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Query: UMLS:C0011854 (
type 1 diabetes
)
20,749
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Insulin-dependent (type 1) diabetes mellitus (
IDDM
) is due to the selective autoimmune-mediated destruction of pancreatic beta cells possibly initiated by viruses. To elucidate the possible role of viruses and cytokines in the pathogenesis of
IDDM
, we have examined the effect of reovirus infection on beta cell major histocompatibility complex (MHC) expression and the effect of interferon-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNF-alpha) on beta cell function in vitro.
Infection
of RIN-m5F (rat insulinoma) cells with reovirus-1 or reovirus-3 was associated with a tenfold increase in class 1 MHC protein and mRNA expression. Reovirus infection did not induced the expression of class 11 MHC by RIN-m5F cells. Exposure of reovirus to ultraviolet light almost completely abolished its ability to induce class 1 MHC protein expression on infected cells. Murine islets cultured for 3 days with IFN-gamma and/or TNF-alpha had a significantly reduced insulin response to glucose, which was more marked with a combination of the cytokines. During 6 days of culture in IFN-gamma plus TNF-alpha islets underwent noticeable degeneration associated with an 80% reduction in insulin content. These findings together with previous data suggest viruses and cytokines may have multiple roles in beta cell destruction, indirectly through enhanced MHC protein expression and directly through functional impairment and loss of viability.
...
PMID:Viruses and cytokines: evidence for multiple roles in pancreatic beta cell destruction in type 1 insulin-dependent diabetes mellitus. 254 35
Polymorphonuclear leucocyte (PMN) ingestion of particles coated with lipopolysaccharide (LPS) from Escherichia coli was compared to other PMN functions in seven patients with
insulin dependent diabetes mellitus
(
IDDM
) during short-term controlled metabolic changes from normo- to hyperglycemia without ketoacidosis. Factors known to interfere with PMN functions were excluded. PMN ingestion of particles coated with both LPS and bovine serum albumin became reduced from normo- to hyperglycemia. PMN motility was impaired in
IDDM
, but did not seem to be affected by short-term changes in metabolic control. PMN metabolism did not change from normo-to hyperglycemia. Particle-uptake by diabetic PMN is impaired after short term hyperglycemia in the range normally occurring in diabetics in every-day life.
Infection
PMID:Polymorphonuclear leucocyte dysfunction during short term metabolic changes from normo- to hyperglycemia in type 1 (insulin dependent) diabetic patients. 284 45
Twenty-four consecutive children with newly diagnosed insulin-dependent (type I) diabetes mellitus (
IDDM
) were investigated for a history of
infectious disease
. Thirteen of the 24 (54%) patients reported symptoms of acute infection within two months before diabetes was diagnosed. The mean age was 8.5 years and 15 (63%) of the patients were girls. No clear seasonal variation in onset was seen. Coxsackie B (CB)-virus-specific IgM responses were detected by reverse radioimmunoassay (RIA) in 16 of the 24 (67%) patients on the day of diagnosis of
IDDM
. The highest titre was usually recorded at that time, but with some the highest titre was found with a second serum obtained three to seven weeks after diagnosis. Thereafter the titres declined, and after six months IgM was detected only in a few patients. Thirteen patients displayed monotypic IgM responses, whereas three patients showed ditypic responses. Among the former, IgM was recorded against Coxsackie B4 (CB4) in four, B5 (CB5) in three, B1 (CB1) in two, B2 (CB2) in two, and B3 (CB3) in two patients. The ditypic responses were against CB2 and CB3, CB3 and CB4, and CB5. No CB-virus-specific IgM was detected in sera, found during the same period, from age-matched nondiabetic children without evidence of infection. In neutralisation (NT) tests, antibodies to the homotypic virus were found in 12 of the 16 diabetic patients showing CB-virus-specific at the time of diagnosis. A significant rise in NT titre was demonstrated in three of these patients. No significant clinical difference was noted between IgM positive and IgM negative patients.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:High frequency of Coxsackie-B-virus-specific IgM in children developing type I diabetes during a period of high diabetes morbidity. 299 22
Using the prospective Hungarian childhood diabetes register, a nationwide case-control study was carried out to investigate the possible role of various non-genetic factors as risk determinants for
type 1 diabetes
in childhood. A questionnaire (covering family characteristics, social status, fetal and perinatal events, breast-feeding habits,
infectious diseases
and stressful life events) was sent by mail to all incident diabetic children in 1990 (n = 163) and to two referent children (for each diabetic child), matched for age, sex and county. Diabetic children had a tendency to have mothers > 35 years of age (odds ratio (OR) = 3.52; 95% confidence intervals (CI) 0.74-16.79), a lower proportion of their mothers had higher education (OR = 1.69; 95% CI 0.95-3.0) and these children tended to move home more frequently (OR = 1.99; 95% CI 0.97-4.1). Although the duration of exclusive breast feeding was similar in both groups, the proportion of diabetic children who received no breast milk tended to be higher (OR = 1.76; 95% CI 0.91-3.4). A higher proportion of diabetic children reported non-specific infections (OR = 2.94; 95% CI 1.19-7.21) and the number of stressful life events was higher in diabetic children aged 10-14 years (OR = 3.9; 95% CI 1.14-13.27). As the risk determinants for childhood insulin-dependent diabetes mellitus identified in our low-risk population appear to be similar to those detected in the genetically different, high-risk Swedish population, our study strongly supports an etiological role for these non-genetic risk factors in
IDDM
.
