Medical Nutrition Therapy for

Rheumatic Disease
Rheumatic disease and related conditions
include more than 100 different
manifestations of inflammation and loss of
function of connective tissue and supporting
body structures, including joints, tendons,
ligaments, bones, muscles, and sometimes
internal organs.

According to the National Arthritis Data
Workgroup, osteoarthritis (OA) affects 27
million Americans; gout, 3 million;
fibromyalgia, 5 million; rheumatoid arthritis
(RA), 1.5 million; Sjogren's syndrome (SS), 1 to
4 million; and systemic lupus erythematosus
(SLE), 161,000 to 322,000.

Arthritis is a generic term that comes from the Greek
word Arthro, which means "joint," and the suffix -itis,
which means "inflammation."
There are two distinct categories of disease: systemic,
autoimmune rheumatic disease and nonsystemic OA.
The more debilitating and autoimmune arthritis group
includes RA, juvenile rheumatoid arthritis gout, SS,
fibromyalgia, SLE, and scleroderma.
The OA group includes OA, bursitis, and tendonitis.
Other rheumatic diseases include
spondyloarthropathies, polymyalgia rheumatica, and
polymyositis.
Body changes associated with aging-including
decreased somatic protein, body fluids, and
bone density, and an increase in total body
fat-may contribute to the onset and
progression of arthritis.
Unfortunately, the cause of most rheumatic
conditions remains unknown.
PATHOPHYSIOLOGY AND
INFLAMMATION
Inflammation plays an important role in health and
disease.
The inflammatory process normally occurs to protect
and repair tissue damaged by infections, injuries,
toxicity, or wounds via accumulation of fluid and cells.
Once the cause is resolved, the inflammation usually
subsides. Whether inflammation is due to stress on the
joints (OA) or to an autoimmune response (RA), an
uncontrolled inflammatoryreaction causes more
damage than repair.
Polyunsaturated fatty acids (PUFAs) play an
important role in inflammation as precursors of a
potent group of modulators of inflammation
termed eicosanoids.
Eicosanoids include the prostaglandins (PGs),
thromboxanes (Txs) and leukotrienes (LTs)
among others.
PG and Tx are the product of the enzyme
cyclooxy genase (COX) and are termed
prostanoids, whereas LTs are the product of the
enzyme lipoxygenase.

For the synthesis of prostanoids, the COX
reaction consumes two double bonds from
the original PUFA, whereas lipoxygenase
reaction consumes none.
Depending on the PUF A used as substrate,
different eicosanoids are produced:
arachidonic acid (ARA) is the precursor of the
series 2 of PG and Tx, and the series 4 ofL T.
If eicosapentaenoic acid is the substrate, series 3 of PG
and Tx and series 5 of LT are produced.
Finally, dihomo-y-linoleic acid (DGLA) is the precursor
of series 1 of PG and Tx, and of series 3 0f LT.
The series 2 compounds (PG2 and TX2) are the most
abundant because ARA is abundant in plasma
membranes of cells involved in inflammation (macro
phages , neutrophils, fibroblasts), and are the most
potent inflammatory eicosanoids.
On the other hand, PGI and TXb derived from DGLA,
have antiinflammatory activities.

Thus diets enriched with PUFAs that enhance
the synthesis of antiinflammatory prostanoids
are, at least theoretically, desirable for the
long-term management of rheumatic disease,
but usually do not replace the use of
medications.
MEDICAL DIAGNOSIS
AND TREATMENT
Laboratory testing can help to further refine the
diagnosis and identify appropriate treatment.
Biochemical Assessment:
Acute-phase proteins are plasma proteins whose
concentration increases of more than 25% during
inflammatory states.
Two acute-phase proteins traditionally used to screen
for and monitor rheumatic disease are rheumatoid
factor (RF) and C-reactive protein (CRP).
The term RF is used to refer to a group of selfreacting
antibodies (an abnormal IgM against normal IgG),
found in the sera of rheumatic patients.

The American College of Rheumatology (ACR)
recommends periodic measurements of RF
and CRP in addition to a detailed assessment
of symptoms and functional status, and
radiographic examination to determine the
current level of disease activity in these
patients.

