A patient is described who had an inhibitor to coagulation factor XIII associated with serum autoantibodies to certain tissues. The relationship of these abnormal findings to practolol therapy suggests that this was practolol-induced lupus erythematosus. Further investigations delineating the site of action of the inhibitor to factor XIII are reported.

Letters to the Editor do not persist for more than three weeks.4 Likewise, there was no evidence of haemosiderin deposition in the stalk which might be expected after haemorrhage. Stalk enlargement could have been an effect of untreated diabetes insipidus, in which the first case might have expected resolution of the abnormality with treatment. However, the swelling persisted for three months despite adequate treatment of the diabetes insipidus. It is possible that unrecognised injury or infection with ensuing inflammation resulted in the swelling observed initially. It is known that insults to the stalk can lead to reorganisation and proximal enlargement.' We may have observed the resolution ofsuch changes. We conclude that pituitary stalk enlargement may occur in idiopathic cranial diabetes insipidus, persist for months, and eventually disappear. Serial imaging with CT or MRI will exclude progressive infiltrative or neoplastic causes. We thank Michael Liddington, Susan Rae, Barbara Beattie and lain McGinley for assistance in preparing the manuscript.

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SYNOPSIS Fatty acid profiles were determined in platelets of 21 patients suffering from Classical Migraine and these results were compared with those obtained in a control group of 24 healthy individuals. Cholesterol levels and the cholesterol/phospholipid ratios of 4 of the migraine patients were investigated and compared with values obtained from 4 age‐matched control persons. No significant differences could be detected between the fatty acid profiles of the migraine and control groups, Analysis of the cholesterol content and the cholesterol/phospholipid ratio of the platelets revealed no significant differences between the two groups. Freeze‐fracture electron microscopy of the platelet membranes of the two groups revealed no striking differences in the protein distribution and environment in the migraine condition. We conclude that the membranes of platelets of migraine‐suffering and control individuals have a similar composition, the symptoms of this disorder thus being mediated by other differences between the platelets.

Family members heterozygous for the congenitally abnormal fibrinogen designated fibrinogen Manchester, A alpha 16Arg----His, have previously been shown by h.p.l.c. and amino acid analysis to release a variant fibrinopeptide, [His16]fibrinopeptide A, from plasma fibrinogen after the addition of thrombin. The present study was designed to determine if the same abnormal phenotype was also present in the intraplatelet fibrinogen pool. Fresh platelets were washed in buffers containing EDTA until it could be shown that all washable plasma fibrinogen was removed. Normal platelets were then lysed by freezing and thawing to release their intracellular proteins, which were then treated with thrombin. The fibrinopeptides, cleaved from the intraplatelet fibrinogen, could be detected by an optimized h.p.l.c. technique. Quantification of the intraplatelet fibrinogen gave a result (means +/- S.D., n = 5) of 110 +/- 30 and 90 +/- 30 micrograms/10(9) platelets, when determined by h.p.l.c. quantification of fibrinopeptide B content and fibrinogen fragment E radioimmunoassay respectively. Examination of fibrinopeptides released from the platelet fibrinogen from the family with fibrinogen Manchester with the same techniques showed elution peaks in the same positions as both [His16]fibrinopeptide A and normal fibrinopeptide A. The identity of these peaks was further substantiated by analysis of the h.p.l.c. peaks by using specific radioimmunoassay to fibrinopeptide A. Our results therefore demonstrate that platelet fibrinogen expresses the heterozygous A alpha 16His phenotype. This supports the view that the A alpha chains of platelet and plasma fibrinogen are produced from a single genetic locus.