[Behcet's disease with neurologic complications in childhood].
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Adolescent↗
Biomedical subjects
H U Fisch
Publications and source records attributed to H U Fisch.
Self-reported somatization symptoms associated with risk for extreme alcohol use.
BACKGROUND: The high rates of alcohol use in the population, the increased general health care utilization associated with untreated alcohol problems, and the often diffuse nature of somatization symptoms led us to hypothesize that somatization symptoms might be associated with alcohol use. OBJECTIVE: To determine whether a relationship exists between somatization symptoms and alcohol use. DESIGN: Multivariable logistic regression models were used to analyze existing cross-sectional and 1-year longitudinal survey data from the National Institute of Mental Health Epidemiologic Catchment Area Program. SETTING: Community households. SUBJECTS: Probability sample. INTERVENTIONS: None. MAIN OUTCOME MEASURES: Prevalent and incident heavy or binge drinking ("extreme alcohol use"). These measures are part of the National Institute of Mental Health Epidemiologic Catchment Area Program public core data set that was collected without regard for specific hypotheses. RESULTS: After control for sex, age, and education, 13 self-reported somatization symptoms showed independent cross-sectional associations to prevalent extreme alcohol use. The greater the number of somatization symptoms, the greater the risk, up to a maximum increased odds ratio of 138 to 1, of having comorbid extreme alcohol use when reporting all 13 somatization symptoms in the model. A smaller set of items was associated with the risk for subsequent new onset of extreme alcohol use. CONCLUSIONS: Self-reported somatization symptoms could add to the detection of extreme alcohol use. In addition, primary care and other physicians should consider somatic complaints as possible indicators of concurrent and future risk for extreme alcohol use. Potential benefits of better detection of extreme alcohol use include supporting primary and secondary prevention efforts and reduced expenditures for the diagnostic workup of somatic complaints.
Alcoholism↗
Mechanism of the excessive sedative response of cirrhotics to benzodiazepines: model experiments with triazolam.
Mechanisms responsible for disproportional sedation resulting from triazolam administration to patients with cirrhosis were investigated. Ordinary sedative doses (0.25 mg) were given p.o. to 8 cirrhotics and 18 controls. Plasma concentrations of unbound drug were assessed by capillary gas chromatography and equilibrium dialysis. Median apparent oral clearances of unbound triazolam were 14.8 ml per min per kg in cirrhotics and 23.9 ml per min per kg in controls (p less than 0.01). Clearances were significantly correlated with severity of liver disease as assessed by the aminopyrine breath test (Rs = 0.77, n = 17, p less than 0.001). At a time when plasma concentrations of unbound triazolam were the same in both groups, i.e., 2.25 hr after dosing, flicker sensitivity at 5 Hz which was used as an index of CNS performance was impaired by a factor of 3.2 in cirrhotics and 1.4 in controls (p less than 0.01 for group difference). Performance was also significantly lower in cirrhotics with the digit symbol substitution test (p less than 0.05). It is concluded that, in patients with cirrhosis, disproportional sedation after benzodiazepine administration may be due not only to impaired drug elimination, but also to hypersensitivity of the brain.
Adult↗
The disulfiram-alcohol reaction: factors determining and potential tests predicting severity.
13 ambulatory alcoholics (3 women, 10 men) who consented to alcohol-aversive treatment with disulfiram were subjected to detailed investigations before, during, and after the disulfiram-alcohol reaction (DAR). The studies included quantitative estimation of liver function (aminopyrine breath test, ABT; galactose elimination capacity, GEC) prior to the DAR, measurement of alcohol and acetaldehyde plasma levels together with pulse rate and blood pressure during the DAR, and the effects of disulfiram on erythrocyte acetaldehyde-oxidizing capacity (AOC). As expected, the severity of the DAR showed considerable interindividual variation. However, the maximal fall in diastolic blood pressure was closely (r = 0.83; p less than 0.001; n = 13) related to peak acetaldehyde plasma level (AAPL). The decrease in systolic blood pressure was age dependent, individuals greater than 40 years exhibiting a larger drop for a given AAPL. The dependence of acetaldehyde formation on liver function was suggested by a significant correlation (r = 0.88; p less than 0.01; n = 8) between ABT and AAPL; this relationship was influenced by the prior intake of enzyme-inducing drugs. Measurements of AOC indicated that a disulfiram-induced maximal suppression is achieved already after 6 days of treatment reaching levels of 0.7 +/- 0.6 nmol/ml/min (SD) (compared to pretreatment values of 4.1 +/- 0.9). Mean values in untreated alcoholics and in subjects with alcoholic or nonalcoholic liver disease were not significantly different from controls.(ABSTRACT TRUNCATED AT 250 WORDS)
Acetaldehyde↗