Antinuclear antibodies (ANA)
Present in many autoimmune diseases and can assist with
proper diagnosis when used correctly; antineutrophil
cytoplasmic antibodies and myositis-specific antibodies can
provide information about the presence of rheumatic
disease as well.
Measurements of RF and anticyclic citrullinated peptide
antibodies may provide unique data in the management of
RA.
Routine blood testing can include complement, a complete
blood count, creatinine, hematocrit, and a white blood cell
count, in addition to analysis of urine or synovial fluid
secreted by the synovial membrane in the joints.
Pharmacotherapy
Acetaminophen (Tylenol) are effective pain
relievers.
Drugs commonly used to reduce inflammation
affect the synthesis of PGs by inhibiting COX
activity, thus diminishing PG production.
Glucocorticoid therapy decreases the release of
ARA from cell membrane phospholipids by
binding to the receptor in the cell cytoplasm.
This forms a complex that moves into the nucleus
as a transcription factor and interferes with
expression for the enzyme phospholipase.

Nonsteroidal antiinflammatory drugs (NSAIDs), which
include ibuprofen (Advil or Motrin) and naproxen
(Aleve), slow down the body's production of PGs by
inhibiting COX-l enzyme activity.
They are considered useful tools in the management of
most rheumatic disorders; however, long-term use of
NSAIDs may cause gastrointestinal problems such as
gastritis, ulcers, abdominal burning, pain, cramping,
nausea, gastrointestinal bleeding, or even renal failure.
Celecoxib (Celebrex) have been shown to provide relief
comparable to other NSAIDs with potentially less
gastrointestinal and cardiovascular toxicity. Naproxen
and celecoxib appear to be safer than other NSAIDs.

Biologic response modifiers are a class of drugs
that selectively target different elements of the
disease, and include those directed against
interleukin (IL)-l such as anakinra (Kineret), or
against tumor necrosis factor (TNF)-a, like
adalimumab (Humira), etanercept (Enbrel), and
infliximab.
Corticosteroids (cortisone [Cortone], prednisone
[Deltasone],methylprednisolone [Medrol], and
hydrocortisone [Cortef]) suppress the immune
system and decrease inflammation, making them
desirable treatments for many of the rheumatic
diseases.
As the most potent of the antiinflammatory drugs used
to treat RA, steroids have extensive catabolic effects
that can result in negative nitrogen balance.
Hypercalciuria and reduced calcium absorption can
increase the risk of osteoporosis
Concomitant calcium (1 g/day) and vitamin D (at least
1000 IU/day) and monitoring of bone status may be
suggested to minimize osteopenia.
Care must be taken to avoid serum calcium levels
greater than 11 mg/dL and 25-0H vitamin D levels less
than 35 ng/mL.
Edema often occurs and may require diet modification,
including a sodium- and fluid-restricted diet.
Other side effects of steroid use include cushingoid
syndrome and gastrointestinal bleeding.
UNCONFIRMED THERAPIES
Willow bark and ginger may relieve pain because
their chemical composition is similar to NSAIDs,
but excessive blood thinning is a concern
It is best to avoid copper or copper salts, shark
cartilage, devil's claw, echinacea, guaifenesin,
alfalfa, wild yam, and methylsulfonylmethane
(MSM).
Both comfrey and alfalfa are herbs that have
been promoted as potential cures for arthritis,
yet both have been deemed toxic by the scientific
community.
Meditation, tai chi, relaxation techniques,
thermotherapy and spiritual practice may
offer pain reduction.

OSTOARTHRITlS
formally known as degenerative arthritis or
degenerative joint disease, is the most prevalent
form of arthritis.
Obesity, aging, female gender, white ethnicity,
greater bone density, and repetitive-use injury
associated with athletics have been identified as
risk factors.
It is caused by joint overuse, whereas RA is a
systemic autoimmune disorder that results in
symmetric joint inflammation.
Pathophysiology
OA is a chronic joint disease that involves the loss of
habitually weight-bearing articular (joint) cartilage.
The loss can result in stiffuess, pain, swelling, loss of
motion, and changes in joint shape, in addition to
abnormal bone growth, which can result in
osteophytes.
The joints most often affected in OA are the distal
interphalangeal joints, the thumb joint, and, in
particular, the joints of the knees, hips, ankles, and
spine, which bear the bulk of the body's weight.
The elbows, wrists, and ankles are less often affected.
OA generally presents as pain that worsens
with weight bearing and activity and improves
with rest, and patients often report morning
stiffness or "gelling" of the affected joint after
periods of inactivity.

