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G S Cooper

Publications and source records attributed to G S Cooper.

At least 19 recordsLinked to original sources

Occupational exposures and risk of systemic lupus erythematosus: a review of the evidence and exposure assessment methods in population- and clinic-based studies.

Epidemiologic and experimental research suggests a potential role of occupational exposures in the development of systemic lupus erythematosus (SLE). A plausible association has been identified in studies of occupational silica exposure and SLE, complemented by experimental studies in lupus-prone mice exploring potential mechanisms related to apoptosis and immune dysregulation. Experimental studies of the solvent trichloroethylene in lupus-prone mice provide evidence of effects on immune function, including increased production of autoantibodies and activation of CD4+ T cells. However, few studies of occupational solvent exposure and SLE have been conducted, and those that are available show little evidence of an association. There is some suggestion from the available studies of the potential influence of pesticides on SLE, but as with solvents, the specific type of pesticides that may be implicated is not known. Our understanding of the role of occupational exposures in SLE could be advanced by the development of larger, multisite or parallel studies that utilize similar questionnaire and exposure evaluation methods. Multiple studies using comparable exposure measures are needed to provide sufficient sample size for examining gene-environment interactions. We provide a general overview of data requirements and methods available for the assessment and evaluation of occupational exposures in clinical and population-based studies of SLE.

Animals↗

Lack of recording of systemic lupus erythematosus in the death certificates of lupus patients.

OBJECTIVE: To determine to what extent the diagnosis of systemic lupus erythematosus (SLE) in deceased lupus patients is under-reported in death certificates, and the patient characteristics associated with such an occurrence. METHODS: The death certificates of 76 of the 81 deceased SLE patients from two US lupus cohorts (LUMINA for Lupus in Minorities: Nature vs Nurture and CLU for Carolina Lupus Study), including 570 and 265 patients, respectively, were obtained from the Offices of Vital Statistics of the states where the patients died (Alabama, Georgia, North Carolina, South Carolina, Tennessee and Texas). Both cohorts included patients with SLE as per the American College of Rheumatology criteria, aged > or =16 yr, and disease duration at enrolment of < or =5 yr. The median duration of follow-up in each cohort at the time of these analyses ranged from 38.1 to 53.0 months. Standard univariable analyses were performed comparing patients with SLE recorded anywhere in the death certificate and those without it. A multivariable logistic regression model was performed to identify the variables independently associated with not recording SLE in death certificates. RESULTS: In 30 (40%) death certificates, SLE was not recorded anywhere in the death certificate. In univariable analyses, older age was associated with lack of recording of SLE in death certificates [mean age (standard deviation) 50.9 (15.6) years and 39.1 (18.6) yr among those for whom SLE was omitted and included on the death certificates, respectively, P = 0.005]. Patients without health insurance, those dying of a cardiovascular event and those of Caucasian ethnicity were also more likely to be in the non-recorded group. In the multivariable analysis, variables independently associated with not recording SLE as cause of death were older age [odds ratio = (95% confidence interval) 1.043 (1.005-1.083 per yr increase); P = 0.023] and lack of health insurance [4.649 (1.152-18.768); P = 0.031]. CONCLUSIONS: A high proportion of SLE diagnoses are not recorded in death certificates. Older patients and those without health insurance are more prone to have SLE not recorded. These findings do have implications for the assessment of the impact of this disease in epidemiological studies conducted using vital statistics records.

Adolescent↗

Single-nucleotide polymorphisms in the C-reactive protein (CRP) gene promoter that affect transcription factor binding, alter transcriptional activity, and associate with differences in baseline serum CRP level.

