Glucose tolerance and plasma insulin levels in subarachnoid haemorrhage.
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Biomedical subjects
Publications and source records attributed to J F Hallpike.
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Two cases of anticonvulsant megaloblastic anaemia are described, showing features of unusual interest. Though both cases were apparently deficient in folic acid, the Figlu tests were negative. One patient had an extremely low serum B(12) concentration apparently associated with defective B(12) absorption due to deficiency of intrinsic factor, and both showed impaired intestinal absorption of D-xylose. There was, however, no evidence of permanent gastro-intestinal dysfunction, and the absorptive defects disappeared completely after treatment with folic acid. Possible reasons for the findings are discussed. It is suggested that absorptive defects produced by the drugs may play some part in initiating anticonvulsant megaloblastic anaemia, and that once deficiencies of haemopoietic factors are established, a vicious circle may be set up owing to the effects of these deficiencies on the gastro-intestinal tract.
Three of five siblings developed a progressive neurological disorder during infancy or early childhood characterized by cerebellar ataxia, choreoathetosis and peripheral neuropathy. Immunological studies revealed a marked selective deficiency of serum IgE in all three affected siblings. There was evidence of chromosomal instability in the three affected siblings and in one of the parents. One of the affected siblings also developed acute lymphoblastic leukaemia. In spite of many resemblances, this syndrome differs from classical or complete ataxia telangiectasia in that oculocutaneous telangiectases were lacking, the serum IgA and alpha-fetoprotein levels in this family were normal, there was no gonadal dysgenesis, and the cytogenetic findings were atypical.