Effect of Vitamin D in a Patient With Classical Adrenal Hyperplasia due to 11-Hydroxylase Deficiency

Thomas, D. S.

doi:10.4021/jmc1352w

Cited by 6 publications

(4 citation statements)

References 64 publications

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“…There is now considerable evidence that Vitamin D is an insulin sensitizer [28]. We recently reported a patient with T2DM, classical 11-hydroxylase deficiency, and severe Vitamin D deficiency [29].…”

Section: Contemporary Gynecologic Practicementioning

confidence: 98%

Treatment of Congenital Adrenal Hyperplasia by ReducingInsulin Resistance and Cysticercosis Induced Polycystic Ovarian Syndrome

Sacerdote¹,

Bahtiyar²

2015

Contemporary Gynecologic Practice

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Among the most common causes of female infertility, anovulation, menstrual irregularity, hirsutism, acne, and alopecia are congenital adrenal hyperplasia (CAH) and polycystic ovarian syndrome (PCOS). These two conditions resemble one another quite a bit, especially the nonclassic forms of CAH (NCAH). Another common cause of such problems is hyperprolactinemia, which results in increased androgen synthesis by both the ovaries and the adrenal cortex, while suppressing gonadotrophin-releasing hormone, gonadotrophin, and estrogen synthesis. Hyperprolactinemia, in turn, may be caused by primary hypothyroidism, prolactinomas, stalk effects of other pituitary and hypothalamic neoplasia, as well as a host of prescription and recreational drugs; it may also be idiopathic. Other, less frequently encountered causes of these problems include Cushing's syndrome and virilizing tumors (ovarian, adrenal, or ectopic). A growing worldwide problem in this sphere is androgen doping to improve athletic performance. Additional causes of menstrual irregularity include uterine leiomyomata, puberty, perimenopause, chronic illnesses eg. poorly controlled diabetes mellitus and sickle cell disease, elite athletics and dancing, eating disorders, endometriosis, and Asherman's syndrome. Infertility may also be caused by stress, tubal factors, Asherman's syndrome, immune response to spermatozoa, luteal phase inadequacy, and male factors. In this chapter we shall focus on 3 novel concepts: • The treatment of the congenital adrenal hyperplasias and the acquired/unmasked adrenal hyperplasias by interventions which reduce insulin resistance.

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Section: Contemporary Gynecologic Practicementioning

confidence: 98%

Treatment of Congenital Adrenal Hyperplasia by ReducingInsulin Resistance and Cysticercosis Induced Polycystic Ovarian Syndrome

Sacerdote¹,

Bahtiyar²

2015

Contemporary Gynecologic Practice

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“…Thus, the magnitude of the increase in bioavailable 25-OHD level may be greater than the magnitude of the increase in total 25-OHD. Our previously published experience with Vitamin D repletion in a patient with another form of congenital adrenal hyperplasia, classic 11-hydroxylase deficiency [11] in whom a modest increase in serum 25-OHD was associated with a dramatic drop in serum 11-deoxycortisol led us to somewhat expect that in the current patient, as well, modest increase in serum 25-OHD would be associated with a dramatic fall in 17-OHP.…”

Section: Discussionmentioning

confidence: 85%

Association of Vitamin D Repletion with Normalization of Elevated Serum 17-OH-Progesterone

Fenteany¹,

Inoue²,

Bahtiyar³

et al. 2017

Med Case Rep

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Insulin resistance is associated with a number of conditions, such as non-classic 21-hydroxylase deficiency and allied disorders. Serum vitamin D is often deficient/ insufficient in insulin resistant individuals. Disorders associated with insulin resistance are often mitigated in association with vitamin D repletion. Here we report a patient with type 2 diabetes mellitus, lower extremity infection, vitamin D insufficiency, and elevated unstimulated serum 17-OH-progesterone (17-OHP), which normalized during vitamin D repletion. Serum 25-OHvitamin D (25-OHD) rose by 32% while serum 17-OHP fell by 87% over the course of four weeks receiving 50,000 IU ergocalciferol orally weekly. Vitamin D repletion in this setting restored normal serum 25-OHD levels and was associated with normalization of elevated serum 17-OHP. Serum 25-OHD levels should be determined before commencing glucocorticoids or mineralocorticoids for the treatment of elevated serum 17-OHP in disorders like non-classic adrenal hyperplasia (NCAH) and levels of 17-OHP, should be re-measured when vitamin D levels are replete to determine whether glucocorticoid/ mineralocorticoid replacement is actually necessary.

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“…Researchers have been studying the effect of 25(OH)D3 status on Insulin resistance (IR) for years [27]. CAH patients, compared with normal individuals with the same BMI, are more prone for the development of IR and greater insulin levels.…”

Section: Discussionmentioning

confidence: 99%

Effect of Vitamin D Supplementation on Insulin Resistance Status in Pubertal Girls with Congenital Adrenal Hyperplasia

Abdou

Hassan

Elatti

et al. 2022

Open Access Maced J Med Sci

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Introduction: Congenital adrenal hyperplasia (CAH) patients especially females are at increased risk for developing obesity and resistance to insulin (IR). Rising evidence indicate that insufficient vitamin D levels are associated with impaired function of β-cells of islets of Langerhans and IR, however, this finding hasn’t been investigated in patients with CAH. The aim was to identify the vitamin D levels and insulin resistance status in pubertal females with CAH, following up at Diabetes Endocrine and Metabolism Pediatric Unit, Abou ElRish Children’s Hospital, Cairo University. We also examined the association between vitamin D level & insulin resistance and the impact of cholecalciferol administration on metabolic abnormalities. Subjects and Methods: Sixteen pubertal CAH females with deficient or insufficient Vitamin D levels were recruited. Follow up was done after a period of 6 months during which oral Vitamin D replacement therapy was prescribed. Results: The serum levels of 25-hydroxyvitamin D (25(OH)D3) were significantly raised following replacement therapy. Significant correlation was detected between HOMA-IR and serum levels of insulin, other IR indices both prior to and following vitamin D supplementation. However, HOMA-IR didn’t correlate with any of the following: 25(OH)D3 levels, 17 hydroxyprogesterone (17-OHP), or steroid dose either prior to or following replacement therapy. Conclusion: Vitamin D replacement therapy didn’t have favorable effects on IR in females with CAH. Future research using randomized controlled trials is required to examine the impact of Vitamin D on IR. This might influence the production of adrenal androgen, resulting in reduction of the therapeutic effect of glucocorticoids and evolution of metabolic derangements.

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Effect of Vitamin D in a Patient With Classical Adrenal Hyperplasia due to 11-Hydroxylase Deficiency

Cited by 6 publications

References 64 publications

Treatment of Congenital Adrenal Hyperplasia by ReducingInsulin Resistance and Cysticercosis Induced Polycystic Ovarian Syndrome

Treatment of Congenital Adrenal Hyperplasia by ReducingInsulin Resistance and Cysticercosis Induced Polycystic Ovarian Syndrome

Association of Vitamin D Repletion with Normalization of Elevated Serum 17-OH-Progesterone

Effect of Vitamin D Supplementation on Insulin Resistance Status in Pubertal Girls with Congenital Adrenal Hyperplasia

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