Medical and Surgical Management
The patient's medical history and level of pain should
determine the most appropriate treatment.
Should include nonpharmacologic modalities (patient
education, physical and occupational therapy),
pharmacologic agents, and surgical procedures with
the goals of pain control, improved function and
health-related quality of life, and avoidance of toxic
effects from treatment.
Weight loss and/or achievement of ideal body weight
(body mass index [BM!] of 18.5-24.9) should be part of
the medical treatment as it improves OA dramatically
Patients with severe symptomatic OA pain who have not
responded adequately to medical treatment and who have
been progressively limited in their activities of daily living
(ADLs), such as walking, bathing, dressing, and toileting,
should be evaluated by an orthopedic surgeon.
Surgical options include arthroscopic debridement (with or
without arthroplasty), total joint arthroplasty, and
osteotomy.
Surgical reconstruction has been quite successful but
should not be viewed as a replacement for overall good
nutrition, maintenance of healthy body weight, and
exercise.
Exercise
OA limits the ability to increase energy
expenditure through exercise.
It is critical that the exercise be done with correct
form so as not to cause damage or exacerbate an
existing problem.
Nonloading aerobic (swimming), range-of-
motion, and weightbearing exercises have all
been shown to reduce symptoms, increase
mobility, and lessen continuing damage from OA.
Medical Nutrition Therapy
Weight and Adiposity Management
Excess weight puts an added burden on the weight-bearing
joints.
Epidemiologic studies have shown that obesity and injury
are the two greatest risk factors for OA.
The risk for knee OA increases as the BMI increases.
Controlling obesity can reduce the burden of OA through
both disease prevention and improvement in symptoms
A well-balanced diet that is consistent with established
dietary guidelines and promotes attainment and
maintenance of a desirable body weight is an important
part of MNT for OA

Anti-Inflammatory Diet
Recently, the anti-inflammatory diet, a diet
resembling the Mediterranean diet, has been
useful.
The diet aims for variety, the inclusion of as much
fresh food as possible, the least amount of
processed foods and fast food, and an abundance
of fruits and vegetables.
When combined with moderate exercise, diet-
induced weight loss has been shown to be an
effective intervention for knee OA.
There is also an anti-inflammatory effect from
weight loss in OA management because the
reduced fat mass results in the presence of less
inflammatory mediators from adipose tissue.
Vitamins and Minerals
Cumulative damage to tissues mediated by
reactive oxygen species has been implicated as a
pathway that leads to many of the degenerative
changes seen with aging.
However, large doses of dietary antioxidants,
including vitamin C, the tocopherols (vitamin E),
b-carotene, and selenium have shown no benefit
for the management of symptomatic OA.
Many patients with OA consume deficient levels
of calcium, and vitamin D. Low serum levels of
vitamin D are being studied for their role in OA
progression.
special attention given to vitamin B6, vitamin D,
vitamin K, folate, and magnesium.
Alternative Therapies
Topical aids, manipulative therapies, and acupuncture.
Capsaicinoids, derived from chili peppers, have a fatty
acid receptor that stimulates, then blocks, small-
diameter pain fibers by depleting them of the
neurotransmitter substance P, thought to be the
principal chemomediator of pain impulses from the
periphery.
Capsaicin, applied with glyceryl trinitrate to reduce
onsite burning, can reduce pain in OA patients
Certain pulsed electromagnetic fields can also affect
the growth of bone and cartilage with potential use in
OA.
S-adenosyl- L-methionine (SAM-e) has also shown
promise for reducing pain and improving mobility in
people with OA at doses of 600 to 1200 mg/day.

