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

Our knowledge on immunopathogenic damage is derived from multiple different sources: experiments in vitro, experiments in vivo, clinical observations, and observations using material from multiple different animal species including man. If we want to analyse an immunological process suspected of causing tissue damage we have critically to evaluate the mechanism of immunologically specific initiating factors and the mechanisms of non-specific mediating factors. It is necessary to have clear information on the identity of the antigen, the location of the antigen, the identity of antibody, the location of antibody and similar information on specifically reactive lymphocytes. With this information in mind it is possible to hypothesize upon mechanisms, which can be responsible for the immunologically specific initiation of immuno-pathogenic damage. The non-specific mediating systems, which are the actual inducers of functional or structural tissue damage, are triggered by the specific, initial immune reaction. These systems comprise for instance complement, coagulation, granulocyte and macrophage lysozomes and function, chemotaxis, the mast cell system, phagocytosis etc. The overall picture of non-specific mediation of tissue damage is extremely complex, since it really makes it necessary to investigate and describe not only these systems but also their co-existence and interaction. Knowledge of immunopathogenic mechanisms in clinical disorders in man is still resting mainly upon analogies and assumptions, although progress is taking place. It is essential to ask the right questions and critically to evaluate the answers. Thereby the understanding of immunopathogenesis in diabetes mellitus and other clinical disorders shall gradually improve.
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PMID:Immunopathogenic mechanisms in tissue damage. 6 10

When the ability of granulocytes from 10 poorly controlled diabetic patients with fasting hyperglycemia and no evidence of ketoacidosis (mean fasting glucose 293 +/- 20 mg. per 100 ml.; mean +/- S.E.M.) to adhere to a nylon fiber column was assessed, the number of adherent granulocytes from whole blood was only 53 +/- 6 per cent of the values observed in controls. After antidiabetic treatment for one to two weeks and lowering of fasting glucose levels (mean 198 +/- 29 mg. per 100 ml.), adherence improved significantly (p less than 0.01) in the diabetics; however, their values were still subnormal (diabetic 74 per cent +/- 8 of control; p less than 0.02). Adherence values before and after treatment correlated with the fasting glucose level (r = 0.88, p less than 0.001). These findings suggest that, in addition to previously reported abnormalities in migration and the ingestion and killing of bacteria, granulocyte adherence may also be impaired in poorly controlled diabetic patients. This functional abnormality correlates directly with the fasting glucose and is reversed by insulin treatment. A defect of this type may compromise the normal inflammatory response in some diabetics and impair their capacity to resist infection.
Diabetes 1978 Jun
PMID:Impaired granulocyte adherence. A reversible defect in host defense in patients with poorly controlled diabetes. 65 13

Behind many clinical cases with recurrent, severe infections, absesses, delayed wound healing and especially in antibiotic resistant sepsis some granulocyte function abnormalities can be detected. The abnormalities are of inherited and acquired origin. The inherited dysfunctions are discussed here in details, but the appearance of some failures in neutrophil functions should be taken into consideration when examining patients with other diseases (e.g. diabetes, infections, periodontal disease, zinc deficiency, malignancies, uremia etc.). The main clinical tools for the diagnosis of the qualitative abnormalities in neutrophil functions are chemotaxis with migration, and an NBT test with and without stimulation, as a first indication. Any deviation in the result of these function tests requires further determinations.
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PMID:When should granulocyte function be checked? 133 55

