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?:abstract
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Thirty two children and adolescents from 14 to 20 years of age, suffering from hepatosplenic schistosomiasis mansoni and bleeding esophageal varicose veins, were evaluated for bone mineral density (BMD), before undergoing medical and surgical treatment. The surgical protocol was splenectomy, autoimplantation of spleen tissue into a pouch of the major omentum and ligature of the left gastric vein. Follow up of these patients ranges from one to ten years with a mean of five years. The BMD was measured at the lumbar spine (L2 - L4) through the dual energy absorptionmetry X-ray (DEXA), using a LUNAR DPX-L densitometer. The degree of Symmers´ fibrosis was assessed by semiautomatic hystomorphometry. In eleven patients, the serum magnesium was measured before an intravenous overload of this ion and subsequently after eight and twenty four hours. Urine was collected 24 hours before and 24 hours after the magnesium overload. Deficiency of magnesium was considered when the uptake of this ion was greater than 40%. There was a significant trend of association between the status of bone mineral content and the Symmers´ fibrosis degree (c² = 6.606 R = 0.01017). There was also a moderate agreement between the greater fibrosis densities ( > the mean percentage) and bone mineral deficits. Although the normal bone mineral content was more found among the patients with better hepatic functional reserve, the results did not reach statistical significance. There was a marked magnesium retention (>95%) in one patient who had severe osteoporosis and a slight depletion ( 5%) in another patient, who presented no bone mineral deficit. It was concluded that the patients included in this series, showed an important BMD deficit, specially among the females which has had a significant improvement after medical and surgical treatment. Bone mineral deficit was associated with the degree of Symmers´ fibrosis. Magnesium depletion was present in two out of eleven patients. It is speculated that magnesium supplementation may be warranted to forestall the progression of bone mineral deficit in patients with more impaired hepatic functional reserve.
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