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

The diabetogenic variant of encephalomyocarditis virus (EMC-D) induces a diabetes-like syndrome in certain strains of mice. A study was done to determine if virus-induced diabetes could be prevented by interferon (IFN). It was found that the production of diabetes by EMC-D was blocked by either IFN beta or a variety of IFN-inducers in SWR/J, but not ICR Swiss mice. The replication of EMC-D in cell culture was inhibited by IFN beta. It is concluded that the response of pancreatic beta cells to the protective effect of IFN, is probably under genetic control.
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PMID:Inhibition of virus-induced diabetes mellitus by interferon is influenced by the host strain. 630 72

The B (nondiabetogenic) and D (diabetogenic) variants of encephalomyocarditis (EMC) virus were studied to further define the role of the interferon (IFN) system in murine virus-induced diabetes mellitus. The relationship between the initial multiplicity of infection with EMC-B and the IFN yield showed that cells infected with one IFN-inducing particle produce a maximum amount of IFN, whereas IFN production is suppressed in cells infected with two or more particles. The IFN yield induced by EMC-D was less than 5% of that induced by EMC-B, allowing the designation of the B and D variants as Ifp+ and Ifp-, respectively. The Ifp+ property of the virion was shown to be responsible for the greater sensitivity of EMC-B to exogenous IFN as a result of primed local IFN induction. The data indicate that different Ifp phenotypes occur in nature and are associated with the development of diabetes in mice.
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PMID:Relationship of interferon-inducing particle phenotype to encephalomyocarditis virus-induced diabetes mellitus. 631 81

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

The repeated administration of interferon (IFN) or an IFN inducer reduced the development of diabetes in mice infected with the D variant of encephalomyocarditis (EMC) virus. Mice treated with the IFN inducer had less infectious virus, fewer pathologic changes, and higher concentrations of immunoreactive insulin in the islets of Langerhans in comparison with untreated mice. Antibody to mouse IFN (MuIFN) suppressed circulating IFN in mice infected with the B variant of EMC virus. Mice treated with antibody to MuIFN had four times more infected islet cells and 10 times more infectious virus in the pancreas compared with untreated mice. Of the surviving animals treated with antibody to MuIFN, approximately 40% developed mild diabetes whereas none of the mice developed diabetes when infected with the B variant of EMC virus alone. The IFN system is an important determinant of the outcome in EMC virus-induced diabetes in mice.
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PMID:The role of interferon in virus-induced diabetes. 633 24

We studied the effect of interferon as an adjunct to conventional insulin therapy on the early course of Type 1 diabetes in 43 newly diagnosed patients. Compared with conventional therapy, interferon administration slightly delayed the improvement of glucose homeostasis and the rise of high density lipoprotein cholesterol, while C-peptide secretion was unaffected. Independent of the type of therapy, 18 patients (42%) entered partial remission. The remission began 2.0 +/- 0.6 months (mean +/- SEM) from the start of therapy and lasted for 4.1 +/- 1.1 months. Seven patients (16%) were still in remission 1 year after diagnosis. The patients who entered remission had higher initial C-peptide secretion, lower glycosylated haemoglobin levels and better initial control than patients without remission. Thus, interferon provided no benefits as an adjunct to conventional insulin therapy in unselected patients with newly diagnosed Type 1 diabetes. An important factor for the development of remission was the presence of C-peptide secretion at the time of diagnosis.
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PMID:Remissions in newly diagnosed type 1 (insulin-dependent) diabetes: influence of interferon as an adjunct to insulin therapy. 638 81

The investigation of interferon status in 54 diabetes mellitus patients gave evidence for high levels of blood serum interferon, leukocyte inhibition of alpha-interferon production against moderate synthesis of gamma interferon. More marked alterations in the interferon status were registered in severe insulin-dependent diabetes mellitus complicated by angiopathies and running more than 5 years. Compensation of metabolic processes was not relevant to interferon status. Variations in the levels of alpha- and gamma-interferons in the course ob observation occurred in 30% of the patients.
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PMID:[The interferon status in diabetes mellitus]. 750 2

We investigated the side effects of interferon (IFN) on the endocrine and respiratory system in 545 cases of chronic hepatitis C. Eleven of 494 (2.2%) patients with chronic hepatitis C who were treated with natural or recombinant interferon (IFN) developed thyroid disease while on treatment. Eight patients developed hyperthyroidism and 3 patients developed hypothyroidism. All 11 patients required definitive therapy, who became euthyroid after the therapy. Two patients received nIFN alpha and one patient received rIFN alpha 2b developed diabetes mellitus. Two patients received rIFN alpha 2a and rIFN alpha 2b, respectively, developed interstitial pneumonia 12 weeks and 24 weeks later, respectively. One patient showed positive reaction for RA test and LE factor and positive LE cell, and complained of fever, arthralgia and dry cough. These phenomenon disappeared after the cessation of IFN therapy.
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PMID:[Side effects of interferon on endocrine and respiratory system in 545 cases of chronic hepatitis C]. 751 24

