1 The effects of oral doses of pindolol (15 mg), metoprolol (200 mg) and propranolol (160 mg) on the response to insulin-induced hypoglycaemia and an oral glucose load were investigated. 2 Serum insulin and serum C-peptide secretion in response to a glucose load were inhibited (2P<0.01) by metoprolol and propranolol but not by pindolol. 3 During hypoglycaemia metoprolol and propranolol inhibited the clearance of insulin (2P<0.01) and caused a delay of glucose nadirs. 4 Adrenaline secretion during hypoglycaemia was markedly increased by metoprolol and propranolol but not by pindolol. 5 The counterregulatory response of growth hormone, ACTH and cortisol was increased following metoprolol and propranolol but not after pindolol. 6 The hypoglycaemic symptoms and signs showed a prevalence of sweating and prolonged changes in skin conductivity whereas palpitations were not observed during P-adrenoceptor blockade.Asymptomatic hypoglycaemia did not occur. 7 The absence of unphysiological rises in adrenaline, growth hormone, ACTH and cortisol supports the use of a P-adrenoceptor blocker with intrinsic sympathomimetic activity.

In order to collect data on (1) the prevalence of lactose malabsorption and (2) the value of indirect diagnostic methods for hypolactasia in diabetics, we compared lactose tolerance tests using serum glucose, serum galactose (after oral ethanol intake) and breath hydrogen excretion as diagnostic cutoff in 144 nondiabetic and 46 diabetic subjects. A good rate of concordance was found for the hydrogen breath test and galactose-dependent lactose tolerance test. The glucose-dependent lactose tolerance test was found to be of satisfactory diagnostic value in nondiabetic subjects and was useless for diagnostic purposes in diabetics. Lactose malabsorption was no more frequent in diabetics than in controls and lactose intolerance was found to be less frequent in the diabetic group. A distinction between hypolactasia and other gastrointestinal disorders in diabetics is possible by ambulatory indirect tests.

Intense immunosuppressive therapy is used frequently for treatment of systemic vasculitides, collagenoses, rapidly progressive glomerulonephritis, and after organ transplantation. Numerous serious treatment-related side effects include localized or disseminated opportunistic infections, and require careful monitoring of immunosuppressed patients. Gastrointestinal infections with Mycobacterium avium complex (MAC) or other nontuberculous mycobacteria have been previously identified in HIV seropositive patients only. We now report the first case of an HIV seronegative patient who received immunosuppressive therapy for rapidly progressive glomerulonephritis. The patient presented with severe lower gastrointestinal bleeding and was diagnosed to have ulcerative colitis due to infection with MAC. The patient recovered promptly after administration of antimycobacterial therapy. MAC infection should be included in the differential diagnosis of gastrointestinal bleeding in all immunodeficient patients. The significance of repeated colonoscopy to obtain multiple biopsy specimens with histological examination for foam cells and specific staining for acid-fast organisms is emphasized.