Complementary and Alternative Medical Lab Testing Part 9: Gynecology
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About this ebook
Complementary and Alternative Medical Lab Testing (CAM Labs) contains summaries of the published research on lab tests, primarily from PubMed trials on humans. Each chapter (disease) begins with a brief summary of conventional lab tests, followed by additional lab tests, including diabetes, insulin resistance, metabolic syndrome, inflammation, etc. There are sections on endocrine hormones (thyroid, adrenal, sex steroids) and environmental medicine (toxic heavy metals). The nutritional assessments section includes minerals, vitamins and amino acids.
CAM Labs 9 - Gynecology
1. Amenorrhea
2. Cervical Dysplasia
3. Dysmenorrhea
4. Endometriosis
5. Female Infertility
6. Fibrocystic Breast Disease
7. Hot Flashes
8. Hypoactive Sexual Desire Disorder (HSDD)
9. Menopause
10. Menorrhagia
11. Polycystic Ovary Syndrome
12. Postmenopausal
13. Postmenopausal Bleeding
14. Postmenopausal Breast Cancer
15. Postmenopausal Osteoporosis
16. Premenstrual Dysphoric Disorder
17. Premenstrual Syndrome
18. Uterine Fibroids
19. Vaginitis
20. Vulvodynia
21. Well Woman
Ronald Steriti
Dr. Ronald Steriti is a graduate of Southwest College of Naturopathic Medicine and currently is researcher for Jonathan V. Wright at the Tahoma Clinic.
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Complementary and Alternative Medical Lab Testing Part 9 - Ronald Steriti
Chapter 1. Amenorrhea
Conventional Lab Tests
FSH and LH, TSH
ESR, liver function tests, BUN, Xreatinine
CBC, Chemistries, Urinalysis
Androgen testing: testosterone, DHEAS, androstenedione, and 17-OH progesterone
Pregnancy test (serum or urinary human chorionic gonadotropin)
Additional Lab Tests
Fasting Glucose, Hemoglobin A1C
A study measured serum LH every 10 min for 24 h and for 2 additional h after the administration of exogenous GnRH in 8 women with IDDM and amenorrhea and compared these to data from 15 eumenorrheic nondiabetic women. Cluster analysis revealed fewer LH pulses per 24 h (14.3 +/- 1.2 vs. 19.9 +/- 0.6; P < 0.001; mean +/- SEM), a greater peak width (63 +/- 4.9 vs. 44 +/- 2.2 min; P < 0.01), and greater peak area (136 +/- 17 vs. 89 +/- 13 IU/L.min; P < 0.01) in the diabetic women. Analysis with Deconv revealed fewer LH secretory episodes per 24 h in the diabetic women (14.4 +/- 0.9 vs. 20.4 +/- 0.5; P < 0.001) and no statistical difference in LH half-lives. The IDDM women responded to a 10-micrograms GnRH bolus with LH pulses of larger total (51 +/- 15.9 vs. 15 +/- 1.4 IU/L; P < 0.01) and incremental (29 +/- 7.6 vs. 9 +/- 1.2; P < 0.001) amplitude. In summary, we observed that amenorrheic diabetic women have fewer LH pulses/secretory episodes than normal women. However, they respond well to exogenous GnRH, suggesting that compromise of the GnRH pulse generator, rather than pituitary dysfunction, is responsible for their menstrual dysfunction. (South et al., 1993)
Celiac Disease
A 20-year-old woman presented with primary amenorrhea and failure of development of secondary sexual characteristics. She had significant weight loss in spite of normal intake of diet. On investigation, she had microcytic hypochromic anemia, and her follicle-stimulating hormone and luteinizing hormone levels were low, while the thyroid-stimulating hormone and prolactin levels were normal. Her duodenal biopsy showed villus atrophy, and IgA antiendomysial antibody was positive, suggestive of celiac disease. The patient's condition improved markedly and attained menarche after 6 months of a gluten-free diet. Celiac disease should be considered in patients presenting with malnutrition and primary amenorrhea. (Pradhan et al., 2007)
Comprehensive Sex Steroid Panel
Among 136 patients presenting with secondary or primary amenorrhea, hyperandrogenemia was found to be the hormonal cause of this specific type of irregular menses in 21 patients. A retrospective study was carried out to investigate the patients' serum androgen findings and body mass index. The ultrasound features of the ovaries were also recorded. Twenty-one of the 136 patients presenting with the most severe form of menstrual irregularity, amenorrhea - defined as an absence of menses for at least 6 months - were found to have elevated serum androgen levels. The androgen profile included elevated levels of total testosterone (TT), or dehydroepiandrosterone sulfate (DHEAS), or calculated free testosterone (cFT), or all three, with or without an elevated luteinizing hormone-follicle-stimulating hormone (LH : FSH) ratio. Six patients with a body mass index > 26 kg/m2 all had elevated cFT, while TT was only increased in three patients. All of the patients had low levels of sex hormone-binding globulin (SHBG). Two patients had abnormal TT, cFT, and DHEAS levels together with polycystic ovaries. Eleven patients with a body mass index (BMI)
