Desquamative inflammatory vaginitis as a manifestation of vitamin D deficiency associated with Crohn disease: case reports and review of the literature.

Desquamative inflammatory vaginitis (DIV) is a chronic disorder associated with yellow vaginal discharge, vulvovaginal burning and pruritus, and dyspareunia. The cause of DIV is unknown; however, infectious, hormonal, and inflammatory etiologies have been proposed. In this series, we observe the association of DIV and vitamin D deficiency by reporting 4 cases of women with DIV and vitamin D deficiency associated with Crohn disease.

Role of calcium metabolism in premenstrual syndrome.

Premenstrual syndrome has been the subject of many myths and misconceptions over the centuries. It is a very common problem affecting millions of young women during their reproductive lives and is characterized by numerous recurrent, cyclical emotional and physical symptoms during the luteal phase of the menstrual cycle. The etiology of this disorder has remained poorly understood until only recently.

Treatment of desquamative inflammatory vaginitis with vitamin D: a case report.

Desquamative inflammatory vaginitis (DIV) is a well-described but poorly understood vaginitis associated with yellow vaginal discharge and vulvovaginal pruritus, burning, and dyspareunia. Although etiologies of an inflammatory, infectious, and hormonal nature have been proposed, response to therapy has been inconsistent and complete resolution of symptoms has been disappointing. We propose that DIV is a mucous membrane manifestation of vitamin D deficiency that results in desquamation of the vaginal epithelium and discharge.

Lower insulin-like growth factor-1 concentrations in women with premenstrual dysphoric disorder.

Objective: Recent evidence suggests that abnormalities in calcium metabolism may be responsible for the luteal phase symptoms in women experiencing premenstrual syndrome. Our objective was to measure the cyclic variations in bone turnover across the menstrual cycle in women with and without luteal phase symptoms consistent with severe premenstrual syndrome or premenstrual dysphoric disorder.

Study Design: We measured the indices of bone metabolism, N-telopeptide, osteocalcin and insulin-like growth factor-1 in women with and without premenstrual dysphoric disorder using a cross-sectional and prospective design.

Differences in free estradiol and sex hormone-binding globulin in women with and without premenstrual dysphoric disorder.

Context: Over the years, different hypotheses involving the ovarian steroid hormones have been proposed to explain the luteal phase occurrence of severe premenstrual syndrome symptoms. Although it had been strongly suspected that differences in the concentrations of the ovarian steroids may underlie the mood and psychological imbalance of this disorder, the evidence for this hypothesis has been inconsistent and remains controversial.

Objective: Our objective was to measure the ovarian steroid hormones across the menstrual cycle in women with and without luteal phase symptoms consistent with premenstrual dysphoric disorder (PMDD).

Cyclical changes in calcium metabolism across the menstrual cycle in women with premenstrual dysphoric disorder.

Context: Alterations in calcium homeostasis have long been associated with affective disorders. Recently, it has been suggested that abnormalities in calcium metabolism may be responsible for some affective and somatic symptoms in women with premenstrual syndrome.

Objective: Our objective was to measure fluctuations and group differences in calcium-regulating hormones across the menstrual cycle in women with and without premenstrual dysphoric disorder (PMDD).

Is premenstrual dysphoric disorder a distinct clinical entity?

Does the evidence now available support the concept of premenstrual dysphoric disorder (PMDD) as a distinct clinical disorder such that the relative safety and efficacy of potential treatment can be evaluated? In a roundtable discussion of this question, a wealth of information was reviewed by a panel of experts. The key characteristics of PMDD, with clear onset and offset of symptoms closely linked to the menstrual cycle and the prominence of symptoms of anger, irritability, and internal tension, were contrasted with those of known mood and anxiety disorders. PMDD displays a distinct clinical picture that, in the absence of treatment, is remarkably stable from cycle to cycle and over time.

Micronutrients and the premenstrual syndrome: the case for calcium.

Premenstrual syndrome afflicts millions of premenopausal women and has been described as one of the most common disorders in women. Research over the past few years suggests that a variety of nutrients may have an important role in the phase related mood and behavioral disturbances of the premenstrual syndrome. There is scientific evidence, at least for a few of these micronutrients, specifically calcium and vitamin D, supporting cyclic fluctuations during the menstrual cycle that may help explain some features of PMS.

Vitamin D and calcium dysregulation in the polycystic ovarian syndrome.

