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Biomedical subjects

S Almog

Publications and source records attributed to S Almog.

66 records · Page 4Linked to original sources
PubMed1982

Methyldopa poisoning.

A case of methyldopa overdose, confirmed by quantitative blood analysis, is presented. The clinical manifestations were coma, hypothermia, hypotension, bradycardia, and dry mouth. This combination of clinical findings, previously considered characteristic of phenothiazines or tricyclic antidepressants poisoning, should also raise the suspicion of methyldopa overdose. Methyldopa is a commonly used antihypertensive agent. Surprisingly, reports on overdose are exceedingly rare [1, 2]. We have recently treated a case of methyldopa overdose in which the presenting signs resembled those of psychotropic drug poisoning.

Adult↗
PubMed1982

Evidence for an extrarenal action of chlorothiazide on serum potassium.

The effects of chlorothiazide and furosemide on serum potassium were studied in fasting anuric patients maintained by chronic hemodialysis and compared to a control period when no drug was administered. Serum potassium levels were significantly lower following oral chlorothiazide (15 mg/kg body weight) than during the control period. After intravenous furosemide (1 mg/kg body weight), potassium levels were midway between those of the chlorothiazide and control periods, but statistical significance was not attained. Comparing the three study periods, there were no significant differences in the changes in body weight, blood pressure, blood pH, hematocrit, urea, glucose, sodium, albumin, insulin, plasma renin activity and aldosterone. This suggests that an extrarenal action of chlorothiazide on the cell membrane promotes cellular uptake of potassium.

Chlorothiazide↗
PubMed1979

Serum concentrations of isosorbide dinitrate produced by a sustained-release capsule.

The bioavailability of isosorbide dinitrate (ISDN) and the time course of its serum concentration produced by a standard 20-mg tablet and a sustained-release capsule were compared in six normal volunteers. Following administration of the tablet, serum ISDN concentrations reached a peak of 29 ng/ml at 0.5 h, declined monoexponentially with a t1/2 of 25.5 min, and disappeared after 2 to 3 h. Following the administration of the sustained-release capsule, serum ISDN concentrations reached a plateau of 4 ng/ml between 2 and 5 h, and declined slowly and nonlinearly up to and including the 10-h point. The total amount of ISDN absorbed was 1.32 times greater with the standard tablet; following the absorption of the capsule, there was truncation of the serum concentration curve due to ongoing absorption at and beyond 10 h.

Administration, Oral↗
PubMed1979

Value of serum digoxin concentration measurement in the control of digoxin therapy in atrial fibrillation.

The association between steady-state serum digoxin concentrations and control of ventricular response rate (VRR) was studied in 53 consecutive patients with atrial fibrillation. Decreases in VRR were significantly correlated with serum digoxin (rs = -0.22, P less than 0.05). Clinical responses were appropriate to serum digoxin concentrations in 37 patients (69.8%) and were inappropriate in 16 (30.2%) (P less than 0.05). Complicating clinical factors were present in all eight patients with inappropriate responses to therapeutic serum digoxin (0.5 to 2.0 ng/ml) (P = 0.046), but were also found in many patients with appropriate responses and thus could not serve to differentiate between the two categories. Digitalis intoxication occurred in one of the three patients with a concentration of serum digoxin greater than 2 ng/ml (P = 0.056). In 30% of our patients with atrial fibrillation, monitoring of serum digoxin was of value in identifying inappropriate therapeutic responses indistinguishable by clinical means and in defining the subgroup of refractory cases, which allows the prevention of digitalis intoxication.

Atrial Fibrillation↗
PubMed1978

Steady state serum concentrations and renal clearance of digoxin in neonates, infants and children.

