Interstitial nephritis, thrombocytopenia, hepatitis, and elevated serum amylase levels in a patient receiving clarithromycin therapy.
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Biomedical subjects
Publications and source records attributed to P Baylor.
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The diffusing capacity for carbon monoxide is partially dependent on lung volume at which it is measured. As a consequence, the diffusing capacity for carbon monoxide is often indexed to the simultaneously measured lung volume (VA), giving rise to the term DL/VA. This reflects the diffusing capacity of carbon monoxide per unit area of lung parenchyma. The authors investigated the pulmonary function of 18 patients who had an elevated DL/VA in order to identify factors that could account for this abnormality. Sixteen of the 18 had a reduction in vital capacity. The vital capacity was reduced because of obesity, pleural disease, and diaphragmatic dysfunction. Eight of nine patients with a body mass index > 30 kg/m2 had a reduction in vital capacity. On the basis of these findings, we believe that an elevated DL/VA should alert the physician to the possibility of 1) an increase in pulmonary capillary blood volume (Vc) (obesity, polycythemia, negative pleural pressure), and 2) reduced VA that does not directly affect the pulmonary capillary bed (pleural disease, neuromuscular disease).
OBJECTIVE: To assess the plasma arterial catecholamine response to nocturnal desaturation in a group of patients with a history suggestive of sleep apnea. PATIENTS AND METHODS: At a Veterans Affairs hospital, 10 patients who had a history consistent with sleep apnea syndrome were involved in the study. Arterial plasma catecholamines were measured at varying intervals during a 5 1/2-hour sleep study. Eighteen samples per patient were analyzed. RESULTS: As the hemoglobin saturation decreased, the variability in plasma norepinephrine increased significantly (r = -.78, P = 0.004). As the hemoglobin saturation fell, there was a trend towards higher concentrations of plasma norepinephrine (r = -.53, P = 0.06). As the hemoglobin saturation decreased, the variability in plasma epinephrine concentration was not significant (r = .42). CONCLUSION: The association between the degree of desaturation and the variability in norepinephrine suggests that norepinephrine is released in response to nocturnal desaturation.
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A patient with symptoms of sleep apnea syndrome had signs of congestive cardiac failure. A sleep study fulfilled the criteria for sleep apnea. Features of Cheyne-Stokes respiration coexisted. Management of the cardiac failure by weight loss principally due to diuretic use eliminated the symptoms of sleep apnea.
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This report describes our experience with 12 patients with thyrotoxic Graves' disease who were prepared for thyroidectomy using only a long-acting orally administered beta-adrenergic blocking agent (nadolol or atenolol); iodides were not used. This form of preparation proved to be very effective, fast acting, and economical. It permitted rapid preparation of patients for surgery and resulted in excellent control of the manifestations of hyperthyroidism in the perioperative period. The surgery was relatively easy and bloodless, and there were no operative complications. We recommend that these long-acting beta-adrenergic blocking agents be considered as the preferred medication for the preparation of thyrotoxic patients for surgery.
Spontaneous or propranolol-induced hypoglycemia can occur in uremic humans. We studied glucose kinetics (using [3-3H]glucose) in five uremic humans 24 h after hemodialysis and in seven normal controls. The effect of glucagon infusion at rates of 3, 6, 12, and 18 ng X kg-1 X min-1 at 60-min intervals was compared with either saline or beta-adrenergic blockade (propranolol infusion). In uremics, plasma glucose increased by 20-25% and by 40-50% at the 3 and 6 ng X kg-1 X min-1 glucagon doses, respectively, with no further increases at higher infusion rates. Glucose production increased transiently and in tandem with glucose uptake at each glucagon increment (P less than 0.0001). During beta-adrenergic blockade, the effect of glucagon in stimulating glucose production was blunted by 14-24% at the 6-18 ng X kg-1 X min-1 doses (P less than 0.05). During saline infusion, plasma insulin concentrations increased progressively to peak levels fourfold above basal at the 18 ng X kg-1 X min-1 dose. This increase in plasma insulin was virtually abolished by concomitant beta-adrenergic blockade (P = 0.0002). In contrast to uremic subjects, normal controls exhibited lesser degrees of hyperglycemia and hyperinsulinemia at all glucagon infusion rates. Propranolol infusion had no effect on the increments in glucose production and uptake nor on the plasma insulin response. These results suggest that in uremic humans propranolol independently reduces the hepatic response to glucagon and the insulin secretory response to hyperglycemia and/or hyperglucagonemia. These observations provide a possible mechanism for the adrenergic regulation of glucose homeostasis in uremia.
We evaluated the effect of treatment with placebo or verapamil (320 mg/day) for 2 weeks on glucose-induced insulin secretion and hypoglycemia-stimulated counterregulatory hormone secretion in hypertensive patients. Verapamil treatment was associated with a significant reduction in diastolic blood pressure (P = 0.02 vs. placebo). During a hyperglycemic clamp (plasma glucose raised 125 mg/dl above basal level) maintained for 90 min, plasma insulin increased 4- to 5-fold (early) and then to values 8- to 10-fold above baseline (late). These increments were identical during placebo or verapamil treatment. The rates of glucose metabolized during each study also were similar, suggesting that no significant change in insulin action occurred during drug treatment. When plasma glucose was allowed to decline precipitously from hyperglycemic levels (220 mg/dl) to nadirs ranging from 42-77 mg/dl, plasma concentrations of glucagon, cortisol, epinephrine, and norepinephrine all increased; however, no consistent differences in the counter-regulatory hormone responses could be attributed to verapamil therapy. We conclude that physiologically effective drug concentrations of verapamil capable of influencing blood pressure do not have a significant effect on secretion of glucoregulatory hormones in man.
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Eleven plasma variables have been studied in 18 elderly patients with cardiac oedema treated with bendrofluazide, frusemide and bumetanide, using a fully balanced, cross-over trial design. Bumetanide caused the least disturbance of plasma potassium and bendrofluazide the greatest. Frusemide produced an intermediate effect. The difference between the changes in plasma potassium produced by bumetanide and bendrofluazide was significant (P less than 0.02).
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