Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal failure developed in a patient treated for worsening spastic dyspnoea, high erythrocyte sedimentation rate and enlarged peribronchial lymph nodes by the antituberculotic regimen. Renal biopsy disclosed rapidly progressive glomerulonephritis with 95% crescents, granulomatous periglomerulonephritis vasculitis and eosinophilic interstitial infiltrates. On the basis of the positivity of antineutrophil cytoplasmic antibodies (ANCA), eosinophilia and profound ventilatory impairment the diagnosis of Churg-Strauss syndrome was established. The patient was treated by plasma exchanges and combined immunosuppression with the profound effect on erythrocyte sedimentation rate, eosinophilia a negativization of ANCA and preservation of at least minimal renal function. Further therapy was complicated by steroid diabetes, repeated leucopenia and exacerbation of spastic bronchitis and eventually by the massive gastrointestinal haemorrhage from asymptomatic gastric ulcer. There were no signs of inflammation in renal autopsy specimens with prevailing glomerulosclerosis a periglomerular fibrosis. Renal impairment is rare in Churg-Strauss syndrome and it is only exceptionally the cause of renal failure.
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PMID:[The Churg-Strauss syndrome with rapidly progressive glomerulonephritis positive for antineutrophil cytoplasmic antibodies]. 829 37

A comparative and retrospective trial of 40 patients with tropical pyomyositis covering studies done between January 1, 1987 and November 31, 1990, at the General Hospital at Cosamaloapan, Veracruz, IMSS, was undertaken. The objectives were to compare predisposing factors, clinical data, morbidity, mortaity and hospital stay among 1) medical (group I) and surgical treatment (II), 2) adult and pediatric populations and 3) the clinical stage of the disease (invasive, suppurative and late). In group I, the family history of diabetes (56%), fever (66%) and hospital stay (6.5 +/- 1.8 days) were significantly different from group II (19%, 100% and 12.8 +/- 5.5 days), respectively. The mean age in adult and pediatric populations was 38 and 8 years, respectively. Pediatric patients had lowest hemoglobin levels (9.7 +/- 1.3). Upper respiratory antecedent was highest in suppurative stage (65%). In the late stage eosinophilia (5.9 +/- 6.9), fluctuance muscles (100%), complication rate of 57%, surgical drainage (100%) and mortality of 29% were found. Cultures were performed in 20 cases with negative results in 55% and the remaining 45% were positive to Staphylococcus aureus. Pyomyositis appears to be multifactorial in origin, the antecedents of trauma and upper respiratory infection were the major predisposing factors. Septicemia caused high morbidity and mortality in the late stage. Surgical treatment was frequently needed, increasing costs.
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PMID:Clinical stage, age and treatment in tropical pyomyositis: a retrospective study including forty cases. 869 59

Alloxan damages insulin-producing cells and has been used as an inducer of experimental diabetes in several animal species. In this study, administration of alloxan (40 mg/kg, i.v.) to rats was followed by a selective and time-dependent reduction in the number of pleural mast cells (50 +/- 2.2%, p < 0.01; mean +/- SEM), while mononuclear cell and eosinophil counts were not altered. As compared to naive rats, the reduction in mast cell numbers was first noted 48 h following alloxan administration and remained unaltered for at least 60 days. It is noteworthy, that the depletion in the mast cell population was not accompanied by alterations in the total amount of histamine stored per cell. Sensitized rats turned diabetic by alloxan treatment performed 72 h before challenge showed a less pronounced antigen-induced mast cell degranulation compared to nondiabetic rats. Moreover, rats injected with alloxan 72 and 48 but not 24 h before challenge, reacted to allergenic challenge with 50% reduction in the number of eosinophils recruited to the pleural cavity within 24 h. We found that the less pronounced eosinophil accumulation did not relate to an intrinsic cell locomotor abnormality since eosinophils from diabetic rats presented similar chemotactic responses to LTB4 and PAF in vitro as compared to matching controls. Insulin (3 IU/rat) restored basal levels of mast cells and reversed the subsequent inhibition of allergen-induced pleural eosinophilia, suggesting a causative relationship between these phenomena. Treatment with insulin also significantly increased the number of mast cells in the pleural cavity of naive rats (from 637 +/- 57 to 978 +/- 79 x 10(3) cells/cavity, p < 0.001). Consistently, previous depletion of mast cells by means of local treatment with compound 48/80 significantly reduced the antigen-induced eosinophil recruitment in sensitized animals. We conclude that the reduction in the pleural mast cell population noted in alloxan-treated rats could be directly implicated in the diminished pleural eosinophil influx following allergen challenge. This hyporesponsiveness is independent of an intrinsic abnormality of cell chemotaxis, but can be imitated by local mast cell depletion.
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PMID:Alloxan diabetes reduces pleural mast cell numbers and the subsequent eosinophil influx induced by allergen in sensitized rats. 875 42