Comprehensive Thyroid Panel
Both hyper- and hypothyroidism may result in menstrual disturbances. In hyperthyroidism, amenorrhea was described as early as 1840 by von Basedow. The most common manifestation is simple oligomenorrhea (decreased menstrual flow). Anovulatory cycles are very common. Increased bleeding may occur, but is rare in hyperthyroidism. Nowadays hyperthyroidism is diagnosed earlier than it once was, and so the clinical picture is generally milder. So, menstrual disorders are less common than in previous series. In a recent paper, 21.5% of 214 patients had disturbances in their cycle, compared to 50% in some older series. In hypothyroidism, on the contrary, polymenorrhea (increased menstrual bleeding) is more common. Defects in hemostasis may contribute to this. Anovulation may be represent. Fertility is reduced in both hyper- and hypothyroidism, and the outcome of pregnancy is more often abnormal than in euthyroid women. It is of interest that in juvenile hypothyroidism precocious puberty has been described. This is probably due to a spillover
effect of the glucoprotein hormones: TSH, which is markedly increased in hypothyroidism, has a small FSH- and LH-like effect. Galactorrhea may also be present in hypothyroidism, possibly because TSH, the hypophyseal TSH-releasing hormone, increases the secretion of both TSH and PRL. (Koutras, 1997)
References
Cupisti, S., et al. (2007), ‘Evaluation of biochemical hyperandrogenemia and body mass index in women presenting with amenorrhea’, Exp Clin Endocrinol Diabetes, 115 (5), 298-302. PubMedID: 17516292
Koutras, D. A. (1997), ‘Disturbances of menstruation in thyroid disease’, Ann N Y Acad Sci, 816 280-84. PubMedID: 9238278
Pradhan, M., et al. (2007), ‘Celiac disease as a rare cause of primary amenorrhea: a case report’, J Reprod Med, 52 (5), 453-55. PubMedID: 17583254
South, S. A., et al. (1993), ‘Alterations in luteinizing hormone secretory activity in women with insulin-dependent diabetes mellitus and secondary amenorrhea’, J Clin Endocrinol Metab, 76 (4), 1048-53. PubMedID: 8473380
Chapter 2. Cervical Dysplasia
Conventional Lab Tests
HPV DNA test
Nutritional Assessments
Zinc and Copper
Serum copper and zinc levels were determined by atomic absorption spectroscopy in 110 women with varying degrees of cervical dysplasia up to carcinoma-in-situ and in 9 women with invasive carcinoma of the cervix, and compared with levels in 21 women with no evidence of cervical dysplasia. The average serum copper and zinc levels in the control group were 1.25 mg/l and 1.02 mg/l (respectively). The mean serum copper level increased with dysplasia to 1.4 mg/l and with invasive carcinoma to 1.47 mg/l. The mean serum zinc levels were decreased in cervical intra-epithelial neoplasia (CIN) grade 1 to 0.81 mg/l and in invasive carcinoma to 0.73 mg/l. The copper:zinc ratios varied significantly between controls, patients with cervical dysplasia and patients with invasive carcinoma (p less than 0.01). Measurement of serum ceruloplasmin revealed no significant differences among the control group and the groups of patients. (Grail and Norval, 1986)
Vitamin A
A study carried out a clinic-based case-control study to assess serum micronutrients as risk factors for cervical dysplasia among Southwestern American Indian women, a group with high rates of cervical preinvasive lesions. Cases were American Indian women with biopsy-proven cervical intraepithelial neoplasia (CIN I or CIN II/III). Controls were from the same Indian Health Service clinics with normal cervical epithelium. We interviewed women about histories of sexually transmitted diseases, sexual behavior, diet, hygienic practices, cigarette smoking, and reproductive factors. Laboratory assays included serum for retinol (vitamin A), ascorbic acid (vitamin C), alpha-tocopherol (vitamin E), and red blood cell folate levels, DNA for human papillomavirus (HPV) typing, and tests for other sexually transmitted diseases. The strongest risks for cervical dysplasia were associated with cervical HPV infection [odds ratio (OR) = 3.2, 95% confidence interval (CI) = 2.2-4.6 and OR = 7.9, 95% CI = 4.8-13.1 for CIN I and CIN II/III, respectively]. With adjustments made for HPV infection and other relevant confounders, subjects in the lowest serum retinol quartile were at increased risk of CIN I compared with women in the highest quartile (OR = 2.3, 95% CI = 1.3-4.1). The data suggest that low serum alpha-tocopherol was associated with CIN I/III, although the adjusted OR was not statistically significant (OR = 2.0, 95% CI = 0.9-4.8). (Yeo et al., 2000)
