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PubMed2005

XRCC1 and XRCC3 polymorphisms and their role as effect modifiers of unsaturated fatty acids and antioxidant intake on colorectal adenomas risk.

Whereas animal and in vitro studies support a role of unsaturated fatty acids in colon carcinogenesis, the epidemiologic evidence is inconclusive. Using a large sigmoidoscopy-based case-control study (753 cases and 799 controls) in Los Angeles County, we investigated possible associations between single-nucleotide polymorphisms in the XRCC1 (codons 194 Arg/Trp and codon 399 Arg/Gln) and XRCC3 (codon 241 Thr/Met) genes and colorectal adenoma risk and their possible role as modifiers of the effect of monounsaturated fatty acid, the ratio of omega-6/omega-3 polyunsaturated fatty acids, and antioxidant intake. We found no evidence of associations between the XRCC1 codon 194 Arg/Trp or Trp/Trp genotypes and the XRCC3 codon 241 Thr/Met or Met/Met genotypes. Subjects with the XRCC1 Gln/Gln genotype were inversely associated with adenoma risk (odds ratio, 0.6; 95% confidence interval, 0.4-0.9; P = 0.01) when compared with subjects with Arg/Arg and Arg/Gln genotypes combined. We found no evidence of gene-dietary fat interactions for the XRCC3 codon 241 polymorphism. However, our data suggest an XRCC1-unsaturated fat interaction. High monounsaturated fatty acid intake was associated with adenoma risk only among subjects with the XRCC1 codon 194 Arg/Arg and codon 399 Gln/Gln combined genotypes (P for interaction = 0.018). High omega-6/omega-3 polyunsaturated fatty acid ratios were associated with adenoma risk among subjects with the XRCC1 codon 194 Arg/Arg and codon 399 Gln/Gln or the codon 194 Arg/Trp or Trp/Trp and codon 399 Arg/Arg or Arg/Gln combined genotypes (P for interaction = 0.026). These interactions were not modified by antioxidant intake. However, low antioxidant intake was associated with an inverse association only among subjects with the XRCC1 codon 194 Arg/Trp or Trp/Trp and codon 399 Arg/Arg or Arg/Gln combined genotypes (P for interaction = 0.022), which was independent of unsaturated fat intake. Our data suggest that the XRCC1 codon 194 and codon 399 single nucleotide polymorphisms may modify the effect of unsaturated fatty acid and antioxidant intake and that this XRCC1 effect modification may explain, in part, previously reported inconsistencies on the role of unsaturated fatty acids and adenoma risk.

Adenoma↗
PubMed2001

The use of common genetic polymorphisms to enhance the epidemiologic study of environmental carcinogens.

Overwhelming evidence indicates that environmental exposures, broadly defined, are responsible for most cancer. There is reason to believe, however, that relatively common polymorphisms in a wide spectrum of genes may modify the effect of these exposures. We discuss the rationale for using common polymorphisms to enhance our understanding of how environmental exposures cause cancer and comment on epidemiologic strategies to assess these effects, including study design, genetic and statistical analysis, and sample size requirements. Special attention is given to sources of potential bias in population studies of gene--environment interactions, including exposure and genotype misclassification and population stratification (i.e., confounding by ethnicity). Nevertheless, by merging epidemiologic and molecular approaches in the twenty-first century, there will be enormous opportunities for unraveling the environmental determinants of cancer. In particular, studies of genetically susceptible subgroups may enable the detection of low levels of risk due to certain common exposures that have eluded traditional epidemiologic methods. Further, by identifying susceptibility genes and their pathways of action, it may be possible to identify previously unsuspected carcinogens. Finally, by gaining a more comprehensive understanding of environmental and genetic risk factors, there should emerge new clinical and public health strategies aimed at preventing and controlling cancer.

Animals↗
PubMed2005

PON1 polymorphism, diabetes mellitus, obesity, and risk of myocardial infarction: Modifying effect of diabetes mellitus and obesity on the association between PON1 polymorphism and myocardial infarction.

