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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The benefit of any medical intervention, particularly drug therapy, must be weighed against its cost. These costs are not only dollar expenditures but effects on lifestyle and overall health. Diuretic therapy for hypertension has been in use long enough to allow long-term clinical evaluation. It is clear from the numerous prospective drug intervention trials involving hypertensive patients that diuretic therapy is not free of "costs." Aside from the fact that 15 to 20% of diuretic-treated patients reportedly drop out of trials because of side effects, including exertional dyspnea, fatigability, lethargy and impotence, numerous metabolic derangements have been reported with these drugs, i.e., potassium, uric acid, lipid, sodium, glucose and magnesium alterations. Perhaps most important are the changes in lipid fractions, which may be responsible for the failure of antihypertensive therapy to decrease the risk of coronary heart disease. Thus, although diuretics are somewhat less expensive than other antihypertensive drugs in terms of dollars, their overall costs are high. The major alternatives, such as the alpha-blocker prazosin or the central nervous system agent clonidine, are preferable, do not impair a patient's lifestyle and are recommended to be used along with changes in diet and an exercise program for control of mild to moderate hypertension.
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PMID:Diuretic therapy for mild hypertension: the "real" cost of treatment. 642 Nov 37

The main purpose of this work was to study changes in the balance of fluids, electrolytes and blood metabolites in neonatal piglets with severe transmissible gastroenteritis. Six two day old conventional piglets were infected with transmissible gastroenteritis virus while six others were used as normal controls. Blood samples were collected in heparin when the infected piglets were moribund. The following variables were measured: packed red cell volume, total plasma protein and bicarbonate, blood pH, blood urea nitrogen and plasma glucose, creatinine, chloride, inorganic phosphorus, sodium, potassium, magnesium and calcium. Vomiting and diarrhea appeared 12 to 24 hours postinoculation in the infected piglets and they were moribund one or two days later. Before becoming moribund, most of the piglets fell rapidly into a lethargic and comatose state. The most evident changes in their blood variables were an increase in packed cell volume, total protein, blood urea nitrogen, phosphorus and magnesium levels and a decrease in pH and bicarbonate concentration as well as a severe hypoglycemia. The results suggest that severe hypoglycemia coupled with metabolic acidosis and dehydration might be an important factor contributing to the high mortality rates caused by transmissible gastroenteritis in neonatal piglets. The hypoglycemia results from a combination of the inadequate glucose metabolism inherent to neonatal piglets and the acute maldigestion and malabsorption resulting from the diffuse and severe villous atrophy induced by the virus.
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PMID:Hypoglycemia: a factor associated with low survival rate of neonatal piglets infected with transmissible gastroenteritis virus. 647 97

Beginning 1 wk postpartum, weekly changes of feed and water intake, body weight, milk production, and electrolyte concentrations in serum, saliva, urine, milk, and feces were observed for 8 to 11 wk. Three dietary treatments differing in sodium chloride and sodium bicarbonate supplementation but containing equal sodium concentrations were used. Dietary chloride percents were low .10%, medium .27%, and high .45%. Consistently changes were significant for feed and water intake, body weight, milk production, and electrolyte concentrations in serum, urine, milk, and feces of cows fed the low chloride diet. By wk 8, body weight had declined from 575.0 +/- 56.7 to 476.7 +/- 54.3 kg, and daily milk production decreased from a peak of 27.7 +/- 2.4 to 19.2 +/- 3.9 kg for cows fed the low chloride diet. Serum chloride decreased from 106.0 +/- 2.8 to 75.5 +/- 6.7 meq/liter during the same time. Cows on the low chloride diet developed clinical signs of a deficiency characterized by depraved appetite, lethargy, hypophagia, emaciation, hypogalactiae, constipation, and cardiovascular depression. Metabolic alterations could be summarized as a severe primary hypochloremic, secondary hypokalemic, metabolic alkalosis.
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PMID:Nutritional chloride deficiency in early lactation Holstein cows. 650 51

