SEARCH · PubMed Health

Results for “DISEASE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 721 records · Page 40Linked to original sources

PubMed1991

Association between autoimmune thyroid disease and familial Alzheimer's disease.

OBJECTIVE: To determine the prevalence of autoimmune thyroid disease in Familial Alzheimer's Disease kindreds and to ascertain whether there is any evidence for genetic linkage between the two conditions. DESIGN: Retrospective study of Familial Alzheimer's Disease kindreds. PATIENTS: Seventy affected and unaffected family members from 12 kindreds. MEASUREMENTS: Anti-thyroglobulin and anti-microsomal autoantibody status was determined using an enzyme-linked immunosorbent assay. Thyrotrophin levels were determined by an immunoradiometric assay. RESULTS: Of the family members, 41.4% had evidence of autoimmune thyroid disease, with significant co-segregation between the presence of thyroid autoantibodies and the development of Alzheimer's disease (P less than 0.01). CONCLUSIONS: This study demonstrates a very high prevalence of autoimmune thyroid disease in Familial Alzheimer's Disease kindreds and suggests that a genetic factor contributing towards the development of autoimmune thyroid disease may be located on chromosome 21 within close proximity to the Familial Alzheimer's Disease gene.

Adult↗

PubMed1983

Investigation of the mode of inheritance of the HLA associated diseases by the method of antigen genotype frequencies among diseased individuals.

Statistical features of the method of antigen genotype frequencies among the diseased, for single and multiple disease associations at a locus, will be presented. A methodology to determine when a true intermediate mode of inheritance can be distinguished from strict recessive or additive inheritance will be developed. The effect of sporadics and ascertainment bias on the observed antigen genotype frequencies will be investigated. Data on ankylosing spondylitis, multiple sclerosis and dermatitis herpetiformis are very close to expectations for an additive (or dominant) mode of inheritance for the HLA-linked disease-predisposing gene, and data on hemochromatosis, insulin dependent diabetes mellitus and celiac disease are close to recessive expectations. If an intermediate model does apply in any of these cases, it must be an intermediate model that is fairly close to a strict recessive or dominant model; as appropriate. DR data for insulin dependent diabetes mellitus (IDDM) strongly indicate that there are two separate "disease" alleles, which exhibit negative complementation, predisposing individuals to IDDM, where the mode of inheritance of the "disease" alleles considered separately is close to recessive. In general, this method cannot rule out the existence of sporadics or a second disease-predisposing gene, when the penetrance values over the two disease-predisposing genes are strictly additive, for diseases showing agreement with additive (or dominant) modes of inheritance.

Arthritis, Juvenile↗

PubMed2005

A comparison of clinically important differences in health-related quality of life for patients with chronic lung disease, asthma, or heart disease.

OBJECTIVE: On the eight scales of the Medical Outcomes Study Short-Form 36-Item Health Survey (SF-36), Version 2, we compared the clinically important difference (CID) thresholds for change over time developed by three separate expert panels of physicians with experience in quality of life assessment among patients with chronic obstructive pulmonary disease (COPD), asthma, and heart disease. STUDY DESIGN: We used a modified Delphi technique combined with a face-to-face panel meeting within each disease to organize and conduct the consensus process among the expert panelists, who were familiar with the assessment and evaluations of health-related quality of life (HRQL) measures among patients with the panel-specific disease. PRINCIPAL FINDINGS: Each of the expert panels first determined the magnitude of the smallest numerically possible change on each SF-36 scale, referred to as a state change, and then built their CIDs from this metric. All three panels attained consensus on the scale changes that constituted small, moderate, and large clinically important SF-36 change scores. The CIDs established by the heart disease panel were generally greater than the CIDs agreed on by the asthma and COPD panels. CONCLUSIONS: These panel-derived thresholds reflect possible differences in disease management among the represented panel-specific diseases, and are all greater than the minimal CID thresholds previously developed for the SF-36 scales among patients with arthritis. If confirmed among patients with the relevant diseases and those patients' physicians, these disease-specific CIDs could assist both researchers and practicing clinicians in the use and interpretation of HRQL changes over time.

