2.33
1.87
Group A Group B
Average Decrease
128
5.4. Statistical Analysis within Group A and Group B
Table 5.22 Wilcoxon Signed Rank Test within the Group A and Group B
Group BT/AT N Mean SD W P
Group A BT 30 2.533 0.507 465 <0.0001
AT 30 0.633 0.614
Group B BT 30 2.600 0.621 465 <0.0001
AT 30 0.300 0.466
Group A
As value of p is far less than 0.05 extremely significant difference
was observed between mean of BT and AT score in Haridra Netra
symptom. Hence it was concluded that Darvi Kwatha is highly effective to
reduce Haridra Netra in Bahupitta Kamala (Hepatocelluar Jaundice).
Group B
As value of p is far less than 0.05 extremely significant difference
was observed between mean of BT and AT score in Haridra Netra
symptom. Hence it was concluded that Vasadi Kwatha is highly effective
to reduce Haridra Netra in Bahupitta Kamala (Hepatocelluar Jaundice).
B) Pita Mutrata
Table 5.23 Wilcoxon Signed Rank Test within the Group A and Group B
Group BT/AT N Mean SD W P
Group A BT 30 2.633 0.490 465 <0.0001
AT 30 0.700 0.651
Group B BT 30 2.667 0.479 465 <0.0001
AT 30 0.366 0.490
129
Group A
As value of p is far less than 0.05 extremely significant difference
was observed between mean of BT and AT score in Pita Mutrata symptom.
Hence it was concluded that Darvi Kwatha is highly effective to reduce
Pita Mutrata in Bahupitta Kamala (Hepatocelluar Jaundice).
Group B
As value of p is far less than 0.05 extremely significant difference
was observed between mean of BT and AT score in Pita Mutrata symptom.
Hence it was concluded that Vasadi Kwatha is highly effective to reduce
Pita Mutrata in Bahupitta Kamala (Hepatocelluar Jaundice).
C) Purisha Pitata
Table 5.24 Wilcoxon Signed Rank Test within the Group A and Group B
Group BT/AT N Mean SD W P
Group A BT 30 2.633 0.490 465 <0.0001
AT 30 1.167 0.530
Group B BT 30 2.667 0.479 465 <0.0001
AT 30 0.733 0.639
Group A
As value of p is far less than 0.05 extremely significant difference
was observed between mean of BT and AT score in Purisha Pitata
symptom. Hence it was concluded that Darvi Kwatha is highly effective to
reduce Purisha Pitata in Bahupitta Kamala (Hepatocelluar Jaundice).
Group B
As value of p is far less than 0.05 extremely significant difference
was observed between mean of BT and AT score in Purisha Pitata
symptom. Hence it was concluded that Vasadi Kwatha is highly effective
to reduce Purisha Pitata in Bahupitta Kamala (Hepatocelluar Jaundice).
130
D) Aruchi
Table 5.25 Wilcoxon Signed Rank Test within the Group A and Group B
Group BT/AT N Mean SD W P
Group A BT 30 2.433 0.626 465 <0.0001
AT 30 0.366 0.490
Group B BT 30 2.600 0.498 465 <0.0001
AT 30 0.133 0.345
Group A
As value of p is far less than 0.05 extremely significant difference
was observed between mean of BT and AT score in Aruchi symptom.
Hence it was concluded that Darvi Kwatha is highly effective to reduce
Aruchi in Bahupitta Kamala (Hepatocelluar Jaundice).
Group B
As value of p is far less than 0.05 extremely significant difference
was observed between mean of BT and AT score in Aruchi symptom.
Hence it was concluded that Vasadi Kwatha is highly effective to reduce
Aruchi in Bahupitta Kamala (Hepatocelluar Jaundice).
E) Avipaka
Table 5.26 Wilcoxon Signed Rank Test within the Group A and Group B
Group BT/AT N Mean SD W P
Group A BT 30 2.433 0.626 465 <0.0001
AT 30 0.333 0.479
Group B BT 30 2.600 0.563 465 <0.0001
AT 30 0.133 0.345
Group A
As value of p is far less than 0.05 extremely significant difference
was observed between mean of BT and AT score in Avipaka symptom.
Hence it was concluded that Darvi Kwatha is highly effective to reduce
Avipaka in Bahupitta Kamala (Hepatocelluar Jaundice).
131
Group B
As value of p is far less than 0.05 extremely significant difference
was observed between mean of BT and AT score in Avipaka symptom.
Hence it was concluded that Vasadi Kwatha is highly effective to reduce
Avipaka in Bahupitta Kamala (Hepatocelluar Jaundice).
