Some cytokines variations in patients with diabetes mellitus

This study comprised eleven newly diagnosed type I diabetics, twelve long-standing type 1 diabetics, eleven long-standing type 2 diabetics, and ten healthy volunteers as control group. For all subjects glycosylated hemoglobin [HbAIc], interleukin-2 [iL-2], soluble interleukin-2 receptor [sIL-2R], and tumor necrosis-alpha [TNF-alfa] were determined aiming to evaluate their role in pathogenesis of diabetes. HbAIc was significantly elevated in all diabetic groups as compared to control group. Newly diagnosed type I and long-standing type 2 diabetics had significantly higher HbAIc levels than long-standing type I diabetics. It was positively correlated with duration of diabetes in long-standing cases of both type I and type 2, and with post-prandial plasma glucose in long-standing type I diabetics. With respect to IL-2, it was significantly decreased in newly diagnosed and long-standing type I diabetics as compared to control group and long-standing type 2 diabetics. Also, it was significantly lower in newly diagnosed type I than long-standing cases of type I. Whereas, sIL-2R was only significantly elevated in Newly diagnosed type I diabetics as compared to control and long-standing type 2. No significant correlation was detected between IL-2 or sIL-2R and other assayed parameters. As regard to TNF-alfa, it was significantly elevated in both newly diagnosed-and long-standing type I diabetics as compared to control group, whereas no significant difference was found when other groups were compared with each other. TNF-alfa was positively correlated with duration of diabetes in long-standing cases of both type 1 and type 2 and with HbAIc in newly diagnosed and long-standing type 1 diabetics. In conclusion, hypoproduction of IL-2 may be attributed to decrease of IL-2-secreting T-lymphocytes, whereas elevated sIL-2R may be related to increased expression and release from the surface of IL-R-bearing T-lymphocytes infiltrating the islets of pancereas and PBMC. These findings indicate imbalance of IL-2-IL-R system which, may be genetically determined and involved in pathogenesis of autoinnune type of diabetes [type 1]. TNF-alfa elevation may be derived from macrophages infiltrating pancreatic islets and mononuclear cells found in percipheral circulation. It may be implicated in B-cell destruction in type I diabetes as well as insulin-resistance in type 2 diabetes

Neutrophil dysfunctions as a result of insulin and glucagon secretory abnormalities in diabetics with infection

The possible role of endocrine pancreatic function [insulin and glucagon] in the pathogenesis of neutrophil dysfunction in diabetics of both types [with or without infection] was the objective of this study. 40 diabetic patients, divided into 20 diabetics with infection [acute and chronic] and 20 diabetics without infection, were studied. Each group was equally subdivided into insulin dependent diabetes mellitus [IDDM], and non insulin dependent diabetes mellitus [NIDDM] groups. 22 subjects as a control group were divided into 12 healthy control and 10 controls with infection. Neutrophil functions [phagocytosis and peroxidase activities] and pancreatic endocrine hormones [insulin and glocagon] were assessed. There was a significant decrease [p < 0.01] in phagocytic activity and peroxides activity in both types of diabetes [with or without infection]. Infection was associated with a higher significant peroxidase stain score in both types of diabetes with a significant higher level in [NIDDM]. Postprandial blood glucose level was significantly [p < 0.01] inversely correlated with peroxidase value being more significant [p < 0.01] with infection but was not correlated with phagocytic function. Hyperglucagonemia [in both types of diabetics] and hyperinsulinemia in NIDDM, had a significant [p < 0.01] negative correlation with phagocytic activity but were not correlated with peroxidase value. These findings were more significant with infection. In conclusion, there is neutrophil dysfunctions in diabetics as indicated by the impairment of both phagocytic and peroxidase activities which is more profound with infection. Hyperglycemia exhibits a negative effect on bactericidal rather than phagocytosis, while the latter is influenced by the disturbed bihormonal profile [insulin and glucagon]

Assessment of the value of the corrected Q-T interval in the diagnosis of cardiac autonomic neuropathy and its relation to microalbuminuria in diabetic patients [type I diabetes mellitus]

The validity of Q-T interval prolongation as a marker of cardiac automatic neuropathy [CAN] as well as its relation to the development of microalbuminuria [early marker of diabetic microangiopathy] are the objectives of this study. The study included 30 patients with insulin dependent diabetes mellitus [17 males and 13 females], and 10 healthy subjects as a control group. Definite CAN [score=5] was found in 13.33% of diabetics, borderline CAN [score > 2] was found in 76.66% of diabetics and normal cardiovascular reflexes was found in 10%. A prolonged corrected Q-T interval [Q-T > 433 ms] was present in 76.7% of diabetics with CAN, and a non prolonged corrected Q-T interval in 6.66% of diabetics with CAN. On the other hand, a prolonged corrected Q-T interval was found in 6.66% of diabetics without CAN and a non prolonged corrected Q-T interval was found in 10% of diabetics without CAN. Corrected Q-T interval prolongation was 92% sensitive and 60% specific in diagnosis of CAN. Microalbuminuria was present in 78.26% of diabetic patients with prolonged corrected Q-T interval and in 50% of diabetic patients without prolonged corrected Q-T interval. In conclusion, corrected Q-T interval prolongation in diabetic patients can be considered as a sensitive marker of cardiac autonomic neuropathy, its presence correlate with microalbuminuria, and hence microangiopathy. The reversibility of Q-T interval prolongation with tight diabetic control may be an objective for further study, if Q-T interval prolongation proves to be reversible with tight control it may then prove to be not only a simple bed side test which indicates microangiopathy but also may guide therapy and monitor diabetic control