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

As a pathogenic factor of type I (insulin-dependent) diabetes cell mediated immunity to pancreatic islet cells, i.e. lymphocytic insulitis has been studied in mice with spontaneous lupus-like autoimmune disease, in mice with experimentally induced immune dysregulation and in mice treated with multiple low doses of streptozotocin or with alloxan. The following conclusions have been reached: Autoimmunity to B-islet cells requires a disturbed immune system. Autoimmune insulitis requires altered B-islet cells. Cellular immunity to B-islet cells apparently involves two different mechanisms: The intrainsular invasion of single lymphocytes and macrophages and the mostly periinsular/periductular infiltration of large numbers of lymphocytes and macrophages. Some observations indicate a primary role of helper and suppressor T lymphocytes as well as of macrophages in B-islet cell destruction. In this paper an attempt will be made to combine observations on the induction and course of insulitis in several animal models in a general scheme of pathological events. Several conclusions on the mechanism of islet autoimmunity have been reached. At the time being however, these "lessons" must be regarded as hypotheses, which may be helpful in understanding the pathogenesis of human type I diabetes.
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PMID:Cell mediated immunity to islet cells: lessons from animal studies. 638 52

Most immunologically-mediated diseases are inflammatory in nature, as assessed by cellular infiltrates at the lesion site. Recent immunohistological studies using monoclonal antibodies on tissue sections and synovial or cerebrospinal fluid reveal that B- and T-lymphocytes (predominantly T) participate in this reaction, together with monocytes and macrophages. The etiopathogenesis of inflammatory diseases of immunological origin can be discussed at two levels. (1) Lesions may be secondary to the cytopathic effect of antibodies, either by direct cytolysis or by opsonization, antigenic modulation, or blockage of functionally-relevant molecules. Immune complexes formed in the circulation or locally at the lesion site may intervene. Direct cellular mechanisms are probably involved, as suggested by evidence in hepatitis (indirect) and in juvenile insulin-dependent diabetes (direct). K-cells may act by antibody-dependent cytotoxicity, particularly in autoimmune diabetes and thyroiditis where lymphocyte-dependent antibodies are demonstrated. Unfortunately, the absence of adequate markers does not permit adequate detection of K-cells in inflammatory reaction sites. (2) Etiological factors are multiple in a given disease and even in a single patient. Deficiency of suppressor T-cells, assessed using monoclonal anti T-cell antibodies, represents a major predisposing factor, although suppressor cell deficit may be restricted to some antigens (EBV) in certain patients. The deficiency of interleukin-2 production in lupus and rheumatoid arthritis is intriguing but the mechanism and its relationship to disease etiology are unknown. Other immunological factors include intrinsic B-cell hyperactivity, anti-T-cell auto-antibodies, and complement deficiencies, whereas non-immunological factors such as viruses, drugs or sex hormones are important but ill-defined.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The immunological basis of inflammatory diseases. 648 71

Complete bilateral, simultaneous and spontaneous rupture of the quadriceps tendon is exceedingly rare; 17 cases have been reported, four with no predisposing cause. This report documents a fifth case, being the first in Dutch literature. Although diabetes, primary or secondary hyperparathyroidism, lupus erythematosus and gout are well-known predisposing factors, this case illustrates that the condition can occur in a previously healthy older patient.
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PMID:Rupture of the quadriceps tendon. 650 84

From March, 1976 to June, 1983, 22 patients (10 males, 12 females) treated by maintenance hemodialysis were autopsied in our department. Primary diseases of the autopsied cases were chronic glomerulonephritis (12 cases), diabetes mellitus (three cases), hydronephrosis (three cases), systematic lupus erythematosus (two cases), myeloma kidney (one case) and atherosclerosing nephropathy (one case). Direct causes of death in maintenance hemodialysis patients were bleeding (six cases), uremia (three cases), infection (three cases), carcinoma (four cases), heart failure (two cases), myocardial infarction (one case), brain ischemia (one case), cardiac tamponade (one case) and unknown (one case).
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PMID:Autopsy findings in maintenance hemodialysis patients. 653 69

The New Zealand Obese (NZO) mouse was studied as a potential model for autoimmune diabetes. NZO mice develop obesity, glucose intolerance, and insulin resistance, and have low-titer IgM antibodies to the insulin receptor. It is shown that they have circulating antibodies to both native DNA and denatured, single-stranded DNA. The antibody levels are higher in females, and, up to 6 mo of age, are comparable to those found in the related NZB X NZW F1 (NZB/W) mouse, a model for systemic lupus erythematosus. After 6 mo of age the antibody levels in NZO mice fall toward normal, in contrast to the persistently elevated levels in NZB/W mice. NZB/W mice are known to succumb to immune complex-mediated proliferative glomerulonephritis before 1 yr of age, whereas NZO mice survive. NZO kidneys exhibit light microscopic features of both diabetic and lupus nephropathies: glomerular proliferation, mesangial deposits, mild basement membrane thickening, glomerulosclerosis, eosinophilic nodules in some glomeruli, occasional hyalinization of the glomerular arterioles, and healing arteriolar inflammation. These changes are associated with glomerular deposition of immunoglobulin, especially IgM, in a granular pattern on fluorescent staining. The NZO mouse, therefore, has evidence of a generalized immune disorder and provides a model for studying the relationship between autoimmunity, obesity, and diabetes.
Diabetes 1980 Oct
PMID:Diabetes is associated with autoimmunity in the New Zealand obese (NZO) mouse. 700 65