Glucosamine and Chondroitin
Sodium chondroitin sulfate (chondroitin sulfate) and
glucosamine hydrochloride (glucosamine) are both
involved in cartilage production, but their mechanism
for eliminating pain has not been identified.
In some cases glucosamine may be equal or superior to
ibuprofen.
Although it is not effective for all afflicted individuals, a
safe dose of glucosamine and chondroitin sulfate is
1500 mg/day and 1200 mg/day in divided doses,
respectively.
chondroitin is chemically similar to commonly used
blood thinners and could cause excessive bleeding if
used in combination with blood thinners.
Chondroitin may also elicit a reaction in those with
shellfish allergies.

Rheumatoid arthritis (RA)
RA affects the interstitial tissues, blood
vessels, cartilage, bone, tendons, and
ligaments, as well as the synovial membranes
that line joint surfaces.
RA occurs more frequently in women than in
men peak onset commonly occurs between 20
and 45 years of age.

Pathophysiology
RA is a chronic, autoimmune, systemic disorder in which
cytoklnes and the inflammatory process playa role.
RA has articular manifestations that involve chronic
inflammation that begins in the synovial membrane and
progresses to subsequent damage in the joint cartilage.
Although the exact cause of RA is still unknown, certain
genes have been discovered that play a role.
The likely trigger is a viral or bacterial infection.
Drinking large amounts of tea may increase the risk of
developing RA (Walitt et al, 2010); however, other studies
have suggested that teas are protective.
More research is clearly needed.
Medical Management
The appearance of rheumatoid factor (RF),
may precede symptoms of RA. Pain, stiffness,
swelling, loss of function and anemia are
common.
RA patients are at increased risk for
cardiovascular disease, explained by the
systemic inflammatory response.
Many of the drugs used to treat RA can result
in hyperhornocysteinemia, hypertension, and
hyperglycemia, all risk factors for
cardiovascular disease.

Pharmacologic Therapy
Medications to control pain and inflammation are
the mainstay of treatment for RA.
Salicylates and NSAIDs are oftenthe first line of
treatment, and methotrexate (MTX) is commonly
prescribed as well, but these drugs may cause
significant side effects.
Disease-modifying antirheumatic drugs
(DMARDs) may be prescribed because of their
unique ability to slow or prevent further joint
damage caused by arthritis.
These include MTX, sulfasalazine (Azulfidine),
hydroxychloroquine (Plaquenil), azathioprine
(Imuran), and leflunomide (Arava).

Surgery
Surgical treatment for RA may be considered if
pharmacologic and nonpharmacologic
treatment cannot adequately control the pain
or maintain acceptable levels of functioning.
Common surgical options include
ynovectomy, joint replacement, and tendon
reconstruction.
Exercise
To maintain joint function, recommendations
may be given for energy conservation, along with
range-of-motion and strengthening exercises.
A loss of body cell mass that accompanies RA,
called rheumatoid cachexia, involves the skeletal
muscle, viscera, and immune system.
This can lead to muscle weakness and loss of
function, which may hasten morbidity and
mortality in RA.
Physical activity, including both aerobic exercise
and strength training, seems to help.
Medical Nutrition Therapy
The association of foods with disease flares
should be discussed. Whether food intake can
modify the course of RA is an issue of continued
scientific debate and interest.
Dietary manipulation by either modifying food
composition or reducing body weight may give
some clinical benefit in improving RA symptoms.
Some literature has suggested that fasting may be
beneficial in reducing pain at the inflammation
site; nevertheless fasting has never been shown
as an effective treatment for RA symptoms.
A vegan, gluten-free diet causes improvement in
some patients, possibly because of the reduction
of immunoreactivity to food antigens.

