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Biomedical subjects

J N Fisher

Publications and source records attributed to J N Fisher.

15 recordsLinked to original sources
PubMed1992

Management of psychotropic-induced hyperprolactinemia.

The effects of individual psychotropic medications on serum prolactin concentrations are described, and recommendations for dealing with adverse effects are provided. Hyperprolactinemia can result in galactorrhea, amenorrhea, irregular menses, and anovulation; in men, impotence and azoospermia, with or without lactation and gynecomastia, can occur. Antipsychotics may block dopamine receptors in the pituitary prolactin-secreting cells and prevent dopamine-induced reduction of prolactin release. The magnitude of the increase in prolactin concentration correlates with the amount of antipsychotic drug given. The treatment of choice is reduction of the antipsychotic dosage or discontinuation of therapy. If adjustments to the antipsychotic dosage fail to resolve symptoms, the dopamine agonists bromocriptine and amantadine may be tried. Antidepressants may produce elevated serum prolactin concentrations, especially with long-term administration. However, the frequency of antidepressant-induced hyperprolactinemia is much lower than that seen with antipsychotics, and serious adverse clinical effects are uncommon. Other psychotropic drugs such as lithium, valproic acid, buspirone, carbamazepine, and benzodiazepines either are only rarely associated with symptomatic hyperprolactinemia or do not produce clinically important changes in prolactin concentrations. Antipsychotic drugs are the psychotropic agents most likely to cause symptomatic hyperprolactinemia. Bromocriptine or amantadine may provide symptomatic relief if withdrawal or adjustment of the antipsychotic dosage does not eliminate the symptoms.

Antidepressive Agents↗
PubMed1990

An immunologic and genetic study of asthma in workers in an aluminum smelter.

The cause or causes of asthma among employees in aluminum smelters is unknown. We attempted to ascertain whether such workers who developed asthma differed in respect to indices of immunological function and certain genetic markers. Data were collected from 33 asthmatic and 127 nonasthmatic potroom workers. Asthmatic workers had significantly lower mean serum levels of immunoglobulin (Ig)M; however, mean levels of IgG and IgA, median levels of IgE, the capacity for recall of delayed type hypersensitivity, levels of immune complexes, and frequency of antinuclear or other autoantibodies did not differ from values for nonasthmatic workers. Asthma was found to develop on a background of atopy in 21 workers (64%), whereas there were no features of atopy in 12 workers (36%). Cigarette smoking had independent effects on immunological function. In respect to genetic markers, there was a higher frequency among asthmatic workers of the alpha-1-anti-trypsin deficiency phenotype MS, but the frequency of blood groups, Gm allotypes, or human leucocyte antigen types was similar. The study established that the profile of immune function, or genetic markers tested, did not differ essentially for workers in an aluminum smelter who did or did not develop asthma; however, there was an indication of heterogeneity in causation, as judged by "atopy-related" and "non-atopy-related" groups in the asthma population.

Adult↗
PubMed1983

A randomized study of phosphate therapy in the treatment of diabetic ketoacidosis.

The use of phosphate therapy in the management of diabetic ketoacidosis (DKA) has been controversial, particularly with respect to the effect of phosphate intermediates on tissue oxygenation. In a prospective randomized study we evaluated the effect of phosphate (8.5 mmol/h or approximately 6 g phosphate/24 h) (experimental group) vs. no phosphate therapy (control group) in 30 DKA patients, 15 in each group. Various determinations including erythrocyte 2,3-diphosphoglycerate (2,3-DPG), oxyhemoglobin dissociation (p50), serum phosphate, calcium, lactate, pyruvate, electrolytes, and response time to reach predetermined values for glucose, bicarbonate, and pH were measured at frequent intervals during the first 24 h of therapy and daily for 5 days after metabolic control. Initial electrolytes, glucose, pH, erythrocyte 2,3-DPG, lactate, and p50 were not different in either group. Whereas the experimental group had a greater level of 2,3-DPG than the control group by 48 h, the difference was not statistically significant. Recovery indices, including hours to reach glucose of 250 mg/dl, bicarbonate greater than 15 meq/liter, pH greater than 7.3, and mental alertness, were not different in the two groups nor were the p50 or lactate measurements. The experimental group exhibited significantly lower plasma ionized calcium values during therapy. We conclude that phosphate therapy may accelerate regeneration of erythrocyte 2,3-DPG but in the relatively small number of patients studied it had no demonstrable influence on tissue oxygenation or clinical response to low dose insulin therapy of DKA. Furthermore, the exaggeration of hypocalcemia seen in phosphate-treated patients may be reason for caution in the use of such therapy.

2,3-Diphosphoglycerate↗
PubMed1979

Similar responsiveness of diabetic ketoacidosis to low-dose insulin by intramuscular injection and albumin-free infusion.

