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    Complementary and Alternative Medical Lab Testing Part 7: Endocrine
    Complementary and Alternative Medical Lab Testing Part 7: Endocrine
    Complementary and Alternative Medical Lab Testing Part 7: Endocrine
    Ebook254 pages5 hours

    Complementary and Alternative Medical Lab Testing Part 7: Endocrine

    By Ronald Steriti

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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 7 – Endocrine

    Endocrine
    1. Growth Hormone Deficiency
    2. Hypopituitarism
    3. Obesity

    Adrenals
    4. Addison's Disease
    5. Cushing's Disease

    Pancreas
    6. Diabetes Type 1
    7. Diabetes Type 2
    8. Hyperglycemia
    9. Hypoglycemia
    10. Insulin Resistance
    11. Metabolic Syndrome

    Thyroid
    12. Euthyroid Sick Syndrome
    13. Grave's Disease
    14. Hashimoto's Thyroiditis
    15. Hyperthyroidism
    16. Hypothyroidism
    17. Subclinical Hypothyroidism

    LanguageEnglish
    PublisherRonald Steriti
    Release dateJun 4, 2016
    ISBN9781311715654
    Complementary and Alternative Medical Lab Testing Part 7: Endocrine
    Author

    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.

    Read more from Ronald Steriti

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      Complementary and Alternative Medical Lab Testing Part 7 - Ronald Steriti

      Chapter 1. Growth Hormone Deficiency

      Conventional Lab Tests

      Insulin-like growth factor-1 (IGF-1)

      Insulin tolerance test (ITT)

      GHRH-arginine test

      Additional Lab Tests

      Insulin Resistance, Metabolic Syndrome

      A cross-sectional study was conducted in 24 GH-naive adult IGHD subjects and 25 controls. During the oral glucose tolerance test, glucose levels were higher in IGHD subjects (P<0.0001), whereas insulin response presented a trend toward reduction (P=0.08). The number of individuals with impaired glucose tolerance was higher in the IGHD group (P=0.001), whereas the frequency of diabetes was similar in the two groups. Homeostasis model assessment index of IR was lower (P=0.04), and quantitative IS check index and OGIS2 showed a non-significant trend toward elevation (P=0.066 and P=0.09, respectively) in IGHD. OGIS3 showed no difference between the groups. Homeostasis model assessment index-beta, insulinogenic index, and ratio of the areas of the insulin and glucose curves were reduced in the IGDH group (P=0.015, P<0.0001, and P=0.02, respectively). Adult subjects with lifetime congenital untreated IGHD present reduced beta-cell function, no evidence of IR, and higher frequency of impaired glucose tolerance. (Oliveira et al., 2012)

      One-hundred and ninety-five moderately-severely obese individuals participated, 149 women and 46 males: body mass index (BMI) 43.0+/-4.4 kg/m2 aged 34.3+/-11.8 yr. Fifty-five subjects (27.3%) were GHD (49 females and 6 males). The prevalence of MetS parameters was 70.9% in GHD subgroup vs 52.9% in GHS (chi2=5.281; p=0.02) and the likelihood of MetS was highest in GHD subgroup (odds ratio: 2.174; 95% confidence interval 1.113 to 4.248). At the multiple regression analysis either GH peak or IGF-I were the major determinants of waist circumference (beta=-0.380, t=-6.110 and beta=-0.326, t=-4.704, respectively; p<0.001), while age and IGFI were the major determinants of MetS (beta=0.255, t= 3.342, and beta=-0.282, t=-3.270; p=0.02, respectively). Among moderately-severely obese individuals the prevalence of the MetS was higher in GHD than in GHS subjects. Thus, in obese subjects, GH status investigation might be considered in the clinical evaluation of their metabolic risk profile. (Di Somma et al., 2010)

      In untreated GHD, cardiovascular risk is increased due to abnormal lipid profile (increased total and low-density lipoprotein cholesterol, increased triglycerides, and reduced high-density lipoprotein cholesterol) and impaired glucose metabolism. (Gazzaruso et al., 2014)