To investigate whether functional polymorphisms exist in the C-reactive protein (CRP) gene, i.e., ones that contribute directly to differences in baseline CRP among individuals, we sequenced a 1,156-nucleotide-long stretch of the CRP gene promoter in 287 ostensibly healthy people. We identified two single-nucleotide polymorphisms (SNPs), a bi-allelic one at nucleotide -409 (G-->A), and a tri-allelic one at -390 (C-->T-->A), both resident within the hexameric core of transcription factor binding E-box elements. Electrophoretic mobility shift assays confirmed that the SNP within the sequence (-412)CACGTG(-407) (E-box 1) modulates transcription factor binding, and that the one within (-394)CACTTG(-389) (E-box 2) supports transcription factor binding only when the -390 T allele is present. The commonest of four E-box 1/E-box 2 haplotypes (-409G/-390T) identified in the population supported highest promoter activity in luciferase reporter assays, and the rarest one (-409A/-390T) supported the least. Importantly, serum CRP in people with these haplotypes reproduced this rank order, i.e., people with the -409G/-390T haplotype had the highest baseline serum CRP (mean +/- SEM 10.9 +/- 2.25 microg/ml) and people with the -409A/-390T haplotype had the lowest (5.01 +/- 1.56 microg/ml). Furthermore, haplotype-associated differences in baseline CRP were not due to differences in age, sex, or race, and were still apparent in people with no history of smoking. At least two other SNPs in the CRP promoter lie within E-box elements (-198 C-->T, E-box 4, and -861 T-->C, E-box 3), indicating that not only is the quality of E-box sites in CRP a major determinant of baseline CRP level, but also that the number of E-boxes may be important. These data confirm that the CRP promoter does encode functional polymorphisms, which should be considered when baseline CRP is being used as an indicator of clinical outcome. Ultimately, development of genetic tests to screen for CRP expression variants could allow categorization of healthy people into groups at high versus low future risk of inflammatory disease.

Adult↗

Pesticide use and menstrual cycle characteristics among premenopausal women in the Agricultural Health Study.

Menstrual cycle characteristics may have implications for women's fecundability and risk of hormonally related diseases. Certain pesticides disrupt the estrous cycle in animals. The authors investigated the cross-sectional association between pesticide use and menstrual function among 3,103 women living on farms in Iowa and North Carolina. Women were aged 21-40 years, premenopausal, not pregnant or breastfeeding, and not taking oral contraceptives. At study enrollment (1993-1997), women completed two self-administered questionnaires on pesticide use and reproductive health. Exposures of interest were lifetime use of any pesticide and hormonally active pesticides. Menstrual cycle characteristics of interest included cycle length, missed periods, and intermenstrual bleeding. The authors used generalized estimating equations to assess the association between pesticide use and menstrual cycle characteristics, controlling for age, body mass index, and current smoking status. Women who used pesticides experienced longer menstrual cycles and increased odds of missed periods (odds ratio = 1.5, 95% confidence interval: 1.2, 1.9) compared with women who never used pesticides. Women who used probable hormonally active pesticides had a 60-100% increased odds of experiencing long cycles, missed periods, and intermenstrual bleeding compared with women who had never used pesticides. Associations remained after control for occupational physical activity.

Adult↗

Atomic force microscopy reveals defects within mica supported lipid bilayers induced by the amyloidogenic human amylin peptide.

To date, over 20 peptides or proteins have been identified that can form amyloid fibrils in the body and are thought to cause disease. The mechanism by which amyloid peptides cause the cytotoxicity observed and disease is not understood. However, one of the major hypotheses is that amyloid peptides cause membrane perturbation. Hence, we have studied the interaction between lipid bilayers and the 37 amino acid residue polypeptide amylin, which is the primary constituent of the pancreatic amyloid associated with type 2 diabetes. Using a dye release assay we confirmed that the amyloidogenic human amylin peptide causes membrane disruption; however, time-lapse atomic force microscopy revealed that this did not occur by the formation of defined pores. On the contrary, the peptide induced the formation of small defects spreading over the lipid surface. We also found that rat amylin, which has 84% identity with human amylin but cannot form amyloid fibrils, could also induce similar lesions to supported lipid bilayers. The effect, however, for rat amylin but not human amylin, was inhibited under high ionic conditions. These data provide an alternative theory to pore formation, and how amyloid peptides may cause membrane disruption and possibly cytotoxicity.