We compared low-dose insulin regimens in a prospective randomized trial in 30 patients with diabetic ketoacidosis. One group received a loading dose of 0.44 U/kg body weight of regular insulin half intramuscularly and half intravenously followed by 7 U/h intramuscularly, whereas the other group received a loading dose of 0.44 U/kg intravenously followed immediately by a constant infusion of 7 U/h in albumin-free saline. The time for metabolic control of the ketoacidosis was not significantly different in the two groups. Five patients in each group developed mild hypokalemia (serum potassium, 3.0 to 3.4 meq/litre). No patient became hypoglycemic, and there were no deaths within the follow-up period (24 h). In the treatment of diabetic ketoacidosis, low doses of insulin administered by the priming dose-intermittent intramuscular route are as effective as the constant infusion method.

Adult↗
PubMed1979

Management of diabetic ketoacidosis.

Many aspects of DKA treatment have become dogma without benefit of critical randomized prospective studies. Although recommendations for low-dose insulin therapy have passed the test of working in practice, many facets of treatment such as bicarbonate vs. no bicarbonate, phosphate replenishment, the merits of rapid vs. slow correction of hyperglycemia and acidosis need to be prospectively studied. In the final analysis, while insulin, fluid, and electrolyte administration are all important in the treatment of DKA, success most often hinges on careful hour-by-hour monitoring of the patient by a concerned and knowledgeable physician.

Bicarbonates↗
PubMed1977

Diabetic ketoacidosis: low-dose insulin therapy by various routes.

Since in normal persons the hypoglycemic effect of low-dose intramuscular exceeds that of subcutaneous insulin we studied the effect of routes of insulin therapy in diabetic ketoacidosis. Forty-five patients with diabetic ketoacidosis entered a randomized prospective protocol with insulin administered either intravenously, subcutaneously or intramuscularly. Initial priming dose of insulin had to be repeated in two of 15, three of 15 and six of 15 of the intravenous, subcutaneous and intramuscular groups respectively. The intravenous group had a more rapid fall in plasma glucose (P less than 0.01) and ketone bodies (P less than 0.05) during the first two hours. Thereafter, there were no significant differences in the rate of decline of plasma glucose or ketones nor in the time required for glucose to reach 250 mg per deciliter or for complete recovery from diabetic ketoacidosis. The data confirm the efficacy of low-dose insulin therapy for diabetic ketoacidosis and indicate that the optimal route of insulin administration is by initial intravenous combined with subcutaneous or intramuscular.

Adult↗
PubMed1976

Familial hyperproinsulinemia. An autosomal dominant defect.

We describe a genetic defect in a kindred in whom proinsulin or a proinsulin-like material constitutes the major fraction of circulating insulin immunoreactivity in both the fasting and stimulated states. The defect, familial hyperproinsulinemia, affects eight males and 10 females in four generations of the kindred, with an autosomal dominant mode of transmission. Familial hyperproinsulinemia is asymptomatic in the affected progeny, with no apparent relation to hypoglycemia or to the development of diabetes mellitus. This genetic defect may represent either a deficiency in the proinsulin cleaving enzyme (or enzymes) within the beta cell, or more probably, an abnormal species of proinsulin.

Adolescent↗
PubMed1976

Periodic apnea, exercise hypoventilation, and hypothalamic dysfunction.

Periodic apnea and exercise hypoventilation were observed in a 14-year-old boy. Hyperphagia, obesity, serum hyperosmolality without diabetes insipidus or appropriate thirst, and retardation of growth and sexual development indicated a hypothalamic disorder. Neurologic evaluation was normal except for electroencephalographic changes induced by apnea. Pulmonary function tests, resting arterial blood gases in the wakeful state, and ventilatory response to inhaled CO2 were also normal. Acute hypoxemia and respiratory acidosis occurred with apnea during sleep and with insufficient ventilation during exercise. The central origin of sleep apneas was shown by esophageal pressure monitoring. The hypothalamic dysfunction and exercise hypoventilation distinguish this patient from others with obesity and periodic apnea.

Adolescent↗
PubMedDate not supplied

Evaluation of a portable insulin infusion pump for outpatient management of brittle diabetes.

Three "brittle" diabetic patients were given constant subcutaneous insulin infusion with a portable battery-driven pump, and their plasma glucose and hemoglobin A1 were measured at frequent intervals during inpatient or outpatient periods. Mean plasma glucose decreased significantly in all inhospital patients and remained significantly less than before pump therapy in two of three as outpatients during the 8--12 wk of follow-ups; however, complete normalization of glucose metabolism was not accomplished in any. All three demonstrated a progressive decline in hemoglobin A1 levels to normal or near-normal values. The need for long-term studies of open loop infusion systems in a research setting before their adaptation to routine care is emphasized.

Adolescent↗