      C-Reactive Protein (CRP) and Cortisol

      A cross-sectional study was conducted at a clinical research center. Thirty girls (15 obese girls and 15 normal-weight controls) 12-18 years old matched for maturity and race were included. The hsCRP levels were higher in obese girls than controls (4.63 +/- 4.81 vs. 0.67 +/- 0.72 mg/liter; P = 0.002 after log conversion), as were other markers of cardiovascular risk. Eight of the 15 obese girls but no normal-weight girl had hsCRP higher than 3 mg/liter (P = 0.002). Body mass index sd score was higher than 4.0 in 87.5% of girls with hsCRP higher than 3 mg/liter and no girls with hsCRP less than 3 mg/liter. Girls with hsCRP higher than 3 mg/liter had higher 24-h urine free cortisol (UFC) and lower peak GH compared with those with hsCRP less than 3 mg/liter. Peak GH was an important negative predictor of most markers of increased cardiovascular risk. In addition to peak GH, UFC and adiponectin independently predicted hsCRP. Relative GH deficiency and cortisol excess are significant contributors to increased levels of markers of cardiovascular risk in obese adolescent girls. (Russell et al., 2009)

      Nutritional Assessments

      Zinc

      An article presented a 13-year-old boy with partial growth hormone deficiency due to chronic mild zinc deficiency. When zinc administration was started, his growth rate, growth hormone levels, and plasma zinc concentrations increased significantly. His poor dietary intake resulted in chronic mild zinc deficiency, which in turn could be the cause of a further loss of appetite and growth retardation. There was also a possibility of renal zinc wasting which may have contributed to zinc deficiency. Zinc deficiency should be carefully ruled out in patients with growth retardation. (Nishi et al., 1989)

      Homocysteine

      A study evaluated in seventy-one GHD children (9.8 +/- 3.6 years) before and after 2 years of GH therapy. Seventy-one healthy controls comparable with patients for age, sex and body mass index (BMI) were enrolled. Compared with controls, GHD children at study entry had higher WHtR (0.52 +/- 0.05 vs 0.45 +/- 0.19, P = 0.004), triglycerides (0.44 +/- 0.98 vs -0.03 +/- 0.73 SDS, P = 0.012), total cholesterol (0.28 +/- 1.08 vs -0.46 +/- 0.98 SDS, P < 0.001), LDL cholesterol (0.20 +/- 0.90 vs -0.39 +/- 1.06 SDS, P = 0.007), AI (3.19 +/- 0.73 vs 2.77 +/- 0.53, P = 0.001), homocysteine (8.45 +/- 1.8 vs 7.72 +/- 1.6 mum, P = 0.003), leptin (8.03 +/- 4.2 vs 5.09 +/- 1.9 ng/ml, P = 0.001) and fibrinogen (292.6 +/- 33 vs 268 +/- 31.4 mg/dl, P = 0.011). No differences were found in adiponectin or hsCRP. GH therapy was associated with a significant reduction in WHtR (P < 0.001), total cholesterol (P < 0.001), LDL cholesterol (P = 0.002), homocysteine (P = 0.044) leptin (P = 0.022) and fibrinogen (P = 0.001). Moreover, GH therapy was associated with a significant increase in adiponectin levels (P = 0.001). Our data suggest that children with untreated GHD exhibit a cluster of early cardiovascular risk factors and that GH treatment exerts beneficial effects on these abnormalities. (Capalbo et al., 2013)