Asthma↗

PubMed2005

Early disease onset and increased risk of other autoimmune diseases in familial generalized vitiligo.

Generalized vitiligo is an autoimmune disorder in which acquired white patches of skin and overlying hair result from autoimmune loss of melanocytes from involved areas. Although usually sporadic, family clustering of vitiligo may occur, in a non-Mendelian pattern typical of multifactorial, polygenic inheritance. Sporadic vitiligo is associated with autoimmune thyroid disease, pernicious anemia, Addison's disease, and lupus; these same disorders occur at increased frequency in patients' first-degree relatives. Here, we studied 133 'multiplex' generalized vitiligo families, with multiple affected family members. The age of onset of vitiligo is earlier in these 'multiplex' families than in patients with sporadic vitiligo. Affected members of the multiplex vitiligo families have elevated frequencies of autoimmune thyroid disease, rheumatoid arthritis, psoriasis, adult-onset insulin-dependent diabetes mellitus, pernicious anemia, and Addison's disease. Probands' unaffected siblings have elevated frequencies of most of these same autoimmune diseases, particularly if the proband had non-vitiligo autoimmune disease. Familial generalized vitiligo is thus characterized by earlier disease onset and a broader repertoire of associated autoimmune diseases than sporadic vitiligo. This mostly likely reflects a greater inherited genetic component of autoimmune susceptibility in these families. These findings have important implications for autoimmune disease surveillance in families in which multiple members are affected with vitiligo.

Addison Disease↗

PubMed2006

Understanding the genetics of autoimmune disease: two loci that regulate late onset Addison's disease in Portuguese Water Dogs.

Addison's disease, an immune-mediated disorder caused by destruction of the adrenal glands, is a rare disorder of Western European populations. Studies indicate that the disorder is polygenic in nature, involving specific alleles of the CTLA-4, DRB1*04 and DQ, Cyp27B1, VDR and MIC-A and -B loci. A similar immune form of Addison's disease occurs in several breeds of domestic dog, with frequencies ranging from 1.5 to 9.0%. The high frequency of the disease in domestic dog breeds likely reflects the small number of founders associated with many breeds, subsequent inbreeding, and the frequent use of popular sires. The Portuguese Water Dog (PWD) is a significantly affected breed. An analysis of 11,384 PWDs surveyed between 1985 and 1996 suggests a breed-specific disease incidence of 1.5%. As with humans, the disease is typically of late onset. This study involves a genetic comparison of Addison's disease in the PWD to the analogous disease in humans. The study is facilitated by the existence of complete pedigrees and a relatively high degree of inbreeding among PWDs. The breed originated from 31 founders, with 10 animals responsible for 90% of the current gene pool. We describe, specifically, the identification of two disease-associated loci, on Canis familiaris (CFA) chromosomes CFA12 and 37, which are syntenic with the human DRB1 histocompatibility locus alleles HLA-DRB1*04 and DRB1*0301, and to a locus for immunosuppression syntenic with CTLA-4. Strong similarities exist therefore in the complex genetic background of Addison's disease in humans and in the PWD. With the completion of the canine and human genome sequence, the purebred dog is set to become an important comparative model for Addison's as well as other human immune disorders.

Addison Disease↗

PubMed2002

Interstitial lung diseases associated with collagen vascular diseases: radiologic and histopathologic findings.