The clinically normal skin of the lower back of 30 patients with diabetes mellitus was examined, using the direct immunofluorescence technique. No deposit of immunoglobulins or complement (C3) could be demonstrated, while other authors have previously reported lupus-like deposits in diabetes mellitus. As other discrepant studies of skin immunofluorescence have been published, it is suggested that the standards of the various immunopathology laboratories are different. This may explain why the actual value of the lupus band test remains controversial.
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PMID:An immunofluorescence study of the skin in diabetes mellitus. 701 83

The salmonella group of bacteria consists of at least 1700 subtypes and causes widespread gastroenteric disease throughout the world, there being approximately two million cases yearly in the United States alone. An uncommon but interesting complication is the hematogenous lodgment of organisms in other sites of the body with resultant localized abscess formation, often months or years later. We present a review of 15 cases seen in our affiliated hospitals over a nine-year period. Remote salmonellosis most often occurs in patients with underlying systemic disease, such as lupus, malignancy, diabetes, and sickle cell disease, or in association with therapy that suppresses host resistance including steroids and cancer chemotherapy. The most frequent sites of involvement are bone marrow, joints, meninges, pleura, and blood vessels, or in an area of locus minoris resistentiae. The latter include scars, hematomas, fracture sites, prosthetic devices, and neoplasms. Our experience would suggest that these infections, which can remote both in location and time from the original gastrointestinal episode, are perhaps more frequent today than is generally realized. Diagnosis is often delayed because of lack of familiarity with this entity. Treatment consist of either drainage or excision of infected tissue often combined with long-term antibiotics.
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PMID:Remote salmonellosis: surgical masquerader. 707 24

The authors report the case of a 22-year-old Guatemalan in whom lupus was diagnosed 8 months after a second pregnancy. The diagnosis of lupus met the criteria of the ARA: Raynaud's syndrome, alopecia, arthralgia, thrombophlebitis, facial erythema, antinuclear factor at 1/100, Farr at 75 p. 100 and immunofluorescent demonstration of IgM binding in healthy skin. Two months after the beginning of the lupus, there was onset of insulin-resistant ketosic diabetes without overweight. The serum insulin was 1.140 mu U/ml. Acanthosis nigricans was noted and confirmed by a biopsy. Insulin-resistance can be attributed to anti-membrane receptor antibodies titrating at 1/200 (R. Khan). The short-term progress of the disease was favorable on corticosteroid treatment. Insulin could be stopped, but high insulin serum levels persisted. This case meets criteria for type B as defined by Flier, Khan and Roth, and is the first European case of lupus with a complete presentation. Short-term progress was favorable, and there is no evidence to affirm that there will be a tardive progression towards hypoglycemia which is, however, possible due to the persistence of elevated serum insulin levels.
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PMID:[Lupus, insulin-resistant diabetes and acanthosis nigricans (author's transl)]. 723 1

Allelic exclusion at the T cell receptor alpha locus TCR-alpha is incomplete, as demonstrated by the presence of a number of T lymphocyte clones carrying two expressed alpha chain products. Such dual alpha chain T cells have been proposed to play a role in autoimmunity, for example, because of a second TCR-alpha beta pair having bypassed negative selection by virtue of low expression. We examined this hypothesis by generating mice of various autoimmunity-prone strains carrying a hemizygous targeted disruption of the TCR-alpha locus, therefore unable to produce dual alpha chain T cells. Normal mice have a low but significant proportion of T cells expressing two cell-surface TCR-alpha chains that could be enumerated by comparison to TCR-alpha hemizygotes, which have none. Susceptibility to various autoimmune diseases was analyzed in TCR-alpha hemizygotes that had been backcrossed to disease-prone strains for several generations. The incidence of experimental allergic encephalomyelitis and of lupus is not affected by the absence of dual TCR-alpha cells. In contrast, nonobese diabetic (NOD) TCR alpha hemizygotes are significantly protected from cyclophosphamide-accelerated insulitis and diabetes. Thus, dual alpha T cells may play an important role in some but not all autoimmune diseases. Furthermore, since protected and susceptible NOD mice both show strong spontaneous responses to glutamic acid decarboxylase, responses to this antigen, if necessary for diabetetogenesis, are not sufficient.
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PMID:Dual T cell receptor alpha chain T cells in autoimmunity. 756 98

During the past decade, experimental and clinical evidence has indicated an important role for the renin-angiotensin system in the progressive destruction of nephrons in a wide variety of chronic renal diseases. Studies have indicated that in the subtotally nephrectomized rat model of progressive glomerulosclerosis, in experimental diabetes mellitus, in the chronic phase of puromycin aminonucleoside-induced nephrotic syndrome and in Heymann's nephritis, angiotensin-converting enzyme (ACE) inhibitors dramatically preserve both nephron structure and function. Clinical studies have similarly noted that chronic administration of ACE inhibitors inhibits progression of renal failure in type I diabetes and type II diabetes as well as primary glomerulopathies, sickle cell nephropathy, systemic lupus erythematosis, chronic pyelonephritis and adult polycystic kidney disease. Current evidence suggests that the beneficial effect of ACE inhibitors is primarily due to inhibition of angiotensin II production, and there is strong suggestive evidence for increases in local intrarenal activation of the renin-angiotensin system in these conditions. In obstructive uropathy, activation of the renin-angiotensin system has also been shown to be an important aspect of the early functional changes and may be of importance in the subsequent generation of interstitial fibrosis. In the obstructed kidney, renin and angiotensinogen production increase and type I angiotensin receptors decrease. Inhibitors of angiotensin II production and angiotensin II action partially reverse the vasoconstriction and the reduced renal blood flow, and abolish the changes in expression of AT1 MRNA induced by obstruction. Studies suggest that the angiotensin-mediated increases in tubulointerstitial fibrosis may be mediated by increased production of transforming growth factor-beta.
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PMID:Angiotensin II-mediated renal injury. 756 81


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