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

Sera of 406 individuals, 174 Type 1 (insulin-dependent) diabetic patients, 125 non-diabetic family members and 107 unrelated control subjects, were screened for the presence of antibodies against glycated albumin. In none of these sera could such antibodies be detected. However, antibodies directed towards monomeric, unmodified human serum albumin were detected in 13 sera. These albumin autoantibodies were of the IgM class, and occurred in sera from nondiabetic persons (0.9-1.6%) and with a five-fold higher frequency in sera from diabetic patients (5.2%). The presence of albumin antibodies was neither related to the presence of diabetic late complications, islet cell antibodies, HLA-status nor duration of diabetes. The albumin antibodies were also found in sera from persons carrying antibodies against mumps (17%) or Epstein-Barr virus.
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PMID:Albumin-directed antibodies in diabetes: demonstration of human serum albumin-directed IgM autoantibodies. 375 31

In the practice of diagnosing occupational deafness resulting from noise effects of factors determining workers' hearing, such as living conditions, working conditions, nutritional and other habits, diseases and their therapy, are often neglected. Discussed in the paper are the significance and ototoxic effects of such factors as: aminoglycoside antibiotics, diuretics, salicylic acid derivatives, fenacetin, quinine, fluorine compounds, cytotoxic drugs, chemical compounds other than drugs (carbon monoxide, carbon disulphide, lead, organic solvents), ethyl alcohol, diseases (abdominal typhus, bacillary dysentery, diphtheria, brucellosis, epidemic parotiditis, poliomyelitis, rubella, aural shingles, syphilis, diabetes mellitus, chronic renopathies, hypothyroidism, serologic conflict, pigmentary retinitis). Exposure to intense noise is more and more frequently juxtaposed with the impact of the mentioned factors. If industrial physicians get aware of this association the prevention of deafness and reliability of treatment may be largely promoted.
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PMID:[Ototoxic factors requiring consideration in the diagnosis of occupational hearing loss]. 390 48

Since mumps virus seems to be one of the most likely candidates in viral etiology of insulin-dependent diabetes (IDDM) we studied the possible relationship of glucose tolerance (75 g oGTT), beta cell function, diabetes associated HLA antigens, haptoglobin phenotype, islet cell antibodies (ICA) and islet cell surface antibodies (ICSA) in 125 subjects with antecedent mumps infection. Impaired glucose tolerance (IGT) was diagnosed in 3.2% (n = 4) but onset of diabetes did not appear within 14 months after mumps infection. There was no relationship between glucose tolerance and complications of antecedent mumps infection (e.g. pancreatitis, meningitis, orchitis). The prevalence rate of ICA was 76%. ICSA were detectable in about 36% of children and 62% of the adults tested (p less than 0.01). There was no relationship between ICA/ICSA and diabetes-associated HLA antigens, haptoglobin phenotype or beta cell function (fasting C-peptide and insulin response to 75 g oGTT). However, adults with circulating ICA were characterized by a significantly lower insulin response to glucose. Fifty two "risk" subjects characterized by IGT, diabetes associated HLA antigen(s), ICA or ICSA either alone or combined were studied again 26 months after mumps infection. No symptomatic diabetes appeared and IGT was diagnosed in one case only. ICA and ICSA persisted in more than 50% of subjects in whom ICA or ICSA were present 14 months after mumps infection. Since the used immunological techniques do not clearly distinguish organ-specific from non-organ-specific antibodies the results must be interpreted with caution. To summarize, the preliminary results do not support a close temporal relationship between mumps infection and the onset of IDDM. The pathogenetic role of mumps virus and ICA/ICSA and their possible relation to a slow progressive beta cell destruction has still to be determined.
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PMID:Metabolic, hormonal, and immunological alterations in subjects with antecedent mumps infection. 391 1

An analysis was conducted of the major findings of a long term follow up study of 3076 subjects who were exposed to viral infections in utero and who at the time of analysis were up to 40 years of age. Mortality and morbidity were compared with those in a control population matched for sex and date and area of birth. An excess of cancers (16 cases against seven) appeared to be clustered among those exposed to herpes viruses (varicella or cytomegalovirus). There was evidence of an increased risk of diabetes among those exposed to mumps during the first trimester (four cases among 128 subjects against none in 148 controls). The most surprising finding was a decrease of diseases of the skin and subcutaneous tissue and of the nervous system among subjects exposed to antenatal varicella zoster infection. The mechanism for the association may include production of fetal anti-idiotype antibodies in response to transplacentally acquired maternal autoantibodies.
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PMID:Long term effects of exposure to viral infections in utero. 391 51

Diagnostic significance of a simple and rapid screening procedure for determining the relative amounts of pancreatic and salivary isoamylase using an amylase inhibitor was evaluated in 242 subjects (controls 84, acute pancreatitis nine, chronic pancreatitis 28, pancreatic cancer 14, peptic ulcer 25, liver cirrhosis 15, cholelithiasis 24, irritable colon syndrome 13, diabetes mellitus 13, mumps seven, and chronic renal failure 10). Electrophoretically separated isoamylases of saliva and pure pancreatic juice were all inhibited at similar degrees to the corresponding unfractionated amylases. Total amylase and pancreatic isoamylase were elevated in all nine patients with acute pancreatitis. Pancreatic isoamylase was decreased in 12 of 28 patients (43%) with chronic pancreatitis and increased in nine of 14 patients (64%) with pancreatic cancer. The mean pancreatic isoamylase activity in the patients with acute pancreatitis was significantly higher (p less than 0.01), while that of chronic pancreatitis was significantly lower (p less than 0.05) when compared with controls. The inhibition method offers simple, rapid, and specific analysis of serum isoamylase for the differential diagnosis of hyperamylasemia in cases of emergency.
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PMID:Differential determination of serum isoamylase using an amylase inhibitor and its clinical application. 396 56