Aluminum Silicates↗

Systemic lupus erythematosus and genetic variation in the interleukin 1 gene cluster: a population based study in the southeastern United States.

BACKGROUND: Interleukin (IL)1alpha and IL1beta, and their endogenous receptor antagonist (IL1Ra), have been related to the pathology of systemic lupus erythematosus (SLE), but the role of IL1 polymorphisms in the aetiology of SLE is unknown. OBJECTIVE: To examine polymorphisms at IL1alpha -889(C-->T), IL1alpha +4845(C-->T), IL1beta -511(C-->T), IL1beta +3953(G-->T), and IL1Ra (86 bp VNTR) in a population based study of SLE in North Carolina and South Carolina. METHODS: Genotypes from 230 cases who met ACR classification criteria, and from 275 controls matched for age, sex, and state, were analysed separately for African Americans and whites. Odds ratios (ORs) were estimated by logistic regression models for each locus alone and also after adjusting for polymorphisms at adjacent loci. RESULTS: An increased risk of SLE for the IL1alpha -889C/C genotype compared with carriage of the -889T allele was found in both African Americans (OR = 3.1, p = 0.001) and whites (OR = 2.9, p = 0.005). In African Americans, carriage of the IL1beta -511T allele was associated with a higher risk of SLE than carriage of the -511C/C genotype (OR = 2.4, p = 0.017), independent of variation at IL1alpha -889. CONCLUSIONS: The observed associations support the hypothesis that genetic variation in IL1 is involved in the aetiology of SLE and merit further investigation.

Adolescent↗

CTLA-4 gene polymorphisms and systemic lupus erythematosus in a population-based study of whites and African-Americans in the southeastern United States.

Cytotoxic lymphocyte antigen-4 (CTLA-4) plays an important role in regulating T cell activation, and may help to limit T cell response under conditions of inflammation. Genetic variability in CTLA-4 has been implicated in the development of several autoimmune diseases. Some studies have described associations between CTLA-4 polymorphisms and systemic lupus erythematosus (SLE), but findings have been inconsistent. We examined polymorphisms in the CTLA-4 gene promoter region (-1722T/C, -1661 A/G, -318C/T) and exon I (+49G/A) with respect to SLE in a population-based case-control study in the southeastern US. Genotypes from 230 recently diagnosed cases and 276 controls were examined separately for African-Americans and whites. We observed no overall associations between SLE and the four CTLA-4 polymorphisms examined. Subgroup analyses revealed effect modification by age for the presence of the -1661G allele, yielding a significant positive association with SLE in younger (<35 years) African-Americans (OR = 3.3). CTLA-4 genotypes also interacted with HLA-DR2 and GM allotype to contribute to risk of SLE. These findings suggest allelic variation in this region of CTLA4 is not a major independent risk factor for SLE, but may contribute to risk of disease in younger African-Americans or in the presence of certain immunogenetic markers.

Adolescent↗

Association between baseline levels of C-reactive protein (CRP) and a dinucleotide repeat polymorphism in the intron of the CRP gene.

Elevation of baseline C-reactive protein (CRP) is associated with increased risk of cardiac disease. This increase might reflect low-grade inflammation, but differences in CRP serum levels might also have a genetic component. To test this possibility, we investigated whether a polymorphic GT-repeat in the intron of the CRP gene contributes to variation in baseline CRP. We found that the polymorphism was associated with differences in baseline CRP in both normal individuals and in patients with the inflammatory disease systemic lupus erythematosus, viz. donors carrying two GT(16) alleles, two GT(21)alleles, or GT(16/21) heterozygotes had two-fold lower serum CRP than those with other genotypes. The frequency of GT(16) and GT(21) was two-fold higher in Caucasians than in African-Americans, but there was no difference in allele distribution between patients and controls. It is not yet known how this genetic polymorphism mediates its effect on CRP expression, and it probably is not a systemic lupus erythematosus susceptibility factor. Rather, the CRP intron polymorphism likely modifies the disease phenotype. On the other hand, the fact that baseline CRP does have a genetic component suggests that in coronary disease, stratification of risk assessment based on CRP levels might be enhanced by consideration of this polymorphism.