F) Sadana
Table 5.27 Wilcoxon Signed Rank Test within the Group A and Group B
Group BT/AT N Mean SD W P
Group A BT 30 1.767 0.430 300 <0.0001
AT 30 0.966 0.182
Group B BT 30 1.933 0.449 465 <0.0001
AT 30 0.166 0.379
Group A
As value of p is far less than 0.05 extremely significant difference
was observed between mean of BT and AT score in Sadana symptom.
Hence it was concluded that Darvi Kwatha is highly effective to reduce
Sadana in Bahupitta Kamala (Hepatocelluar Jaundice).
Group B
As value of p is far less than 0.05 extremely significant difference
was observed between mean of BT and AT score in Sadana symptom.
Hence it was concluded that Vasadi Kwatha is highly effective to reduce
Sadana in Bahupitta Kamala (Hepatocelluar Jaundice).
G) Daha
Table 5.28 Wilcoxon Signed Rank Test within the Group A and Group B
Group BT/AT N Mean SD W P
4Group BT 30 2.300 0.794 435 <0.0001
A AT 30 0.533 0.507
Group B BT 30 2.667 0.479 465 <0.0001
AT 30 0.133 0.345
132
Group A
As value of p is far less than 0.05 extremely significant difference
was observed between mean of BT and AT score in Daha symptom. Hence
it was concluded that Darvi Kwatha is highly effective to reduce Daha in
Bahupitta Kamala (Hepatocelluar Jaundice).
Group B
As value of p is far less than 0.05 extremely significant difference
was observed between mean of BT and AT score in Daha symptom. Hence
it was concluded that Vasadi Kwatha is highly effective to reduce Daha in
Bahupitta Kamala (Hepatocelluar Jaundice).
H) Daurbalya
Table 5.29 Wilcoxon Signed Rank Test within the Group A and Group B
Group BT/AT N Mean SD W P
Group A BT 30 2.033 0.668 465 <0.0001
AT 30 0.466 0.860
Group B BT 30 2.267 0.449 465 <0.0001
AT 30 0.166 0.379
Group A
As value of p is far less than 0.05 extremely significant difference
was observed between mean of BT and AT score in Daurbalya symptom.
Hence it was concluded that Darvi Kwatha is highly effective to reduce
Daurbalya in Bahupitta Kamala (Hepatocelluar Jaundice).
Group B
As value of p is far less than 0.05 extremely significant difference
was observed between mean of BT and AT score in Daurbalya symptom.
Hence it was concluded that Vasadi Kwatha is highly effective to reduce
Daurbalya in Bahupitta Kamala (Hepatocelluar Jaundice).
133
I) Hrullas
Table 5.30 Wilcoxon Signed Rank Test within the Group A and Group B
Group BT/AT N Mean SD W P
Group A BT 30 2.100 0.661 465 <0.0001
AT 30 0.433 0.504
Group B BT 30 2.167 0.833 430 <0.0001
AT 30 0.200 0.406
Group A
As value of p is far less than 0.05 extremely significant difference
was observed between mean of BT and AT score in Hrullas symptom.
Hence it was concluded that Darvi Kwatha is highly effective to reduce
Hrullas in Bahupitta Kamala (Hepatocelluar Jaundice).
Group B
As value of p is far less than 0.05 extremely significant difference
was observed between mean of BT and AT score in Hrullas symptom.
Hence it was concluded that Vasadi Kwatha is highly effective to reduce
Hrullas in Bahupitta Kamala (Hepatocelluar Jaundice).
A) Sr. Billirubin
Table 5.31 Shows Paired t Test within the Group A and Group B
Group BT/AT N Mean SD t P
Group A BT 30 6.840 1.817 21.33 <0.0001
AT 30 2.427 1.315
Group B BT 30 7.407 2.074 21.90 <0.0001
AT 30 1.723 1.031
134
Group A
As value of p is far less than 0.05 extremely significant difference
was observed between mean of BT and AT score in Sr. Billirubin. Hence it
was concluded that Darvi Kwatha is highly effective to decrease Sr.
Billirubin level in Bahupitta Kamala (Hepatocelluar Jaundice).
Group B
As value of p is far less than 0.05 extremely significant difference
was observed between mean of BT and AT score in Sr. Billirubin. Hence it
was concluded that Vasadi Kwatha is highly effective to decrease Sr.
Billirubin level in Bahupitta Kamala (Hepatocelluar Jaundice).