Collagen vascular diseases that demonstrate features of interstitial lung disease include systemic lupus erythematosus, rheumatoid arthritis, progressive systemic sclerosis, dermatomyositis and polymyositis, ankylosing spondylitis, Sjögren syndrome, and mixed connective tissue disease. At histopathologic analysis, interstitial lung diseases associated with collagen vascular diseases are diverse and include nonspecific interstitial pneumonia, usual interstitial pneumonia, bronchiolitis obliterans organizing pneumonia (BOOP), apical fibrosis, diffuse alveolar damage, and lymphocytic interstitial pneumonia. Although proportions of interstitial pneumonias vary, nonspecific interstitial pneumonia accounts for a large proportion, especially in progressive systemic sclerosis, dermatomyositis and polymyositis, and mixed connective tissue disease. The more favorable prognosis in interstitial pneumonia associated with collagen vascular diseases than in idiopathic interstitial pneumonias may be explained by the larger proportion of nonspecific interstitial pneumonia than of usual interstitial pneumonia. High-resolution computed tomography seems to help characterize and determine the extent of interstitial lung disease in collagen vascular diseases.

Arthritis, Rheumatoid↗

PubMed2025

Deciphering microbial and metabolic influences in gastrointestinal diseases-unveiling their roles in gastric cancer, colorectal cancer, and inflammatory bowel disease.

INTRODUCTION: Gastrointestinal disorders (GIDs) affect nearly 40% of the global population, with gut microbiome-metabolome interactions playing a crucial role in gastric cancer (GC), colorectal cancer (CRC), and inflammatory bowel disease (IBD). This study aims to investigate how microbial and metabolic alterations contribute to disease development and assess whether biomarkers identified in one disease could potentially be used to predict another, highlighting cross-disease applicability. METHODS: Microbiome and metabolome datasets from Erawijantari et al. (GC: n = 42, Healthy: n = 54), Franzosa et al. (IBD: n = 164, Healthy: n = 56), and Yachida et al. (CRC: n = 150, Healthy: n = 127) were subjected to three machine learning algorithms, eXtreme gradient boosting (XGBoost), Random Forest, and Least Absolute Shrinkage and Selection Operator (LASSO). Feature selection identified microbial and metabolite biomarkers unique to each disease and shared across conditions. A microbial community (MICOM) model simulated gut microbial growth and metabolite fluxes, revealing metabolic differences between healthy and diseased states. Finally, network analysis uncovered metabolite clusters associated with disease traits. RESULTS: Combined machine learning models demonstrated strong predictive performance, with Random Forest achieving the highest Area Under the Curve(AUC) scores for GC(0.94[0.83-1.00]), CRC (0.75[0.62-0.86]), and IBD (0.93[0.86-0.98]). These models were then employed for cross-disease analysis, revealing that models trained on GC data successfully predicted IBD biomarkers, while CRC models predicted GC biomarkers with optimal performance scores. CONCLUSION: These findings emphasize the potential of microbial and metabolic profiling in cross-disease characterization particularly for GIDs, advancing biomarker discovery for improved diagnostics and targeted therapies.

Humans↗

PubMed2006

The role of disease burden measures in future estimates of endemic waterborne disease.

The 1996 Safe Drinking Water Act amendments require the US Environmental Protection Agency and the Centers for Disease Control and Prevention to develop a national estimate of the occurrence of waterborne infectious disease that is attributable to public drinking water systems in the United States. Much of the information for developing the national estimate will be derived from epidemiologic data, and the primary outcome of this effort will be an estimate of the number of cases of gastrointestinal illness. While quantifying the number of these cases provides some measure of waterborne disease impact, the usefulness of this measure may be limited because the full spectrum of societal impact also involves consideration of the additional effects of these diseases such as hospitalization costs and lost productivity. If decision-makers wish to compare the impact of waterborne infectious diseases to the impact of some other public health concern (e.g. to aid in resource allocation decisions), then a comparison of case numbers may prove inadequate. Case numbers alone do not provide sufficient information about the severity of different illnesses. Society may value the avoidance of a few cases of severely debilitating illness more than it values the avoidance of many cases of mild illness. In order to compare disparate public health concerns, "burden of disease" measures that incorporate indicators of disease severity, costs, or societal values may prove essential for some types of decisions. We describe epidemiologic measures of severity, quality adjusted life years (QALYs), disability adjusted life years (DALYs), willingness-to-pay, and cost-of-illness methods commonly used for burden of disease estimates, and discuss how some of these summary measures of burden might be used for waterborne disease estimates.