PURPOSE: Previous studies on PON1 gene polymorphism and the risk of coronary atherosclerotic diseases have been inconsistent. This may be in part due to population difference in prevalence of high oxidative stress and its modifying effect on the association. Diabetes and obesity are two major risk factors of myocardial infarction (MI) and associated with high oxidative stress. We investigated the association between PON1 Q192R polymorphism and the risk of myocardial infarction (MI) and in particular, whether the association can be modified by diabetes mellitus (DM) and obesity. METHODS: We conducted a case-control study, including 154 MI cases and 154 controls enrolled in Beijing, China. Epidemiological and clinical data and PON1 Q192R genotype were obtained from each subject. RESULTS: Without considering the modifying effect of DM and obesity, PON1 Q192R polymorphism was not associated with MI. When simultaneously examining the joint association of this polymorphism, DM, and obesity with MI, as compared to subjects with QQ genotypes and without DM and obesity, subjects with QR/RR genotypes and with either DM or obesity had significantly higher risk of MI (OR = 3.6, 95% CI: 1.5-8.7). CONCLUSION: Our data suggest that PON1 Q192R polymorphism was not independently associated with MI but further increased the risk of MI among the subjects with DM, obesity, or both, the conditions associated with high oxidative stress.

Aryldialkylphosphatase↗
PubMed2004

Reliability of sickness certificates in detecting potential sick leave reduction by modifying working conditions: a clinical epidemiology study.

BACKGROUND: Medical sickness certificates are generally the main source for information when scrutinizing the need for aimed intervention strategies to avoid or reduce the individual and community side effects of sick leave. This study explored the value of medical sickness certificates related to daily work in Norwegian National Insurance Offices to identify sick-listed persons, where modified working conditions might reduce the ongoing sick leave. METHODS: The potential for reducing the ongoing sick leave by modifying working conditions was individually assessed on routine sickness certificates in 999 consecutive sick leave episodes by four Norwegian National Insurance collaborators, two with and two without formal medical competence. The study took place in Northern Norway in 1997 and 1998. Agreement analysed with differences against mean, kappa, and proportional-agreement analysis within and between groups of assessors was used in the judgement. Agreements between the assessors and the self-assessment of sick-listed subjects were additionally analysed in 159 sick-leave episodes. RESULTS: Both sick-listed subjects and National Insurance collaborators anticipated a potential reduction in sick leave in 20-30% of cases, and in another 20% the potential was assessed as possible. The chance corrected agreements, however, were poor (k < 0.20) within and between groups of National Insurance collaborators. The agreement between National Insurance collaborators and the sick-listed subjects was no better than chance. Neither extended medical information nor formal medical competence increased agreement in cases where modified working conditions might have reduced sick leave. CONCLUSION: Information in medical sickness certificates proved ineffective in detecting cases where modified working conditions may reduce sick leave, and focusing on medical certificates may prevent identification of needed interventions. Strategies on how to communicate directly with sick-listed subjects would enable social authorities to exploit more of the sick leave reduction potential by modifying the working conditions than strategies on improving medical information.

Adult↗
PubMed1997

[Surgical therapy of the peptic ulcer in a hospital specializing in gastroenterology. Effects of therapy with h2 antagonists].

To evaluate how the introduction of H2-receptor antagonists has modified the epidemiology of surgical management of peptic ulcer, we examined data records of patients operated on for gastric or duodenal ulcer in our Institute. Patients were divided into two groups: a) patients operated from 1970 to 1979 and b) patients operated from 1980 to 1992. The comparison between the two groups showed the following variations: decrease in male/female ratio from 8 to 4.4:1 (p = 0.0009); decrease in duodenal/ gastric ulcer ratio from 5 to 3.5:1 (p = 0.02); decrease in elective/emergency surgery ratio from 16 to 6.4:1 (p = 0.00006); increase in mean age of patients undergoing emergency operations from 51 to 58 years (p = 0.05); decrease in elective/emergency surgery ratio for gastric ulcer from 17.5 to 5.3:1 (p = 0.03), above all for the increase in emergency operations for hemorrhage; decrease in the prevalence of operations for refractory duodenal ulcer from 49% to 36% (p = 0.00009). Our findings show that H2-receptor antagonists have greatly modified the epidemiology of surgical treatment of peptic ulcer with a clear decrease in elective surgery for refractory duodenal ulcer in men and an increase in emergency surgery for gastric ulcer.