B) Bile salt / Bile pigments
Table 5.32 Shows Paired t Test within the Group A and Group B
Group BT/AT N Mean SD T P
Group A BT 30 2.633 0.490 17.89 <0.0001
AT 30 0.766 0.626
Group B BT 30 2.700 0.466 26.65 <0.0001
AT 30 0.366 0.490
Group A
As value of p is far less than 0.05 extremely significant difference
was observed between mean of BT and AT score in Bile Salts and Bile
Pigments. Hence it was concluded that Darvi Kwatha is highly effective to
decrease Bile Salts and Bile Pigments level in Bahupitta Kamala
(Hepatocelluar Jaundice).
Group B
As value of p is far less than 0.05 extremely significant differences
was observed between mean of BT and AT score in Bile Salts and Bile
Pigments. Hence it was concluded that Vasadi Kwatha is highly effective
to decrease Bile Salts and Bile Pigments level in Bahupitta Kamala
(Hepatocelluar Jaundice).
135
5.5. Statistical Analysis in between the Group A and Group B
A) Haridra Netra
Table 5.33 Mann Whitney‟s Test in between the Group A and Group B
Group N Mean SD U P
Group A 30 1.900 0.607 304.5 0.0294
Group B 30 2.300 0.596
B) Pita Mutrata
Table 5.34 Mann Whitney‟s Test in between the Group A and Group B
Group N Mean SD U P
Group A 30 1.933 0.520 307.5 0.0312
Group B 30 2.300 0.466
136
C) Purisha Pitata
Table 5.35 Mann Whitney‟s Test in between the Group A and Group B
Group N Mean SD U P
Group A 30 1.467 0.507 248 0.0023
Group B 30 1.933 0.365
137
As value of p is less than 0.05, highly significant difference was
observed between the mean of difference of Group A and Group B in
Avipaka symptom. Mean difference score of Group B is more than that of
Group A. Hence it was concluded that Vasadi Kwatha is more effective
than Darvi Kwatha to reduce Avipaka in Bahupitta Kamala (Hepatocellular
Jaundice).
F) Sadana
Table 5.38 Mann Whitney‟s Test in between the Group A and Group B
Group N Mean SD U P
Group A 30 0.800 0.406 96 <0.0001
Group B 30 1.767 0.504
G) Daha
Table 5.39 Mann Whitney‟s Test in between the Group A and Group B
Group N Mean SD U P
Group A 30 1.767 0.626 184 <0.0001
Group B 30 2.533 0.507
138
H) Daurbalya
Table 5.40 Mann Whitney‟s Test in between the Group A and Group B
Group N Mean SD U P
Group A 30 1.567 0.504 229.5 0.0008
Group B 30 2.100 0.305
I) Hrullas
Table 5.41 Mann Whitney‟s Test in between the Group A and Group B
Group N Mean SD U P
Group A 30 1.667 0.479 315 0.0431
Group B 30 1.967 0.889
139
5.5.2 Objective Parameters (By Student’s t Test for Unpaired
data)
A) Sr. Billirubin
Table 5.42 Shows Unaired t Test within the Group A and Group B
Group N Mean SD t P
Group A 30 4.413 1.133 3.827 0.0003
Group B 30 5.683 1.421
140
5.6. Effect of therapy
141
25 24 5 19 79.17 25 21 2 19 90.48
26 24 5 19 79.17 26 23 1 22 95.65
27 14 2 12 85.71 27 22 2 20 90.91
28 18 2 16 88.89 28 14 0 14 100
29 16 1 15 93.75 29 23 2 21 91.3
30 19 3 16 84.21 30 21 0 21 100
31 74.63 31 90.04
Average Relief (A)
% Average Relief (B) %
The relieved symptom score and percent relief are given in the
Table 5.44. Overall average relief in Patients‟ score in Group A is 74.63%
and in Group is 90.04%.
142
Table 5.46 Relieved score and %relief in Symptoms‟ score in Group B
S/O Symptoms B.T. A.T. Relieve %
No. (Group B) d Relief
1 Haridra Netra 78 9 69 88.46
2 Mutra Pitata 80 11 69 86.25
3 Purisha Pitata 80 22 58 72.5
4 Aruchi 78 4 74 94.87
5 Avipaka 78 4 74 94.87
6 Sadana 58 5 53 91.38
7 Daha 80 4 76 95
8 Daurbalya 68 5 63 92.65
9 Hrullas 65 6 59 90.77
10 Average Relief (B) 89.63 %
The relieved symptom score and percent relief are mentioned in the
Table 5.45 and Table 5.46. Overall average relief in Symptoms‟ score in
Group A is 72.65% and in Group is 89.63%.
