Diabetes mellitus factors inducing

Perhaps the most satisfying hypothesis for the formation of atherosclerotic lesions is that of response to injury in which lesions are precipitated by some form of injury to endothelial cells. The injury may be caused by elevated plasma levels of LDL and modified LDL (oxidized LDL), free radicals (e.g., caused by cigarette smoking), diabetes mellitus, hypertension-induced shear stress, and other factors that lead to focal desquamation of endothelial cells such as elevated plasma homocysteine levels, genetic... 

Burge MR, Schmitz-Fiorentino K, Fischette C, Qualls CR, Schade DS. A prospective trial of risk factors for sulfonylurea-induced hypoglycemia in type 2 diabetes mellitus. JAMA I998 279(2) l 37 13. 

Insulin-dependent diabetes mellitus (IDDM) is an example of a metabolic disease under active consideration for inducible gene therapy strategies. In this disorder, inflammatory cytokines have been shown to activate apoptosis in pancreatic beta cells. Experimental studies indicate that expression of insulinlike growth factor-1 (IGF-1) can prevent the cytokine-mediated destruction of beta cells of the pancreas (Giannoukakis et al., 2001). Regulated expression of IGF-1 in human pancreatic islets, to preserve beta cell function, may be a useful approach in the treatment of certain types of diabetes (Demeterco and Levine, 2001). 

Iwamoto T, Kagawa Y, Naito Y, et al. Steroid-induced diabetes mellitus and related risk factors in patients with neurologic diseases. Pharmacotherapy. 2004 24 508-514. 

Contrast-induced nephropathy has been defined as an increase in serum creatinine of at least 25% or an absolute increase in serum creatinine of at least 0.5 mg/dL within 48 to 72 hours of iodinated contrast administration and is associated with significant morbidity and mortality (75). Important risk factors include diabetes mellitus, chronic renal insufficiency, administration of large volumes of high osmolar contrast agents, and intravascular volume depletion. Numerous pharmacologic preventive measures have been studied, but consistent benefits have not been demonstrated. In a recent large retrospective study, preprocedural statin therapy was independently associated with a lower risk of contrast nephropathy and nephropathy requiring dialysis (76). 

Polypeptides are substrates for receptor-mediated transcytosis. Cerebral insulin reaches the brain from the circulation via receptor-mediated transcytosis through the BBB on the brain endothelial insulin receptor. This receptor is upregulated in development and downregulated in streptozotocin-induced diabetes mellitus. Similarly a BBB transferrin receptor mediates the transcytosis of transferrin across the BBB and this explains how the brain is able to extract iron from the circulation. Other RMT pathways consituting portals of entry to the brain for circulating peptides include receptors for insulin-like growth factors, cationic proteins, lectins, acetyl-low density lipoprotein and leptin. 

The nonsalicylate NSAIDs can also affect renal function. Risk factors fc>r NSAID-induced acute renal failure include congestive heart feilure, glomerulonephritis, chronic renal insufficiency, cirrhosis, systemic lupus erythematosus, diabetes mellitus, significant atherosclerotic disease in the elderly and use of diuretics. NSAIDs can adversely affect cardiovascular homeostasis and can be a risk factor for the onset or exacerbation of heart feilure. 

The following factors are decisive in achieving a favourable prognosis for all forms of alcoholic liver disease (7.) total abstention from alcohol, (2.) extent of irreversible loss of liver parenchyma, (S.) exclusion of other risk factors (e. g. obesity, diabetes mellitus, malnutrition), 4.) additional effects of hepatotoxic substances (e.g. medication, chemical agents), and (5.) coexistence of further alcohol-induced organ damage. (5, 23, 37, 80, 81, 86, 99, 102, 108)... 

Mechanism and susceptibility factors The mechanism of cisplatin-induced neurotoxicity has not been fully explained. Cisplatin appears to affect neurons in the dorsal root ganglia. It has also been suggested that it can act as a calcium channel blocker, altering intracellular calcium homeostasis and leading to apoptosis of exposed neurons, such as those of the dorsal root ganglia. Cisplatin-induced sensory neuropathy is predominantly characterized by symptoms such as numbness and tingling, paresthesia of the upper and lower extremities, reduced deep-tendon reflexes, and leg weakness with gait disturbance. The first symptoms are often observed after a cumulative dose of 300-600 mg/m. Risk factors include diabetes mellitus, alcohol consumption, or inherited neuropathies. Advanced age has not been identified as an independent risk factor when there is no co-morbidity (67-70). 

The pathogenesis of vincristine-induced neuropathy has not been fully elucidated, but very probably altered axoplasmic transport processes are of major importance, since neurons treated with vincristine lose portions of their axonal microtubules (35). There is marked interindividual variability in sensitivity to this toxic effect, partially based on different predisposing factors, for example diabetes mellitus, pretreatment with other potentially neurotoxic agents (such as cisplatin and taxanes), or familial disorders (such as Charcot-Marie-Tooth syndrome) (37,51,52). 

Corticosteroids and CIs can impair glucose control in previously diabetic patients, as well as cause new-onset post-transplant diabetes mellitus (PTDM) in 4% to 20% of patients. Corticosteroids induce insulin resistance and impair peripheral glucose uptake, whereas CIs appear to inhibit insulin production. " TAC seems to be more diabetogenic than CSA, although recent studies have failed to show a statistical difference." " Other possible risk factors that have been identified for PTDM include ethnicity (African-American or Hispanic), age (>40 years), pretransplant diabetes status, family history, and weight. " ... 

Imai S, Tezuka H, Fujita K (2001) A factor of inducing IgE from a filarial parasite prevents insulin-dependent diabetes mellitus in nonobese diabetic mice. Biochem Biophys Res Commun, 286(5) 1051-1058. 

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