Energy
Although traditional measures to assess energy
requirements can be used, weight should be
monitored and energy intake modified as needed
to achieve desirable or usual body weight.
For patients who are totally sedentary,
calculations should be estimated at the resting
energy expenditure and adjusted for weight
changes that occur over time.
When intakes are poor, enteral or parenteral
supplementation may be required, and home
nutrition support is beneficial for chronic cases
Protein
Well-nourished individuals require protein at
levels comparable to the DRIs for age and sex.
Patients with RA tend to have increased
whole-body protein breakdown (regardless of
age) from growth hormone factor, glucagon,
and TNF-a production.
Protein may be needed at levels of 1.5 to 2
g/kg/day.
Lipids
Low-fat diets (including use of low-fat substitutes) lead to
low serum levels of vitamins A and E and actually stimulate
lipid peroxidation and eicosanoid production, thus
aggravating RA.
Therefore low-fat or fat-free dieting may actually be
counterproductive for patients susceptible to or afflicted by
RA.
Changing the type of fat in the diet is useful and likely
offers advantages for both the arthritis and cardiovascular
systems.
Omega-3 fatty acids have increased in popularity in the
management of RA because of their role in inflammatory
pathways.
Fish oil alleviates RA symptoms and reduces the use of
NSAIDS in RA patients The beneficial effects are generally
delayed for up to 12 weeks after they are started but last
up to 6 weeks after discontinuing therapy .

Minerals, Vitamins, and Antioxidants
Several vitamins and minerals function as antioxidants
and therefore affect inflammation.
Vitamin E is just such a vitamin, and along with O-3 and
O-6 fatty acids, may affect cytokine and eicosanoid
production by decreasing proinflammatory cytokines
and lipid mediators.
RA patients often have nutritional intakes below the
DRIs for folic acid, calcium, vitamin D, vitamin E, zinc,
vitamin B, and selenium.
Adequate intakes of folate and vitamins B6 and Bl2
should be encouraged. Calcium and vitamin D
malabsorption and bone demineralization are
characteristic of advanced stages of the disease,
leading to osteoporosis or fractures.
Supplementation with calcium and vitamin D should be
considered.
Alternative Therapies
Gamma-linolenic acid (GLA) is an (0-6 fatty
acid found in the oils of black currant, borage,
and evening primrose that can be converted
into the antiinflammatory PG E, or into ARA, a
precursor of the inflammatory PG E2.
This antiinflammatory PGEI may relieve pain,
morning stiffness, and joint tenderness with
no serious side effects.
Thunder god vine (Tripterygium wilfordit) has
been used in China to treat patients with a
number of autoimmune diseases.
SJOGREN'S SYNDROME
Sjogren's syndrome (55) is a chronic
autoimmune disease characterized by
lymphocytic infiltration of the exocrine glands,
particularly the salivary and lacrimal glands,
leading to dryness of the mouth (xerostomia)
and of the eyes (xerophthalmia).

Pathophysiology
Common signs include thirst, burning sensation in the oral
mucosa, inflammation of the tongue (glossitis), and lips
(cheilitis), cracking of the corners of the lips (cheilosis),
difficulties in chewing and swallowing (dysphagia), severe
dental caries, progressive dental decay, and nocturnal oral
discomfort.
SS can be present alone (primary SS) or as secondary SS, as
a result of another rheumatic disorder (RA, lupus).
Nutrient insufficiency may playa role in the development or
progression of SS.
Altered consumption of several nutrients has been noted in
SS patients including higher intake of supplemental calcium
and lower intake of nonsupplemental vitamin C, PUFAs,
linoleic acid, and (0-3 fatty acids.
Biochemical deficiency of vitamin B6 (pyridoxine) has also
been observed
Medical Management
Medications for SS address the issues of dry eyes
and dry mouth. These include artificial tears and
immunosuppressant drops such as cevimeline
(Evoxac) and pilocarpine (Salagen), respectively.
Medical Nutrition Therapy
The goal of dietary management in patients with
SS is to relieve symptoms and reduce eating
discomfort, which can result in lack of appetite,
weight loss, fatigue, difficulty chewing and
swallowing, mouth infections, and anemia.
Sugary foods should be reduced or eliminated
from the diet to minimize cavities.
Ready-to-eat foods may be useful.
Foods should all be moist, and extremes in
temperature should be avoided.
The most common modifications include soaking or
overcooking certain foods to make them softer;
chopping and cutting meats and fruits to make them
smaller; and limiting consumption of citrus fruits,
irritant foods, and spices.
Iron and vitamin deficiencies such as vitamin C, vitamin
B12, vitamin B6 and folate are possible, but these can
be easily avoided with a well-balanced diet or
appropriate vitamin supplementation.

