Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study compared the effects of saccharose and glucose on the recovery from insulin hypoglycemia. 17 normal volunteers (12 men, 5 women, 25-40 years old) received the same dose (0.1 IU i.v.) of semisynthetic rapid-acting human insulin on two different days after an overnight fast. Blood glucose and C peptide were measured in venous blood samples before as well as at regular time intervals after insulin administration. 30 min after the injection, 20 g saccharose or 20 g glucose p.o. (diluted in water) were given. The mean glucose values were at most time intervals higher after glucose than after saccharose administration. In addition, glucose ingestion resulted in an earlier and steeper blood glucose rise (mean recovery rates during the first 5 min 3.10 and 1.38 mg/dl/min for glucose and saccharose, respectively). The C peptide values decreased progressively and did not achieve baseline levels even at 120 min in spite of blood sugar normalization. It is concluded that glucose acts faster than saccharose in insulin-induced hypoglycemia. Exogenous insulin results in a prolonged depression of C peptide which lasts longer than the hypoglycemic effect.
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PMID:Recovery from insulin-induced hypoglycemia after saccharose or glucose administration. 210 1

Four insulin-treated diabetic patients presented over a 2-year period in hypoglycaemic coma and died secondary to this. At autopsy, there were widespread neuropathological changes, in all four cases consistent with hypoglycaemic damage. Abnormalities were also found in areas regarded as generally being spared in hypoglycaemic brain injury, particularly the brain stem, thalamus, globus pallidus, and cerebellum, and these lesions may relate to seizure activity and cardio-respiratory depression secondary to the hypoglycaemia. Although more than one aetiological factor may be contributing, it is concluded that the neuropathological changes in diabetic patients dying in hypoglycaemic coma are extremely diverse.
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PMID:Fatal hypoglycaemia in insulin-treated diabetes mellitus: clinical features and neuropathological changes. 214 89

A wide variety of conditions seen in medical practice can produce memory impairment (amnesia). Normal aging, depression, and anxiety are commonly associated with memory difficulties, as are many neurologic conditions. Systemic illnesses can impair memory by injuring vulnerable limbic regions sensitive to hypoxia or hypoglycemia. Commonly used over-the-counter and prescription medications can likewise cause amnesia. These conditions disrupt memory in characteristic ways. Recent studies suggest that immediate, recent, and remote memory functions have different neuroanatomic substrates, as do the processes of registration, retention, and retrieval. New classifications have emerged to explain the evidence for multiple memory subsystems. The neuropharmacology of memory now includes several peptides in addition to cholinergic and noradrenergic pathways. Critical limbic regions have been discovered that mediate memory consolidation, and neuronal mechanisms such as long-term potentiation are being implicated in the unique capacity of these areas to permit new learning to take place.
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PMID:Amnestic disorders. Pathophysiology and patterns of memory dysfunction. 215 98

Behavioral and electrophysiological evidence implicating the GABA-benzodiazepine receptor complex in the pathogenesis of hepatic encephalopathy was obtained using an improved rat model of hepatic encephalopathy caused by thioacetamide-induced fulminant hepatic failure. After the administration of thioacetamide together with supportive therapy, acute hepatocellular failure developed in rats as a result of massive hepatocellular necrosis without evidence of renal failure or hypoglycemia. The evolution of hepatic encephalopathy in this model was sufficiently slow to readily permit the staging of the syndrome. Prominent features of the encephalopathy include a marked reduction in open field activity and an abnormal visual evoked response. Both the deficits in spontaneous motor function and visual evoked response abnormalities of rats in stages III to IV hepatic encephalopathy were significantly improved after the administration of the benzodiazepine receptor ligands flumazenil or Ro 15-4513. Doses of flumazenil or Ro 15-4513 that produced these effects in rats with hepatic encephalopathy had no detectable action on either the behavior or the visual evoked responses of normal rats. The ability of benzodiazepine receptor ligands to ameliorate both the behavioral depression and the visual evoked response abnormalities associated with hepatic encephalopathy in the thioacetamide-induced rat model suggest an involvement of the GABA/benzodiazepine receptor complex in the pathogenesis of hepatic encephalopathy. In addition, the similarity of these observations to those in rabbits with hepatic encephalopathy caused by galactosamine-induced fulminant hepatic failure is compatible with the hypothesis that the mechanisms of hepatic encephalopathy in these two distinct models share a common final pathway, the allosteric enhancement of GABAergic tone through the benzodiazepine receptor.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reversal of the behavioral and electrophysiological abnormalities of an animal model of hepatic encephalopathy by benzodiazepine receptor ligands. 215 65

Although changes in hypothalamic-pituitary-adrenal axis function have frequently been reported in alcoholics, the majority of studies have used recently detoxified subjects in whom abstinence phenomena and clinical depression may contribute to observed stress axis alterations. To isolate the primary effects of alcohol dependence on the stress axis, the ACTH and cortisol responses to insulin-induced hypoglycemia were measured in seven actively drinking male alcoholics recruited from the general public through a newspaper advertisement along with eight age-matched male controls. The alcoholic subjects met current American Psychiatric Association diagnostic criteria for alcohol dependence, were stably employed, and had no concurrent psychiatric disorders, cognitive impairment, or psychometric evidence of depression. While relatively young (30.0 yr; range, 22-48 yr), they had lengthy histories of alcohol-related problems (11.9 yr; range, 5-30 yr). Insulin administration resulted in similar nadirs in blood sugar in both alcoholic and control groups. However, the plasma ACTH response was markedly blunted in the alcoholics (P = 0.040, by Mann-Whitney U test). There was a nonsignificant trend toward increased cortisol levels in the alcoholic group. The findings suggest that altered hypothalamic-pituitary-adrenal axis function in alcoholics is a primary results of chronic ethanol exposure rather than a confounding effect of clinical depression or recent detoxification.
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PMID:Diminished adrenocorticotropin response to insulin-induced hypoglycemia in nondepressed, actively drinking male alcoholics. 216 34