A simple, direct assay for T-lymphocyte reactivity to islet antigen(s) in human insulin-dependent diabetes mellitus (IDDM) should facilitate preclinical diagnosis and the evaluation of intervention therapy to avert autoimmune-mediated beta-cell destruction. In subjects with preclinical or clinical IDDM, we measured the reactivity of peripheral blood mononuclear cells (PBMCs) incubated over 6 days with either adult human islets or fetal pig proislets, or other fetal pig tissues, and with human insulin. With islets, the stimulation index (SI) of [3H]thymidine uptake by PBMCs exceeded the mean + 2SD of control subjects in 6 of 6 preclinical subjects (SI 8.7 +/- 3.7), 7 of 11 clinical subjects (SI 5.2 +/- 3.4), and 1 of 12 control subjects (SI 2.7 +/- 1.7); with insulin, the responses were less in frequency and magnitude, being 4 of 6 (2.7 +/- 1.6), 3 of 11 (2.2 +/- 1.1), and 0 of 12 (1.20 +/- 0.55), respectively. The mean responses to islets of PBMCs from preclinical and clinical subjects differed significantly from control subjects (P less than 0.02 by 2-tailed Kruskal-Wallis test). Secretion of granulocyte macrophage colony-stimulating factor by PBMCs over 6 days was assayed in the preclinical group and generally paralleled the uptake of [3H]thymidine. PBMC reactivity to islets appeared to be at least as sensitive a marker of preclinical IDDM as autoantibodies to a 64,000-Mr protein, presumably the enzyme glutamic acid decarboxylase, in fetal pig proislets. In conclusion, islet-reactive T lymphocytes in subjects with preclinical and clinical IDDM can be identified in bulk culture of PBMCs.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1991 Sep
PMID:Reactivity to human islets and fetal pig proislets by peripheral blood mononuclear cells from subjects with preclinical and clinical insulin-dependent diabetes. 193 20

Sixteen-years-old female with severe aplastic anemia received a therapy combined with antilymphocyte globulin (ALG), high-dose methylprednisolone (m-PSL) and danazol. At the hospitalization, hematological examination demonstrated as follows; reticulocyte 21,000/microliters, granulocyte 350/microliters, platelet 10,000/microliters and hypocellular bone marrow. Treatment schedule were 1) m-PSL 1,000 mg (day 1-4), 500 mg (5-8)--then tapered. 2) ALG lg/day (day 4-8) 3) danazol 600 mg/day. During ALG administration, leukocytopenia and thrombocytopenia appeared but thereafter hematological recovery was obtained and the patient was free from supportive care. She developed mild diabetes mellitus and moderate liver dysfunction, nevertheless, both of which were controlled. At 3 months after the beginning of the treatment, hematological examination demonstrated as follows; reticulocyte 236,000/microliters, granulocyte 1,900/microliters, platelet 56,000/microliters and normocellular bone marrow. Although this immunosuppressive therapy was remarkably effective to this patient, immunological relation to the onset of aplastic anemia was not demonstrated in in vitro examination. This combined therapy seems to be effective one for patients with severe aplastic anemia.
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PMID:[Severe aplastic anemia remarkably improved by a treatment with antilymphocyte globulin, high-dose methylprednisolone and danazol]. 271 2

The phagocytic activity of granulocytes and mononuclear blood cells was compared in probands at risk for insulin-dependent Type 1 diabetes mellitus and in newly diagnosed diabetics before and during short-term insulin treatment. Healthy persons without family history of Type 1 diabetes were used as controls. Furthermore, the relationship between phagocytic activity and the proportion on monocytes in the granulocyte- and mononuclear blood cell fractions was estimated. The phagocytic activity of the mononuclear cells from the risk subjects was reduced. This observation suggests that defective phagocytosis might be important in the pathogenesis of Type 1 diabetes. But the phagocytic activity of mononuclear cells from newly diagnosed diabetics was not severely impaired and was fully normal under insulin treatment. We found no differences in the phagocytic activity of the granulocytes between patients and healthy probands. The proportion of monocytes in the mononuclear cell fraction was significantly enhanced in newly diagnosed diabetics and remained high throughout the 6-month period of insulin therapy. We assume that the increased monocyte level and the phagocytic activity of mononuclear cells in diabetics are not related to each other. But the increased monocyte level could also be interpreted as a compensatory reaction against the impaired phagocytic activity observed in the risk probands.
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PMID:Phagocytic activity of blood cells in diabetic risk probands and newly diagnosed type 1 diabetics. 325 67

