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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sera were collected from 49 pairs of identical twins, 27 of whom were discordant (only one twin affected) and 22 concordant (both diabetic) for insulin-dependent diabetes. All were tested for antibodies to mumps, cytomegalovirus, rubella, Coxsackie virus types B1-5, and Mycoplasma pneumoniae. The diabetic co-twins had no more antibodies to any of the viruses than the non-diabetic co-twins of the discordant pairs. Antibodies to Coxsackie B2, rubella virus, and M pneumoniae were found more often in the discordant than in the concordant twins. In 30 of the 71 diabetic twins symptoms began when they were aged 4-6 years or 10-15 years. More concordant than discordant twins were diagnosed during the months January to March. Hence there was no direct evidence of a virus aetiology of juvenile onset diabetes in these twins, and the difference in antibody titres between the concordant and discordant twins was in keeping with a genetic difference between them. The age and time of onset suggested that environmental factors may be important in causing diabetes in the twins.
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PMID:Viruses and the aetiology of diabetes: a study in identical twins. 17 83

Pathologists have confirmed the specific nature of the insulitis lesion in diabetes requiring insulin. Data from genetic studies implicate both genetic and environmental influences as important in the appearance of overt disease. Certain HLA histocompatibility antigens are associated with insulin-dependent diabetes and have been interpreted as markers for closely linked immune response genes, a situation that may lead to beta cell susceptibility to viral injury or to uncontrolled beta cell autoaggression following beta cell damage. There is much circumstantial evidence that viruses may precipitate the disease (coxsackie) or may precede the disease onset by a long interval (mumps, rubella). However, susceptibility to virus, if it exists in human insulin-requiring diabetes, would appear on clinical grounds to be localized to the pancreas. Autoimmune phenomena are common in insulin-requiring diabetes, and there is both human and animal evidence that suggest that cell-mediated immunity may have a central pathogenic role. The recent explosion of new findings should lead to a clearer understanding of the nature of the disease, and this knowledge will hopefully lend itself to the prevention or arrest of the disease through immunological intervention, vaccination programs, or other means yet to be discovered.
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PMID:Viral and immunological bases of beta cell failure in insulin-dependent diabetes. 33

Age, sex, and estimated time of onset of insulin-dependent diabetes were determined for children in Pittsburgh (N = 673), Gainesville (N = 976), Galveston (n = 741), and Melbourne (N = 851). The US cities had a decrease in new cases during the summer and peak incidence in January through April. In Melbourne, monthly trends were reversed: there were more cases during May through August. In US cities, but not in Melbourne, children less than 6 years old showed a greater variation by season than children 6 years old and older. Observations of the same fall and winter onset (in different calendar months) of insulin-dependent diabetes in Australia and the United States, and exaggeration of seasonal differences in young US children, suggest that onset of insulin-dependent diabetes is associated with seasonally varying viral diseases. Mumps and rubella infections do not seem to be responsible for much of the seasonal variation. Seasonal peaks of mumps and rubella are later than those observed for insulin-dependent diabetes, and immunization with live mumps and rubella viruses has not been associated with changes in incidence of insulin-dependent diabetes. An increase in disease incidence in boys over girls below age 6 years and in girls over boys at ages 6 through 11 years was consistently observed but not explained.
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PMID:Age, sex, and season of onset of juvenile diabetes in different geographic areas. 44 Aug 39

Data are collected here that may support the hypothesis that there is an infectious component in the genesis of insulin-dependent diabetes mellitus. The clinical and experimental data on which that hypothesis is based referring to viruses such as: mumps virus, rubella virus, encephalomyocarditis virus, and Coxsackie B viruses, are presented. The authors mention the pathogenic mechanism, which extends over the existence of diabetogenic genes linked to the major complex of the histocompatibility HLA system, as well as the existence of an autoimmune reaction induced by the infecting virus. This review shows up the large gaps that exist in the accurate knowledge we have about the possible infectious etiology of diabetes. However, it also offers different pathogenic possibilities for further experimental investigations on bases that are reasonably scientifically consistent.
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PMID:[Viral etiology of insulin-dependent diabetes (author's transl)]. 45 6