Chronic Disease↗

PubMed2004

Reports of zoonotic disease outbreaks associated with animal exhibits and availability of recommendations for preventing zoonotic disease transmission from animals to people in such settings.

OBJECTIVE: To assess the number of zoonotic disease outbreaks associated with animal exhibits and identify published recommendations for preventing zoonotic disease transmission from animals to people in exhibit settings. DESIGN: Literature review and survey of state public health veterinarians and state epidemiologists. PROCEDURE: MEDLINE and agriculture databases were searched from 1966 through 2000. Retrieved references and additional resources provided by the authors were reviewed. A survey was sent to state public health veterinarians and state epidemiologists to determine whether their states had written recommendations or guidelines for controlling zoonotic diseases in animal exhibition venues, whether their states maintained a listing of animal exhibitors in the state, and whether they had any information on recent outbreaks involving animals in exhibitions. RESULTS: 11 published outbreaks were identified. These outbreaks occurred in a variety of settings including petting zoos, farms, and a zoological park. An additional episode involving exposure to a potentially rabid bear required extensive public health resources. A survey of state public health veterinarians identified 16 additional unpublished outbreaks or incidents. Most states did not have written recommendations or guidelines for controlling zoonotic diseases or any means to disseminate educational materials to animal exhibitors. CONCLUSIONS: Recent outbreaks of zoonotic diseases associated with contact with animals in exhibition venues highlight concerns for disease transmission to public visitors. Only a handful of states have written guidelines for preventing zoonotic disease transmission in animal exhibition venues, and published recommendations currently available focus on preventing enteric diseases and largely do not address other zoonotic diseases or prevention of bite wounds.

Animal Diseases↗

PubMed1993

Prevalence of peripheral artery disease in patients with coronary artery disease.

The incidence of coronary artery disease in Singapore has shown a rapid rise in recent years, however, there is a subjective impression that the prevalence of atherosclerotic peripheral artery diseases, although sharing common aetiological factors with coronary artery disease, has not shown a similar rise. We set out to determine the incidence of occlusive peripheral artery diseases of the lower limb in a selected population of Asian patients using a non-invasive test and we analysed the risk factors. The overall prevalence of peripheral artery disease of the subjects as determined by an abnormal ankle brachial index less than 0.9 in at least one limb was 19.1%. Increasing age, hypercholesterolemia and smoking were risk factors. In patients with proven coronary artery disease, abnormal ankle brachial indices were present in 21.3% of patients with angiographic evidence of coronary artery disease but in only 13.0% of those without. In this study, the incidence of peripheral artery disease in this selected Asian population was high. With the increasing availability of vascular laboratories and awareness of the diseases, we can expect to see increasing numbers of patients presenting with these problems.

Adult↗

PubMed2003

Serum osteoprotegerin and its ligand in Paget's disease of bone: relationship to disease activity and effect of treatment with bisphosphonates.

OBJECTIVE: To test the following hypotheses: 1) osteoprotegerin (OPG) and receptor activator of nuclear factor kappa B ligand (RANKL) serum levels in patients with Paget's disease are related to disease activity and are different from those in healthy individuals; 2) interleukin-6 (IL-6), a cytokine that has been shown to have higher levels in Paget's disease, modulates these factors; and 3) the antiresorptive effect of bisphosphonates in Paget's disease of bone may be mediated through these local factors. METHODS: The study group comprised 31 patients with Paget's disease who received 400 mg/day of oral tiludronate for 3 months. Serum levels of OPG, RANKL, IL-6, bone alkaline phosphatase (AP), N-terminal type I procollagen propeptide, urinary N-terminal crosslinking telopeptide of type I collagen, and urinary alpha-C-terminal crosslinking telopeptide of type I collagen were measured at baseline and 1 month after the end of therapy. In addition, the RANKL:OPG ratio was calculated, and disease activity was evaluated at baseline by quantitative bone scintigraphy. RESULTS: Mean baseline OPG values were higher in patients with Paget's disease than in healthy control subjects (P < 0.005), but RANKL and IL-6 values and RANKL:OPG ratios in the 2 groups were similar. OPG concentrations decreased significantly after treatment with tiludronate (P < 0.005), whereas no significant changes were observed in serum RANKL values. No correlation was found between either bone markers or quantitative scintigraphic indices and serum levels of OPG, RANKL, IL-6, and RANKL:OPG ratios. Serum OPG decreased significantly only in those patients with baseline OPG values >4.1 pM/liter. CONCLUSION: Serum OPG increases in Paget's disease and decreases after treatment with tiludronate, especially in patients with the highest OPG values. In contrast, RANKL serum levels and RANKL:OPG ratios are unmodified in patients with Paget's disease. Although serum OPG, RANKL, and IL-6 values were unrelated to disease activity, the increase in OPG may reflect a protective mechanism of the skeleton to compensate for increased bone resorption.