      Seventeen prepubertal children with GHD (11 boys and six girls) aged 8.6 +/- 1.9 years were studied before and after 12 months of GH replacement therapy at a dose of GH of 30 microg/kg/day. Seventeen healthy children acted as controls and were matched for age, sex and body mass index (BMI). At study entry height and serum IGF-I were significantly lower, as expected, in GHD patients than in controls (P < 0.0001 and P < 0.007, respectively). Serum Hcy levels were significantly higher in GHD patients than in healthy children (8.4 +/- 2.9 vs. 6.0 +/- 2.9 micromol/l; P < 0.03), although the absolute values were within the normal values for age and sex. After 12 months of GH replacement therapy height and serum IGF-I increased significantly compared to pretreatment values (P < 0.0001); serum Hcy levels decreased significantly (6.0 +/- 3.3 micromol/l; P < 0.002) compared to baseline values, becoming similar to control values. Total cholesterol (3.5 +/- 0.6 mmol/l) and the AI (2.5 +/- 0.8) decreased significantly with respect to both pretreatment (4.2 +/- 1.0 mmol/l; P < 0.0002 and 3.4 +/- 0.8; < 0.002, respectively) and control values (4.2 +/- 0.4 mmol/l; P < 0.0005 and 3.3 +/- 1.1; P = 0.02, respectively). GHD in children is associated with higher serum levels of Hcy compared to controls, without significantly affecting the lipid profile. GH replacement for 12 months significantly decreased the Hcy levels and improved the lipid profile with a decrease of total cholesterol and the total/HDL cholesterol ratio, compared to pretreatment values. Given the small number of patients, further larger studies are needed to clarify whether these results may have significant effects in the prevention of cardiovascular disease in adulthood. (Esposito et al., 2004)

      Vitamin A

      A study compared plasma vitamin A with physiological nocturnal and stimulated GH secretion in 68 short prepubertal children. Fasting plasma vitamin A correlated with nocturnal GH secretion but not with stimulated GH secretion. Total dietary vitamin A intake was significantly lower in short children with abnormal nocturnal GH secretion than in normal children and in endocrinologically-normal short children. 9 of 12 children with low nocturnal GH secretion and normal stimulated GH peaks who were supplemented with vitamin A 3000 micrograms for 3 months had increased nocturnal GH secretion. (Evain-Brion et al., 1994) (Evain-Brion, 1998)

      References

      Capalbo, D., et al. (2013), ‘Cluster of cardiometabolic risk factors in children with GH deficiency: a prospective, case-control study’, Clin Endocrinol (Oxf), PubMedID: 24372071

      Di Somma, C., et al. (2010), ‘Prevalence of the metabolic syndrome in moderately-severely obese subjects with and without growth hormone deficiency’, J Endocrinol Invest, 33 (3), 171-77. PubMedID: 19794297

      Esposito, V., et al. (2004), ‘Serum homocysteine concentrations in children with growth hormone (GH) deficiency before and after 12 months GH replacement’, Clin Endocrinol (Oxf), 61 (5), 607-11. PubMedID: 15521964

      Evain-Brion, D., et al. (1994), ‘Vitamin A deficiency and nocturnal growth hormone secretion in short children’, Lancet, 343 (8889), 87-88. PubMedID: 7903782

      Evain-Brion, D. (1998), ‘Vitamin A deficiency and growth hormone in children’, Nutrition, 14 (3), 314-16. PubMedID: 9583378

      Gazzaruso, C., et al. (2014), ‘Cardiovascular risk in adult patients with growth hormone (GH) deficiency and following substitution with GH--an update’, J Clin Endocrinol Metab, 99 (1), 18-29. PubMedID: 24217903

      Nishi, Y., et al. (1989), ‘Transient partial growth hormone deficiency due to zinc deficiency’, J Am Coll Nutr, 8 (2), 93-97. PubMedID: 2708733

      Oliveira, C. R., et al. (2012), ‘Insulin sensitivity and beta-cell function in adults with lifetime, untreated isolated growth hormone deficiency’, J Clin Endocrinol Metab, 97 (3), 1013-19. PubMedID: 22170707

      Russell, M., et al. (2009), ‘Relative growth hormone deficiency and cortisol excess are associated with increased cardiovascular risk markers in obese adolescent girls’, J Clin Endocrinol Metab, 94 (8), 2864-71. PubMedID: 19435823

      Chapter 2. Hypopituitarism

      Conventional Lab Tests

      ACTH (Cortrosyn) stimulation test (or morning cortisol and ACTH)

      TSH and T1 (thyroxine)

      FSH, LH and estradiol (female) or testosterone (male)

      GH provocative test

      Prolactin

      Water Deprivation Test (differentiate psychogenic polydipsia from diabetes insipidus and nephrogenic diabetes insipidus)