Adolescent↗
PubMed2003

Molecular epidemiology of pancreatic cancer.

Pancreatic cancer is the fourth leading cause of cancer-related death in the United States. Currently there is no early diagnostic test and no effective treatment options for this deadly disease. Prevention of pancreatic cancer is difficult because little is known about its etiology. The main modifiable risk factors for pancreatic cancer include cigarette smoking and dietary factors. Information from molecular epidemiological study of pancreatic cancer is very limited. DNA adducts derived from exposure to polycyclic aromatic hydrocarbon, aromatic amines, and heterocyclic amines have been detected in human pancreatic tissues. DNA damages derived from oxidative stress and lipid peroxidation are also present in the pancreas. No study has demonstrated a main effect of carcinogen-metabolizing genes and DNA repair genes on the risk of pancreatic cancer thus far. However, significant effects of these genes have been observed among individuals with known carcinogen exposure, such as smoking. A number of environmental and lifestyle factors, such as smoking, alcohol, coffee consumption, and exposure to organochlorine or hydrocarbon solvent, have been associated with the frequency and spectrum of K-ras mutation in pancreatic tumors. Dietary folate intake and serum levels of folate have been associated with the risk of pancreatic cancer among male smokers. These findings demonstrate the potential of the molecular epidemiology approach in understanding the etiology of pancreatic cancer. Further efforts should be made to understand the interactive relationship between genetic and environmental factors in the etiology of pancreatic cancer, which will in turn be important in identifying the high-risk population for the primary prevention of this deadly disease.

Carcinogens↗
PubMedDate not supplied

Immune activation as effect modifier of atherogenesis in chronic infection.

Although no study has proven that infections cause atherosclerotic disease, findings suggest that exposure to infections such as Chlamydia pneumoniae, Helicobacter pylori, and bacterial infections related to periodontal disease or smoking might influence the development of heart, carotid, and peripheral vascular disease. Epidemiological data convincingly demonstrate risk for atherosclerotic disease associated with bacterial infection and endotoxemia; however, the independent contributions to disease and pathogenic mechanisms of endotoxin remained elusive. Investigation into this relation tested the correlation between endotoxin and neopterin. Data indicated that neopterin, which reflects immune activation of monocytes/macrophages, functions as atherogenic effect modifying factor on the effects of endotoxin. We hypothesize that immune activation via induction of endotoxin hyperresponsiveness determines the atherogenic potential of Gram-negative infections.

Arteriosclerosis↗
PubMed2006

The timing of maternal depressive symptoms and mothers' parenting practices with young children: implications for pediatric practice.