Adult↗

PubMed1997

Polymorphism of the LMP2 gene and disease phenotype in ankylosing spondylitis: no association with disease severity.

Although a number of reports have now described an association between polymorphism of the LMP2 gene and disease phenotype in HLA-B27 positive individuals with ankylosing spondylitis (AS), some describe associations with acute anterior uveitis, others with juvenile onset disease, and one report provides no association. A recent study describes yet a further association with disease severity in patients with juvenile rheumatoid arthritis. We therefore hypothesized that the discrepant findings in adult disease may be a reflection of an underlying association with disease severity. Our study population consisted of 100 HLA-B27 positive Caucasians with AS of ten or more years duration. Clinical assessment of disease severity was based on a metrology index scoring five measurements, the modified health assessment questionnaire for the spondyloarthropathies, and a disease activity index consisting of a visual analog scale to score the amount of pain, stiffness and fatigue. LMP2 genotypes were assigned following polymerase chain reaction amplification from genomic DNA and restriction enzyme digestion with CfoI. Despite confirmation of a significantly higher prevalence of the LMP2 BB genotype in AAU positive (66.0%) versus AAU negative (45.2%) patients (P < 0.05), we observed no association between LMP2 genotypes and any of the indices of disease severity. Furthermore, although a significant association was noted between the presence of peripheral synovitis and the functional index score (P < 0.05), a history of AAU was not associated with more severe disease. Our data is thus internally consistent in demonstrating no association between LMP2 genotypes and either disease severity or peripheral arthritis, and supports the notion that polymorphism of LMP2 primarily influences the development of AAU and not some other phenotype of AS.

Adult↗

PubMed2004

Paget's disease of bone in New Zealand: continued decline in disease severity.

We have reported previously that severe Paget's disease of bone had become less common at our center between 1973 and 1993. Data from several countries support the view that there are important secular trends in the prevalence and severity of Paget's disease. In this paper we describe recent trends in the demography of newly referred patients with Paget's disease to determine if the secular trend toward milder disease has continued. A database of all newly referred patients (n = 1487) with Paget's disease (1973 to 2002 inclusive, 30 years) was examined. Of these, 832 subjects (56%) had scintiscans. Plasma total alkaline phosphatase (total ALP) activity, disease extent on scintiscan, and a derived index of average ALP activity of pagetic bone were used as indices of severity. The number of new referrals with Paget's disease declined sharply from 1994 onward and is currently at half the rate seen 20 years earlier, while the mean age at presentation has progressively increased by 4 years per decade (P < 0.0001). Total ALP at diagnosis, disease extent on scintiscan, and the number of bones involved were all negatively correlated with both date of birth (P < 0.0001) and year of presentation (P < 0.0001), indicating that more recently born and presenting subjects had substantially less severe bone disease. The average activity of pagetic bone was only weakly correlated with year of presentation, but not with year of birth or age at presentation. Although there are a number of potential biases, these data are consistent with a continued secular trend to presentation in older subjects with less extensive skeletal involvement, and a declining prevalence of Paget's disease.