Adult↗

Familial aggregation of Barrett's oesophagus, oesophageal adenocarcinoma, and oesophagogastric junctional adenocarcinoma in Caucasian adults.

BACKGROUND: Although familial clusters of Barrett's oesophagus and oesophageal adenocarcinoma have been reported, a familial predisposition to these diseases has not been systematically investigated. AIMS: To determine whether Barrett's oesophagus and oesophageal (or oesophagogastric junctional) adenocarcinoma aggregate in families. PATIENTS AND METHODS: A structured questionnaire eliciting details on reflux symptoms, exposure history, and family history was given to Caucasian case (n=58) subjects with Barrett's oesophagus, oesophageal adenocarcinoma, or oesophagogastric junctional adenocarcinoma, and to Caucasian control (n=106) subjects with symptomatic gastro-oesophageal reflux disease without Barrett's oesophagus. Reported diagnoses of family members were confirmed by review of medical records. RESULTS: The presence of a positive family history (that is, first or second degree relative with Barrett's oesophagus, oesophageal adenocarcinoma, or oesophagogastric junctional adenocarcinoma) was significantly higher among case subjects compared with controls (24% v 5%; p<0.005). Case subjects were more likely to be older (p<0.001) and male (74% v 43% male; p<0.0005) compared with control subjects. In a multivariate logistic regression analysis, family history was independently associated with the presence of Barrett's oesophagus, oesophageal adenocarcinoma, or oesophagogastric junctional adenocarcinoma (odds ratio 12.23, 95% confidence interval 3.34-44.76) after adjusting for age, sex, and the presence of obesity 10 or more years prior to study enrollment. CONCLUSIONS: Individuals with Barrett's oesophagus, oesophageal adenocarcinoma, or oesophagogastric junctional adenocarcinoma are more likely to have a positive family history of Barrett's oesophagus, oesophageal adenocarcinoma, or oesophagogastric junctional adenocarcinoma than individuals without Barrett's oesophagus, oesophageal adenocarcinoma, or oesophagogastric junctional adenocarcinoma. A positive family history should be considered when making decisions about screening endoscopy in patients with symptoms of gastro-oesophageal reflux.

Adenocarcinoma↗

Differences by race, sex and age in the clinical and immunologic features of recently diagnosed systemic lupus erythematosus patients in the southeastern United States.

We examined the prevalence of clinical and immunologic features of systemic lupus erythematosus (SLE) by race, sex and age in a population-based study of 265 SLE patients. Patients fulfilled the American College of Rheumatology classification criteria. The median time between diagnosis and study enrollment was 13 months. The clinical and hematologic data were limited to occurrences up to 6 months after the diagnosis date, as documented in medical records. We used sera collected at study enrollment from 244 (92%) patients for serologic testing of autoantibodies. The associations between clinical and immunological features of SLE and age, sex and race were examined using logistic regression. The effect of each of these variables was examined adjusting for the other two demographic factors. Mean age at diagnosis was 6 years younger among African-Americans and other minorities compared with white patients (P < 0.01). Discoid lupus, proteinuria, anti-Sm and anti-RNP autoantibodies were more commonly seen in African-American patients, with odds ratios higher than 3.0. Photosensitivity and mucosal ulcers were noted less often in African-American patients. Proteinuria, leukopenia, lymphopenia and thrombocytopenia were approximately three times more common in men compared with women. The prevalence of oral or nasal ulcers and anti-DNA autoantibodies declined with age. The extent to which the differences we observed reflect genetic or environmental influences on the disease process should be investigated.