A study followed up on 134 women who had been diagnosed with cervical dysplasia to examine the relationship of dietary and serum vitamin A to subsequent cervical cancer. The subjects were women attending the Papanicolaou test screening for residents in Miyagi, Japan and histologically diagnosed as having cervical dysplasia between October 1987 and September 1988. During the follow-up, 8 women (5.9%) developed cancer in situ or invasive cervical cancer and 106 (79.1%) reverted to normal. The rate of progression of the cancer in situ or invasive cervical cancer was 4.5 times higher in women with lower serum retinol levels than those with higher serum retinol levels (p = 0.08). The results suggest an association of low serum retinol level with development of cervical cancer. (Nagata et al., 1999)
To examine the relationship of dietary and serum vitamin A to the risk of cervical dysplasia, a case-control study was conducted in Miyagi, Japan. Cases were 137 women who were found by Papanicolaou test screening and histological examination provided by Miyagi Cancer Society between October 1987 and September 1988 to have cervical dysplasia. Controls were selected from participants of the general health examination provided by the Society and individually matched to cases on age and screening date. The consumption of retinol or carotene-rich foods during the past 7 days was assessed at interview. Information was also collected about other risk factors of cervical dysplasia, such as reproductive histories and sexual behaviour. The mean serum retinol levels were significantly lower among cases compared with controls, although dietary intake levels of retinol and carotene were not different between the two groups. When examined by tertile, the risk of cervical dysplasia was significantly higher among women in the highest tertile of dietary vitamin A level. An inverse association was observed between serum retinol level and risk of cervical dysplasia, although it did not achieve statistical significance. (Shimizu et al., 1996)
Homocysteine
Through the years 2007-2008, 122 women who have admitted to Gynecology Clinic were evaluated for cervical cytology, demographical characteristics, HPV infection, serum folate, vitamin B12, homocysteine, albumin, and neopterin levels. Considering all the cases, the highest percentage of the HPV-infected patients was in high-grade squamous intraepithelial lesion (HSIL) group (83%, n = 25). The serum folate levels in all patient groups [HSIL 10.0 +/- 0.4 ng/ml, low-grade squamous intraepithelial lesion (LSIL) 10.6 +/- 0.5 ng/ml, atypical squamous cells-undetermined significance (ASCUS) 11.1 +/- 0.8 ng/ml] were lower than control group (11.9 +/- 0.5 ng/ml; p < 0.05). The vitamin B12 levels were not significantly altered in any of the patient groups. The serum homocysteine levels in all patient groups (HSIL 10.4 +/- 0.5 Umol/l, LSIL 10.1 +/- 0.5 Umol/l, ASCUS 10.5 +/- 0.7 Umol/l) were higher than the control group (7.9 +/- 0.5 Umol/l; p < 0.05). The neopterin levels of HSIL group (1.0 +/- 0.2 ng/ml) were lower than the control group (1.5 +/- 0.2 ng/ml; p < 0.05). The serum neopterin concentrations of HSIL with HPV group (0.6 +/- 0.1 ng/ml) were significantly lower than HSIL without HPV (2.4 +/- 0.9 ng/ml) and other study groups (p < 0.05). The serum homocysteine levels of HSIL HPV(+) group and LSIL HPV(+) were higher than control group (p < 0.05). The serum albumin levels of HSIL with HPV group are lower than control and other groups (p < 0.05). In all cervical dysplasia groups, folate levels in patients infected with HPV are lower than in HPV(-) patients (p < 0.05). Folic acid deficiency could be caused by insufficient cellular immunity. In case of folate deficiency, the predisposition of HPV infection persistency and progression of cervical dysplasia increase. The fact that neopterin is a strong cellular immunity marker and it was detected in patients with HPV persistence and cervical dysplasia in lower levels shows that these patients may have relatively insufficient immune system. In order for dysplasia progression to be prevented, folate fortification on diets may be advised to HPV-infected women. (Abike et al., 2011)
