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

The present study describes the results achieved 6 months after the establishment of a health examination, with different features depending on age and sex groups, which was progressively applied to the population of the C.A.P. "Virgen de la Fuensanta" (Valencia). The preventive activities included: vaccination (rubella, tetanus and influenza), tuberculin skin testing, determination of body weight and mass (BMI), measurement of blood pressure and heart rate, cervical cytology, breast examination and search for occult blood in feces. Among the 388 evaluated individuals (69.4% females and 30.6% males), 10 cases of hypertension, 2 of diabetes, 65 of obesity, 20 of hypercholesterolemia, 23 women with benign breast abnormalities and 8 instances of occult blood in feces were detected. In the age group of 15-26 years, 7 positive tuberculin reactions were detected. In 175 cytological studies no case of malignant disease was discovered. The degree of acceptance of the program by the users was satisfactory, as assessed by the compliance with both the appointments (85%) and the individual interventions (88-100%).
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PMID:[Results of health examination by age and sex groups]. 251 28

A high incidence of insulin-dependent diabetes mellitus (IDDM) has been reported in children and young adults previously afflicted with congenital rubella syndrome (CRS). The authors have studied the effect of rubella virus infection on human pancreatic islet cells in tissue culture. These experiments were performed with the use of both monolayers and free-floating human fetal islets of Langerhans tissue. Levels of production of immunoreactive insulin by islet cells that had been infected by rubella virus were lower than those observed in control cultures, under conditions of high glucose concentration (11.1 mmol/L) in the medium. The presence of rubella viral antigens in human pancreatic beta and non-beta cells was demonstrated by double-label immunofluorescence. These results suggest that rubella virus can infect human pancreatic islet cells and that such infection may lead to significant reductions in levels of secreted insulin.
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PMID:Infection of cultured human fetal pancreatic islet cells by rubella virus. 264 1

Type 1 diabetes results from the destruction of insulin-producing pancreatic beta cells. Genetic and environmental factors are implicated in the beta cell destruction. As environmental factors affecting the induction of type 1 diabetes, diabetogenic viruses, chemicals, toxins, and diet are likely candidates as either primary injurious agents of beta cells or triggering agents for the induction of autoimmunity. Regarding viruses as a triggering factor of type 1 diabetes, there are at least two different pathogenic mechanisms in virus-induced diabetes: cytolytic infection of beta cells, leading to their destruction, and triggering of autoimmunity, leading to the autoimmune-mediated destruction of beta cells. Since there is no correlation between the induction of antibodies to Coxsackie B viruses and the presence of islet cell autoantibodies in patients with type 1 diabetes, the induction of diabetes by Coxsackie B viruses may be due to cytolytic infection of beta cells rather than an autoimmune response. In contrast, rubella virus and cytomegalovirus (CMV) do appear to be somehow associated with autoimmune type 1 diabetes since there is a strong correlation between the presence of islet cell autoantibodies and persistent infections. Regarding genetic factors, there are distinct markers related to the susceptibility to Coxsackie B4 virus-associated type 1 diabetes and CMV-associated type 1 diabetes. Four specific DNA restriction endonuclease fragments (BamHI-DQ-beta 6.6, TaqI-DR-beta 4.3, TaqI-DR-beta 2.5 and TaqI-DR-beta 1.5 kb) are related to the susceptibility to Coxsackie B4 virus-associated type 1 diabetes while six specific DNA restriction endonuclease fragments (BamHI-DQ-alpha 12.5, -beta 3.7 and -beta 3.2 kb, TaqI-DQ-alpha 7.2, -beta 7.2 and -beta 5.4 kb) are related to the susceptibility to CMV-associated type 1 diabetes.
Diabetes Res Clin Pract 1989
PMID:Viruses as a triggering factor of type 1 diabetes and genetic markers related to the susceptibility to the virus-associated diabetes. 268 Mar 67