      Vasopressin Stimulation Test (differentiate central and nephrogenic diabetes insipidus)

      Additional Lab Tests

      C-Reactive Protein (CRP)

      A study investigated whether inflammatory and traditional cardiovascular risk markers are elevated in women with hypopituitarism. Fifty-three women with hypopituitarism and 111 healthy control women were included in this cross-sectional study. IL-6 and CRP levels were higher in women with hypopituitarism than in healthy controls (P < 0.0001 for comparison between groups). In a multivariate model, CRP levels depended on hypopituitarism, body mass index (BMI), and estrogen use. There was an interaction between the effect of BMI and hypopituitarism on CRP levels, such that the importance of hypopituitarism in determining CRP levels disappeared at high BMIs. In a similar multivariate model, IL-6 levels depended on hypopituitarism and BMI. Total cholesterol, the total to HDL cholesterol ratio, and triglycerides were higher in hypopituitary patients, but only triglycerides and the total to HDL cholesterol ratio depended on hypopituitarism when controlling for BMI. There was no significant difference in lipoprotein(a) levels between hypopituitary women and control subjects. However, when controlling for estrogen use, lipoprotein(a) levels showed a trend toward being lower in the hypopituitary group (P = 0.075). In patients with hypopituitarism, CRP correlated negatively with IGF-I (r = -0.35; P = 0.010), total T (r = -0.42; P = 0.0020), and free T (r = -0.30; P = 0.031). Similarly, IL-6 correlated negatively with total T (r = -0.39; P = 0.0040) and androstenedione (r = -0.27; P = 0.048) in hypopituitary patients. In conclusion, hypopituitary women have increased levels of IL-6 and CRP, both of which are inflammatory markers of atherosclerosis. GH deficiency and androgen deficiency may contribute to these findings. Chronic inflammation may contribute to the high cardiovascular risk seen in this population. (Sesmilo et al., 2001)

      Anti-Pituitary Antibodies and IGF-1

      A total of 119 patients with CD (0.9-15.8 years old) attending the inpatient clinic of University Hospital were recruited for the cross-sectional study. Anti-pituitary antibodies (APA) were detected in 50 patients (42.0%), 15 of them with high titer (30%) and 35 with low titer (70%), and in 2 control subjects at low titer (2%) (P<0.001). IGF-1 was higher in patients with negative than with low titer (P=0.02) or high titer APA (P=0.03). Height was more reduced in high-titer APA patients than in the negative ones (P<0.01). Height was positively correlated with IGF-1 (P<0.01) and negatively with chronological age (P=0.001). IGF-1 was positively correlated with BMI (P<0.001). For height prediction the regression analysis showed the rank order 1 for chronological age and 2 for IGF-1. (Delvecchio et al., 2010)

      Digestive Assessments

      Celiac disease

      The status of prolactin in patients with coeliac disease was investigated by obtaining serum samples from 48 patients with active and non-active coeliac disease. These were compared with samples from 20 children with familial Mediterranean fever and 65 normal controls. Serum prolactin in patients with active coeliac disease was significantly higher than in the other groups studied and reference values. Serum prolactin correlated well with the degree of mucosal atrophy and with the serum concentration of antiendomysial antibodies. Prolactin may play a part in immune modulation in the intestinal damage of coeliac disease and serve as a potential marker for disease activity. (Reifen et al., 1997)