143
Figure 5.14 Shows Average Relief % in Patients‟ and Symptoms‟ score
Avg. % Relief
Avg. Patient Score (%) Avg. Symptom score (%)
90.04 89.73
74.63 72.65
15.41 17.08
144
DISSCUSSION
Research Question
Does the treatment of Bahupitta Kamala (Hepatocellular Jaundice)
with Vasadi Kwatha is significantly effective than treatment with Davrvi
Kwatha or not?
145
6.1. General Observations
A) Distribution of patients
60 patients were included in the study. Further they were classified
in two equal groups viz. Group A and Group B. Group A was Control group
whether Group B was Trial group, each comprising 30 patients. (Table
5.1)
B) Age
In Group A: 7 patients were of age group 18 to 31 yrs, 17 of age group
32 to 46 yrs and 6 of age group 47 to 60 yrs.
In Group B: 11 patients were of age group 18 to 31 yrs, 15 of age group
32 to 46 yrs and 4 of age group 47 to 60 yrs.
146
Housewives (16), Servicemen (12), Labors (10) and Students (10)
were found maximum among all occupations. (Table 5.5)
E) Prakruti
In Group A: 0 patients were having Kapha-Pitta, 0 were having Kapha-
Vata, 8 were having Pitta-Kapha, 9 were having Pitta-Vata, 4 were having
Vata-Kapha and 9 were having Vata-Pitta prakruti.
In Group B: 2 patients were having Kapha-Pitta, 0 were having Kapha-
Vata, 8 were having Pitta-Kapha, 9 were having Pitta-Vata, 6 were having
Vata-Kapha and 6 were having Vata-Pitta prakruti.
Maximium patients were found having Pitta-Vata (18), Pitta-Kapha
(16), Vata-Pitta (14) and Vata-Kapha (10) prakriti. Total patients having
Pitta dosha dominant in Prakruti are 34, total patients having Pitta dosha
as at least one of the constituents in prakruti were 48. It is clear that
patients having Pitta dosha in prakruti are more prone to Bahupitta
Kamala in future. Bahupitta Kamala is mentioned as Pitta pradhan vyadhi
by all Acharyas. (Table 5.5)
F) Addiction
In Group A: 3 patients were addicted to Tea, 0 were addicted to Tea and
Alcohol, 2 were addicted to Tea and Tobacco, 2 were addicted to Tea,
Alcohol and Tobacco, 1 was addicted to Tobacco and Alcohol, 1 was
addicted to Tobacco, Alcohol and Gutakha, 3 were addicted to Tobacco
and Gutkha and 18 were non-addicted.
In Group B: 2 patients were addicted to Tea, 4 were addicted to Tea and
Alcohol, 3 were addicted to Tea and Tobacco, 0 were addicted to Tea,
Alcohol and Tobacco, 0 were addicted to Tobacco and Alcohol, 0 were
addicted to Tobacco, Alcohol and Gutakha, 0 were addicted to Tobacco
and Gutkha and 21 were non-addicted.
Maximium patients (39) were found non-addicted. It doesn‟t mean
that non-addicted people are more prone to Bahupitta Kamala. It was by
chance only. Among addicted none addiction have been shown significant
incidence. (Table 5.6)
147
G) Religion
In Group A: 24 patients were Hindu, 6 patients were Muslim and 0
patients were from other religion.
In Group B: 28 patients were Hindu, 2 patients were Muslim and 0
patients were from other religion.
Hindu patients (52) were found maximum. But it doesn‟t at all
mean that Bahupitta Kamal is common in Hindu people. It was only by
chance as most of the population was Hindu. (Table 5.7)
H) Diet
In Group A: 12 patients were Vegetarian while 18 were having mixed
diet.
In Group B: 14 patients were Vegetarian while 16 were having mixed
diet.
Mixed diet patients (34) were found maximum. It can be said that
meat, eggs, fish etc in diet causes pitta prakopa and there by rakta
dushti, which may lead to disease like Bahupitta Kamala. (Table 5.8)
I) Agni
In Group A: 7 patients were having mand, 15 patients were having
tikshna and 8 patients were having vishama agni.
In Group B: 3 patients were having mand, 17 patients were having
tikshna and 10 patients were having vishama agni.
Maximum patients (32) were found with tikshna agni. Tikshna agni
is seen dominant in Pitta pradhan prakruti and Bahupitta Kamala is also
Pitta pradhan vyadhi. Hence incidence of Bahupitta Kamala could have
been found maximum in Tikshna agni patients. (Table 5.9)
J) Koshtha
In Group A: 18 patients were having mrudu, 2 patients were having
Madhya and 10 patients were having krura koshtha.
In Group B: 16 patients were having mrudu, 5 patients were having
Madhya and 9 patients were having krura koshtha.
