Summary. Twelve patients are described who developed well‐marked micro‐angiopathic haemolytic anaemia in association with metastatic carcinoma. The tumours originated in the stomach in six cases, in the breast in two cases, in the lung in one case and the origin was uncertain in three cases. All 11 tumours studied were found to be mucin‐secreting adenocarcinomas. Ten out of the 12 patients were thrombocytopenic. Fibrinogen metabolism was studied in four patients and in each patient the catabolism of fibrinogen was found to be greatly increased despite normal or near normal plasma fibrinogen levels and an absence of overt fibrinolysis. Fibrin degradation products were demonstrated in the serum of five out of six patients. Hyaline thrombi were seen in the small blood vessels in the kidneys and suprarenals in one patient and in the myocardium in two patients, while changes suggestive of organized thrombi were present in the interlobular arteries of the kidneys in three patients. It is thought likely that the microangiopathic haemolytic anaemia develops secondarily to intravascular coagulation brought about by thromboplastins derived from mucin‐forming tumour cells which have entered blood vessels, and that contact between circulating red cells and tumour emboli within blood vessels may be an additional cause of red‐cell damage.

SUMMARY A study of splenic function in 28 patients with adult coeliac disease showed no significant correlation between the half life of heat-damaged red cells and either the duration of pre-treatment exposure to gluten or the length of time on a gluten free diet. A significant correlation was found between splenic size and duration of treatment; those patients who had been taking a gluten free diet for the longest time had the smallest spleens. Blood films from 11 of these 28 patients taken before treatment with a gluten free diet were compared with those taken between two and 15 years after the start of treatment. There was no tendency for the hyposplenic changes to regress. In the majority, the changes became more prominent despite strict adherence to the gluten free diet. These findings suggest that splenic atrophy in adult coeliac disease is not reversed by treatment with a gluten free diet and is unlikely to be related to the state of the jejunal mucosa or the duration of initial exposure to gluten.Splenic atrophy is now widely recognised as an accompaniment of adult coeliac disease. It has been demonstrated using quantitative techniques such as measuring the half life of heat-damaged red cells and splenic size as defined by area of radioactivity on a rectilinear scan.' The recognition of the changes in red cell morphology characteristic of hyposplenism may first alert the physician to the possibility that the patient has adult coeliac disease.6The mechanism of splenic atrophy is not known. In inflammatory bowel disease, where splenic atrophy may also occur, improvement in splenic function may follow excision of the diseased bowel.7 However, in coeliac disease the small intestinal lesion is presumed to develop in early childhood after weaning onto gluten containing foods. Even if the hyposplenism were related to the mucosal lesion, the factors determining hyposplenism could have been operating long enough to produce irreversible changes by the time a gluten free diet is started in adult life.In this study we have examined the serial changes in red cell morphology which occur when patients with adult coeliac disease are treated with a gluten free diet. In patients already taking a gluten free diet we

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