...
PMID:Non-genetic risk determinants for type 1 (insulin-dependent) diabetes mellitus in childhood. Hungarian Childhood Diabetes Epidemiology Study Group. 794 3
The mechanism of beta-cell destruction leading to
insulin dependent diabetes
is probably a cell mediated auto-immune process occurring in genetically susceptible individuals. Since 50-70% of monozygotic twins will not get the disease non-genetic risk factors must play an important role in the etiology of the disease. During the past decade population based epidemiological studies have identified several risk determinants for
insulin dependent diabetes
. Based on these studies a multifactorial hypothesis of causation is proposed. Some risk determinants (maternal child blood group incompatibility, fetal viral infections, early exposure to cow's milk proteins, a high exposure level of nitrosamines) may independently initiate the autoimmune process by causing the initial damage of the beta-cell, leading to antigen release. Other risk determinants may promote an already ongoing autoimmune destructive process through induction of lymphokine release or by causing an increased work load on the beta-cell. Risk factors that may increase the peripheral need for insulin (
infectious diseases
, cold environment, a high growth rate and stressful life events) may act as promoters of the beta-cell destruction but also disclose the beta-cell impairment and make the disease clinically overt. Possibilities of different risk profiles in different age groups and of synergism between different risk factors are also discussed.
...
PMID:Etiological aspects of insulin-dependent diabetes mellitus: an epidemiological perspective. 821 32
A 76 years old patient suffering from
insulin dependent diabetes
presents a multiple, bilateral and asymmetric cranial neuropathy involving on the left side the cranial nerves VIII, IX with a participation of the efferent autonomic fibers of the nerves VII and IX (xerostomia) and the nerve XII, and involving on both sides the nerves VII and X. Like it is known from literature the nerve XI was spared, probably because of the more caudal emergence from the brainstem. The disease was preceded by a violent otalgia on the left side which was initially interpretated as a malignant external otitis. This affection was associated with an inflammatory syndrome that was easily monitored by the blood sedimentation rate. The course was favorable but marked by fluctuations of the neurological deficits. The MRI shows a pachymeningitis localised at the beginning in the medial fossa and on the cerebellar tentorium, later on the left parieto-occipital convexity. The diagnosis of a focal idiopathic pachymeningitis was confirmed by excluding different other affections like inflammatory, tumoral and
infectious diseases
, by using MRI examinations, CSF analysis and especially meningeal biopsy. It is a rare inflammatory disease of unknown origin with potentially persistent neurological deficits. We discuss the differential diagnosis and the therapeutical possibilities, which consist in a long term immunosuppression with corticosteroids and azathioprine.
...