An analysis of genetic and non-genetic factors which might be of importance for the aetiology of hypospadias was performed in a clinical and in a registered material comprising altogether 893 hypospadiacs. Of 213 index patients in the clinical material, the probable aetiology was known in 11: in 3 patients chromosomal aberrations, in 2 well-defined syndromes with a known genetic background, in one maternal diabetes, in 2 maternal rubella, and 2 of the hypospadiacs were born after the mothers' use of anticonvulsant drugs and one after the mother's use of thalidomide. Other hypospadiacs were identified in 28 of the families of the remaining 202 index patients. As regards inheritance, 10 cases of hypospadias associated with clinodactyly were found in one family and this suggests an autosomal dominant gene as the cause of hypospadias. In the great majority (174/213) of index patients neither genetic nor non-genetic factors could be demonstrated but a significant cyclic trend for the month of birth and the month of the last menstrual period was found.
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PMID:On aetiological factors in hypospadias. 60 94

In spite of a history of more than 100 years, the pathoaetiology of multiple sclerosis is still unknown today. Research is based on three working hypotheses, i.e. on an immunopathological disease origin, on the conception that MS, as an infectious disease, is caused by a specific pathogen (slow virus infection) and on the assumption of a disturbance of basal metabolism or utilisation. The present position of the scientific foundation of the working hypotheses is presented in detail and supplemented by the results of our own investigations. Of particular interest are the geomedical studies which show that MS occurs more frequently in temperate climatic regions. In Europe, a latitude of 46 degrees forms a conspicuous boundary; in the USA this boundary is found at 38 degrees. North of this line there is a morbidity rate of 30 to 60 patients per 100 000 inhabitants, while south of it 15 cases at most per 100 000 inhibitants are found. Asia, especially in China and Japan, and tropical countries, where Multiple Sclerosis is practically unknown in the native populations, are exceptions. The observation that immigrants from areas with a low MS incidence into regions with a high risk of MS fall ill with the disease after years remains also unexplained. These peculiarities have given rise to the consideration whether there is a still unknown factor in the soil of high-risk areas or a specific pathogenic spectrum. In this connection, the question is also discussed whether the risk of MS in northern countries is associated with the excessive consumption of animal fat. The possible therapeutic and prophylactic significance of unsaturated fatty acids is emphasized. Our own results with the Schilling-test, determination of gastric acids, rubella titres in serum and cerebrospinal fluid, the immunofluorescence test of the serum and CSF, determination of tissue antigens (HLA) in families with multiple incidence of Multiple Sclerosis are discussed. On evaluation of a large series of patients, it is striking that Multiple Sclerosis and juvenile diabetes seem to be mutually exclusive (Schrader). Likewise, in MS statistics no other immunopathologic disease such as rheumatic diseases or bronchial asthma was found. Interestingly, also in 400 MS patients examined, hyperuricaemia or gout, which are widespread among the populace, were not found in a single case.
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PMID:[Pathogenesis of multiple sclerosis. Work-hypotheses and experimental data]. 84 79