BACKGROUND: The prevalence of maternal depressive symptoms and its associated consequences on parental behaviors, child health, and development are well documented. Researchers have called for additional work to investigate the effects of the timing of maternal depressive symptoms at various stages in the development of the young child on the emergence of developmentally appropriate parenting practices. For clinicians, data are limited about when or how often to screen for maternal depressive symptoms or how to target anticipatory guidance to address parental needs. PURPOSE: We sought to determine whether concurrent maternal depressive symptoms have a greater effect than earlier depressive symptoms on the emergence of maternal parenting practices at 30 to 33 months in 3 important domains of child safety, development, and discipline. METHODOLOGY: Secondary analyses from the Healthy Steps National Evaluation were conducted for this study. Data sources included a self-administered enrollment questionnaire and computer-assisted telephone interviews with the mother when the Healthy Steps children were 2 to 4 and 30 to 33 months of age. The 30- to 33-month interview provided information about 4 safety practices (ie, always uses car seat, has electric outlet covers, has safety latches on cabinets, and lowered temperature on the water heater), 6 child development practices (ie, talks daily to child while working, plays daily with child, reads daily to child, limits child television and video watching to <2 hours a day, follows > or = 3 daily routines, and being more nurturing), and 3 discipline practices (ie, uses more reasoning, uses more harsh punishment, and ever slapped child on the face or spanked the child with an object). The parenting practices were selected based on evidence of their importance for child health and development, near complete data, and sample variability. The discipline practices were constructed from the Parental Response to Misbehavior Scale. Maternal depressive symptoms were assessed using a 14-item modified version of the Center for Epidemiologic Studies-Depression Scale. Multiple logistic regression models estimated the effect of depressive symptoms on parenting practices, adjusted for baseline demographic characteristics, Healthy Steps participation, and site. No significant interactions were found when testing analytic models with dummy variables for depressive symptoms at 2 to 4 months only, 30 to 33 months only, and at both times; reported models do not include interaction terms. We report main effects of depressive symptoms at 2 to 4 and 30 to 33 months when both are included in the model. RESULTS: Of 5565 families, 3412 mothers (61%) completed 2- to 4- and 30- to 33-month interviews and provided Center for Epidemiologic Studies-Depression Scale data at both times. Mothers with depressive symptoms at 2 to 4 months had reduced odds of using car seats, lowering the water heater temperature, and playing with the child at 30 to 33 months. Mothers with concurrent depressive symptoms had reduced odds of using electric outlet covers, using safety latches, talking with the child, limiting television or video watching, following daily routines, and being more nurturing. Mothers with concurrent depressive symptoms had increased odds of using harsh punishment and of slapping the child on the face or spanking with an object. CONCLUSIONS: The study findings suggest that concurrent maternal depressive symptoms have stronger relations than earlier depressive symptoms, with mothers not initiating recommended age-appropriate safety and child development practices and also using harsh discipline practices for toddlers. Our findings, however, also suggest that for parenting practices that are likely to be established early in the life of the child, it may be reasonable that mothers with early depressive symptoms may continue to affect use of those practices by mothers. The results of our study underscore the importance of clinicians screening for maternal depressive symptoms during the toddler period, as well as the early postpartum period, because these symptoms can appear later independent of earlier screening results. Providing periodic depressive symptom screening of the mothers of young patients has the potential to improve clinician capacity to provide timely and tailored anticipatory guidance about important parenting practices, as well as to make appropriate referrals.

Adult↗
PubMed1985

Risk assessment for indoor exposure to radon daughters.

Approaches to and results for the estimation of healths risks from indoor exposure to radon and its daughter products are discussed. Particular weight is given to the derivation of exposure-time-effect relationships using a modified proportional hazard model which has been adapted to account for relevant epidemiological data. The results of this analysis indicate that about (10 +/- 5) % of the lung cancer rate observed in the general public might be correlated to the enhanced exposure to radon daughters in dwellings (at 10 - 20 Bq/m3 (Rn-eq] and in outdoor air. A chronic exposure to indoor Rn-levels at home of about 300 - 500 Bq/m3 (Rn-eq) might possibly double the normal lung cancer rates. The relative fractions of radiogenic lung cancer rates might be nearly the same for smokers and non-smokers, and for men and women.

Climate↗
PubMed2003

Glutathione-S-transferase genotypes, smoking, and their association with markers of inflammation, hemostasis, and endothelial function: the atherosclerosis risk in communities (ARIC) study.

Recent epidemiologic studies suggest that polymorphisms of glutathione-S-transferases M1 and T1 (GSTM1/GSTT1) modify the effects of cigarette smoking on risk of coronary heart disease (CHD). Since GSTs are able to detoxify numerous toxic compounds and products of oxidative stress, it is possible that GST genotypes may also modify the capacity of smoking to invoke a chronic inflammatory response. A cross-sectional analysis, using a subset of participants (n = 989) in a large (n = 15, 792) biracial cohort, was used to evaluate levels of nine markers of inflammation, hemostasis, and endothelial function by different combinations of GST genotypes and cigarette smoking status. Participants with the GSTM1 null (GSTM1-0) genotype and > or = 20 pack-years of smoking had the highest mean levels of CRP, fibrinogen, von Willebrand factor, ICAM-1, and VCAM-1 and lowest mean levels of albumin compared to other combinations of genotype and smoking. However, a formal test for interaction between GSTM1 genotype and smoking was statistically significant only for albumin. By contrast, participants who had the functional GSTT1 genotype (GSTT1-1) and smoked > or = 20 pack-years had the highest mean levels of only CRP and fibrinogen. The results of this study provide some limited evidence that GSTM1 and GSTT1 polymorphisms modify the effect of smoking on inflammation, hemostasis, and endothelial function.

