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245attacks. Oestrogens may increase the plasma concentrations of some of the coagulation factors with shortening of the prothrombin time. Toy et al2 found this effect with synthetic oestrogens but not with "natural" oestrogen (oestriol succinate). Thus it is improbable that this mechanism was responsible for thromboembolic episodes in our patient. The oestrogen preparation she was taking was a naturally occurring one (conjugated equine oestrogen), and the patient's prothrombin times remained within the therapeutic range, at levels similar to those maintained in the past without embolic symptoms.An increase in platelet adhesiveness, which can be shown during oestrogen therapy,3 was probably responsible for the appearance of embolic phenomena in our patient. The importance of platelets in the genesis of emboli from prosthetic heart valves is further illustrated by reports that patients being treated with dipyridamole in addition to oral anticoagulants derive greater protection from nonfatal thromboembolism than those taking anticoagulants alone.4In an extensive review of reports on oestrogen treatment in postmenopausal women, Shoemaker et a15 concluded that there was no proved risk of thromboembolic disease on such treatment. While this may be true for most women, it does not necessarily apply in those with an additional predisposing factor, such as a prosthetic heart valve. Our case illustrates the potential risks of oestrogen therapy in patients with valve prostheses. Anticoagulation with warfarin or phenindione alone should not be considered to protect these patients adequately against thromboembolic complications of oestrogen treatment. Non-essential oestrogen administration should be avoided in all patients with prosthetic heart valves.We are grateful to Dr J P Lee-Potter for providing haematological data, and to Mrs B Davies for her help in preparing this paper. Case reportsCase 1-A 30-year-old Caucasian housewife presented with a three-week history of blurring of vision of the left eye, two weeks' morning nausea and vomiting, and three days' haematuria. She had no history of hypertension and was taking no medication. She smoked five cigarettes daily. She had a sinus tachycardia of 124/min, blood pressure of 270/175 mm Hg, and clinical and electrocardiographic features of left ventricular hypertrophy. Fundoscopy showed grade IV hypertensive retinopathy, and visual acuity was decreased in the left eye. After admission to hospital she received methyldopa 500 mg by mouth six-hourly (figure). The next day she was confused and drowsy but there were no new focal neurological signs. Methyldopa was withdrawn and propranolol 80 mg eight-hourly and Moduretic two tablets daily given. Thirty-six hours after admission her conscious level was normal but she complained of total loss of vision and hallucinations. The pupils were bilaterally dilated and unresponsive to light. Fundal appearances were unchanged. Dexamethasone 4 mg six-hourly was given from the fourth day without measurable benefit. The only other neurological...

SUMMARY. The referral of a patient with features of Cushing's syndrome but with suppressed plasma cortisol and adrenocorticotrophic hormone concentrations prompted us to study the effect of medroxyprogesterone acetate (MPA) therapy on the adrenal axis. II women (aged 54--82 years) who were receiving 200-400 mgj day MPA were studied. Of these, four had subnormal plasma cortisol responses to a short synacthen test, and two more had borderline responses (30 min post-synacthen plasma cortisol results of 411 and 511 nmol/L), We conclude that suppression of the adrenal axis occurs relatively frequently in patients on MPA and that such patients should be checked for evidence of suppression before MPA therapy is withdrawn.

index of an increase in circulating adrenal oxysteroids.' Depression of eosinophil concentrations has been shown in response to surgery,2 trauma,3 exercise,4 and emotional stress.4 The low eosinophil counts found in acute severe asthma are compatible with a stress response related to the higher cortisol concentrations.5 The authors' argument that eosinophilia has a beneficial effect in chronic asthma while eosinopenia allows the development of acute asthma might lead one to expect that corticosteroids would produce an exacerbation of chronic asthma in association with their action of decreasing eosinophil counts. Yet even the authors agree that corticosteroids are beneficial in chronic asthma, and the recent controlled trial of Fanta et a16 also shows their importance in the treatment of acute asthma.

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