A study examined correlates of total plasma homocysteine (tHcy) in 294 subjects with cervical intraepithelial neoplasia and 170 control subjects. Plasma and red blood cell folate and plasma B(12) were strong inverse correlates of tHcy (r = -0.35, -0. 31, and -0.27, respectively). Plasma copper and severity of dysplasia were positively correlated with tHcy (r = 0.14 and 0.21, respectively). A stepwise regression model that included red blood cell folate, plasma copper, grade of dysplasia, ethnicity, intake of polyunsaturated fatty acids, plasma vitamin B(12), intake of fat, and oral contraceptive use explained 29% of the variation in tHcy. Two hundred thirty-five subjects with cervical intraepithelial neoplasia were randomized to receive folic acid (10 mg/d) or placebo for 6 mo. After 2, 4, and 6 mo, mean tHcy in the folate-supplemented group (7.2 +/- 1.8, 7.0 +/- 1.9, and 7.0 +/- 2.3 micromol/L, respectively) was significantly lower than baseline and the placebo group at 2, 4, and 6 mo (8.9 +/- 3.1, 8.4 +/- 3.0, and 8.9 +/- 3.1 micromol/L, respectively). Supplementation lowered tHcy even in subjects in the highest quintile of baseline folate. Folate, vitamin B(12), copper, and severity of dysplasia are associated with tHcy. Folate supplementation significantly lowers tHcy even in folate-replete subjects. (Thomson et al., 2000a)
A study investigated whether total plasma homocysteine (tHcy) is associated with risk for cervical intraepithelial neoplasia (CIN). tHcy was evaluated, along with numerous risk factors for CIN and biochemical indexes of nutrients, in a previously reported study population of 294 subjects with CIN and 170 female controls without CIN. tHcy was significantly higher in cases than in controls (9.1 vs. 8.3 mumol/l, p = 0.002). Human papillomavirus type 16 infection [odds ratio (OR) = 6.7], oral contraceptive use (OR = 6.0), parity (OR = 2.2), and cigarette smoking (OR = 1.9) were significantly associated with CIN after adjustment for each other and for age, number of sexual partners, and plasma tHcy, folate, iron, and zinc. Human papillomavirus type 16 positivity increased risk for CIN more when tHcy was > 9.12 mumol/l (OR = 4.7) than when it was < or = 9.12 mumol/l (OR = 3.0). Cigarette use increased risk for CIN when tHcy was > 9.12 mumol/l (OR = 3.9), but not when tHcy was < or = 9.12 mumol/l (OR = 1.5). Parity increased risk for CIN more when tHcy was > 9.12 mumol/l (OR = 4.0) than when tHcy was < or = 9.12 mumol/l (OR = 2.0). These results suggest that elevated plasma tHcy is a risk factor for cervical dysplasia and that it enhances the effects of other risk factors. It is unknown whether tHcy is serving as a marker of folate deficiency or is acting through other mechanisms. (Thomson et al., 2000b)
A study estimated the concentrations of folic acid and free homocysteine in the blood serum of women with CIN III (cervical intraepithelial neoplasia-Burghard's classification) infected with DNA HPV (human papillomaviruses) of type 16 and/or 18. The control group consisted of 49 patients with normal cytological smears without HPV infection. Types 16 and/or 18 DNA HPV were found in 50 patients. This women qualified for the studied group. The sequence of DNA HPV type 16 and/or 18 was identified with the PCR method (polymerase chain reaction). The high-performance liquid chromatography (HPLC) method was employed to evaluate the levels of folic acid and free homocysteine in the blood serum of the examined patients. Significantly lower levels of folic acid and higher levels of free homocysteine were observed in the blood serum of HPV-positive patients with CIN III. The correlation was found between serum concentrations of folic acid and free homocysteine in both groups. (Kwasniewska et al., 2002)
Vitamin B12
The study included 376 premenopausal women of childbearing age who tested positive for infections with high-risk (HR) human papillomaviruses (HPVs) and were diagnosed with cervical intraepithelial neoplasia (CIN) grade 2 or higher (CIN 2+, cases) or
The vitamin B12 statuses of Thai women with high- and low-grade cervical dysplasia were studied and compared with women with normal cytological smears. Serum vitamin B12 and vitamin B12 intakes were assessed, as well as demographic characteristics, sexual behavior, reproductive and menstrual history, exogenous hormone use, personal and familial medical history, smoking habit, and other risk factors. The presence or absence of genital HPV DNA was determined by polymerase chain reaction (PCR). Serum vitamin B12 levels in women with normal cytological smears were significantly higher than those with both high- and low-grade cervical dysplasia (p<0.001). Low vitamin B12 serum levels were significantly statistically associated with increased low-grade (OR = 4.08; 95% CI = 1.41-11.79; p < 0.05) and increased high-grade cervical dysplasia risk (OR = 3.53; 95% CI = 1.24-10.04; p< 0.05) for the highest vs lowest quartiles of serum vitamin B12. This study