Sera from 123 patients with diabetes mellitus of recent onset, 155 patients with diabetes of more than two years' duration, and 250 normal persons were collected over a period of two and a half years. All sera were tested for neutralizing antibody to Coxsackie virus types B1-6, and a sample was tested for complement-fixing antibody to a number of viral, rickettsial, and mycoplasmal antigens.In diabetics of recent onset no evidence was found of any excess of antibodies to mumps virus or some common respiratory viruses. Insulin-dependent diabetes within three months of onset were found to have higher antibody titres to Coxsackie B virus, particularly of type B4, than either normal subjects or patients with diabetes of longer duration.
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PMID:Viral antibodies in diabetes mellitus. 581 81

Autoimmunity is frequently involved in the pathogenesis of insulin-dependent diabetes, and viral infections have been implicated in some cases. We have investigated the possibility that islet cells and viruses share antigenic determinants with the result that antiviral antibodies would cross-react with islet cells. Antibody titers to Coxsackie B2, B3, B4, and B5, Influenza A and B, and mumps viruses were compared with islet cell antibody (ICA) titers in newly diagnosed insulin-dependent diabetic patients and in some diabetic patients followed prospectively for 1 yr postdiagnosis. Nondiabetic patients, with culture-proven Coxsackie B4 infections and large rises in Coxsackie B4 antibody titers, were evaluated for islet cell antibodies. No relationship between ICA and viral antibody titers was found either in diabetic or nondiabetic patients. We conclude that it is unlikely that islet cells and the viruses tested share antigenic determinants and other mechanisms relating viral infection and autoimmunity in insulin-dependent diabetes must be sought.
Diabetes Care
PMID:Antibodies to viruses and to pancreatic islets in nondiabetic and insulin-dependent diabetic patients. 618 49

Accumulating evidence strongly suggests that viruses may play an etiologic role in some cases of diabetes mellitus. The importance of environmental factors in the pathogenesis of the disease is suggested by genetic and epidemiological observations. Group B Coxsackie viruses and mumps virus have been implicated, and the evidence suggests that several other agents also could play a role in the disease. In experimental animals, a picornavirus similar to the Coxsackie viruses exhibits specific tropism for the beta cells of the islets of Langerhans, causing a disease in mice that is similar to juvenile-onset diabetes. In these animals, genetic and metabolic factors appear to influence the severity of beta cell injury. Immunopathologic considerations also may be important. In man, histocompatibility genes are important determinants of juvenile-onset diabetes and abberations of immune responsiveness to beta cells have been demonstrated. In experimental animals, cell-mediated immunity develops subsequent to the occurrence of viral-induced lesions in the islets. Viewed in concert, the evidence supports the notion that certain "wild" viruses may possess specific tropism for beta cells and destroy them during the course of a systemic infection. Host factors clearly play a role, but their relative importance in the pathogenesis of the disease remains to be defined.
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PMID:Viral diabetes mellitus in man and experimental animals. 625 11

Serological studies were carried out in the time course of insulin-dependent diabetes mellitus in 419 children, among whom paired sera from 66 were studied in the very beginning of diabetes mellitus. By seroconversion in 83% of the children early in the disease, different, frequently mixed virus infections were diagnosed: Coxsackie B2, B3, B4 (46%), rubella (41%), influenza A, B, C (38%), parainfluenza types 1-3 (35%), mumps (23%), adenovirus infection (18%), HB virus infection (4.5%). Acute respiratory diseases preceded or coincided with the onset of diabetes in half of the children with diagnosed acute respiratory and enterovirus infections. No clinical signs of rubella, mumps, or hepatitis immediately before the onset of diabetes or early in the disease were found. A possible role of virus infection diagnosed early in diabetes, in the etiology of chronic insulitis, in provocation of its exacerbation, and manifestation of diabetes mellitus is discussed.
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PMID:[Antibodies to viruses in children with diabetes mellitus]. 631 65

Much clinical and experimental data is in support of a significant role played by viruses in the etiology of diabetes mellitus. This hypothesis is borne out by the association of diabetes mellitus with Coxsackie B, mumps, rubella and herpes simplex virus infections, the presence of high persistent titers of neutralizing antibodies in diabetic patients, the in vitro permissiveness of human beta cells to viruses, and the recovery of viruses from the pancreas of diabetic patients. Viral multiplication is facilitated in HLA B8, B15, B18, Dw3 and Dw4 carriers. Experimental inoculation of EMC and Coxsackie B viruses to mice shows that beta cell involvement is dependent upon viral strains, viral membrane receptors, interferon production, immunological response and less essential factors such as age and sex. The virus is responsible for a specific immunological response and produces autoimmunological phenomena. These result in a decrease in the number and activity of insulin-producing cells through cytotoxic mechanisms. Pathological findings corroborate these physiopathological hypotheses.
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PMID:[Viruses and juvenile diabetes mellitus]. 632 9


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