PMID:[Neuritis of multiple cranial nerves in idiopathic focal pachymeningitis]. 886 57
In this prospective analysis we investigated the clinical characteristics of black South African diabetic patients admitted to hospital with hyperglycaemic emergencies. The study cases were selected from the medical admissions to an urbanized, Johannesburg academic hospital over a period of 12 months. Only patients with severe diabetic ketoacidosis (DKA) or hyperosmolar non-ketotic hyperglycaemia (HNKH) as defined in the text were included. Over the study period, we identified 58 patients with severe DKA (M: 32, F: 26) and 24 with HNKH (M: 14, F:10). Thirty-two of the patients with DKA (55.2%) were classified as having non-insulin dependent (Type 2) diabetes mellitus (NIDDM). Compared to the 26 subjects with insulin-dependent (Type 1) diabetes mellitus (
IDDM
), the NIDDM patients were older (51.7 vs 27.7 years) and had a significantly higher body mass index (BMI) (29.4 vs 23.5 kg m(-2), p = 0.002), and glucose levels 47.5 vs 34 mmol l(-1) p = 0.004). Mortality from DKA was 6.8 % and from HNKH 16.6%.
Infection
was the leading precipitating factor for both DKA and HNKH, followed by first presentation and noncompliance. We conclude that the majority of urban African patients admitted to hospital with DKA have NIDDM. Mortality from DKA among the black Africans in Johannesburg is low and comparable to the mortality in western Europe.
...
PMID:Clinical characteristics and outcome of hyperglycaemic emergencies in Johannesburg Africans. 922
Forty-three cases of diabetic ketosis were analysed to determine the mode of presentation, treatment modalities and outcome. Among these cases 62.8% were non-insulin dependent diabetes mellitus (NIDDM) patients and 37.2% belonged to the
insulin dependent diabetes mellitus
(
IDDM
) group. Six patients had blood glucose levels of more than 250 mg/dl but less than 300 mg/dl who were grouped separately for analysis under the term "euglycaemic diabetic ketoacidosis (EGDK)".
Infection
was the commonest precipitating factor in diabetic ketosis in all groups. Abdominal pain and vomiting occurred with NIDDM and EGDK cases. Drowsiness was common and coma was rare. Acute myocardial infarction (MI) and pulmonary oedema occurred with NIDDM cases. Shock, acidosis, acquired respiratory distress syndrome (ARDS) and mucor mycosis were seen with
IDDM
cases. Mortality was 7 out of 43(16.3%). Saline requirement was lower in NIDDM and EGDK cases. Intensive insulin therapy with hourly intravenous doses were needed for
IDDM
cases while majority of NIDDM cases could be managed with 6 hourly doses of insulin given subcutaneously or intramuscularly.
...
PMID:Changing profile of diabetic ketosis. 956 97
During the last years the intensified insulin therapy has proven to be more successful than standard insulin treatment in patients with
type I diabetes mellitus
. For this kind of insulin therapy, intermediate and short acting insulin is injected in an independent manner. The basic need for insulin of the organism is covered with the intermediate insulin while application of the short acting insulin depends on carbohydrate intake and blood glucose levels. The patients are learning the intensified insulin therapy by structured guidance that they are able to modify the insulin dosage by themselves. The patients have to take several parameters into account to calculate the actual insulin need such as physical activity, interval between meal and injection,
infectious diseases
, or the circadian rhythm. An intensified insulin therapy involves a great deal of time for the patient since he has to perform insulin injections and measurements of blood glucose levels up to four times a day. However, this kind of treatment increases the flexibility of the patient's food intake and metabolic control which reduces the onset of diabetic side effects.
...
PMID:[Intensified insulin therapy in type I diabetes: when and how?]. 984 92
The spontaneous development of
insulin dependent diabetes mellitus
in non-obese diabetic (NOD) mice has been shown to be mediated by a Th1 response against beta cell antigens. It is known that in murine models of Schistosoma mansoni infection, egg production is associated with a switch from a Th1 to Th2 response. This subsequent dominance of a Th2 response in S.mansoni infected mice has been shown to influence the response to other infectious agents or antigens. We therefore determined whether infection with S.mansoni could influence the spontaneous incidence of
insulin dependent diabetes mellitus
(
IDDM
) in NOD mice.
Infection
with this helminth significantly reduced the spontaneous incidence of
IDDM
.
IDDM
was also prevented by injecting parasite eggs alone. Because until relatively recently humans might expect to succumb to a variety of infectious agents, the current freedom from infection might permit the expression of a genetic predisposition to autoimmune pathology and be responsible for the increased incidence of
IDDM
.
...
PMID:Infection with Schistosoma mansoni prevents insulin dependent diabetes mellitus in non-obese diabetic mice. 1032 Jun 14
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