Steady state serum concentrations of digoxin were determined repeatedly in 34 infants with congenital heart disease. Simultaneous measurements of renal clearances of digoxin, creatinine and urea were obtained in 29 of the subjects. Serum digoxin concentrations were markedly higher in children under the age of 3 months than in those over this age, despite equal weight--adjusted 24 h doses. This finding was explained by a very rapid increase in renal digoxin clearance in the first 3 months--32 +/- 7 ml/min/1.73m2 at 1 week to 65.6 +/- 30 at 3 months. The subsequent increase in digoxin clearance was much slower, e. g. to 87.7 +/- 43 ml/min/1.73m2 at 12 months. Renal clearance of digoxin was equally well correlated with creatinine clearance (r = 0.87) as with urea clearance (r = 0.83), but it exceeded that of creatinine in all age groups. The findings indicate that both glomerular and tubular function is involved in the renal elimination of digoxin in young children, and that development of renal elimination of the drug parallels that of the maturation of renal function in the early months of life. The neonate and infant with congestive heart failure display impaired ability to eliminate digoxin. The impairment lessens rapidly with the development of renal function over the first 3 months of life. Diminished doses of digoxin should be advocated in this age group if therapeutic serum concentrations of the drug are to be maintained and toxicity avoided.

Aging↗
PubMedDate not supplied

Omeprazole has no effect on acetaminophen kinetics in the rat.

We investigated in the rat the effect of the H+/H(+)-ATPase inhibitor, omeprazole, on the kinetics of acetaminophen. Two groups of rats were treated with either omeprazole 50 mg/kg/day or the vehicle for 7 days. On day seven, the pharmacokinetic parameters of acetaminophen clearance were determined in the conscious rat. Elimination rate constant, elimination half life time, clearance and volume of distribution of acetaminophen were not disturbed by omeprazole. It is concluded that in the rat, omeprazole does not affect acetaminophen kinetics and, therefore, will not increase susceptibility to acetaminophen toxicity.

Acetaminophen↗
PubMedDate not supplied

Oral magnesium intake reduces permanent hearing loss induced by noise exposure.

INTRODUCTION: Following animal experiments where correlations were observed between serum magnesium level and noise-induced permanent hearing threshold shifts (NIPTS), we tested the prophylactic effect of magnesium in human subjects exposed to hazardous noise. METHODS: Subjects were 300 young, healthy, and normal-hearing recruits who underwent 2 months of basic military training. This training necessarily included repeated exposures to high levels of impulse noises while using ear plugs. During this placebo-controlled, double-blind study, each subject received daily an additional drink containing either 6.7 mmol (167 mg) magnesium aspartate or a similar quantity of placebo (Na-aspartate). RESULTS: NIPTS was significantly more frequent and more severe in the placebo group than in the magnesium group, especially in bilateral damages. NIPTS was negatively correlated to the magnesium content of blood red cells but especially to the magnesium mononuclear cells. Long-term additional intake of a small dose of oral magnesium was not accompanied by any notable side effect. CONCLUSION: This study may introduce a significant natural agent for the reduction of hearing damages in noise-exposed population.

Administration, Oral↗
PubMedDate not supplied

Malaria antibodies and mefloquine levels among United Nations troops in Angola.

BACKGROUND: The United Nations deployed about 8,000 soldiers in a peacekeeping mission in Angola. Malaria is the most common disease there and consequently it was the major risk to the UN troops. Most of them are from malaria free areas. As a result of improper prophylactic measures there were many cases of malaria, including some deaths in 1995. In February-March 1996, an Israeli team was sent to Angola to evaluate the malaria situation among UN soldiers. This paper deals specifically with some aspects of chemoprophylaxis and diagnosis. The efforts were concentrated in one particular area where malaria incidence had been reported as the highest. METHODS: Blood samples were collected from nonimmune soldiers who were using mefloquine as a prophylactic drug and were exposed to malaria. The mefloquine and the antimalarial antibody plasma levels were monitored. RESULTS: While the local laboratory indicated that about 80% had a malaria episode, the serological results revealed that only 5 soldiers of the 56 (9%) examined had antimalarial antibodies, of which 3 were Angolans. Despite a controlled prophylactic regimen there was considerable variability in mefloquine plasma levels: 46% of the samples were below the required prophylactic level and 26% above it. All patients who were proven positive with malaria by both microscopic and serologic observation had a low level of mefloquine. CONCLUSIONS: In field conditions, a kit which identifies plasmodial antigens, is preferable, to a microscopic diagnostic method. Controlled mefloquine prophylaxis may not prevent malaria, especially when blood levels are low. The reason for the low mefloquine blood levels is not clear and needs further evaluation.