Adult↗

Determination of county-level prostate carcinoma incidence and detection rates with Medicare claims data.

BACKGROUND: To the authors' knowledge, national-level population-based data regarding prostate carcinoma incidence and detection currently are not available. The availability of such data could identify those regions with a disproportionately high cancer incidence as well as the population-level association between prostate carcinoma detection and incidence. METHODS: Inpatient, hospital outpatient, and physician/supplier Medicare claims from 1997 were used to identify incident cases of prostate carcinoma in men age > or = 65 years and to calculate state and county-level incidence rates. The 1991 and 1997 claims data were used to determine small area rates of prostate-specific antigen (PSA) testing and prostate biopsy and to determine their correlation with incidence. RESULTS: The calculated incidence rates for 1997 were 890 per 100,000 and 1196 per 100,000, respectively, in white males and African-American males and varied substantially between counties (i.e., 25--75th percentile, 676--1124 per 100,000). Rates of PSA and prostate biopsy increased markedly from 1991 to 1997 in both white men (1580 per 100,000 to 24,286 per 100,000) and African-American men (1277 per 100,000 to 15,190 per 100,000), and considerable variation in detection between counties was observed. Counties that had higher rates of prostate biopsy also had higher age-adjusted incidence rates, and county-level PSA testing was found to be associated with incidence in African-American patients, but not in white patients. CONCLUSIONS: Medicare claims may provide an alternative source of population-based data, particularly for areas in which registry data are not readily available or are of limited scope. In addition, claims provide otherwise unavailable national data concerning cancer detection.

Aged↗

Measures of menopausal status in relation to demographic, reproductive, and behavioral characteristics in a population-based study of women aged 35-49 years.

The purpose of this cross-sectional analysis of women aged 35-49 years from the Third National Health and Nutrition Examination Survey, conducted between 1988 and 1994, was to assess associations with menopausal status based either on menstrual cycle patterns or on elevated (>20 IU/liter) follicle-stimulating hormone. Menstrual cycle-based menopausal status was defined for women who had not had surgical menopause by months since the last period (<2, 2-12, and >12 months for pre-, peri-, and postmenopause, respectively). Logistic regression was adjusted for age, smoking, and unilateral oophorectomy. Higher body mass index (> or =30 kg/m(2) compared with < 25.0 kg/m(2)) was associated with a lower likelihood of elevated follicle-stimulating hormone (odds ratio (OR)=0.6, 95% confidence interval (CI): 0.4, 0.9) but this association was not seen with the menstrual measure of menopause. Exercise (three or more times per week) was associated with a lower likelihood of being postmenopausal on the basis of menstrual (OR = 0.3, 95% CI: 0.2, 0.7) and hormonal (OR = 0.6, 95% CI: 0.4, 1.0) measures. Alcohol use also tended to be associated with postmenopausal status by either measure, but not significantly so. There was little evidence of associations with ethnicity, education, age at menarche, number of livebirths, and oral contraceptive use. Menstrual-based definitions of menopause can be misclassified for women with menstrual irregularity. This might explain why obese women were classified menstrually as menopausal while remaining hormonally premenopausal.

Adult↗

Impact of a guideline-based disease management team on outcomes of hospitalized patients with congestive heart failure.

BACKGROUND: Congestive heart failure is the most common reason for hospitalization in the United States, and guidelines to improve the quality of care for patients with congestive heart failure have been developed. However, adherence is typically low. We hypothesized that a guideline-based care management team would result in greater quality and efficiency of care than guidelines alone. METHODS: A faculty cardiologist and nurse care manager at an academic medical center reviewed each patient's data and made guideline-based recommendations. Hospital length of stay, total costs, and use of recommended guidelines were compared between 173 patients before team implementation but with available guidelines, 283 care-managed patients, and 126 concurrent non-care-managed patients. RESULTS: Care-managed patients achieved higher rates of use of angiotensin-converting enzyme inhibitor than baseline or non-care-managed patients (95%, 60%, and 75%, respectively; P<.001), as well as increased adherence to guidelines for daily weight monitoring and assessment of left ventricular function. Hospital length of stay was lower (median, 3, 4, and 5 days, respectively; P<.001) as were costs of hospitalization (median, $2934, $3209, and $4830, respectively; P<.01). These differences persisted after adjustment for severity of illness. CONCLUSIONS: When compared with dissemination of guidelines alone, an active care management approach was associated with significant improvements in quality and efficiency of care for hospitalized patients with congestive heart failure.