Genetic factors and environmental factors are thought to be involved in the pathogenesis of insulin-dependent diabetes mellitus Type 1. Viruses, as one environmental factor, may act as primary injurious agents to beta cells or as triggering agents for autoimmunity. Some viruses such as EMC-D and Coxsackie B4 can induce Type 1 diabetes by infecting and destroying beta cells in genetically susceptible mice. In addition, certain species of monkey, such as Patas, show elevated blood glucose levels and depressed insulin secretion after infection with Coxsackie B4 virus. An occasional case of Type 1 diabetes mellitus appears to be associated with the infection of beta cells with Coxsackie B viruses. In addition, Coxsackie B4 virus may also generate viral antigen-specific cytotoxic T cells which may cross-react with a beta cell-specific autoantigen leading to autoimmune Type 1 diabetes. In the case of viral triggering of autoimmune Type 1 diabetes, certain viruses (eg, retrovirus in NOD mice and rubella virus in hamsters and humans) may alter a normally existing beta cell antigen into an immunogenic form or might induce a new antigen, leading to beta cell-specific autoimmune insulin dependent diabetes mellitus. In addition, other viruses (eg, Kilham's rat virus in DR-BB rats) could generate antigen-specific T effector cells which may cross-react with a beta cell-specific autoantigen. In contrast to the induction of diabetes, viruses can prevent the development of diabetes. Inoculation of DP-BB or NOD mice with lymphocytic choriomeningitis virus reduced the incidence of diabetes or prevented the disease by disordering particular lymphocyte subsets.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Induction and prevention of type 1 diabetes mellitus by viruses. 129 46

A number of practical office and bedside clues to cardiac disease in infants and children have been passed on through the years. They relate to the history, to the inspection and palpation components of the physical examination, and to knowledge of the specific cardiac defects that are likely to be associated with certain clinical syndromes. With the possible exception of coarctation of the aorta, the clues are not diagnostically specific. In many instances, however, they serve to narrow a broad array of diagnostic possibilities to 2 or 3 and, with the aid of other clues and auscultation, they can often be distinguished from one another. When a primary care physician is confronted with a child who has an incidental murmur that is "probably" innocent but could be organic, useful clues favoring an organic murmur are a history of congenital heart disease in a first-degree relative; a history of maternal rubella syndrome, alcohol use, or teratogenic drug use during pregnancy; a history of inappropriate sweating; a history of syncope, chest pain, or squatting; maternal diabetes mellitus; premature birth; birth at a high altitude; cyanosis; abnormal pulsations; recurrent bronchiolitis or pneumonia; chronic unexplained hoarseness; asymmetric facies with crying; and a physical appearance suggestive of a clinical syndrome.
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PMID:Clues in diagnosing congenital heart disease. 157 99

Viral infection has been suggested to play a triggering role in the pancreatic beta cell destruction which occurs in insulin-dependent diabetes (IDDM). However, the underlying mechanism of this phenomenon is unknown. In this study a human insulinoma cell line has been infected with measles, mumps and rubella viruses since a temporal association is reported between the clinical onset of IDDM and diseases caused by these viruses. The infection with measles and mumps viruses induced the release of interleukin-1 (IL-1) and interleukin-6 (IL-6) by the cell line as assessed by a bioassay and up-regulated the expression of human leucocyte antigen (HLA) class I and class II antigens as evaluated by cytofluorimetric analysis. Stimulation with rubella virus induced the release of IL-6 only and had no effect on HLA antigen expression. These data show for the first time that IL-1 and IL-6 secretion by an insulinoma cell line may occur after viral infection and suggest that cytokine release and increased expression of HLA molecules by beta cells may act to induce the immune response towards beta cells in IDDM.
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PMID:Viral infection induces cytokine release by beta islet cells. 159 39

In this study, antibody levels to Epstein-Barr virus (EBV) capsid antigen (VCA) and EBV early antigens (EA) were analysed by enzyme immunoassay in 54 newly diagnosed type 1 diabetic children and in matched controls. The patients had significantly lower EBV VCA IgG-class antibody levels (p less than 0.02). This was true particularly in young patients and in boys (p less than 0.005). VCA IgA-class antibody levels were also decreased in young patients (p less than 0.02). VCA IgM-class antibodies were observed in two of the patients only. IgG- and IgA-class antibodies to EBV EA or rubella virus antigen showed no differences between patients and controls. The results suggest that EBV infections coincide with the onset of clinical diabetes relatively rarely. However, the abnormally low antibody response to EBV VCA in diabetic children suggests abnormalities in the EBV-specific immune response.
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PMID:Decreased antibody reactivity to Epstein-Barr virus capsid antigen in type 1 (insulin-dependent) diabetes mellitus. 164 69


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