case of persistent urogenital sinus: pitfalls and challenges in diagnosis

Persistent urogenital sinus [PUGS] is a rare anomaly whereby the urinary and genital tracts fail to separate during embryonic development. We report a three-year-old female child who was referred to the Sabah Women and Children Hospital, Sabah, Malaysia, in 2016 with a pelvic mass. She had been born prematurely at 36 gestational weeks via spontaneous vaginal delivery in 2013 and initially misdiagnosed with neurogenic bladder dysfunction. The external genitalia appeared normal and an initial sonogram and repeat micturating cystourethrograms did not indicate any urogenital anomalies. She therefore underwent clean intermittent catheterisation. Three years later, the diagnosis was corrected following the investigation of a persistent cystic mass posterior to the bladder. At this time, a clinical examination of the perineum showed a single opening into the introitus. Magnetic resonance imaging of the pelvis revealed gross hydrocolpos and a genitogram confirmed a diagnosis of PUGS, for which the patient underwent surgical separation of the urinary and genital tracts

Histomorphometric changes in the perirenal adipocytes of adrenalectomized rats treated with dexamethasone

INTRODUCTION: Prolonged steroid treatment administered to any patient can cause visceral obesity, which is associated with metabolic disease and Cushing's syndrome. Glucocorticoids have a profound negative effect on adipose tissue mass, giving rise to obesity, which in turn is regulated by the 11β-hydroxysteroid dehydrogenase type 1 enzyme. Adrenalectomized rats treated with dexamethasone exhibited an increase in visceral fat deposition but not in body weight. OBJECTIVES: The main aim of this study was to determine the effect of dexamethasone on the histomorphometric characteristics of perirenal adipocytes of adrenalectomized, dexamethasone-treated rats (ADR+Dexa) and the association of dexamethasone treatment with the expression and activity of 11 β-hydroxysteroid dehydrogenase type 1 (11 β-hydroxysteroid dehydrogenase type 1). METHODS: A total of 20 male Sprague Dawley rats were divided into 3 groups: a baseline control group (n = 6), a sham-operated group (n = 7) and an adrenalectomized group (n=7). The adrenalectomized group was given intramuscular dexamethasone (ADR+Dexa) 2 weeks post adrenalectomy, and the rats from the sham-operated group were administered intramuscular vehicle (olive oil). RESULTS: Treatment with 120 μg/kg intramuscular dexamethasone for 8 weeks resulted in a significant decrease in the diameter of the perirenal adipocytes (p<0.05) and a significant increase in the number of perirenal adipocytes (p<0.05). There was minimal weight gain but pronounced fat deposition in the dexamethasone-treated rats. These changes in the perirenal adipocytes were associated with high expression and dehydrogenase activity of 11β-hydroxysteroid dehydrogenase type 1. CONCLUSIONS: In conclusion, dexamethasone increased the deposition of perirenal fat by hyperplasia, which causes increases in the expression and dehydrogenase activity of 11 β-hydroxysteroid dehydrogenase type 1 in adrenalectomized rats.