RESUMEN

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. We further show that the DIV symptoms resolve when the circulating concentrations of 25-hydroxyvitamin D (25-HD) returned to normal. These data provide further support for the notion that DIV can be associated with vitamin D deficiency and DIV symptoms reflect altered vaginal mucous membrane function.

Asunto(s)

RESUMEN

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. Moreover, we suggest that the loss of this epithelium leads to altered vaginal pH levels, mucous membrane fragility, inflammation, and secondary infection. Because vitamin D is a known transcriptional activator, we suggest that vitamin D is necessary for the synthesis of specific vaginal structural proteins, such as cytokeratins. Vitamin D deficiency results in decreased amounts of these proteins, resulting in loss of epithelial structural integrity and desquamation. Correction of the vitamin D deficiency ultimately leads to regeneration of the vaginal epithelium and cessation of desquamation.

Asunto(s)

RESUMEN

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. Participating women underwent 2 months of self-assessment symptom screening and 1 month of hormonal evaluation. RESULTS: Overall serum insulin-like growth factor-1 (mean +/- standard deviation) was significantly lower in the premenstrual dysphoric disorder group compared with controls (205.7 +/- 56.8 vs 240.2 +/- 76.9 ng/ mL, P = .01) and was significantly lower throughout all 5 phases of the menstrual cycle in the premenstrual dysphoric disorder group compared with controls. In both groups of women, serum insulin-like growth factor-1 concentrations were highest and urinary N-telopeptide levels were lowest during the luteal phase. Bone remodeling indices of formation and resorption during the menstrual cycle were greater and appeared earlier in the control compared with the premenstrual dysphoric disorder group. CONCLUSION: Significantly lower insulin-like growth factor-1 concentrations in premenstrual dysphoric disorder subjects compared with controls may hold insights about how premenstrual dysphoric disorder subjects differ from asymptomatic controls.

Asunto(s)

RESUMEN

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). DESIGN: We measured estradiol (E2), progesterone, and SHBG in women with and without PMDD using a cross-sectional and prospective experimental design. Participating women underwent 2-month self-assessment symptom screening and 1-month hormonal evaluation. RESULTS: Overall means for LH, progesterone, E2, peak E2, and free E2 were not different between groups. Across the menstrual cycle, overall percent free E2 was significantly lower and SHBG significantly greater in the PMDD group compared with controls (1.39 +/- 0.26 vs. 1.50 +/- 0.28, P = 0.03; 61.4 +/- 25.1 vs. 52.4 +/- 21.3 nmol/liter, P = 0.046, respectively). During the luteal phase, free E2 was significantly lower in the PMDD group compared with controls (PMDD 7.6 +/- 7.0 vs. controls 8.9 +/- 8.4 pmol/liter; P = 0.032). For both follicular and luteal phases, SHBG was significantly higher in the PMDD group (follicular phase 60.5 +/- 31.7 vs. 51.4 +/- 38.2 nmol/liter, P = 0.047; luteal phase 65.1 +/- 32.3 vs. 55.1 +/- 38.9 nmol/liter, P =0.03). In both groups, SHBG significantly increased from the follicular to luteal phase. CONCLUSION: Luteal phase concentrations of free E2, percent free E2, and SHBG differ significantly between women with and without PMDD.

Asunto(s)

RESUMEN

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. Alterations in calcium homeostasis have long been associated with many affective disorders. Cyclical fluctuations of the ovarian steroid hormones across the menstrual cycle influence calcium metabolism, affect intestinal calcium absorption and modulate 1,25-dihydroxyvitamin D synthesis. Evidence now strongly suggests that abnormalities in calcium and vitamin D metabolism, specifically calcium and vitamin D deficiency, are responsible for these luteal-phase symptoms. Calcium and vitamin D supplementation may offer a simple solution to millions of women affected with premenstrual syndrome.

RESUMEN

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). DESIGN: We conducted a cross-sectional and prospective study of women with and without PMDD. Participating women underwent 2 months of self-assessment symptom screening and 1 month of hormonal evaluation. RESULTS: Calcium-regulating hormones varied significantly across the menstrual cycle in both groups. Total serum, ionized and urine calcium, pH, intact PTH, and 1,25-dihydroxyvitamin D [1,25(OH)(2)D] varied significantly over the menstrual cycle. The PMDD group, when compared with controls, had significantly lower ionized calcium at phase 1 (menses) (1.166 +/- 0.072 vs. 1.182 +/- 0.087 mmol/liter; P = 0.027), significantly lower urine calcium excretion at three of the five phases (late follicular phase 2, midcycle phase 3, and early luteal phase 4), and significantly lower 1,25(OH)(2)D at luteal phase 4 (45.0 +/- 27.5 vs. 50.6 +/- 33.8 pg/ml; P = 0.032). CONCLUSIONS: Cyclical fluctuations of the calcium-regulating hormones may help us better understand some of the psychological and somatic features of PMDD. The lack of responsiveness in vitamin D metabolism resulting in a decline in 1,25(OH)(2)D during the luteal phase of the menstrual cycle may serve as the biological trigger for the classical features of PMDD.

Asunto(s)