Successful removal of single metastasis in recurrent parathyroid carcinoma.
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Biomedical subjects
Publications and source records attributed to C E Dent.
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A 23-year-old woman presented with an 11-year history of peripheral joint pains and stiffness slowly progressing to the development of gross calcinosis circumscripta. She had no definite evidence of systemic scleroderma. She was first treated for one year with frequent intravenous sodium EDTA, which increased urinary calcium and enhanced negative calcium balance but did not lessen her calcinosis. She was then treated with probenecid up to 2 g daily and her calcinosis lessened steadily over three years. Plasma levels of both phosphorus and urate fell during this time.
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Five patients suffering from alpha chain disease are described. Clinically the patients presented with clubbing and the symptoms of malabsorption. There was a characteristic, predominantly plasma cell infiltrate of the wall of the small intestine. Spread of the plasmacytosis beyond the small intestine to bone marrow (1), peripheral blood (1), and probably the nasopharyngeal lymphoid tissue (1) is described. Fragments of the heavy chain of IgA (alpha chain) were found in serum (5), urine (3), jejunal fluid (2), and saliva (1). The jejunal biopsy of one patient was shown to synthesize free alpha chain in tissue culture. A new and simple immunoselection technique for the identification of free alpha chain is described. Marked clinical remissions were achieved in two patients treated with intermittent cytotoxic and steroid therapy, and in a third patient who received intermittent cytotoxic therapy and tetracycline.
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Further causes of rickets or osteomalacia need to be added to the list previously published by the author. These include phosphate deficiency osteomalacia from prolonged consumption of aluminum hydroxide, rickets and osteomalacia from prolonged therapy by antiepileptic drugs, rickets associated with the severe form of osteopetrosis, further rare causes of the Fanconi syndrome, congenital rickets occurring when the mother has osteomalacia from dietary causes or has celiac disease and temporary neonatal rickets probably due to enzymic immaturity. The importance is stressed of defining as closely as possible the type of rickets or osteomalacia one is dealing with, especially when considering therapy and detailed pathogenesis.
The investigation and treatment of osteomalacia are described in four patients with epilepsy treated with long-term anticonvulsant therapy. It is suggested that drug-mediated enzyme induction may be the mechanism responsible by causing a greatly increased inactivation of vitamin D in these patients.
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