Cohort Studies↗
PubMed1995

Complex segregation analysis of Gerbera flower colour.

The distribution of hue (CIELAB colour notation) classes among flowers of the Davis population of gerbera (Gerbera jamesonii H. Bolus ex Hooker) appears bimodal. This suggests that the genetic control of hue is determined by the segregation of a gene with large effect modified by additional genes with smaller effects. Complex segregation analysis (CSA), routinely employed in human genetic epidemiology, was used to study both qualitative and quantitative variation. CSA applies pedigree analysis through the consideration of transmission probabilities to optimize likelihood functions of various genetic models. Applying this technique to study flower hue of a sample representing generations 14, 15 and 16 of the Davis population, allowed identification of a putative dominant major gene with genotypic values for the dominant homozygote, heterozygote and recessive homozygote of 32, 32 and 71 degrees, respectively. This corresponds to the modes of the hue frequency distribution for the population. The putative major gene represents 0.66 of the total variation. The residual parent-offspring correlation (rho po = 0.2) measures the genetic contribution to the remainder of the variance.

Heterozygote↗
PubMedDate not supplied

Chronic estrogen replacement inhibits aortic intimal hyperplasia independent of serum lipids.

The role of estrogens in providing atheroprotection has been well documented in both epidemiologic and experimental studies. This phenomenon has traditionally been attributed to the beneficial lipid-modifying effects of estrogens. Yet lipid alterations may not be the sole mechanism of estrogen-mediated cardiovascular protection. Previous studies have utilized models of either diet- or injury-induced atherosclerosis. As such, the interrelationship between estrogens, lipids, and atherosclerosis remains unclear. The purpose of this study was to determine the effect of ovariectomy with or without estrogen replacement on the development of aortic intimal hyperplasia. Although we acknowledge the influence of estrogens on the lipid profile, we hypothesized that estrogens are atheroprotective independent of changes in serum lipids. Twelve Warhill ewes (7-11 years old) were randomized to sham (2 sheep) operation, ovariectomy (OVx-5 sheep), or ovariectomy with 17 beta-estradiol replacement (OVxE-5 sheep). Serum cholesterol and triglyceride levels were measured at 0, 6, and 12 months. Necropsy was performed at 6 and 12 months with histologic morphometric analysis of the aortoiliac bifurcation. Ovariectomy resulted in intimal thickening in comparison to the sham (p < 0.0001) and hormone replacement group (p < 0.0001). Serum cholesterol and triglyceride levels were similar and normal (40-60 mg/dl) among all groups. Estradiol abrogates aortic intimal hyperplasia following ovariectomy independent of the hormone's effects on lipid metabolism.

Animals↗
PubMed2004

Manganese superoxide dismutase Ala-9Val polymorphism and risk of breast cancer in a population-based case-control study of African Americans and whites.

INTRODUCTION: A polymorphism in the manganese superoxide dismutase (MnSOD) gene, Ala-9Val, has been examined in association with breast cancer risk in several epidemiologic studies. Results suggest that the Ala allele increases the risk of breast cancer and modifies the effects of environmental exposures that produce oxidative damage to DNA. METHODS: We examined the role of the MnSOD Ala-9Val polymorphism in a population-based case-control study of invasive and in situ breast cancer in North Carolina. Genotypes were evaluated for 2025 cases (760 African Americans and 1265 whites) and for 1812 controls (677 African Americans and 1135 whites). RESULTS: The odds ratio for MnSOD Ala/Ala versus any MnSOD Val genotypes was not elevated in African Americans (odds ratio = 0.9, 95% confidence interval = 0.7-1.2) or in whites (odds ratio = 1.0, 95% confidence interval = 0.8-1.2). Greater than additive joint effects were observed for the Ala/Ala genotype and smoking, radiation to the chest, and occupational exposure to ionizing radiation. Antagonism was observed between the Ala/Ala genotype and the use of nonsteroidal anti-inflammatory drugs. CONCLUSIONS: The MnSOD genotype may contribute to an increased risk of breast cancer in the presence of specific environmental exposures. These results provide further evidence for the importance of reactive oxygen species and of oxidative DNA damage in the etiology of breast cancer.