Over the past 30 years, numerous studies in invertebrates and vertebrates have established a role of calcium in oocyte maturation as well as in the resumption and progression of follicular development. Polycystic ovarian syndrome (PCO) is characterized by hyperandrogenic chronic anovulation, theca cell hyperplasia, and arrested follicular development. The aim of this observational study was to determine whether vitamin D and calcium dysregulation contribute to the development of follicular arrest in women with PCO, resulting in reproductive and menstrual dysfunction.

Calcium carbonate and the premenstrual syndrome: effects on premenstrual and menstrual symptoms. Premenstrual Syndrome Study Group.

Objective: Previous reports have suggested that disturbances in calcium regulation may underlie the pathophysiologic characteristics of premenstrual syndrome and that calcium supplementation may be an effective therapeutic approach. To evaluate the effect of calcium carbonate on the luteal and menstrual phases of the menstrual cycle in premenstrual syndrome, a prospective, randomized, double-blind, placebo-controlled, parallel-group, multicenter clinical trial was conducted.

Study Design: Healthy, premenopausal women between the ages of 18 and 45 years were recruited nationally across the United States at 12 outpatient centers and screened for moderate-to-severe, cyclically recurring premenstrual symptoms.

Short-term inhibition of parathyroid hormone secretion by a calcium-receptor agonist in patients with primary hyperparathyroidism.

Background: Surgery is the usual therapy for patients with primary hyperparathyroidism. We investigated the ability of a calcimimetic drug that inhibits parathyroid hormone secretion in vitro to decrease serum parathyroid hormone and calcium concentrations in patients with this disorder.

Methods: We performed a randomized, placebo-controlled study of single oral doses of 4 to 160 mg of the calcium-receptor agonist drug R-568 in 20 postmenopausal women with mild primary hyperparathyroidism.

Calcium-regulating hormones across the menstrual cycle: evidence of a secondary hyperparathyroidism in women with PMS.

Calcium metabolism across one menstrual cycle was studied in 12 healthy, premenopausal women. Seven women had documented premenstrual syndrome (PMS), and five were asymptomatic controls. Fasting blood samples were drawn at six points throughout the ovulatory cycle.

Comparative analysis of three PMS assessment instruments--the identification of premenstrual syndrome with core symptoms.

Premenstrual syndrome (PMS) is a commonly encountered complaint among women. This study compared the PMS Diary (PMSD), which measures core menstrual symptoms (negative affect, water retention, and pain symptoms), with two commonly used self-rating forms, the Menstrual Distress Questionnaire (MDQ) and the Daily Rating Form (DRF). Thirty-seven premenopausal women with documented PMS completed the forms.

Alleviation of migraines with therapeutic vitamin D and calcium.

Two postmenopausal migraineurs who developed frequent and excruciating migraine headaches (one following estrogen replacement therapy and the other following a stroke) were treated with combination vitamin D and calcium. Therapeutic replacement with vitamin D and calcium resulted in a dramatic reduction in the frequency and duration of their migraine headaches.

Vitamin D and calcium in menstrual migraine.

Two premenopausal women with a history of menstrually-related migraines and premenstrual syndrome were treated with a combination of vitamin D and elemental calcium for late luteal phase symptoms. Both cited a major reduction in their headache attacks as well as premenstrual symptomatology within 2 months of therapy. These observations suggest that vitamin D and calcium therapy should be considered in the treatment of migraine headaches.

Premenstrual and menstrual symptom clusters and response to calcium treatment.

Fourteen perimenstrual symptoms were rated daily by 33 women in a randomized, double-blind, crossover trial of calcium supplementation. Factor analysis was performed on these symptoms using 2,413 daily ratings during the luteal and menstrual phases with at least one symptom present. Four factors (negative affect, water retention, food, and pain) accounting for 67 percent of the total variance were extracted.

Calcium supplementation in premenstrual syndrome: a randomized crossover trial.

Objective: To determine the efficacy of calcium supplementation in women with premenstrual syndrome (PMS).

Design: Randomized, double-blind crossover trial.

Setting: Outpatient medical clinic of a large city hospital.

Evaluation of isradipine (PN 200-110) in mild to moderate hypertension.

The efficacy and safety of isradipine (PN 200-110), a new dihydropyridine calcium antagonist, was evaluated in 87 hypertensive patients in a placebo-controlled, double-blind, randomized multicenter trial. After a 3-week single-blind washout phase, isradipine (or matching placebo) was administered for 4 weeks, beginning at 2.5 mg b.