TEMPOROMANDIBULAR
DISORDERS
Temporomandibular disorders (TMDs) affect
the temporomandibular joint, which connects
the lower jaw (mandible) to the temporal
bone.
TMDs can be classified as myofascial pain,
internal derangement of the joint, or
degenerative joint disease.
Pathophysiology
Besides experiencing a severe jaw injury, there is
little scientific evidence to suggest a cause for
TMD. It is generally agreed that physical or
mental stress may aggravate this condition.
Medical Nutrition Therapy
The goal of dietary management is to alter food
consistency to reduce pain while chewing.
Diet should be mechanically soft in consistency;
all foods should be cut into bite-size pieces to
minimize the need to chew or open the jaw
widely; and chewing gum, sticky foods, and biting
hard foods such as raw vegetables, candy, and
nuts should be avoided.
Intake of fiber is often reduced.
CHRONIC FATIGUE SYNDROME
AND FIBROMYALGIA
Chronic fatigue syndrome (CFS) and fibromyalgia have
rheumatic symptoms.
The etiology and pathogenic mechanisms of
fibromyalgia and CFS are to date not fully understood.
In fibromyalgia, central nervous system dysfunction,
mitochondrial dysfunction, nutrient deficiencies, and
other systemic abnormalities have been suggested.
Mitochondrial dysfunction can result in lack of energy
(ATP) for muscular work.
Some symptoms include poor growth, loss of muscle
coordination and muscle weakness
Pathophysiology
In fibromyalgia, nonarticular aches at specific
pressure points and fatigue cause disabling
symptoms including muscle tenderness, sleep
disturbances, fatigue, morning stiffness,
numbness and tingling, symptoms of anxiety
and depression, chronic headaches, irritable
bowel, and irritable bladder.
In CFS, chronic fatigue is the major symptom.
It lasts 6 months or longer and is accompanied
by hypotension, sore throat, multiple joint
pains, headaches, postexertion lethargy,
muscle pain, and impaired concentration.
Medical Management
Treatment program for CFS should be
multidisciplinary and include exercise, MNT,
appropriate sleep hygiene, low dose tricyclic
antidepressants or selective serotonin reuptake
inhibitors (SSRIs), and cognitive behavior therapy.
Serotonin norepinephrine reuptake inhibitors
(SNRIs) such as duloxetine (Cymbalta) and
milnacipran (Savella) and the anticonvulsant
pregabalin (Lyrica) have been suggested for
fibromyalgia patients and are FDA approved for
this purpose.
Exercise is helpful; supervised moderate-intensity
graded aerobic exercise, or water aerobics
(minimum 12 weeks, 3x/ week) is suggested.
Medical Nutrition Therapy
Data regarding MNT for CFS are extremely
limited.
When hypotension is identified medically in CFS
patients, increases in sodium and fluid intakes
have been suggested.
Vegetarian diets could have some beneficial
effects probably due to the increase in
antioxidant intake.
Weight control seems to be an effective tool to
improve the symptoms in these patients.
Vitamin therapies such as riboflavin, coenzyme Q,
and carnitine (a specialized amino acid) may
provide subjective improvement in fatigue and
energy levels in some patients.
GOUT
A disorder of purine metabolism in which
abnormally high levels of uric acid accumulate
in the blood (hyperuricemia).
Renal disease is common, and uric acid
nephrolithiasis can occur.
As the disease advances, symptoms occur
more frequently and are more prolonged.
The disease usually occurs after the age of 35
years and predominantly affects men.
Pathophysiology
Gout is characterized by the sudden and acute
onset of localized arthritic pain that usually
begins in the big toe and continues up the leg.
The urate deposits can destroy joint tissues,
leading to chronic symptoms of arthritis.
As a consequence, sodium urates are formed and
deposited as tophi in the small joints and
surrounding tissues.
In chronic gout a classic site is the helix of the ear.
Genetic factors play an important role in the
pathogenesis of gout and regulation of serum
uric acid levels.
One comorbidity of gout is obesity.
Medical Management
The goals of treatment are to reduce the pain
associated with acute attacks, to prevent future
attacks, and to avoid the formation of tophi and
nephrolithiasis.
The primary treatment for gout involves
pharmacologic therapy (colchicine, allopurinol,
NSAIDs, and others depending on the acute or
chronic condition and renal function).
Maintaining a serum urate level of less than 6
mg/ dL may reduce the risk of recurrent gout
attacks.
Probenecid (Benemid) and sulfinpyrazone
decrease the blood uric acid level by increasing
elimination through the kidneys.
Allopurinol inhibits uric acid production.