Since their initial description in 1957, the interferons (IFNs) have been increasingly used to treat a wide array of diseases. Acute adverse effects, i.e. 'flu-like' syndromes, hypo- or hypertension, tachycardia, headache, myalgias and gastrointestinal disorders, occur within the first hour or day after starting treatment. They are seldom treatment-limiting and are easily manageable. Sub-acute and chronic effects develop after several days, usually within 2 and 4 weeks of therapy. The most typical is neurological toxicity, including fatigue/asthenia, and behavioural and cognitive changes. Such symptoms may seriously impair quality of life and result in treatment discontinuation. Seizures have seldom been described. Other infrequent central nervous system adverse effects include vertigo, cramp and oculomotor nerve paralysis. Distal paraesthesias and peripheral neuropathy have been reported. IFN-associated autoimmunity is quite rare but a matter of concern. Biological or clinical manifestations usually require several months to become apparent. Autoantibodies have been shown to develop in most patients but have been inconsistently associated with clinical symptoms of systemic lupus erythematosus, rheumatoid-like arthritis and thyroiditis. Both hypo- and hyperthyroidism have been described but are usually reversible. Other infrequent autoimmune reactions include diabetes, pemphigus and worsening of multiple sclerosis. Although several patients present with a pre-existing autoimmune disorder, no predisposing factor has been clearly established. While hypotension and tachycardia are the most frequent acute cardiovascular complications, a few additional cases of cardiac arrhythmias and myocardial ischaemia have been reported after a short course or several weeks of treatment. These latter complications do not appear to be dose-dependent or age-related. Isolated cases of congestive heart failure have also been described. Mild proteinuria has been observed in 15 to 25% of patients, but acute renal toxicity is uncommon. A transient rise in serum aminotransferase levels is frequently noted during the first stage of therapy, especially in patients receiving the highest dosages. Direct hepatotoxicity is extremely rare. Autoimmune hepatitis, which is ill-diagnosed as chronic viral hepatitis, and de novo induction of autoimmune hepatitis, account for the majority of liver diseases. Haematotoxicity is relatively common but mild to moderate, and develops gradually during the first weeks of treatment. Neutropenia is the most common haematological toxicity, but is usually not dose-limiting and resolves rapidly upon drug discontinuation. Myelosuppression, autoimmune and immune allergic haemolytic anaemias and thrombocytopenias have seldom been described. Cutaneous adverse effects comprised nonspecific erythema and hair loss and, less frequently, vasculitis, local ulcerations at the site of injection and exacerbation of psoriasis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical toxicity of the interferons. 751 63

Fifty patients treated with interferon for chronic type C hepatitis, chronic type B hepatitis and renal cell carcinoma were examined for retinal complications. Retinal hemorrhages or cotton wool spots were observed in 23 (46%) of the patients. Retinal hemorrhages without cotton wool spots were found in 14 patients, cotton wool spots without retinal hemorrhages in 5 patients, and both hemorrhages and cotton wool spots in four patients. These findings were potentially reversible. There was one case of branch retinal artery occlusion and one case with microaneurysm. Red blood cell count decreased significantly in the patients with retinopathy compared with those without retinopathy (p < 0.05%). Patients with diabetes, hypertension, retinal arterial sclerosis, and anemia were at risk for retinopathy.
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PMID:[Interferon-induced retinal changes]. 751 88

During interferon (IFN) treatment for chronic hepatitis C, retinopathy develops in about one half of the patients. This "IFN-associated retinopathy" is characterized by cotton-wool spots (ischemic lesions) and superficial hemorrhage around the optic disc. It usually occurs 1 to 3 months after initiation of IFN therapy. Most of the patients with retinopathy have no symptoms, while some complain of impairment of visual acuity or flying specks. IFN-associated retinopathy tends to improve without any ophthalmic treatment and IFN therapy can be continued under careful observation. A complication of diabetes mellitus or a decrease in platelet count during IFN treatment may aggravate IFN-associated retinopathy. We emphasize that careful ophthalmologic follow-up is needed for all patients under IFN therapy.
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PMID:[Interferon-associated retinopathy]. 752 39


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