Developmental enamel defects in primary teeth have been found at least twice as frequently in children with cerebral palsy or mental retardation as in control children, and frequently also in children with sensori-neural hearing deficits. The developing tooth germ is sensitive to a range of systemic disturbances, some of which may also affect neurologic development. Because the enamel cannot recover once it is damaged, it may provide a repository of information on the timing and nature of insults potentially affecting other ectodermally derived structures, including the brain. This paper reviews the literature on developmental defects of enamel in primary teeth, asking whether these might be useful as biological markers of the timing and in some cases the nature of insults. Among systemic factors related to development of enamel that might also have implications for neurologic development are certain genetic disorders including tuberous sclerosis, premature birth, neonatal nutritional disturbances (especially hypocalcemia), viral infections (such as rubella and cytomegalovirus during gestation), thyroid disorders, and maternal diabetes. It is concluded that further research is warranted concerning whether developmental defects of dental enamel can be useful markers for the timing of intra-uterine or perinatal events associated with certain neurologic and sensory disorders of children.
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PMID:Developmental enamel defects in primary teeth in children with cerebral palsy, mental retardation, or hearing defects: a review. 270 Nov 56

Insulin-dependent diabetes mellitus results from destruction of pancreatic beta cells. Viruses and autoimmunity have been implicated as possible causes of beta cell destruction in genetically predisposed individuals. The evidence for viruses comes largely from experiments in animals, but several studies in humans point to viruses as triggers in the pathogenesis of diabetes in some cases. In animal models, at least 4 different possible mechanisms for virus-induced diabetes have been proposed. The first mechanism is direct cytolytic infection of pancreatic beta cells. One group of viruses, including encephalomyocarditis virus, Mengovirus 2T, and Coxsackie B viruses, can directly infect and destroy pancreatic beta cells independent of autoimmune processes. The second mechanism is triggering of autoimmune responses. In contrast to the encephalomyocarditis virus-induced diabetes, reovirus type 1 and rubella virus seem to be somehow associated with autoimmunity in the genesis of a diabetes-like syndrome in a certain strain of suckling mice and hamsters, respectively. The third mechanism is cumulative environmental insults. The cumulative environmental insults with viruses and beta cell toxic chemicals can result in diabetes in genetically predisposed non-human primates and certain inbred strains of mice. The fourth mechanism is persistent infection. A certain virus, such as lymphocytic choriomeningitis virus, persistently infects murine pancreatic beta cells and produces hyperglycemia. The evidence that viruses cause diabetes in humans is more circumstantial.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Possible mechanisms in the pathogenesis of virus-induced diabetes mellitus. 282 13

Analysis of sequence variation in the polymorphic second exon of the major histocompatibility complex genes HLA-DQ alpha and -DQ beta has revealed 8 allelic variants at the alpha locus and 13 variants at the beta locus. Correlation of sequence variation with serologic typing suggests that the DQw2, DQw3, and DQ(blank) types are determined by the DQ beta subunit, while the DQw1 specificity is determined by DQ alpha. The nature of the amino acid at position 57 in the DQ beta subunit is correlated with susceptibility to insulin-dependent diabetes mellitus. This region of the DQ beta chain contains shared peptides with Epstein-Barr virus and rubella virus.
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PMID:Allelic sequence variation of the HLA-DQ loci: relationship to serology and to insulin-dependent diabetes susceptibility. 284 56

Alterations in T-lymphocyte subsets have been connected to the autoimmune pathogenesis of Type 1 (insulin-dependent) diabetes. In this study peripheral blood lymphocytes were analysed by flow cytometry using OKT3, OKT4, OKT8, anti-HLA-DR, anti-IL-2 receptor and anti-membrane immunoglobulin antibodies in newly diagnosed Type 1 diabetic children, their healthy siblings and healthy control children. The results were compared to the occurrence of serologically verified recent virus infections, some of which can induce lymphocyte subset alterations and have also been connected with the onset of diabetes. In most diabetic patients the amounts of OKT3, OKT4, OKT8 and membrane-Ig-positive cells were within the normal range. Exceptional helper/inducer and suppressor/cytotoxic T cell profiles were observed in a few patients, most of whom had serologically verified recent Epstein-Barr, rubella, mumps or Coxsackie B virus infection. In addition, increased numbers of activated IL-2 receptor-positive cells were observed in the patient group. These results suggest that significant lymphocyte subset alterations are not characteristic of Type 1 diabetes but can occasionally be induced by recent virus infections in newly diagnosed patients. However, the slight increase in activated lymphocytes could reflect the activation of cellular immune systems to the autoantigens in the pancreas.
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PMID:Flow-cytometric analysis of lymphocyte subsets in relation to virus infections at the onset of type 1 (insulin-dependent) diabetes. 284 9

