[A clinical analysis of insulin antibody in type 2 diabetic patients].

This study was conducted to evaluate the relationship between serum insulin levels and the production of insulin antibody (IA) in type 2 diabetes (T2DM). A total of 647 T2DM were included. Among them, 20.9% patients were IA positive, who were elder and had a longer duration, lower BMI, a higher positive rate of glutamic acid decarboxylase antibody(GADAb) and higher serum insulin levels during an insulin secretion test. More patients were treated with insulin in IA positive group than in IA negative group (65.9% vs 41.0%, P=0.000). Fasting serum insulin level was associated with occurrence of IA in all patients (OR=1.02, P=0.001) and insulin treated patients (OR=1.033, P=0.002). The cut-off point of fasting serum insulin level for predicting IA positive was 17.87 mIU/L (sensitivity 55.1%, specificity 89.0%). Exogenous insulin use is associated with the presence of IA. Fasting serum insulin level can be used as a predictor for the production of IA in insulin-treated patients.

Delayed gastric emptying is related to cardiovascular autonomic neuropathy in Chinese patients with type 2 diabetes.

BACKGROUND AND STUDY AIMS: Delayed gastric emptying (DGE) is the commonest gastrointestinal (GI) complication in type 2 diabetes. We aimed to evaluate the association between DGE and cardiovascular autonomic neuropathy (CAN) in type 2 diabetes. PATIENTS AND METHODS: A total of 71 Chinese patients (39 men and 32 women, aged 60-90 years) and 30 controls (12 men and 18 women, aged 50-79 years) were studied in Nanjing, China. The gastric emptying was assessed by 13C-octanoic acid breath test (OBT) and gastric emptying ultrasonography (GEU). Cardiovascular autonomic neuropathy (CAN) was assessed by a scoring system being validated before. RESULTS: The diabetic patients, except for a higher plasma glucose level, had similar characteristics compared to the non-diabetic controls. Diabetic patients had higher incidence of DGE and CAN than controls (48.5% vs. 10.7%, p = 0.001). Among diabetic patients with DGE (n = 27), 18 (66.7%) had CAN and 9 (33.3%) did not. Corresponding figures for those without DGE (n = 39) were 14 (35.9%) and 25 (64.1%), respectively (p = 0.014). Diabetes was independently associated with the risk of DGE with odd ratio (95% CI) of 15.6 (1.92, 127.06) (p = 0.010). The presence of diabetes or CAN was independently associated with the half gastric emptying time after adjusting for age, gender, plasma glucose and blood pressure. CONCLUSIONS: We found a much prolonged gastric emptying time in Chinese patients with type 2 diabetes as compared to non-diabetic controls. There was a high rate of CAN in diabetic patients, and it was associated with gastric emptying.

Large granular lymphocyte proliferation with the natural killer-cell phenotype.

Lymphoproliferated disorders involving large granular lymphocytes (LGL) can be divided into a common T-cell subset (CD3+, CD8+) and a rarer natural killer (NK)-cell subset (CD2+, CD3-). The immunophenotype, clinical pathologic features, and cytogenetic and molecular genetic analyses are reported for seven patients with NK-cell-LGL proliferation. The typical immunophenotype was CD2+, CD3-, CD4-, CD11b+, and CD16+ or CD56+. A low but variable percentage of cells were CD8+ or CD57+. Unusual phenotypes with CD2- (1 of 7), CD11b- (1 of 7), or CD16-/CD56- (1 of 7) cells were seen. Strong NK-cell activity was observed in all cases, indicating that none of the NK-cell markers (CD11b, CD16, CD56, CD57) is essential for NK-cell activity. One patient died shortly after diagnosis from coexistent refractory multiple myeloma and another patient died within 1 month from the LGL proliferation. The other patients had been followed for 12 to 70 months, with a median follow-up period of 38 months. There was no progression of their LGL proliferation. Lymphocyte counts varied from 3.3 x 10(3)/microL to 58.4 x 10(3)/microL at the time of diagnosis. Unexplained anemia and neutropenia were observed in one patient. Cytogenetic abnormalities were detected in two of four patients studied with t(6;12) in one and der(5), der(6), and der(11) in the other. The approximately T gamma and T beta genes were in the germline configuration and Epstein-Barr virus DNA was undetectable in five of five patients studied. Natural killer-cell LGL proliferations were morphologically indistinguishable from T-cell LGL proliferations. However, the two were immunophenotypically and genotypically distinct and NK-cell activity was consistently observed in the former. Most of the NK-cell proliferations also were chronic indolent disorders and the incidence of associated cytopenias seemed to be lower than T-cell LGL proliferations.

Influence of cytokines and immunosuppressive drugs on major histocompatibility complex class I/II expression by human cardiac myocytes in vitro.

Human cardiac myocytes do not express detectable levels of major histocompatibility complex (MHC) class II antigens and express low levels, if any, of MHC class I antigens. During rejection episodes, cardiac biopsies show massive increases of MHC antigens, which are thought to be induced by cytokines released by donor-sensitized recipient mononuclear cells. In efforts to determine the nature of the cytokines that induce MHC expression on cardiac myocytes, human fetal cardiac myocyte cultures were established. Interferon-alpha (IFN-alpha), interferon-gamma (IFN-gamma), interleukin (IL)-1, IL-2, IL-3, IL-4, and tumor necrosis factor (TNF)-alpha were added to these cultures and dose/kinetics of MHC class I/II induction quantitated. Data show that IFN-gamma induces both MHC class I and II expression, and all the other cytokines (except IL-2) induce only MHC class I but not class II. Cytokines used in combination showed that IFN-alpha with TNF-alpha was the only combination that induced MHC class II expression. Addition of immunosuppressive drugs such as cytoxan, azathioprine, cyclosporine-A, and FK-506, even when added at the initiation of the cultures, did not appreciably affect the ability of the appropriate cytokines to induce MHC expression by the myocytes in vitro.