148
Maximum patients (34) were found Mrudu koshtha. Mrudu Koshtha
is seen dominant in Pitta pradhan prakruti and Bahupitta Kamala is also
Pitta pradhan vyadhi. Hence incidence of Bahupitta Kamala could have
been found maximum in Mrudu Koshtha patients. (Table 5.10)
149
C) Changes in Purisha Pitata (BT and AT) in Group A and Group B
Group A: Before treatment, 19 patients were of Grade Three, 11 of
Grade Two, 0 of Grade One and 0 of Grade Zero, while After treatment,
0 patients were of Grade Three, 7 of Grade Two, 21 of Grade One and 2
of Grade Zero.
150
0 patients were of Grade Three, 0 of Grade Two, 10 of Grade One and 20
of Grade Zero.
Group B: Before treatment, 19 patients were of Grade Three, 10 of
Grade Two, 1 of Grade One and 0 of Grade Zero, while After treatment,
0 patients were of Grade Three, 0 of Grade Two, 4 of Grade One and 26
of Grade Zero.
It was observed that, Avipaka has decreased more in Group B than
in Group A. It suggests that, Vasadi Kwatha has better efficacy than Darvi
Kwatha to reduce Avipaka in Bahupitta Kamala. (Table 5.15)
151
It was observed that, Daha has decreased more in Group B than in
Group A. It suggests that, Vasadi Kwatha has better efficacy than Darvi
Kwatha to reduce Daha in Bahupitta Kamala. (Table 5.17)
152
6.3. Changes in objective parameters before and after treatment
153
6.4. Statistical Analysis within Group A and Group B
154
Group A
Null Hypothesis (H0)
Darvi Kwatha is not effective to reduce symptoms in Bahupitta
Kamala (Hepatocelluar Jaundice).
Group B
Null Hypothesis (H0)
Vasadi Kwatha is not effective to reduce symptoms in Bahupitta
Kamala (Hepatocelluar Jaundice).
155
6.4.2. Objective Parameters (By Student’s t Test for Paired data)
Table 6.2 Statistical analysis within the Group A and B by Paired t Test
Sr. Parameters Gr. T P Significance
No.
1 Sr. A 21.33 <0.0001 Significant
Billirubin B 21.90 <0.0001 Significant
2 Bile Salts, A 17.89 <0.0001 Significant
Pigments B 26.65 <0.0001 Significant
Group A
Null Hypothesis (H0)
Darvi Kwatha is not effective to reduce objective parameters in
Bahupitta Kamala (Hepatocelluar Jaundice).
Alternate Hypotheis (H1)
Darvi Kwatha is effective to reduce objective parameters in
Bahupitta Kamala (Hepatocelluar Jaundice).
In the caseof all objective parameters Sr. Billirubin and Bile Salts-
Bile Pigments the test has shown highly significant difference between BT
and AT symptom scores. H1 is accepted and H0 is rejected here.It was
hence concluded that Darvi Kwatha is effective to reduce objective
parametersSr. Billirubin and Bile Salts-Bile Pigments in Bahupitta Kamala
(Hepatocelluar Jaundice).
Group B
Null Hypothesis (H0)
Vasadi Kwatha is not effective to reduce symptoms in Bahupitta
Kamala (Hepatocelluar Jaundice).
156
Alternate Hypotheis (H1)
Vasadi Kwatha is effective to reduce symptoms in Bahupitta Kamala
(Hepatocelluar Jaundice).
In the caseof all objective parameters Sr. Billirubin and Bile Salts-
Bile Pigments the test has shown highly significant difference between BT
and AT symptom scores. H1 is accepted and H0 is rejected here.It was
hence concluded that Vasadi Kwatha is effective to reduce objective
parametersSr. Billirubin and Bile Salts-Bile Pigments in Bahupitta Kamala
(Hepatocelluar Jaundice).
157
Null Hypothesis (H0)
There is no difference between efficacy of Vasadi Kwatha and Darvi
Kwatha to reduce symptoms in Bahupitta Kamala (Hepaticellular
Jaundice).
Alternate Hypothesis (H1)
Vasadi Kwatha is significantly effective than Darvi Kwathato reduce
symptoms in Bahupitta Kamala (Hepatocellular Jaundice).
158
Alternate Hypothesis (H1)
Vasadi Kwatha is significantly effective than Darvi Kwathato reduce
objective parameters in Bahupitta Kamala (Hepatocellular Jaundice).