Patients from England, Austria, and Australia with recently diagnosed juvenile-onset insulin-dependent diabetes (type 1) mellitus (IDDM) and matched controls were tested for specific IgM responses to Coxsackie B1-5 viruses. 37 of 122 (30%) patients aged less than 15, but only 15 of 204 (6%) controls, were positive (p less than 0.005). Differences in Coxsackie B virus specific IgM responses between patients and controls were statistically significant for patients in England and Austria (p less than 0.005). Coxsackie B virus specific IgM responses were detected in only 3 of 31 patients aged greater than 16. Virus-specific IgM responses were directed against a single serotype, usually Coxsackie B4 or 5, in 23 of 37 (62.5%) children aged less than 15; 10 of 13 (77%) of children aged less than 7 had monotypic responses. Among families of Austrian patients with IDDM, 8 of 79 (10%) siblings had Coxsackie B virus specific IgM responses, 1 of whom subsequently had IDDM, but none of the 80 parents was positive. In contrast, there was no evidence of recent infection by mumps, rubella, or cytomegalovirus (CMV), since mumps-virus specific IgM was present in only 2 of 100 children with IDDM and 5 of 139 controls; no rubella or CMV specific IgM responses were detected in 60 sera from patients with IDDM.
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PMID:Coxsackie B, mumps, rubella, and cytomegalovirus specific IgM responses in patients with juvenile-onset insulin-dependent diabetes mellitus in Britain, Austria, and Australia. 286 61

Routine obstetric screening for all patients should include a Pap smear, urinalysis and urine culture, complete blood count, blood type, Rh factor and direct Coombs' test. Patients should also be screened for syphilis, rubella, gonorrhea and diabetes. For patients at high risk for certain conditions, additional studies of value include obstetric ultrasound, amniocentesis, serum alpha-fetoprotein level and screening for sickle cell anemia, herpes, hepatitis B, Chlamydia and human immunodeficiency virus.
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PMID:Prenatal screening. 328 2

The major goal of rubella immunization is the prevention of the congenital rubella syndrome. As many as 20 per cent of women in the reproductive age group in the United States continue to be susceptible to rubella despite the immunization programs currently in place. Intensified efforts are therefore needed to identify persons at risk for infection and to vaccinate them. Women who develop a rubella-like illness during pregnancy should have the diagnosis confirmed serologically because a diagnosis based on clinical criteria alone is unreliable and because of the serious implications of gestational rubella infection. The rubella virus can infect the fetus at any stage of pregnancy, but defects are rarely noted when this occurs after the 16th week of gestation. The most common abnormalities in the congenital rubella syndrome are hearing loss, mental retardation, cardiac malformations, and eye defects. Diabetes mellitus, thyroid disease, glaucoma, and other delayed manifestations of congenital rubella syndrome are common, thereby necessitating long-term followup of these patients. The detection of rubella-specific IgM antibodies in fetal blood is helpful in establishing the diagnosis prenatally and can aid in the management of pregnancies complicated by this infection. Susceptible women identified through screening during pregnancy should be immunized in the immediate postpartum or postabortion period. Although the live, attenuated rubella vaccine is contraindicated during pregnancy, pregnant women who are inadvertently immunized are not candidates for pregnancy termination because no defects consistent with congenital rubella have been reported to date in the offspring of other similarly vaccinated women.
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PMID:Maternal rubella and the congenital rubella syndrome. 328 22


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