Adult↗
PubMed2005

Smoking and age-related macular degeneration: a review of association.

PURPOSE: Age-related macular degeneration (AMD) is the leading cause of severe and irreversible vision loss in the Western world. As there is no effective treatment for all types of AMD, identifying modifiable risk factors is of great importance. This review evaluates the epidemiological evidence associating smoking with AMD. METHODS: Systematic review of published epidemiological studies evaluated against established criteria for evidence of a causal relationship. RESULTS: In total, 17 studies (cross-sectional studies, prospective cohort studies, and case-control studies) were included in the review. A total of 13 studies found a statistically significant association between smoking and AMD with increased risk of AMD of two- to three-fold in current-smokers compared with never-smokers. Five studies found no association between smoking and AMD. There was also evidence of dose-response, a temporal relationship and reversibility of effect. CONCLUSION: The literature review confirmed a strong association between current smoking and AMD, which fulfilled established causality criteria. Cigarette smoking is likely to have toxic effects on the retina. In spite of the strength of this evidence, there appears to be a lack of awareness about the risks of developing eye disease from smoking among both healthcare professionals and the general public.

Aged↗
PubMed1997

The hypertensive patient with multiple risk factors: is treatment really so difficult?

Multiple risk factors for cardiovascular disease, particularly hypercholesterolemia, are often present in the hypertensive patient. Recent guidelines, ranging from those prepared by the World Health Organization/International Society of Hypertension to those of the three European Societies of Cardiology, Atherosclerosis, and Hypertension, stress the importance of evaluating global risk, based on the presence of all cardiovascular risk factors in an individual or in a group of subjects. It has also been suggested that treatment should aim to correct all modifiable risk factors. This is a reasonable recommendation, but although observational epidemiologic studies have shown that the effects of concomitant risk factors are additive, if not multiplicative, it is surprising that no intervention trial has been undertaken to determine whether the benefits of treating more than one risk factor are also additive. The Plaque Hypertension Lipid-Lowering Italian Study (PHYLLIS) is the first such study. Its aim is to investigate the potential benefit of lowering blood pressure and plasma cholesterol on the progression of carotid plaque in hypertensive patients with elevated plasma cholesterol. Using a factorial design, the antiatherosclerotic effect of two different antihypertensive drugs, the angiotensin-converting enzyme (ACE) inhibitor fosinopril and the diuretic hydrochlorothiazide will be compared. The study aims to confirm animal experiments demonstrating the benefit of ACE inhibitors on experimental atherosclerosis. PHYLLIS will also compare the effects of two lipid-lowering regimens, diet plus placebo and diet plus pravastatin, in the study population. This 3-year, multicenter, double-blind, randomized Italian study, using B-mode ultrasound evaluation of the carotid walls with central reading of the ultrasound scans (Bowman Gray University, Winston-Salem, NC) is now underway and should provide useful evidence about the benefits of multiple risk factor treatment in the hypertensive patient.

Aged↗
PubMed1996

Is this finding relevant? Generalisation and epidemiology.

The decision about whether the findings from analytical epidemiological studies can be extrapolated to another setting is an important one. We discuss some of the issues involved in the process of generalisation. A critical systematic qualitative approach should be used. This involves an assessment of the internal validity of the study and of the nature of the study base. The study subject matter and choice of epidemiologic measure should be considered. A study base similar to the target population is essential if the study is descriptive or if there is concern about effect modifiers whose effects cannot be predicted. In addition, data from quantitative tests of study findings in different populations should be considered.