The first reported case, in an adult, of cholestyramine induced hyperchloremic metabolic acidosis is a 70 year old female with a two year history of primary biliary cirrhosis confirmed by histologic and immunologic criteria. After taking cholestyramine II sachets twice daily for two months she presented with lethargy, confusion and drowsiness. Examination revealed confusion, jaundice, signs of chronic liver disease, portal hypertension and hepatic encephalopathy. Laboratory investigations confirmed a metabolic acidosis (pH 7.15) and hyperchloremia. Multiple cultures failed to reveal sepsis and a urinary pH of 4.85 together with tests of renal acidification, excluded renal tubular acidosis. She received 600 mEq of sodium bicarbonate intravenously over 36 hours by which time her mentation, electrolytes and pH were normal. It is presumed that her hyperchloremic metabolic acidosis was secondary to cholestyramine because of the similarity to pediatric reports; the rapid and lasting response to intravenous sodium bicarbonate; the absence of another etiology; normal serum potassium, chloride and bicarbonate despite continued spironolactone therapy after recovery.
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PMID:Cholestyramine induced hyperchloremic metabolic acidosis. 659 13

Cold insolubility of a serum IgA cryoimmunoglobulin was found to be inhibited by the addition of 1.5 mM sodium decanedicarboxylate in vitro. The patient with the cryoglobulin had advanced multiple myeloma complicated by severe hyperviscosity that caused lethargy and episodic loss of consciousness. Decanedicarboxylic acid administered orally resulted in transient relief of symptoms and the loss of cryoprecipitability of the paraprotein. Further in vitro studies revealed that sodium salts of long-chain monocarboxylic acids with a minimum of eight carbons, and dicarboxylic acids with a minimum of 12 carbons inhibited cryoprecipitation. Salts of short-chain carboxylic acids, by contrast, enhanced cryoprecipitation. Sodium phenolate and sodium salts of benzoic acid, 2,4-DNP, phenylpropionic acid, and salicylic acid were also inhibitory. These latter compounds, which have a ring structure, did not cause precipitation at any concentration. It was demonstrated that the presence of a free carboxylic group was required for these activities; conversion of carboxylic acid to amide resulted in the loss of both the inhibitory and cryoprecipitation-enhancing effects. Normal plasma, or plasma from five other patients who had IgG, IgM, or mixed-type cryoglobulinemia, were not affected by any of these compounds. It is suggested that in selected cases of hyperviscosity syndrome associated with cryoglobulinemia, some of these compounds, especially monocarboxylic acids with appropriate chain lengths, or those with a ring structure, may have therapeutic applications.
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PMID:Inhibition of cold insolubility of an IgA cryoglobulin by decanedicarboxylic acid and related compounds. 663 13

Twenty beef calves weighing approximately 180 kg were allotted to 3 groups. In group A, 6 calves were given 25 mg of mycelial monensin/kg of body weight orally and were evaluated at 1, 2, and 4 days for clinical, ECG, clinicopathologic, and pathologic alterations. In group B, 7 calves were given a single dose of monensin (40 mg/kg) and 5 were given a 2nd 40 mg/kg dose on day 7; calves were evaluated at days 1, 2, 4, 7, 8, 9, and 11. In group C, 2 calves served as controls. Monensin-treated calves developed anorexia, diarrhea, and lethargy after day 1. One group B calf died on day 7 with lesions of congestive heart failure. Electrocardiographic abnormalities were not observed in group A calves; in group B, prolongation of Q-T and QRS intervals occurred from days 2 to 11 and first degree heart block was seen from days 7 to 11. Clinicopathologic alterations included: increased serum activities of aspartate aminotransferase and creatine kinase in group B calves after day 2; decreased serum K+, Na+, and Ca2+ concentrations in both groups, and postdosing occurrence of leukocytosis. Calves were euthanatized sequentially and the lesions of monensin toxicosis were present in the heart, skeletal muscles, and rumen in groups A and B. Disseminated pale yellowish-brown areas of necrosis were present in the ventricular myocardium of 6 of 12 group B calves. Gross lesions were not present in the skeletal muscles or rumen. Microscopically, the myocardial and skeletal muscular lesions were characterized by sarcoplasmic vacuolation from mitochondrial swelling and lipid accumulation in calves killed after day 1 in groups A and B, and by myocardial necrosis with contraction bands, but without calcification, in group B calves killed by day 4. Acute rumenitis was present in groups A and B calves. Myotoxic effects of monensin may be related to its action as an ionophore producing altered intracellular ion concentrations and initiating degeneration and necrosis in striated muscle fibers.
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PMID:Clinical, clinicopathologic, and pathologic alterations in acute monensin toxicosis in cattle. 665 Sep 60