Aged↗

Age at natural menopause and the risk of epithelial ovarian cancer.

OBJECTIVE: To investigate the relationship between age at natural menopause and risk of developing epithelial ovarian cancer. METHODS: Using data from six population-based, case-control studies conducted in the United States, age at natural menopause among 1411 women with epithelial ovarian cancer and 6380 control subjects were analyzed using survival analysis methods, including Kaplan-Meier and proportional hazards models. Subjects ranged from 20 to 81 years of age. RESULTS: The median age at natural menopause was 50 years among cases compared with 51 years among controls, a difference of borderline statistical significance (P =.06). The hazard ratio for the relationship between case-control status and age at natural menopause was 1.09 (95% confidence interval 0.99, 1.20). Controlling for potential confounders including parity, oral contraceptive use, tubal ligation, smoking, and body mass index did not appreciably change this association. There was little evidence of an association between early age at natural menopause and early onset ovarian cancer (diagnosis age under 48 years). CONCLUSION: We observed a weak association between ovarian cancer risk and age at natural menopause and, among women with early onset disease, there was little evidence to suggest that early menopause is related to ovarian cancer. Thus, there seems little need for increased surveillance or screening for ovarian cancer among women with early natural menopause.

Adult↗

The delivery of preventive services for patient symptoms.

BACKGROUND: Although data are available on rates of delivery of preventive services by primary care physicians, the proportion of services delivered because of related symptoms or signs, rather than for primary or secondary prevention of disease is not known. METHODS: Research nurses directly observed 4454 consecutive visits to 138 practicing family physicians. Direct observation was used to identify delivery of 36 different services recommended by the U.S. Preventive Services Task Force and to assess whether delivery of these services was associated with related signs or symptoms. RESULTS: One or more preventive services were delivered in 33% of visits, with rates ranging from 0.2% (HIV prevention) to 19.9% (tobacco counseling). In contrast to pure prevention, services were frequently performed for assessment or care of symptoms or signs, with the ratio ranging from 0% (eye examination; car seat, poison control, and HIV prevention counseling) to 66.7% (hearing test). Physicians varied considerably in the frequency at which their delivery of recommended preventive services was associated with patient symptoms, from 0% to 100% for screening services and from 0% to 100% for counseling services. CONCLUSIONS: Because of the illness focus of most primary care visits, preventive service delivery is often associated with related signs or symptoms. Care of illnesses appears to present an important impetus and perhaps teachable moments for providing preventive care. Clinician variability in preventive service delivery for patient symptoms shows an opportunity to improve the primary and secondary prevention focus of practice to meet public health prevention goals.

Adolescent↗

Effectiveness of endoscopy in patients admitted to the intensive care unit with upper GI hemorrhage.