In the caseof all objective parameters Sr. Billirubin and Bile Salts-
Bile Pigments the test has shown highly significant difference between BT
and AT symptom scores. H1 is accepted and H0 is rejected here because
mean difference score of Group B is more than that of Group A.It
was hence concluded that Vasadi Kwatha is significantly effective than
Darvi Kwathato reduce objective parameters Sr. Billirubin and Bile Salts-
Bile Pigments in Bahupitta Kamala (Hepatocellular Jaundice).
159
In Group B, 28 patients have shown Excellent improvement, 2 patients
have shown Good improvement, none patients have shown Moderate
improvement while none patients have shown Poor improvement.
It suggest that Group B has shown overall good effect than Group A
to reduce patients‟ score.
160
6.6.3 Effect of therapy according to Average Relief %
Table 6.5 Shows Average Relief % in Patients‟ and Symptoms‟ score
Sr. Group Avg.Patient Avg. Symptom
No. Score (%) score (%)
1 Group A 74.63 72.65
2 Group B 90.04 89.73
161
6.6. Mode of Action:-
Drug description of Vasadi Kwath:-
LATIN
DRAVYA GUNA RASA VIRYA VIPAKA KARMUKTA
NAME
Pitta shaman
Adhatoda Laghu Tikta
Vasa Sheeta Katu & Rakta
vasica Ruksha Kashaya
Prasadan
Mrudu Tikta Pitta shaman
Tinospora
Amruta Laghu Katu Ushna Madhur & Yakruta
cordifolia
Ruksha Kashaya Uttejana
Deepan,
Pachan,
Tikta
Terminalia Laghu Yakrut-
Haritki Katu Ushna Madhur
chebula Ruksha Uttejan,
Kashaya
Anuloman,
Mruduvirecha,
Deepan,
Pachan,
Terminalia Guru,
Bibhitak Kashaya Ushna Madhur Anuloman,
belerica Ruksha
chhardi
nigrahan
Lavanrahit
Agnideepan,
Embelica Laghu 5 rasa
Amalaki Sheet Madhur Ruchikar,
officinalis Ruksha mainly
Amanpachan
Amla
Tikta Raktagataa &
Azadiracta Laghu
Nimba Katu Sheeta Katu Yakrutastha
indica Ruksha
Kashaya Pitta Shaman
Pitta Saraka
Swertia Laghu
Bhunimba Tikta Sheeta Katu Shodhan
chiraita Ruksha
Agnideepan
Yakruta
Picrorrhiza Laghu
Kutki Tikta Sheeta Katu Uttejana
kurroo Ruksha
Pitta Sarak
Guru, Madhur Tridosha
Madhu Sheeta Madhur
Ruksha Kashaya Shamaka
162
Drug Description for Darvi Kwath:
LATIN
DRAVYA GUNA RASA VIRYA VIPAKA KARMUKTA
NAME
Berberis Laghu Tikta Kapha Pitta
Darvi Ushna Katu
aristata Ruksha Kashaya Shaman
Guru, Madhur Tridosha
Madhu - Sheeta Madhur
Ruksha Kashaya Shamaka
LIMITATIONS OF STUDY:-
The present study was conducted with limited facilities and limited no. of
patients.Larer the representative sample drawn from lare population
would have been yielded more fruitful results.
Here only oral intervention was studied without any Shodhan. Oral
intervention against shodhan or any other dravya formulation along with
shodhan may be studied in future.
163
CONCLUSION
164
SUMMARY
Control group A 30 patients were given 60ml Darvi kwath with 5ml
Madhu for 60 days. Both groups were advised same pathya diet.
Due analysis of the results of both trial group and control group was
done and comparison of results of both groups were assessed by
applying Mann Whitney”s test for paired data and Student”s t-test
for unpaired data (unpaired t-test) at 5% level of significance.
165
normal level. Only 2 patients had shown good improvement and
none shown moderate or poor improvement.
166
ABBRIVATIONS
Sr. - Serum
P - Probability
t test - Student t test
167
W - Wilcoxon Signed Rank test
U - Mann Whitney”s test
S.D. - Standard Deviation
S. E. - Standard Error
B. T. - Before Treatment
A. T. - After Treatment
BS/BP - Bile salts and bile pigments
168
REFRENCES
xÉÑ. zÉÉ. 9
xÉÑ.ÌlÉ. 2/11
169
8. aÉpÉïxrÉ rÉM×üimsÉÏWûÉlÉÉæ zÉÉåÍhÉiÉeÉÉæ |
(QèsWûhÉ) xÉÑ.ÌlÉ.