Alkaline Phosphatase↗

PubMed2006

Serum cholinesterase activity helps to distinguish between liver disease and non-liver disease aberration in liver function tests.

The diagnostic usefulness of a single determination of serum cholinesterase activity to distinguish between overt liver disease and non-liver disease clinical problems in which a few of the traditional liver function tests are abnormal was assessed. Using three groups of subjects comprising liver disease, non-liver disease, and healthy controls, we have shown that serum cholinesterase activity helped to distinguish between liver disease and non-liver disease in subjects who had abnormality of a few liver function tests. Serum cholinesterase activity helped also to distinguish between the liver disease subjects and healthy controls. There was no statistically significant difference between the mean serum cholinesterase activities of non-liver disease subjects and healthy controls. We suggest that determination of serum cholinesterase activity is a cost-effective diagnostic means of differentiating between overt liver disease and non-liver diseases where there may be aberration of some liver function tests.

Journal Article↗

PubMed2003

Different patterns of oesophageal acid exposure distinguish complicated reflux disease from either erosive reflux oesophagitis or non-erosive reflux disease.

BACKGROUND: The reason why less than one-half of patients with gastro-oesophageal reflux disease develop complicated reflux disease (ulcerative oesophagitis, oesophageal strictures and Barrett's oesophagus) and erosive reflux oesophagitis is not fully understood. Supine nocturnal oesophageal acid reflux is considered to be critically involved in this phenomenon, but reliable data are lacking. AIM: To clarify whether high levels of supine nocturnal oesophageal acid exposure are associated with complicated reflux disease. METHODS: Ambulatory 24-h oesophageal pH monitoring was performed in 220 patients with gastro-oesophageal reflux disease (56 with complicated reflux disease, 76 with erosive reflux oesophagitis and 88 with non-erosive reflux disease). The total, supine nocturnal and upright diurnal percentage acid reflux times were calculated. RESULTS: The total percentage acid reflux time was significantly greater in complicated reflux disease than in either erosive reflux oesophagitis (P = 0.024) or non-erosive reflux disease (P = 0.000). These differences were entirely due to a greater supine nocturnal percentage acid reflux time (P = 0.038 and P = 0.000, respectively), whereas no difference was observed in the upright diurnal percentage acid reflux time. CONCLUSIONS: Complicated reflux disease is characterized by high levels of supine nocturnal percentage acid reflux time. Prospective studies would be appropriate to clarify whether the normalization of this parameter is relevant to the effective management of this subset of patients with gastro-oesophageal reflux disease.

Circadian Rhythm↗

PubMed2005

What does "active disease" mean? patient and parent perceptions of disease activity in the systemic arthritis form of juvenile idiopathic arthritis (SO-JIA).

OBJECTIVE: The systemic onset form of juvenile idiopathic arthritis (SO-JIA) is a very serious chronic illness of childhood. At present, there is no specific tool to measure disease activity for SO-JIA. Our long-term goal is to develop a disease activity measure for SO-JIA using a consensus (Delphi) approach. In preparation for the development of this measure, we interviewed both patients and their parents. We sought to elicit specific items reflecting their perceptions of active disease that may be considered for inclusion in a disease activity measure for SO-JIA. METHODS: SO-JIA patients followed at The Hospital for Sick Children and their parents were chosen by purposive sampling. A trained research coordinator interviewed all participants using open-ended questions to elicit aspects of disease activity (defined as reversible manifestations of disease) of relevance to families. A list of these aspects was then generated and organized by categories to allow item reduction. RESULTS: Fourteen patients (eight females) with a mean age of 11.8 yr (mean disease duration 5.2 yr) and their parents were interviewed. A total of 292 items were generated, with an average of 11 items generated per interview. Arthralgia, ambulation difficulties, rash, decreased energy level and fever were the most common items mentioned by patients and their parents. Mood disturbances, decreased activity levels, arthritis severity and decreased school attendance were also common items identified as relevant aspects of disease activity. CONCLUSION: This study has allowed us to include patient and parent perspectives in preparation for developing a disease activity measure for SO-JIA. The resulting items will be added to future physician surveys in the further development and validation of a disease activity measure for SO-JIA.