Of 13 patients with complex partial seizures who experienced stuporous states during treatment with sodium valproate (VPA), 4 received VPA only, 4 VPA and phenobarbital (PB) and 5 VPA, PB, and a third anticonvulsant. Seven cases were described in detail. Side effects-stupor or confusion-appeared a few days after efficacious drug plasma levels were attained, persisted until therapy was readjusted, and disappeared 24 to 72 h after VPA withdrawal. Therapeutic trials established the role of VPA in the onset of stuporous states. The adverse effects of VPA were potentiated by the concomitant administration of other anticonvulsants. Stupor was not due to VPA overdoses, and plasma concentration of the drugs were not correlated with the electroclinical signs. The EEG showed spike and wave discharges or continuous sharp theta and delta waves persisting during VPA treatment. The fact that all 13 stuporous, VPA-treated patients were subjected to partial seizures with complex symptomatology, and none were cases of generalized epilepsy, together with the observations that the disturbances of consciousness started with focal symptoms and EEG signs resembling those of spontaneously occurring partial seizures, suggest that VPA given alone or in association with other antiepileptics has a paradoxical epileptogenic effect in certain forms of epilepsy.
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PMID:Stuporous episodes during treatment with sodium valproate: report of seven cases. 680 87

7 cases of stuporous states or coma induced in epileptic subjects by the rapid administration of high doses of sodium valproate are described. Progressive impairment of consciousness began 2 to 7 days after the administration of sodium valproate and induced a slowing of background EEG activity until the delta activity became of high amplitude, generalized, continuous and areactive. The authors believe that the impairment of consciousness in their patients was related to the rapid administration of high doses and a direct intrinsic action of sodium valproate on the brain, as no increase in plasma levels of the drugs in association with valproate was observed.
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PMID:Stuporous states or coma induced by the rapid administration of high doses of sodium valproate. 681 49

We encountered an apparent bilateral internuclear ophthalmoplegia (INO) in a stuporous patient who used narcotics and benzodiazepines and had taken phenytoin sodium for drug-withdrawal seizures. The INO was promptly reversed by administration of the narcotic antagonist naloxone, which binds opiate receptors. This suggests the INO resulted from a specific toxic effect of narcotics, but opiate receptors have not been anatomically demonstrated within the medial longitudinal fasciculus or associated structures. Stimulation of inhibitory GABA-ergic (alpha-aminobutyric acid) vestibulo-ocular fibers may have been related to INO in this case.
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PMID:Bilateral internuclear ophthalmoplegia reversed by naloxone. 683 Apr 74

Chronic depletion of body chloride developed in a group of infants ingesting a diet consisting almost exclusively of chloride deficient Neo-Mull-Soy. Ten of the 12 infants were on this diet three to five months before loss of appetite, failure to thrive, muscle weakness, and lethargy led to a diagnostic evaluation. The outstanding laboratory features were severe hypokalemic metabolic alkalosis, low urinary chloride concentrations (< 10 mEq/liter), and erythrocyturia. There was marked decrease in weight for age in all 12 infants. Head circumference for age had decreased in five of six and length for age in five of ten infants for whom earlier measurements were available. The biochemical abnormalities reverted to normal following dietary supplementation with either sodium or potassium chloride. Appetite, affect, and muscle strength improved, and weight gain resumed. Head circumference for age has moved toward the percentile level present prior to starting Neo-Mull-Soy in all instances. With one exception, length measurements show a similar pattern. The erythrocyturia has decreased or vanished. Chloride deficiency led to contraction of the extracellular volume and the substitution of poorly reabsorbable anions for readily reabsorbable chloride. These alterations caused development of the negative hydrogen ion and potassium balances which led to the hypokalemic metabolic alkalosis.
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PMID:The dietary chloride deficiency syndrome. 693 41


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