11. ̲iÉÏrÉÉ U£ükÉUÉlÉÉqÉç, qÉÉÇxÉxrÉÉprÉliÉUiÉ: iÉxrÉÉÇ zÉÉåÍhÉiÉÇ ÌuÉzÉåwÉ´cÉ ÍxÉUÉxÉÑ rÉM×üimsÉÏlWûÉå´cÉ pÉuÉÎliÉ |
xÉÑ. zÉÉ. 4
xÉÑ. E. 6/14
13. ¤ÉzÉÏiÉaÉÑÂxuÉÉSÒurÉÉrÉÉqÉæuÉåïaÉÌlÉaÉëWæû:|
SÉWûÌuÉmÉÉMüSÉæoÉïsrÉxÉSlÉÉÂÍcÉ MüwÉÏïiÉ: |
(rÉÉå.U. 12/1-2
170
16. urÉrÉÉrÉqÉqsÉÇ sÉuÉhÉÉÌlÉ qÉkÉÇ qÉ×SÇ ÌSuÉÉxuÉmlÉqÉiÉÏuÉiÉϤhÉqÉç |
SÉæoÉïsrÉÉsmÉÉÎalÉmÉÉ´uÉïÌiÉïÌWû‚üɵÉÉxÉÉÂÍcÉeuÉUæ: |
cÉ.ÌlÉ. 1/10
A. WØû. ÍcÉ. 16
171
23. rÉSÉ iÉÑ mÉÉhQûÉåuÉïhÉï: xrÉÉSWûËUiÉzrÉÉuÉmÉÏiÉMü: |
x§ÉÏwuÉWûwÉÉåïÅ…ûqÉïS´cÉ ´uÉÉxÉiÉ×whÉÉÅÂÍcÉpÉëqÉ: |
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zÉÑwMüqÉÑsÉMüÉæsÉijÉærÉÑïwÉæ´cÉɳÉÉÌlÉ pÉÉåeÉrÉåiÉ |
ÄrÉÉå. U.mÉÉhQÒûÍcÉÌMüixÉÉ 17 ||
172
29. mÉÉhQÒûUÉåaÉÌ¢ürÉÉÇ xɱÉå rÉÉåeÉrÉåŠ WûsÉÏqÉMåü |
rÉÉå. U. 12
173
BIBLIOGRAPHY
174
9) Sharangdharsamhita of Shrangdhar with Dipika commentary,
Editor BrahamanadTripathi ,Chaukhamba prakashan Varanasi,year
2004 –Madhyama khanda, Chapter no.2,Page no.133
10) BhaişhajyaRatnãvalî with Vidyotinî commentary, Editor Ambika
Dutta Shastri, published by Chaukhambã Sanskrita
Sansthãna,Vãrãņasî-18th Edition, Page no.269.
11) AshtãngaSamgraha –InduTîkã edited by A.D. Ãthavale, published
by Ãtreya Prakãśana-1980, chapter no.16 of Chikitsa sthana,
Shloka no.613.
12) BhavprakashNighantu of Shri.Bhavmishra commentary by
Dr.K.C.Chunekar edited by Dr.G.s.Pandey, 2004 edition,
Chaukhambaprakashan.
13) Dravya gun vidnyan voi.2 16th edition 1994, by Prof.P.V.Shrama,
sChaukhamba Bhrati academy, Varanasi.
14) Raj Nighantu by Pandit narhari, Editor Dr. Indradev Tripathi,
Krishnadas academy, Varanasi, 1st edition, Page no.71.
15) Principles of Anatomy and Physiology Tortora Garbowiski,
Published by John Wiley & sons 10th edition.
16) Harrisons principles of Internal Medicine
17) Davidsons principles and practice of Medicine
,19thedition.Christopher R.W. edwords et al, W.B. Sounders
company Ltd.London 2002
18) Harsh mohan text book of Pathology, 5th edition. New Delhi;
jaypee Brothers Medical Publishers pvt Ltd. 2005.
19) Indian MateriaMedica by Sri. K.M. Nãdakarnî, pulished by Popular
Prakaśaņa -3rd Edition, 1999
20) Dravya gun vidnyan vol.2 16th edition 1994, by prof. P. V.
Shrama, ChaukhambaBhrati academy, Varanasi.
