Obesity, adiposity, and lengthening of the QT interval: improvement after weight loss.

OBJECTIVES: To determine the prevalence of QT interval prolongation in patients referred to an outpatient clinic for treatment of obesity; and to describe the change in the QT interval during rapid weight loss with a very-low-calorie diet. DESIGN: Retrospective and prospective review of charts and electrocardiograms. SUBJECTS: Five hundred twenty-two obese patients (411 female, 112 males) with a mean age 44 (18-78 y) and a mean initial weight of 116 kg (63-285 kg) completing 26 weeks of treatment between September, 1989 through to December, 1993. MEASUREMENTS: We reviewed the EKGs of all patients and serially monitored the QTc if greater than 0.44 s or if more than 23 kg was lost during treatment. The QTc interval was calculated with Bazzett's formula using both a manual method and an automated software program. In some patients, body composition was measured by hydrodensitometry. RESULTS: The QTc interval before treatment was 0.42 +/- 0.026 s by manual measurement and 0.41 +/- 0.021 s by automated measurement. Forty-one to 53% of patients showed a QTc interval of greater than 0.42 s and 10-24% demonstrated moderate prolongation (> 0.44 s). In those patients for whom repeat EKG were performed, QTc showed shortening with weight loss by both methods (mean +/- s.e. of 0.42 +/- 0.003 to 0.41 +/- 0.003 s, P < 0.01 manually and 0.41 +/- 0.003 to 0.40 +/- 0.003 s, p < 0.005 by automated program). Analyses were repeated excluding 179 patients with a cardiovascular-related diagnosis or intraventricular block and the results were similar. By regression analysis, gender and fat mass (FM) percentage above normal predicted the QTc. CONCLUSIONS: QT Interval prolongation is common in obesity. For each 50% increase in FM% above normal, there is a 5 ms increase in the QTc above a 'normal' upper limit of 0.40 and 0.38 s in women and men, respectively. Moreover, the QT interval shortens with weight loss. This change may represent an additional benefit of weight loss along with the improvement in other cardiovascular risk factors.

Analysis of Michigan Medicaid costs to treat HIV infection.

To obtain better understanding of the nature and cost of health care related to human immunodeficiency virus (HIV) infection, medical payment records were analyzed for 204 men, women, and children older than 60 months who had indications of HIV infection. The records were those of Michigan Medicaid, the General Assistance Medical Program, and the Resident County Hospitalization Program, with service dates on or after January 1, 1984, and which were processed by November 30, 1987. Patient payment records were coded according to whether the patient's condition was considered to be pre-HIV, HIV unrelated, possibly HIV related, or HIV related. Average monthly payments were found to be $150 for pre-HIV patient payment records, $114 for those HIV unrelated, $57 for those possibly related, and $1,213 for those related to HIV infection. HIV-related monthly payments rose from about $1,500 per month in the period 3 months prior to the patient's death to more than $8,000 in the last month of life. Men were found to have twice as many claims as women, and men's claims cost about three times as much. A higher percentage of women than men (91 percent versus 37 percent) received pre-HIV paid services, indicating a higher percentage of women were at least initially receiving Medicaid for reasons other than an HIV-related disability. Diagnostic categories that accounted for the bulk of the HIV-related health care utilization included infectious and parasitic diseases, acquired immunodeficiency syndrome, diseases of the respiratory system, and non-HIV-specific immunity disorders. Inpatient hospitalization accounted for more than 75 percent of the payments, followed by physician costs (11 percent), pharmacy costs (5 percent), and outpatient costs (3 percent). A total of 45, or about 22 percent of the recipients, received zidovudine (AZT) prescriptions at an average monthly cost of $404.

Self-poisoning: outcome and complications in the community hospital.

One hundred sixty cases of self-poisoning of patients aged 15 years and older were treated on the wards of the four community hospitals of Lansing, Michigan, in 1981. Most cases (91 percent) were intentional and represented suicide attempts. The complication rate was 13.8 percent and the overdose-related mortality rate 0.6 percent. Aspiration pneumonia was the most common complication, followed by respiratory failure and seizures. No patient with a level of consciousness stage 0 or 1 in the emergency room had a major overdose-related complication with permanent sequelae, and this group represented 80 percent of the cases. One possible guideline for managing the self-poisoner is level of consciousness in the emergency room.

Suicide attempt by drug overdose.

Suicide attempts by drug overdose are a growing health care problem, now reaching epidemic proportions. The patient who attempts suicide is typically a young, single adult female with interpersonal conflicts who takes an overdose of a prescribed drug, frequently a benzodiazepine. Patients who have recently been separated or divorced and those who are alcoholic, depressed or previously suicidal are also at risk. The family physician is in the best position to prevent suicide.

Transport of D- and L-tryptophan in Bacillus megaterium by an inducible permease.

Tryptophan-grown cells of Bacillus megaterium ATCC 19213 contain a permease system that transports both D- and L-tryptophan and is inhibited by sodium azide. Arginine-grown cells contain little tryptophan permease activity, suggesting that the system is inducible. Arginine represses the tryptophan permease as well as the transport system for leucine and phenylalanine. Kynurenine was a more effective inducer of the tryptophan transport system than either D- or L-tryptophan.

Tryptophan catabolism in Bacillus megaterium.

Bacillus megaterium grows in a medium containing L-tryptophan as the sole carbon, nitrogen, and energy source. Kynurenine, anthranilic acid, and catechol are metabolic intermediates, suggesting that this organism used the anthranilic acid pathway for tryptophan degradation. Cells that grow on L-tryptophan oxidize kynurenine, alanine, and anthranilic acid and the presence of tryptophan oxygenase (EC 1.13.1.12), kynureninase (EC 3.7.1.3), and catechol oxygenase (EC 1.13.1.1) in cell extracts provide additional evidence for the degradative pathway in B. megaterium. Tryptophan oxygenase is inhibited by sodium azide, potassium cyanide, and hydroxylamine, indicating that the enzyme has a functional heme group. D-Tryptophan is not a substrate for tryptophan oxygenase, and the D-isomer does not inhibit this enzyme. Formamidase (EC 3.5.1.9) and anthranilate hydroxylase are not detectable in extracts. Tryptophan catabolism is inducible in B megaterium and is subject to catabolite repression by glucose and glutamate. Arginine does not cause repression, and kynurenine induces both tryptophan oxygenase and kynureninase.