Feminizing adrenal tumors (FAT) are extremely rare tumors prevailing in males. Clinical manifestations are gynecomastia and/or other hypogonadism features in adults. They are rarer in pediatric population and their main manifestation is peripheral sexual precocity.In women genital bleeding, uterus hypertrophy, high blood pressure and/or abdomen mass may be the only manifestations.On the biological point, estrogen overproduction with or without increase in other adrenal hormones are the main abnormalities. Radiological examination usually shows the tumor, describes its limits and its eventual metastases. Adrenal and endocrine origins are confirmed by biochemical assessments and histology, but that one is unable to distinguish between benign and malignant tumors, except if metastases are already present. Immunostaining using anti-aromatase antibodies is the only tool that distinguishes FAT from other adrenocortical tumors. Abdominal surgery is the best and the first line treatment. For large tumors (≥10 cm), an open access is preferred to coeliosurgery, but for the small ones, or when the surgeon is experienced, endoscopic surgery seems to give excellent results. Surgery can be preceded by adrenolytic agents such as ortho paraprime dichloro diphenyl dichloroethane (Mitotane), ketoconazole or by aromatase inhibitors, but till now there is not any controlled study to compare the benefit of different drugs. New anti-estrogens can be used too, but their results need to be confirmed in malignant tumors resistant to classical chemotherapy and to conventional radiotherapy. Targeted therapy can be used too, as in other adrenocortical tumors, but the results need to be confirmed.

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Feminizing adrenal tumors (FATs) are very rare as they account for less than 2% of all the adrenal neoplasms. Their prognosis is deemed to be very poor. We aimed to present a mono centre (adult and pediatric) experience over a long period of time (January 1980 to Jun 2012). During the study period, we observed only three cases in men aged 22 (2 cases) and 45 (1 case). They all consulted for a painful gynecomastia, decreased libido and impotency. Estradiol was high in two cases at presentation, and after a relapsing tumor in the third one. All had big adrenal tumors (5.9, 6, and 17 cm), and a mixed secretion composed by high estradiol and cortisol. The pathological study argued for malignancy in two cases. But, only one had diffuse metastasis and died 4 years after diagnosis; the others diagnosed one and three years ago are still alive without any metastasis or relapsing.

Vitamin D deficiency is a major public health issue affecting large proportions of the population. Therefore, maternal vitamin D deficiency is not uncommon. Infants born to mothers who are deficient in vitamin D are at risk of developing vitamin D deficiency and hypocalcaemia. We reported here a case of neonatal hypocalcaemic seizures secondary to vitamin D deficiency. A 25-day old, full term male infant presented two episodes of generalized seizures. Laboratory investigations in blood, revealed low calcium level at 5.5 mg/dl, elevated phosphatemia level at 9.6 mg/dl and high parathormone (PTH) level at 133.4 pg/ml. Unfortunately 25 hydroxy vitamin D assay was not available in the infant but it was low in the mother at 12.9 ng/ml. The infant was commenced on vitamin D and calcium supplements during some weeks which allowed normalization of calcium levels. After several months of treatment cessation, the infant was doing well, and his development was according to his chronological age. His calcium, phosphatemia and PTH levels were within normal ranges without any treatment. Hypocalcemia in this infant was presumably due to vitamin D deficiency as other causes were unlikely. Neonatal hypocalcaemic seizures are a rare presentation of vitamin D deficiency. This case could have been preventable had the mother been given vitamin D supplementation during pregnancy and early lactation.

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