BACKGROUND: Esophagogastroduodenoscopy (EGD) is generally indicated for the management of patients admitted to intensive care units (ICUs) with upper gastrointestinal (GI) hemorrhage but its impact in community practice has not been measured. Thus, the effectiveness of 3 EGD factors, viz., accurate initial diagnosis, performance within 24 hours of admission (early EGD), and appropriate intervention, was examined. METHODS: Records of 214 patients admitted to the ICU of 10 metropolitan hospitals with upper GI hemorrhage were reviewed. Unadjusted and severity-adjusted associations of the 3 EGD factors with length of hospital stay, length of ICU stay, readmission to ICU, recurrent bleeding, surgery, and death were evaluated. RESULTS: Inaccurate diagnosis occurred in 10% of patients at initial EGD and was associated with significant increases in risk of recurrent bleeding (70% vs. 11%, p < 0.001), rate of surgery (20% vs. 4%, p < 0.05), length of hospital stay (median 7.5 vs. 5 days, p < 0.005), length of ICU stay (median 4 vs. 2 days, p < 0.005), and rate of readmission to ICU (20% vs. 0.6%, p < 0.001). These associations persisted after adjusting for severity of illness. Early EGD performed in 82% of patients was associated with significant severity-adjusted reductions in hospital (-33%: 95% CI [-45%, -18%]) and ICU (-20%: 95% CI [-24%, -3%]) stay. Appropriate intervention at initial EGD, performed in 84% of patients, was associated with reductions in severity-adjusted length of ICU stay (-18%: 95% CI [-32%, 0%]) and rate of recurrent bleeding (odds ratio = 0.37, 95% CI [0.13, 1.06]). CONCLUSIONS: Early, accurate EGD with appropriate therapeutic intervention is effective as practiced in the community and is associated with improved outcomes for patients with upper GI hemorrhage admitted to the ICU. Inaccurate diagnosis at initial EGD is uncommon but has a significant adverse association with all outcome measures.

Endoscopy, Digestive System↗

Evaluation of a rapid urine amylase test using post-ERCP hyperamylasemia as a model.

OBJECTIVE: The initial diagnosis of acute pancreatitis is often based on clinical criteria together with elevations of serum amylase and lipase. A reliable bedside urine test could facilitate the early diagnosis of pancreatitis. We evaluated a rapid urine amylase test (Rapignost) by using post-ERCP hyperamylasemia as a human model of acute development of hyperamylasemia suggestive of pancreatitis. METHODS: Seventy-five patients undergoing ERCP were prospectively evaluated. Patients with renal insufficiency, hyperlipidemia, or hyperglycemia were excluded. Before ERCP, patients had serum amylase and lipase measured, and urine amylase tested with the Rapignost test strip. At 4 and 16-24 h post-ERCP, a serum and urine (test strip) amylase were measured again; the adequacy of urine collection was verified by measuring a 2-h creatinine clearance. Patients were clinically assessed for the development of clinical pancreatitis. The concordance of the strip result with post-ERCP hyperamylasemia was assessed. RESULTS: The sensitivity of the test strip for the detection of hyperamylasemia was greatest at 16-24 h post-ERCP (78%). Specificity was uniformally high (100% specificity at 16-24 h post-procedure). The test strip was positive in all cases of clinical pancreatitis. Of three cases of clinically evident ERCP-induced pancreatitis, only one was urine test strip positive by 4 h post-procedure. CONCLUSIONS: Using post-ERCP hyperamylasemia as a model, the Rapignost rapid urine amylase test strip was only marginally sensitive but highly specific for hyperamylasemia. The urine test strip was positive in all cases of clinical pancreatitis and may be a useful bedside test for the diagnosis of acute pancreatitis.

Adolescent↗

Immunoglobulin GM and KM allotypes in systemic lupus erythematosus.

Genetic variation in immunoglobulin gamma (GM) and kappa (KM) chains was associated with systemic lupus erythematosus (SLE) in some studies. However, the data are conflicting, and only one study examined associations in African-Americans. We examined GM and KM allotypes, by race, in a population-based case-control study of SLE. Sera from patients (n = 222) and controls (n = 273) were typed for GM and KM allotypes by a hemagglutination inhibition method. GM phenotypes were not significantly associated with SLE in African-Americans or Caucasians. However, the frequency of KM phenotypes in Caucasian patients was significantly different from that in controls (p = 0.032). KM3,3 was associated with an increased risk, whereas KM1,3 was associated with a lower relative risk of SLE. In African-Americans, however, the pattern of associations with KM phenotypes differed from that in Caucasians, and the overall difference between patients and controls was not statistically significant.

Adolescent↗