Bone metabolism and osteopenia in eating disorders.

Bone loss is a potentially debilitating condition in women with eating disorders. Complications may include failure to achieve peak bone mass, increased risk of premature fractures, and inability to reach the height potential. We therefore conducted a comprehensive evaluation of 58 women with anorexia nervosa (AN), bulimia (BUL) and anorexia/bulimia (AB), comparing bone mineral density (BMD) to physical parameters, biochemical indices, and markers for bone formation and resorption. BMDs were significantly lower in patients with AN than in those with AB and BUL, and overt osteopenia was uncommon in AB and BUL. Hypercortisolism was the best laboratory marker to assess the risk of osteopenia in patients with AN. However, there were no associated changes in bone formation or resorption parameters. No direct correlation was found between BMD and body mass index, estrogen deficiency, tubular reabsorption of phosphorus, serum vitamin D, PTH, BGP, or alkaline phosphatase levels. Although the prognosis for complete recovery to normal BMD is poor, treatment of the underlying depressive disorder, improvement in nutrition with increased weight, and spontaneous resumption of menses are associated with restoring bone health.

Osteomalacia and osteitis fibrosa in a man ingesting aluminum hydroxide antacid.

A 53-year-old man with a history of long-term aluminum hydroxide antacid ingestion reported diffuse bone pain and multiple stress fractures over a two-year period. An undecalcified transiliac bone biopsy specimen revealed osteomalacia with osteitis fibrosa; plasma parathyroid hormone and cyclic AMP levels were normal. Following withdrawal of antacids and treatment with calcium and phosphorus, an initially elevated plasma, 1,25-dihydroxyvitamin D level fell to within the normal range, accompanied by decreased bone pain, healed stress fractures, and increased axial bone mineral content as determined by computed tomography of lumbar trabecular bone. Phosphate deprivation and 1,25-dihydroxyvitamin D excess may contribute to the poor mineralization and exaggerated resorption of bone observed in this syndrome. The clinical, biochemical, radiologic, and histologic features of previously reported cases are reviewed. Early recognition of this syndrome is important, since appropriate therapy promotes skeletal remineralization and prevents morbidity.

Pericardial tamponade, a new complication of amyloid heart disease.

With advancing age of the population and with echocardiographic means of diagnosis, amyloid disease of the heart is of increasing clinical interest. Advanced age, restrictive myocardiopathy, arrhythmias, and conduction disorders are familiar features of this disease. A 92 year old man with past history of hemiblock followed by complete heart block and transvenous pacemaker was admitted to the hospital because of increasing fatigue and the abrupt development of dyspnea. Examination revealed paradoxic pulse, markedly elevated central venous pressure, and echocardiographically demonstrated large pericardial effusion. Shortly after admission signs of tamponade developed; 1,000 ml of pericardial fluid was removed with prompt relief of dyspnea dna disappearance of paradoxic pulse and return of central venous pressure to normal. However, dyspnea soon recurred and subsequent hemodynamic measurements indicated increased right ventricular and left ventricular filling pressures. Echocardiography revealed no recurrent effusion or ventricular hypokinesis. Left ventricular ejection fraction by radionuclide ventriculogram was 64 percent. Echocardiography revealed ventricular wall thickening, normal chamber size, and glittering, sparkling myocardial echoes. On postmortem examination, there was extensive myocardial amyloidosis. There was no evidence of constrictive pericarditis or recurrent effusion. The unique aspect of this case was the combined presence of restrictive myocardiopathy and pericardial tamponade. To our knowledge, no previous case of tamponade due to amyloid heart disease had been reported.

Situs inversus and appendicitis.

Two cases of left lower quadrant appendicitis associated with situs inversus totalis are presented. Historic, genetic, and embryologic aspects of situs inversus, as well as recent theories regarding etiology are discussed. The clinical recognition of appendicitis in situs inversus is often difficult because of the unusual location of the appendix and abnormal pain localization. The differentiation of situs inversus totalis and abnormal rotation of the abdominal viscera (situs indeterminus) is important surgically because fixation of the midgut loop may be indicated in patients with situs indeterminus.