The cause of toxic oil syndrome (TOS) has not yet been definitively determined, but some genetic susceptibility factors (certain HLA antigens and female sex) have been identified in 236 patients. Similarities with genetic factors for scleroderma and hydralazine-induced lupus (i.e. in TOS female sex and HLA-A24, Pcorrected = 0.00001 and DR4, Pcorrected = 0.04, respectively) may provide a clue to the responsible xenobiotic and its pathogenesis, and may also help in understanding the basis of the related eosinophilia-myalgia syndrome associated with tryptophan ingestion. In this paper it is also established that a human class I antigen (HLA-A24) and, independently, an HLA class II haplotype (DR4-DQ8, Pcorrected = 0.04) and arginine 52 in the alpha-DQ chains (Pcorrected = 0.03) are associated with TOS susceptibility, similarly to insulin-dependent diabetes. This further supports the classification of TOS as an autoimmune disease. Also, the increased frequency of a particular set of low-frequency HLA class I antigens in chronic TOS patients (i.e. B27, B37, B38 and B49) and the probable decrease in the frequency of HLA-B homozygotes in surviving patients (Pcorrected = 0.008) may provide an objective model to explain the maintenance of the HLA polymorphism: less frequent HLA alleles may be more advantageous in the event of unexpected human contact with unusual xenobiotics (not only microbes); however, other mechanisms working together to preserve and generate HLA polymorphism may coexist.
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PMID:Frequencies of HLA-A24 and HLA-DR4-DQ8 are increased and that of HLA-B blank is decreased in chronic toxic oil syndrome. 880 34

Primary adrenal insufficiency (Addison's disease) may initially present with cutaneous hyperpigmentation. Addison's disease, when associated with autoimmune thyroid disease and/or insulin-dependent diabetes mellitus, is referred to as polyglandular autoimmune syndrome type II. We present the case of a patient who initially was diagnosed as having Grave's disease and eventually Addison's disease due to persistent cutaneous hyperpigmentation, fatigue, weight loss, hypotension, hyponatremia, peripheral eosinophilia, and positive results of a synthetic corticotropin stimulation test. Addison's disease, polyglandular autoimmune syndrome type II, and cutaneous hyperpigmentation are reviewed.
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PMID:Cutaneous hyperpigmentation and polyglandular autoimmune syndrome type II. 904 Sep 76

In the lungs, neuronal M2 muscarinic receptors limit ACh release from parasympathetic nerves. In antigen-challenged animals, eosinophil proteins block these receptors, resulting in increased ACh release and vagally mediated hyperresponsiveness. In contrast, diabetic rats are hyporesponsive and have increased M2 receptor function. Because there is a low incidence of asthma among diabetic patients, we investigated whether diabetes protects neuronal M2 receptor function in antigen-challenged rats. Antigen challenge of sensitized rats decreased M2 receptor function, increased vagally mediated hyperreactivity by 75%, and caused a 10-fold increase in eosinophil accumulation around airway nerves. In antigen-challenged diabetic rats, neuronal M2 receptor function was preserved and there was no eosinophil accumulation around airway nerves. Insulin treatment of diabetic rats completely restored loss of M2 receptor function, vagally mediated hyperresponsiveness, and eosinophilia after antigen challenge. These data demonstrate that insulin is required for development of airway inflammation, loss of neuronal M2 muscarinic receptor function, and subsequent hyperresponsiveness in antigen-challenged rats and may explain decreased incidence of asthma among diabetic humans.
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PMID:Role of insulin in antigen-induced airway eosinophilia and neuronal M2 muscarinic receptor dysfunction. 980 73

A 58-year-old man with diabetes mellitus was treated with acarbose 300 mg daily. 13 days after the start of treatment with acarbose, generalised erythema multiforme developed with blood eosinophilia. Tissue eosinophilia was also found histologically. A challenge test for acarbose confirmed allergic reaction clinically and histologically.
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PMID:Acarbose-induced generalised erythema multiforme. 1043 76

