451permission to include their patients in the study, Mr A Lawton for statistical advice, and the staff of the medical photography department for preparing the illustration. ReferencesRowan RM, Fraser Failure of bromocriptine to maintain reduction in size of a macroprolactinoma HARALD D BREIDAHL, DUNCAN J TOPLISS, JOHN W PIKE Abstract A patient with a macroprolactinoma was treated with bromocriptine 15 mg daily. Both the size of the tumour as shown by computed tomography and the serum prolactin concentration decreased over several months but then increased. The dose of bromocriptine was increased to 40 mg daily but tumour growth continued, and the tumour was resected. Production of prolactin by cultured cells was not inhibited by high concentrations of bromocriptine, suggesting that regrowth of the tumour was due to cells resistant to dopamine agonist action. This case of regrowth of a prolactinoma during bromocriptine treatment after an initial reduction in size indicates the need for close surveillance especially of patients whose serum prolactin concentration fails to fall into the normal range with bromocriptine treatment.

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A 34-year-old woman with longstanding untreated thyroprivic hypothyroidism and pituitary enlargement is reported here in whom visual failure coincided with thyroid hormone replacement. Visual fields were normal after 30 years untreated hypothyroidism, but severe concentric field constriction developed during the first 6 months of therapy and was relieved by hypophysectomy. Plasma TSH and prolactin remained elevated during 10 months replacement therapy, but both were suppressed by preoperative hyperreplacement with T3 and T4. The paradoxical pressure symptoms suggest imbalance between pituitary TSH content and TSH release during treatment with thyroid hormone; a finding previously reported in animal studies. This sequence suggests that patients with known pituitary enlargement secondary to thyroid hypofunction should be observed for pressure symptoms during thyroid hormone treatment.

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The purpose of this communication is to describe our experiences in the clinical management of sixty diabetic patients who have been treated with chlorpropamide for periods varying from a few weeks to six months. In addition, the results of some comparative experiments on the action of tolbutamide and chlorpropamide ilz vitro are given. These suggest that the mode of action of the two drugs upon hepatic enzyme systems is similar, but there seems to be a quantitative difference between them.Clinical observations have been made on sixty adult diabetic patients: twenty-one males and thirty-nine females. In view of earlier experiences with tolbutamide and carbutamide, no attempt has been made to treat any juvenile patient; with few exceptions, the persons included in this series have been middle-aged or elderly. Within these limits a random selection has heen made from patients attending the routine practice of the diabetic service of this hospital.In contrast with earlier clinical trials conducted in the Diabetic and Metabolic Unit of the Alfred Hospital,', many of the patients in this series were not admitted to hospital for continuous observation. I t was felt that experience gained during the past three years was sufficient to enable us to assess the efficacy of chlorpropamide without the need for hospitalization. In consequence, a number of patients were instructed to present the results of urine tests taken a t regular times each day, and spot blood sugar estimations were made at frequent intervals. Subsequent interrogation enabled us to detect the incidence of side effects and the degree of control achieved. A significant number of patients were closely observed, and laboratory investigations were undertaken for evidence of hepatic, renal, and hematological abnormalities. Patients transferred from maintenance doses of insulin were instructed to report daily either in person or by telephone and to present the results of urinalyses performed four times each day.Almost without exception the loading dosage prescribed was 1.0 gm. per day and the maintenance dose 0.5 gm. per day, given in divided doses of 0.25 gm. morning and evening. I n any case that failed to respond, the dosage was raised gradually to 0.75 gm. per day and, in a few instances, to 1.5 gm. per day. Dosage for 1 case was raised to 3 gm. per day for a short time. FIGURE 1 shows the duration of treatment of the patients considered in this series and indicates the number responding to treatment and the number failing to do so. The relatively large number not responding within the first 4 weeks of treatment can be related to several such factors as inappropriate selection of patients, and attempts to transfer cases from insulin therapy. TABLE 1 shows the distribution of the patients by age and sex 810