Medical Nutrition Therapy
Although gout has traditionally been treated with
a low-purine diet, drugs have largely replaced the
need for rigid restriction of the diet.
However, the patient can takean active role by
adhering to the nutrition guidelines for the
management of gout as well.
Higher levels of meat and seafood consumption
were associated with increased serum uric acid.
High intake of fluids (8 to 16 cups of fluid/day, at
least half as water) should be encouraged to
assist with the excretion of uric acid and to
minimize the possibility of renal calculi formation
SCLERODERMA
Scleroderma is a chronic, systemic sclerosis or
hardening of the skin and visceral organs characterized
by deposition of fibrous connective tissue.
Scleroderma is considered an autoimmune rheumatic
disease with a genetic component.
Free-radical, oxidative damage from cytokines, in
which fibroblast proteins are modified, is involved
Gastrointestinal symptoms include gastroesophageal
reflux, nausea and vomiting, dysphagia, diarrhea,
constipation, fecal incontinence, and small intestine
bacterial overgrowth.
Joint stiffness and pain, renal dysfunction,
hypertension, pulmonary fibrosis, and
pulmonary arterial hypertension are also
common.
Treatment
Some studies have been undertaken with the
use of anti- TNF therapies with some
promising results.
Treatments for the pulmonary hypertension
and renal crises have shown good results
overall
Medical Nutrition Therapy
Dysphagia requires nutrition intervention
Dry mouth with resultant tooth decay, loose
teeth, and tightening facial skin can make eating
difficult.
Consuming adequate fluids, choosing moist
foods, chewing sugarless gum, and using saliva
substitutes help moisten the mouth and may
offer some relief.
A high-energy, high-protein supplement or
enteral feeding may prevent or correct weight
loss.
Home enteral or parenteral nutrition is often
required when problems such as chronic diarrhea
persist.
SYSTEMIC LUPUS
ERYTHEMATOSUS
Systemic lupus erythematosus (SLE) is
commonly known as lupus. Lupus is most
prevalent in women of childbearing age and is
more common in blacks and women of Hispanic,
Asian, and Native American descent than in
whites.
Common symptoms include extreme fatigue,
painful or swollen joints, unexplained fever, skin
rashes, mouth ulcers, and kidney problems.
Pathophysiology
SLE has a genetic predisposition and
overproduction of type 1 interferon and other
cytotoxic cells
SLE is considered to be an autoimmune
disease that affects all organ systems.
Renal function is deranged in lupus, thus
causing excessive excretion of protein and
often renal failure.
Medical Management
Lupus itself and the medications used
(corticosteroids, NSAIDs, immunosuppressants,
antimalarials) affect nutrient metabolism, needs,
and excretion.
Plaquenil, an antimalarial drug, appears to be
effective in clearing up skin lesions for some
individuals with lupus but has side effects that
include nausea, abdominal cramping, and
diarrhea.
Immunosuppressives such as cyclophosphamide
may be useful when there is renal involvement,
but gastrointestinal and fertility problems may
occur.
Medical Nutrition Therapy
No specific dietary guidelines for managing
SLE exist.
Rather, the diet needs to be tailored to the
individual needs of the patient.
Protein, fluid, and sodium requirements are
altered as a result of disordered renal function
and steroid-induced side effects.
The goal should be to attain and maintain the
usual body weight.
Enteral nutrition support may be required in
chronic cases
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