Angola↗
PubMedDate not supplied

Survey of symptoms following intake of pyridostigmine during the Persian Gulf war.

Pyridostigmine bromide, a reversible inhibitor of acetylcholinesterase (AChE), is effectively used as a pre-treatment to organophosphate intoxication. Previous studies have shown that an oral dose of 30 mg twice a day produces a sufficient inhibition of the enzyme activity (20-40%) without causing any significant adverse effect. During the Persian Gulf war pyridostigmine was taken for the first time under a chemical warfare threat. We searched for symptoms and complaints that may be related to the medication. Our survey included 213 soldiers who completed a questionnaire regarding possible symptoms and their severity. AChE inhibition level was compared between groups of soldiers with and without complaints. The most frequent symptoms were nonspecific and included dry mouth, general malaise, fatigue and weakness. Typical effects, such as nausea, abdominal pain, frequent urination and rhinorrhea, were infrequent. The severity of the symptoms was generally mild. The symptoms appeared around 1.6 h after taking the medication and recurred after each intake. No correlation was found between levels of cholinesterase and type or severity of complaints. Anxiety, which accompanies wartime, may have contributed to the appearance of significant symptoms. Further investigations concerning the effects of pyridostigmine ingestion under stressful conditions are warranted.

Adolescent↗
PubMedDate not supplied

Acute pyridostigmine overdose: a report of nine cases.

Pyridostigmine is known as a pre-treatment drug against intoxication with organophosphorus nerve agents. During the Persian Gulf war, we encountered a cluster of nine cases of pyridostigmine self-poisoning, of which three presented with mixed drug poisoning. The clinical and laboratory features of pyridostigmine toxicity are presented. Doses ranged between 390 and 900 mg. Pyridostigmine ingestion resulted in mild to moderate cholinergic symptoms such as abdominal cramps, diarrhea, emesis, nausea, hypersalivation, urinary incontinence, fasciculations, muscle weakness and blurred vision. No central nervous system manifestations were evident. The symptoms developed within several minutes and lasted up to 24 h. All patients underwent gastric emptying followed by administration of activated charcoal. Atropine (1-8 mg) was required in only three patients. Measurement of serum cholinesterase inhibition was found to be a reliable and sensitive diagnostic tool in pyridostigmine poisoning. No clear correlation was found between the extent of cholinesterase inhibition and the incidence or severity of the cholinergic signs. The clinical recovery was faster than the spontaneous recovery of the enzyme. Pyridostigmine intoxication is self-limited and well tolerated by young healthy adults.

Adolescent↗
PubMedDate not supplied

The effect of pyridostigmine on respiratory function in healthy and asthmatic volunteers.

Respiratory function was evaluated in 12 healthy and 13 asthmatic volunteers following a single oral dose of pyridostigmine in a double-blind, placebo-controlled cross-over study. Respiratory function tests were performed at rest and after submaximal exercise at the time corresponding to the expected peak cholinesterase inhibition by pyridostigmine. A single dose of 60 mg pyridostigmine given to nonasthmatic subjects led to a decrease of 28.4% in cholinesterase activity when compared to the baseline and a statistically (but not physiologically) significant decrease in FEV1 (forced expiratory volume in 1 sec) both at rest (P less than 0.015) and after exercise (P less than 0.05). This effect showed a strong correlation to the degree of cholinesterase inhibition (r = -0.936, P less than 0.0001). According to these findings, a smaller dose of pyridostigmine (30 mg) was given to subjects with mild bronchial asthma. At that dose, pyridostigmine resulted in a similar inhibition of cholinesterase activity to a mean of 76.7% of the baseline. A significant decrease in the pulse rate was also found (P less than 0.005). However, no changes in respiratory function were observed when compared with the effects of placebo. The effect of post-exertion atropine inhalation on respiratory function was also unchanged with pyridostigmine at that dose. We conclude that, in general, at this dose pyridostigmine is a safe drug for asthmatics; however, the distribution of individual results in this group cannot preclude the existence of a subpopulation of asthmatic patients who are more vulnerable to the effects of pyridostigmine.

Administration, Oral↗