Widespread utilization of short-chain alcohols in solvents and alcoholic beverages provides small animals with numerous opportunities for exposure. Toxicosis most commonly occurs following ingestion but may also arise from inhalation and/or dermal absorption. The actions of short-chain alcohols are believed to result from nonspecific interactions with biomembranes altering the function of membrane-bound proteins, including the GABAA receptor. Mortality in alcohol toxicosis typically occurs because of respiratory and cardiac arrest as a result of profound CNS depression; therefore, general measures for resuscitation prevail in the initial treatment of severe alcohol toxicosis. Metabolism of alcohols alters the redox state in the liver, leading to hypoglycemia and lactic acidosis in some cases. In primates, treatment for methanol toxicosis is aimed at reducing accumulation of formate, thereby diminishing the metabolic acidosis and ocular damage characteristic in these species.
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PMID:Toxicology of selected pesticides, drugs, and chemicals. Short-chain alcohols. 218 Jan 93

We review the English-language literature on antibiotic-associated adverse reactions in patients with renal insufficiency in order to highlight this important but often overlooked clinical problem. Because many adverse reactions to antibiotics are not dependent on renal function, we have attempted to review only those reactions that are believed to be associated with renal insufficiency or that have been reported in patients with impaired renal function. Adverse effects of antibiotics in this setting can be divided into six major categories: neurologic toxicity, coagulopathy, nephrotoxicity, hypoglycemia, hematologic toxicity, and aminoglycoside inactivation by penicillins. Neurologic toxicity can be further divided into central nervous system toxicity consisting primarily of encephalopathy and seizures, ototoxicity, peripheral neuropathy, and neuromuscular blockade/respiratory depression. We explore the factors in uremia that may contribute to the susceptibility of patients with renal insufficiency to the adverse effects of antibiotics. Moreover, we make general recommendations regarding the use of the discussed antibiotics in patients with compromised renal function.
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PMID:Adverse antibiotic effects associated with renal insufficiency. 192 3

Previous prognostic studies of infants with intrauterine growth retardation (IUGR) have not adequately considered the heterogeneity of IUGR in terms of cause, severity, and body proportionality and have been prone to misclassification of IUGR because of errors in estimation of gestational age. Based on a cohort of 8719 infants with early-ultrasound-validated gestational ages and indexes of body proportionality standardized for birth weight, the consequences of severity and cause-specific IUGR and proportionality for fetal and neonatal morbidity and mortality were assessed. With progressive severity of IUGR, there were significant (all P less than .001) linear trends for increasing risks of stillbirth, fetal distress (abnormal electronic fetal heart tracings)O during parturition, neonatal hypoglycemia (minimum plasma glucose less than 40 mg/dL), hypocalcemia (minimum Ca less than 7 mg/dL), polycythemia (maximum capillary hemoglobin greater than or equal to 21 g/dL), severe depression at birth (manual ventilation greater than 3 minutes), 1-minute and 5-minute Apgar scores less than or equal to 6, 1-minute Apgar score less than or equal to 3, and in-hospital death. These trends persisted for the more common outcomes even after restriction to term (37 to 42 weeks) births. There was no convincing evidence that outcome among infants with a given degree of growth retardation varied as a function of cause of that growth retardation. Among infants with IUGR, increased length-for-weight had significant crude associations with hypoglycemia and polycythemia, but these associations disappeared after adjustment for severity of growth retardation and gestational age.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Impact of intrauterine growth retardation and body proportionality on fetal and neonatal outcome. 223 24

Cases of alcohol intoxication in children are common; they are encountered every day in Finland. Studies other than case studies of alcohol intoxication in children are few. Metabolic acidosis was a frequent finding in juvenile alcohol intoxication. Capillary or arterial blood pH was below normal (less than 7.36) in 61.4% of patients and bicarbonate (less than 22) in 55.3% of patients. pCO2 was varied; the higher the blood alcohol concentration the higher the pCO2. Metabolic acidosis and blood pH correlated with the blood alcohol concentration and consciousness. The lower the blood pH the higher the serum glucose. Hypoglycemia is the most common reported symptom in children under 5 years of age. In the present study three patients were slightly hypoglycemic. Hypokalemia was the most important change (in 12.2%) in serum electrolytes. Alcohol intoxication causes metabolic acidosis and respiratory depression in children. Metabolic acidosis reduces consciousness.
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PMID:Acute alcohol intoxications in children treated in hospital. 223 82

A study of acute alcohol influence (heavy drinker) on sudden unexpected death were analyzed as to age, sex, cause of death and along with the lethal blood alcohol content. Excess alcohol abuse by adults or middle aged women causatived acute intoxication with actual toxic depression of brainstem function (high blood levels, means 3,6 mg/g). Others (alcohol abuse) die by drowning, trauma, sudden coronary death (drinking spirits), cardiomyopathy, hypothermia or hypoglycemia (Diabetes). The autopsy findings are discussed.
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PMID:[Cause of death in severe acute ethanol intoxication]. 224 82


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