Practice patterns for the elicitation of sexual history, education, and counseling among providers of STD services: results from the gonorrhea community action project (GCAP)

BACKGROUND: The frequently asymptomatic nature and high incidence of severe complications of sexually transmitted diseases (STD) calls for targeted efforts to identify those at greatest risk. Earlier studies have shown inconsistencies regarding STD evaluation by primary care clinicians and physicians. However, the literature regarding the consistency of practice patterns regarding elicitation of sexual history is limited. We examined practice patterns for the elicitation of sexual history among providers across seven sites nationwide. METHODS: As part of a multisite study to encourage health seeking for populations specifically at risk for gonorrhea (GC) and other STDs, semistructured interviews that included questions regarding sexual history elicitation were conducted with 208 service providers in a total of 121 publicly and privately funded clinics, managed care organizations (MCOs), hospital clinics, community- and school-based clinics in Denver, New York, Los Angeles, Birmingham, St. Louis, Indianapolis, and Prince Georges County, MD. RESULTS: Among the providers interviewed, practice patterns for the elicitation of sexual history were inconsistent. Sexual histories were described as routine (i.e., solicited from every client regardless of reason for visit) in 57% of sites. Providers most frequently asked clients their number of sex partners (57%), their contraceptive history (55%), and STD history (34%). Client discomfort among 46% and provider discomfort among 13% was cited as barriers to the elicitation of sexual history. A quarter (26%) of providers agreed that the elicitation of sexual history can be fostered by improved provider communication skills and 16% agreed increasing training and experience for providers is needed. CONCLUSIONS: These findings suggest that interventions with providers to standardize sexual history elicitation can help to reduce barriers to prevention, diagnosis, and treatment of STD.     

Mass spectrometric analysis of tobacco-specific nitrosamine-DNA adducts in smokers and nonsmokers

A gas chromatography, negative ion chemical ionization mass spectrometry (GC-NICI-MS) based assay for tobacco-specific nitrosamine adducts of DNA is described. The assay is based on the observation that acid hydrolysis of DNA from animals treated with tobacco-specific nitrosamines releases 4-hydroxy-1-(3-pyridyl)-1-butanone (HPB). HPB and the internal standard [4,4-D2]HPB are derivatized with pentafluorobenzoyl chloride and the resulting HPB-pentafluorobenzoate is purified by high-performance liquid chromatography prior to GC-NICI-MS analysis. DNA from human peripheral lung and tracheobronchial tissue, collected at autopsy, was analyzed for acid-released HPB. The mean HPB level (fmol/mg of DNA) for peripheral lung DNA was 11 +/- 16 (SD, n = 9) for smokers and 0.9 +/- 2.3 (n = 8) for nonsmokers. Mean adduct levels in tracheobronchus were 16 +/- 18 (n = 4) for smokers and 0.9 +/- 1.7 (n = 4) for nonsmokers. These are the first measurements of tobacco-specific nitrosamine-DNA adducts in humans. Further studies comparing the levels of DNA and globin adducts will provide a better understanding of the metabolic activation of tobacco-specific nitrosamines in humans and may provide a more accurate indication of an individual's risk of developing tobacco-related cancer.     

Ethylnitrosourea-induced transplacental carcinogenesis in the mouse: tumor response, DNA binding, and adduct formation

We have confirmed previous results which suggest that transplacental exposure of fetal mice to carcinogens does not cause an increase in tumor incidence as they mature unless treatment occurs after midorganogenesis. In C3HeB/FeJ mice we found a negligible increase in tumor incidence and multiplicity following transplacental exposure to the direct-acting carcinogen ethylnitrosourea (ENU) on gestation day 10, but significant increases in lung and liver tumor incidence following exposure on days 13 or 15 or in adults. To explore the possibility that this observed difference is due to differences in the biodistribution of the carcinogen or its interaction with cellular macromolecules, the level of covalent binding between ENU and fetal and maternal DNA following an i.p. injection of a dose of 50 mg/kg of tritium-labeled ENU was measured 30 min after its injection into pregnant females on days 10, 13, and 15 of gestation. The DNA from fetal and maternal lung, liver, and brain was isolated and the amount of covalent binding estimated from the dpm/mg DNA recovered. Samples of DNA were hydrolyzed and chromatographed to determine that the bound tritium was associated with ENU-DNA adducts and not as a product of DNA synthesis. The level of binding of ENU to fetal DNA was equivalent at all gestation days studied but was significantly less than maternal tissues. Binding to the DNA of maternal liver was 4-fold greater than to fetal DNA while maternal lung and brain DNA were bound at intermediate levels. We conclude that the lack of carcinogenic response to ENU documented here, in fetal mice exposed early in gestation (day 10), is not due to differences in ENU binding to fetal DNA during development.     