Adolescent↗

PubMed1999

Nitric oxide production in meningococcal disease is directly related to disease severity.

OBJECTIVES: Meningococcal disease is a homogeneous and well-characterized form of sepsis. Cardiovascular collapse is prominent in severe meningococcal disease. Nitric oxide overproduction may be a mediator of cardiovascular collapse. We relate the level of nitric oxide metabolites, nitrates and nitrites, to disease severity in meningococcal disease. DESIGN: Prospective, nonrandomized study. SETTING: Tertiary referral pediatric intensive care unit. PATIENTS: Children admitted with a clinical diagnosis of meningococcal disease. INTERVENTIONS: Blood was sampled from children with meningococcal disease. Disease severity was scored using the Glasgow meningococcal septicemia prognostic score and pediatric risk of mortality score. Plasma nitrates and nitrites were measured in stored plasma using the Greiss reaction after conversion of all the nitrate to nitrite. MEASUREMENTS AND MAIN RESULTS: Twenty-two children were studied. In 19, the final diagnosis was meningococcal disease. Of the 19 children with meningococcal disease, 7 had a Glasgow meningococcal septicemia prognostic score of <8 (mild) and 12 had a Glasgow meningococcal septicemia prognostic score > or = 8 (severe). Three children died, all of these being in the severely affected group. Higher levels of nitrates and nitrites were seen in the more severely affected children (median admission nitrates and nitrites, 27.5 vs. 59.7 nmol/mL; p = 0.063; median peak nitrates and nitrites, 49.9 vs. 114 nmol/mL; p = .01) or those with an increased predicted mortality using pediatric risk of mortality (Spearman's p 0.742; p = .0003). CONCLUSIONS: Higher levels of nitrates and nitrites are seen in sicker children with meningococcal disease.

Child↗

PubMed1999

Relation of Chlamydia pneumoniae serology to mortality and incidence of ischaemic heart disease over 13 years in the caerphilly prospective heart disease study.

OBJECTIVES: To investigate the effect of Chlamydia pneumoniae infection on future development of ischaemic heart disease and mortality. DESIGN: Prospective longitudinal study. SETTING: Caerphilly, South Wales. SUBJECTS: Plasma specimens were collected during 1979-83 from 1773 men aged 45-59 years. These were tested for IgG and IgA antibodies to C pneumoniae (TW183) by microimmunofluorescence. OUTCOME MEASURES: 13 year mortality and incident ischaemic heart disease events were ascertained from death certificates, hospital records, and electrocardiographic changes at follow up every 4 to 5 years. RESULTS: 642 men (36.2%) had IgG antibodies at a titre of >/=1 in 16, of whom 362 (20.4% of all men) also had detectable IgA antibodies. The prevalence of ischaemic heart disease (a history of past or current disease) at entry was similar at all IgG antibody titres but was positively related to IgA antibody titre. IgA antibody titre was positively correlated with plasma viscosity but not with other cardiovascular risk factors. Incidence of ischaemic heart disease was not associated with either IgG antibody titre or IgA antibody titre, but there were stronger and significant relations of IgA antibodies with all cause mortality and fatal ischaemic heart disease, which persisted after adjustment for conventional cardiovascular risk factors. The odds ratios associated with detectable IgA antibodies were 1.07 (95% confidence interval 0.75 to 1.53) for all incident ischaemic heart disease, 1. 83 (1.17 to 2.85) for fatal ischaemic heart disease, and 1.50 (1.10 to 2.04) for all cause mortality. CONCLUSION: This is the first prospective demonstration of an association between IgA antibodies to C pneumoniae, a putative marker of chronic infection, and subsequent risk of death from ischaemic heart disease. In contrast to earlier case-control studies, IgG antibodies were not associated with either prevalent or incident ischaemic heart disease.

Antibodies, Bacterial↗