Sixty-five insulin-dependent diabetes mellitus (IDDM) patients at the Steno-Memorial Hospital entered the present study. Of these, 43.1 percent had one or more late diabetic complication, 19.3 percent had circulating immune complexes (CIC)--there was a tendency for CIC to be related to late diabetic complications (P = 0.1) - and 16.9 percent had elevated total S-IgG. Elevated S-IgG values were related neither to CIC, to complications, nor to IgG deposits in the skin. Three patients had elevated total S-IgM, IgD and, IgE, respectively. No patients had elevated total S-IgA. Insulin antibodies were present in 41.9 percent. They were related to neither CIC nor clinical complications. No patients had rheumatoid factors (RF) or granulocyte-specific antinuclear antibodies (ANA). 12.3 percent had a low titre of organ non-specific ANA. No relationship could be established between ANA and complications or CIC. As regards skin deposits IgG was present at the dermo-epidermal junction zone (DEJ) and/or in the dermal vessels in 75.4 percent of the patients; IgA was present in 35.4 percent; and IgM in 32.3 percent. IgD and IgE were absent in all patients. Fibrinogen deposits were found in 80 percent and complement C3 in 32.3 percent. No correlation was found between skin deposits and CIC, on one hand, or clinical complications, on the other. From the present work, we conclude that humorally mediated immunological processes are active in IDDM. However, the exact role of this activity still remains to be defined.
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PMID:Circulating immune complexes, insulin antibodies, and deposits of immunoglobulins in the skin in diabetes. 372 Mar 67

BB rats spontaneously develop an insulin dependent diabetes which resembles in many features human type I diabetes. We have tested the effect of the immunomodulatory drug Ciamexone, a 2-cyan-aziridine-derivative, on the development of diabetes in BB rats. Ciamexone was given once daily during 6 days per week beginning with the age of 42 or 50 days up to 120 days. For comparison cyclosporin A (10 mg/kg) was applied following the same protocol. At 1 mg/kg ciamexone administration led to complete prevention of diabetes in females but was not beneficial in males. At 10 mg/kg the drug caused significant suppression of diabetes development in males but more pronounced in females. Both, a reduction of the incidence of diabetes and a delay in the onset of hyperglycaemia was observed only in females. After administration of cyclosporin A none of the animals developed diabetes. Ciamexone treatment did not affect granulocyte and lymphocyte counts and subsets in the peripheral blood except for a tendency to suppress eosinophilia. The growth of animals was not retarded. It is concluded that ciamexone seems to influence the autoimmune state of the BB rat resulting in partial suppression of the disease.
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PMID:Suppression of spontaneous insulin-dependent diabetes in BB rats by administration of ciamexone. 376 May 92

Diabetic patients are said to be prone to infections. Several studies of different host defense mechanisms report defects in individual granulocyte functions and cell mediated immunity, especially in patients with poorly controlled diabetes. Diabetic females have an increased risk of developing urinary tract infections. This high susceptibility is probably due to local risk factors such as diabetic cystopathy and vaginitis, the latter being frequently associated with glucosuria. Urinary tract infections in diabetic individuals often have a complicated course which may be explained by the aforementioned compromised host defense mechanisms. Diabetics have an increased risk not only of lower, but also of upper urinary tract infections. Urinary tract infections such as emphysematous cystitis and pyelonephritis, as well as papillary necrosis as a complication of pyelonephritis, are not uncommon in diabetic patients. Rapid recognition and management of such complicated urinary tract infections is important.
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PMID:[Urinary tract infection in the diabetic patient]. 637 86

To assess the immune system's involvement in the causation of diabetes in the genetically diabetic Chinese hamster, "prediabetic" animals were immunosuppressed with cyclophosphamide, starting several weeks prior to the expected onset of hyperglycemia. The immunosuppressant dose was titrated to maximally depress the lymphocyte count without significant deleterious effects on food consumption, body weight or granulocyte count. Immunosuppression did not prevent or postpone the development of hyperglycemia or glucosuria. This suggests that if there is an autoimmune component in the etiology of diabetes in the genetically diabetic Chinese hamster, it takes place earlier or is of a more specific nature than that investigated in the present study.
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PMID:Cyclophosphamide treatment of prediabetic Chinese hamsters. 674 81


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