Factors affecting the plasma insulin concentration shortly after accidental injury in man.

There are conflicting reports on plasma insulin concentrations in the acutely injured. Plasma insulin and glucose concentrations have been measured in 504 patients within 8 h of injury, and related to the severity of injury as assessed by the injury severity score (ISS). As in previous surveys of injured patients, an extremely wide range of insulin concentrations was found (2-141 mU/l). Most of the variability occurred at lower severities of injury. In very severely injured patients (ISS greater than or equal to 30), insulin concentrations were uniformly suppressed (less than 20 mU/l), especially in relation to the hyperglycaemia in these patients. Two small subgroups, patients dying within 3 h of injury and known psychiatric patients on psycho-active drugs, differed from the general pattern in displaying elevated insulin concentrations despite very severe injuries. The results bear out the idea that insulin secretion is usually acutely suppressed by adrenaline after severe injury; after less severe injuries, however, the response is much less uniform.     

Adherence to guidelines for continuous morphine sulfate infusions

A retrospective chart audit evaluating the degree of adherence of health-care personnel to guidelines for continuous intravenous infusion of morphine sulfate was conducted. The audit was conducted one year after implementation of guidelines for administering morphine sulfate by continuous i.v. infusion. Audit criteria were developed from these guidelines and used to evaluate justification of use, adherence of physicians, pharmacists, and nurses to procedures, and patient outcome. Audits were completed for 11 of 13 patients who received morphine sulfate infusions during the one-year study period. All patients met the standard for justification of use. Adequate patient outcome, defined as chart-documented pain relief within 24 hours, was achieved in six patients. The median time to pain control was 20 hours (range 4-168 hours). Physicians' and pharmacists' adherence to the guidelines was acceptable in over 80% of patients, but documentation of hourly monitoring of blood pressure and respiratory rate and rhythm by nurses met the standard in only 55% of patients; this may have been related to lack of a designated place in the chart for recording this information. The morphine sulfate infusion guidelines appear to contribute to safe and effective therapy.     

Hormonal and metabolic responses to glucose infusion in sepsis studied by the hyperglycemic glucose clamp technique

Although nutritional support is vital to treatment of severe sepsis, the septic patient does not respond normally to glucose infusion. We have used the hyperglycemic glucose clamp technique to investigate the initial hormonal and metabolic responses of the septic patient to glucose under controlled conditions. The plasma glucose concentration was raised to and maintained at 12 mmol/liter for 2 hr in 12 septic patients and 11 normal controls. Glucose utilization, assessed from the amount infused, was significantly depressed in the patients, despite similar plasma insulin concentrations in the two groups. Forearm glucose uptake was similarly impaired. Despite very similar plasma free fatty acid concentrations in the two groups, which were suppressed equally by the glucose infusion, whole-body fat oxidation was elevated in the patients compared with the controls, and suppressed to a lesser extent in response to glucose. Glycerol and ketone body concentrations were elevated in the patients in keeping with a picture of accelerated release, clearance, and oxidation of fatty acids. Plasma cortisol, epinephrine, and norepinephrine concentrations were elevated in the septic patients in a severity-related manner, but not to high levels compared with experimental work. Norepinephrine showed no response to the glucose infusion in either group. Plasma glucagon concentrations were not significantly elevated in the septic patients. We conclude that the hyperglycemic glucose clamp provides a useful model for studying glucose intolerance in sepsis. Impaired glucose utilization in septic patients is associated with increased fat oxidation, although the hormonal basis for these changes is still unclear.     

Activation of the Ki-ras protooncogene in spontaneously occurring and chemically induced lung tumors of the strain A mouse.

The strain A mouse has a high incidence of spontaneous lung tumors and is susceptible to lung tumor induction by chemical carcinogens. By utilizing transfection assay, Southern blot analysis, and DNA amplification techniques, we have detected an activated Ki-ras gene in the DNAs of both spontaneously occurring and chemically induced lung tumors of strain A mice. The point mutations in the spontaneous lung tumors were in both codon 12 (60%) and codon 61 (30%). In contrast, 100% of the mutations in the Ki-ras gene detected in methylnitrosourea-induced lung tumors and 93% of the mutations in the Ki-ras genes detected in benzo[a]pyrene-induced lung tumors were in codon 12, whereas 90% of the mutations in the Ki-ras genes detected in ethyl carbamate-induced lung tumors were in codon 61. The selectivity of mutations in the Ki-ras oncogene observed in chemically induced tumors, as compared to spontaneous tumors, suggests that these chemicals directly induce point mutations in the Ki-ras protooncogene. These data indicate that the strain A mouse lung tumor model is a very sensitive system to detect the ability of chemicals to activate the Ki-ras protooncogene in lung tissue.