21) Ayurvedic pharmacology and theurapeutic uses of Medicinal
plant (Dravyagunavignyan)Vaidya V.M. Gogate, First English
edition Oct.2000
175
Website
22) www.phcog.com/article
23) www.jpsionline.com/pdf
24) WWW.eMedicine.com
25) www.pubmed.org
26) www.ayurveda.hu/api
176
ANNEXURE
qÉsÉÉ uÉUÏsÉ qÉÉÌWûiÉÏ mÉÔhÉïmÉhÉå xÉqÉeÉÉuÉÔlÉ xÉÉÇaÉhrÉÉiÉ AÉsÉÏ AxÉÔlÉ rÉÉÌuÉwÉrÉÉ xÉÇSpÉÏïrÉ mÉëzlÉ ÌuÉcÉÉUhrÉÉcÉÏ xÉÇkÉÏ
qÉÏ ÍcÉÌMüixÉÉ bÉåhrÉÉxÉ iÉrÉÉU AÉWåû. qÉsÉÉ rÉÉ AÉæwÉkÉÉÇcÉÉ mÉËUhÉÉqÉ AÉÍhÉ xÉÑUͤÉiÉiÉÉ qÉÉlÉuÉÉÇqÉkrÉå mÉëxjÉÉÌmÉiÉ
AxÉsrÉÉcÉÏ eÉÉhÉÏuÉ AÉWåû. qÉsÉÉ rÉÉ xÉÇqÉiÉÏmɧÉÉcÉÏ mÉëiÉ SåhrÉÉiÉ AÉsÉÏ AÉWåû.
ÂahÉÉcÉå lÉÉuÉ................................................................................................................
ÂahÉÉcÉÏ xuÉɤÉëUÏ
qÉÏ ZÉÉsÉÏ xÉWûÏ MüUhÉÉU, rÉÉÇlÉÏ ÂahÉÉxÉ sÉbÉÑmÉëoÉÇkÉÉcrÉÉ xÉÇSpÉÉïiÉÏsÉ xÉÇmÉÔhÉï qÉÉÌWûiÉÏ ÂahÉÉxÉ/ÂahÉÉxÉWû AxÉhÉÉ-rÉÉ
xÉÇqÉiÉÏ bÉåiÉsrÉÉ eÉÉhÉÉ-rÉÉ eÉoÉÉoÉSÉU urÉ£üÏxÉç xÉqÉeÉÉuÉÔlÉ xÉÉÇÌaÉiÉsÉÏ AÉWåû. rÉÉÌuÉwÉrÉÏ qÉÏ mÉëÍzÉͤÉiÉ AÉWåû.
...........................................................
ÌSÇlÉÉMü:
xÉɤÉÏSÉU:
ÂahÉÉzÉÏ lÉÉiÉå:
mɨÉÉ: xÉɤÉÏSÉUÉcÉÏxuÉɤÉUÏ
177
CASE RECORD FORM
178
History of Present illness:
Past History
Drug History
Family History
Personal History
a) Aahar –
Time: Regular/Irregular
Kshudha: Samyakpravartan/Mandya/Visham
Rasapriti: Madhur/Amla/Lavan/Katu/Tikta/Kashaya
Vegetarian/Mixed
Adhyshan/Alpashan/Vishamashan/Atimatrashan
Paryushitanna/Abhishyandi/Virudhaaaharasevan
Ushapan/nishapan
Atiruksha/Atisnigdha/Atiushana/Atiguru
b) Vihar-
c) Vyasan-
1. Tea 4. Gutkha 7. Alcohol
3. Cold-drink 6. Smoking
General Examination:
Ashtavidha Parikshan:
i) Nadi -/min ii) Mala
iii) Mutra iv) Jivha
v) Shabda vi) Sparsha
vii) Druk viii) Akruti
179
Dashavidha Parikshana
i) Prakrititah :
ii) Saratah : Pravar / Madhya / Avar
iii) Samhanana : Pravar / Madhya / Avar
iv) Satmyatah : Pravar / Madhya / Avar
v) Satvatah : Pravar / Madhya / Avar
vi) Pramanatah : ht - wt –
vii) Aharshaktitah : Pravar / Madhya / Avar
viii) Vyayamshaktitah : Pravar / Madhya / Avar
ix) Vayatah (Age) : Bal / Madhyam / Vriddha
x) Balatah : Pravar / Madhya / Avar
SROTAS PARIKSHNA:
1) Pranavaha Srotas :
6) MamsavahaSrotas :
7) MedovahaSrotas :
8) AsthivahaSrota :
9) MajjavahaSrotas :
180
10) Shukravaha / Artavaha Srotas:
11) MutravahaSrotas :
12) PurishvahaSrotas :
13) SwedvahaSrotas :
14) ManovahaSrotas :
INVESTIGATION:
DLC N L E B M
Sr.Billirubin
Urine test-Bile salts, Bile pigments
SGOT, SGPT
181
DOSHA-DUSHA SAMUCCHAYA:
●Purvaroopa :
●Roop :
●Samprapti :
●Upashaya / Anupashaya:
CHIKITSA:
182
OBSERVATION TABLES:
RESULT:
183
MASTER CHARTS
184
185
186