Data Interpretation, Statistical↗
PubMed2005

The molecular epidemiology of gliomas in adults.

In this paper the authors highlight recent findings from molecular epidemiology studies of glioma origin and prognosis and suggest promising paths for future research. The reasons for variation in glioma incidence according to time period of diagnosis, sex, age, ancestry and ethnicity, and geography are poorly understood, as are factors that affect prognosis. High-dose therapeutic ionizing irradiation and rare mutations in highly penetrant genes associated with certain rare syndromes--the only two established causes of glioma--can be called upon to explain few cases. Both familial aggregation of gliomas and the inverse association of allergies and immune-related conditions with gliomas have been shown consistently, but the explanations for these associations are inadequately developed or unknown. Several biomarkers do predict prognosis, but only evaluation of loss of 1p and 19q in oligodendroglial tumors are incorporated in clinical practice. Ongoing research focuses on classifying homogeneous groups of tumors on the basis of molecular markers and identifying inherited polymorphisms that may influence survival or risk. Because most cases of glioma have yet to furnish either an environmental or a genetic explanation, the greatest potential for discovery may lie in genomic studies in conjunction with continued evaluation of environmental and developmental factors. Large sample sizes and multidisciplinary teams with expertise in neuropathology, genetics, epidemiology, functional genomics, bioinformatics, biostatistics, immunology, and neurooncology are required for these studies to permit exploration of potentially relevant pathways and modifying effects of other genes or exposures, and to avoid false-positive findings. Improving survival rates for patients harboring astrocytic tumors will probably require many randomized clinical trials of novel treatment strategies.

Adult↗
PubMed1998

Accuracy of ICD-9-CM coding for the identification of patients with acute ischemic stroke: effect of modifier codes.

BACKGROUND AND PURPOSE: Discharge ICD-9-CM (International Classification of Diseases, 9th Revision, Clinical Modification) codes have been used to identify patients with acute stroke for epidemiological, quality of care, and cost studies. The aim of this study was to determine if the accuracy of the primary ICD-9-CM codes for ischemic stroke is improved by modifier codes and how specific codes reflect stroke subtype diagnoses. METHODS: Available hospital charts for all patients discharged from a single hospital between May 1995 and June 1997 with ICD-9-CM codes 433 (occlusion and stenosis of precerebral arteries), 434 (occlusion of cerebral arteries), or 436 (acute but ill-defined cerebrovascular disease) listed in the first position were reviewed. The primary discharge diagnosis was verified, and a presumed stroke subtype was assigned on the basis of information provided in the medical record. RESULTS: Charts were available for 175 of the 198 identified patients (88%). Of these, 61% had an acute ischemic stroke (code 433, 4%; 434, 82%; 436, 79%) with the remaining patients having other conditions. Of the 130 patients with a modifier code indicating cerebral infarction, 79% had an acute stroke; of the 45 patients with a modifier code indicating an absence of cerebral infarction, 7% had acute stroke (sensitivity, 0.97; specificity, 0.60). The codes with the highest proportions of ischemic stroke cases were 434.11 (embolic occlusion of cerebral arteries with infarction, 85%), 434.91 (unspecified occlusion of precerebral arteries with infarction, 82%), and 436 (79%), with a combined sensitivity of 0.81 and specificity of 0.90. On review, 73% of patients with code 434.11 had embolic strokes, and 47% of those with code 436 had an identified stroke cause. Of patients with code 434.91, 39% had stroke of uncertain cause, 25% "lacunar," 17% atherothrombosis, and 15% embolism. CONCLUSIONS: Despite the use of modifier codes, 15% to 20% of patients with the indicated primary ICD-9-CM codes have conditions other than acute ischemic stroke. Although the proportion of patients with acute stroke increased from 61% to 79% with the use of modifier codes, the inclusion of modifier codes did not have an appreciable effect on the accuracy of the coding if patients with code 433 are excluded. Assignment of presumed ischemic stroke subtype is particularly inaccurate.

Acute Disease↗