      Pituitary regulation of gonadal function was investigated in 39 consecutive men with treated and untreated coeliac disease and in an intestinal disease control group of 19 men with Crohn's disease of similar age and general nutritional status. Basal serum FSH concentration was increased in 10 of the coeliacs (26%) compared to only two of 19 men with Crohn's disease (11%). This abnormality was observed with equal frequency in both treated and untreated coeliacs, and was not associated with oligospermia. Serum LH concentration was increased in eight of 15 untreated coeliacs (53%) with sub-total villous atrophy, an abnormality which unlike the elevation of serum FSH, appears to return towards normal after gluten withdrawal. Serum LH was high in coeliacs despite marked elevation of the free testosterone index. Exaggerated responses of FSH and LH to LHRH were found in 89% and 45% respectively, of coeliacs with sub-total villous atrophy. However, exaggerated responses of LH alone were found more frequently in coeliacs than in men with Crohn's disease (P less than 0.02) and unlike the exaggerated FSH responses, LH responses were closely related to jejunal morphology. Exaggerated responses of FSH and LH in coeliacs were commonly found when basal gonadotrophin concentrations were normal. The occurrence of exaggerated gonadotrophin responses could not be related to plasma concentration of testosterone, dihydrotestosterone, oestradiol or the free testosterone index. Serum prolactin was modestly raised in 25% of untreated and partially treated coeliacs and in the same proportion of men with Crohn's disease. Elevated serum prolactin concentrations never exceeded 809 mU/l and were not associated with impotence or infertility. This study provides further evidence that in men with coeliac disease there is a derangement of pituitary regulation of gonadal function. (Farthing et al., 1983)

      Nutritional Assessments

      Asymmetrical Dimethylarginine (ADMA)

      Plasma from 44 patients with hypopituitarism with (n = 30) and without growth hormone deficiency (GHD) (n = 14) and from 25 age- and sex-matched healthy controls was taken for analysis of L-arginine, ADMA, symmetrical dimethylarginine (SDMA) and clinical parameters. Further plasma from 10 hypopituitary patients was examined before and after treatment with 9 g of oral L-arginine for 14 days. Asymmetrical dimethylarginine was significantly higher in the hypopituitary patients than in the controls (0.63 +/- 0.12 vs. 0.51 +/- 0.15 micromol L(-1); P < 0.005). L-arginine and the L-arginine/ADMA ratios were lower in the subjects with hypopituitarism (53 +/- 18 vs. 90 +/- 29 micromol L(-1) and 87 +/- 31 vs. 185 +/- 59; both P < 0.0001). Symmetrical dimethylarginine was comparable between the patients and the controls. L-arginine and dimethylarginines were associated with 2-h stimulated glucose levels in a glucose tolerance test (r = 0.33; P < 0.05), but not other cardiovascular risk factors. Oral L-arginine supplementation normalized the reduced L-arginine/ADMA ratio in the hypopituitary patients. Asymmetrical dimethylarginine is elevated in patients with hypopituitarism independent of GHD and traditional risk factors. This might contribute to the increased cardiovascular morbidity in hypopituitary patients. (Krzyzanowska et al., 2005)

      References

      Delvecchio, M., et al. (2010), ‘Anti-pituitary antibodies in children with newly diagnosed celiac disease: a novel finding contributing to linear-growth impairment’, Am J Gastroenterol, 105 (3), 691-96. PubMedID: 19904244

      Farthing, M. J., L. H. Rees, and A. M. Dawson (1983), ‘Male gonadal function in coeliac disease: III. Pituitary regulation’, Clin Endocrinol (Oxf), 19 (6), 661-71. PubMedID: 6418418

      Krzyzanowska, K., et al. (2005), ‘Circulating ADMA concentrations are elevated in hypopituitary adults with and without growth hormone deficiency’, Eur J Clin Invest, 35 (3), 208-13. PubMedID: 15733076

      Reifen, R., et al. (1997), ‘Serum prolactin in coeliac disease: a marker for disease activity’, Arch Dis Child, 77 (2), 155-57. PubMedID: 9301358

      Sesmilo, G., et al. (2001), ‘Inflammatory cardiovascular risk markers in women with hypopituitarism’, J Clin Endocrinol Metab, 86 (12), 5774-81. PubMedID: 11739438

      Chapter 3. Obesity

      Conventional Lab Tests

      Total, HDL and LDL cholesterol, Triglycerides

      Liver and Thyroid function tests

      Fasting glucose, hemoglobin A1C (Esposito and Giugliano, 2005) (Lefebvre et al., 1994)

      Diagnostic criteria for metabolic syndrome include three or more of the following.

      Abdominal obesity: A waist/hip ratio >1.0 for men and > 0.8 for women

      Triglycerides > 150 mg/dl

      Low HDL cholesterol:

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