Troglitazone, a thiazolidinedione, is a novel agent for the oral treatment of non-insulin-dependent (Type II) diabetes mellitus; it works by increasing cell sensitivity to available insulin. Previous studies have shown that rodents treated with high doses of troglitazone develop increased heart weight and increased interscapular brown fat. This study investigated cellular proliferation in heart and brown fat of troglitazone-treated mice as well as possible interactions with an angiotensin-converting enzyme inhibitor (quinipril). B6C3F1 female mice were treated daily with either vehicle control, 125 mg/kg quinipril, 1,200 mg/kg troglitazone, or troglitazone/quinipril combination per os for up to 14 days. Four days before necropsy, mice were dosed with bromodeoxyuridine (BrdU) using osmotic pumps. Cell proliferation in heart, brown fat, and retroperitoneal white fat was investigated by means of light microscopic anti-BrdU immunolabeling techniques. Immunoelectron microscopy was used to determine the cell phenotypes and cellular distribution of BrdU label in heart and brown fat. Treatment with troglitazone for 2 wk resulted in increased heart and brown fat weights but in decreased white fat weight. Combination treatment with troglitazone and quinipril also resulted in decreased white fat weight compared with controls. Histologically, brown fat adipocytes in troglitazone- and troglitazone/quinipril-treated mice had coalescent lipid vacuoles and increased eosinophilia of the cytoplasm. White fat adipocytes in troglitazone- and troglitazone/quinipril-treated mice had decreased cell size and increased cytoplasmic eosinophilia. BrdU labeling revealed increased cell proliferation in troglitazone-treated hearts after 1 wk but did not reveal increased cell proliferation in quinipril- or troglitazone/quinipril-treated animals. Brown fat BrdU labeling after 1 wk was increased in troglitazone- and troglitazone/quinipril-treated mice. Ultrastructural anti-BrdU immunogold labeling demonstrated that troglitazone-treated heart and brown fat had greater populations of BrdU-labeled cells that were identified as endothelial cells. These results demonstrated that troglitazone-induced increased cardiac weight in mice can be prevented by quinipril and that increased cardiac weight coincides with early increased endothelial cell proliferation.
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PMID:Troglitazone-induced heart and adipose tissue cell proliferation in mice. 1052 34

Drinking water contamination by arsenic remains a major public health problem. Acute and chronic arsenic exposure via drinking water has been reported in many countries of the world; especially in Argentina, Bangladesh, India, Mexico, Thailand, and Taiwan, where a large proportion of drinking water (ground water) is contaminated with a high concentration of arsenic. Research has also pointed out significantly higher standardized mortality ratios and cumulative mortality rates for cancers of the bladder, kidney, skin, liver, and colon in many areas of arsenic pollution. General health effects that are associated with arsenic exposure include cardiovascular and peripheral vascular disease, developmental anomalies, neurologic and neurobehavioral disorders, diabetes, hearing loss, portal fibrosis of the liver, lung fibrosis, hematologic disorders (anemia, leukopenia, and eosinophilia), and carcinoma. Although, the clinical manifestations of arsenic poisoning appear similar, the toxicity of arsenic compounds depends largely u[on the chemical species and the form of arsenic involved. On the basis of its high degree of toxicity to humans, and the non-threshold dose-response assumption, a zero level exposure is recommended for arsenic, even though this level is practically non-attainable. In this review, we provide and discuss important information on the physical and chemical properties, production and use, fate and transport, toxicokinetics, systemic and carcinogenic health effects, regulatory and health guidelines, analytical methods, and treatment technologies that are applied to arsenic pollution. Such information is critical in assisting the federal, state and local officials who are responsible for protecting public health in dealing with the problem of drinking water contamination by arsenic and arsenic-containing compounds.
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PMID:Important considerations in the development of public health advisories for arsenic and arsenic-containing compounds in drinking water. 1074 34

Parasitic helminth infections are characterized by eosinophilia and markedly elevated levels of circulating antigen-nonspecific immunoglobulin E (IgE), responses from which concern helminth protection. We previously purified a factor from Dirofilaria immitis that induces antigen-nonspecific IgE in mice and rats. Recombinant DiAg (rDiAg) has various biological activities. It is also known that parasitic helminth infection generates tremendous Th2 responses. The nonobese diabetic (NOD) mouse spontaneously develops Th1 cell-dependent autoimmune diabetes. Here we investigated the effects of rDiAg on the initiation and progression of this disease. rDiAg treatment of 6-week-old NOD females (the age at which insulitis typically begins) completely prevented insulitis and diabetes. Thus, rDiAg impaired the islet Ag-specific Th1 cell response in vivo, and the prevention of diabetes by rDiAg was associated with switching of the response from a Th1 to a Th2 profile. Since rDiAg clearly prevented insulitis by inhibiting the development and further accumulation of pathogenic Th1 cells to islets of Langerhans, we conclude that DiAg is a native Th2 inducer in filarial helminth and that Th1 responses are required for early events in the development of spontaneous autoimmune diabetes. In conclusion, the presence of parasitic helminth infections may play an important role as an immunomodulator in some autoimmune diseases or allergies.
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PMID:A factor of inducing IgE from a filarial parasite prevents insulin-dependent diabetes mellitus in nonobese diabetic mice. 1152 7


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