Stroke is a serious complication of diabetes but the risk factors for stroke in these patients are not fully defined. The aim of this retrospective study was to investigate the risk factors for stroke in patients with type 2 diabetes mellitus (T2DM). The group comprised 208 patients with T2DM, and the mean duration of followup was seven years (range 4-11 years). The incidence of stroke was investigated according to lymphocyte proliferation in response to insulin.Using cimetidine to inhibit cells with histamine receptors and indometacin to inhibit prostaglandin-synthesising cells, a higher incidence of stroke was found in patients with indirect cell-mediated immunity to insulin. Therefore, one of the risk factors for stroke in patients with T2DM is high activity of cells with histamine receptors and prostaglandin-synthesising cells. These cells suppress cell-mediated immunity to insulin and may have a role in promoting the development of insulin resistance. 2006;3:57-60 Diabetes Vasc Dis Res
Objective. To study risk factors of death in diabetes mellitus (DM). Materials and methods. This prospective cohort study included 337 patients with compromised carbohydrate metabolism (36 with impaired fasting glycemia or impaired glucose tolerance, 80 with type 1 diabetes, 194 with type 2 diabetes, 27 with diabetes due to chronic pancreatitis). Mean follow-up was 11.2±4.8 years (from 1 January 1995 through 31 December 2014). We investigated causes and risk factors of death in patients with impaired carbohydrate metabolism. Results. 115 patients died during the study period. The most common causes of death of patients with type 1 and 2 diabetes are cardiovascular diseases and cancer. Risk factors of death in type 1 DM include cardiovascular disease, diabetic nephropathy and retinopathy. Patients die at a younger age due to early onset of the disease. In type 2 diabetes risk factors of death are cardiovascular and oncologic diseases, nephropathy, the use of insulin. Patients die in elderly and senile age due to the late onset of diabetes. Gender differences in mortality associated with type 1 and 2 diabetes mellitus were not observed. Conclusion. Main causes of death in patients with type 1 and 2 DM are cardiovascular diseases and cancer. Risk factors of death include macro - and microvascular complications.
The literature review presents the possibilities of using non - steroidal anti - inflammatory drugs (NSAIDs) for polymorbid pathology. The mechanism of NSAIDs action, risk factors for the development of undesirable effects on the cardiovascular, digestive, urinary and other systems are considered; prevention measures and drug selection options are discussed, NSAIDs prescribing algorithm is considered.
AIM: To study the structure of mortality not caused by coronavirus infection, in patients with polymorbid pathology during the period of self-isolation (lockdown). MATERIALS AND METHODS: Outpatient records of 2 423 patients with polymorbid pathology (841 males and 1 582 females, aged from 18 to 99 years) were examined. The mortality and its causes during three years including a period of lockdown were investigated. RESULTS: The overall mortality rate among patients with polymorbid pathology was 10.2% without differences in gender. The structure of the causes of death in patients with polymorbidity: cardiovascular diseases accounted for 50.8%, oncological diseases 21%, nervous system diseases 7.3%. During the lockdown, an increase in overall mortality by 34.3% was recorded (p 0.05), with an increase in the number of deaths of patients with cardiovascular diseases by 19.5% (p 0.05) (mostly patients with ischemic heart disease). CONCLUSION: An increase in the number of deceased patients with polymorbidity during the lockdown may be due to the limitation of physical activity, of the possibility of examination and consultation by profile specialists. Taking into account the vulnerability of this group of patients, there is an urgent need to develop preventive measures when the situation recurs.
АннотацияСигаретный дым обусловливает активацию врожденного и адаптивного иммунитета и развитие воспаления бронхо-легочной ткани. Разрушение альвеолярной стенки в процессе воспаления способствует формированию аутоиммунной реакции. Никотин, являясь компонентом сигаретного дыма снижает активность всех клинических проявлений, за счет активации холинергического противовоспалительного пути. Под влиянием никотина отмечается снижение реакций врожденного иммунитета, проявляющееся в нарушении фагоцитарной активности, снижении активности NK-клеток, что повышает риск инфекционных осложнений. Никотин снижает синтез провоспалительных цитокинов, экспрессию костимулирующих молекул, все это отражается на презентации антигена Т-клеткам. Нарушение адаптивного иммунитета под влиянием никотина заключается в анергии как клеточного, так и гуморального иммунитета. Возможно, именно действием никотина на систему иммунитета и объясняется вялотекущее, прогредиентное течение хронической обструктивной болезни легких, ассоциированной с курением (вне инфекционного обострения). Участие аутоиммунных реакций в генезе заболевания делает процесс необратимым. Ключевые словаКурение, система иммунитета, никотин, патогенез хронического обструктивного заболевания легких Summary Cigarette smoke causes the activation of innate and adaptive immunity as well as the development of lung tissue inflammation. The destruction of the alveolar wall during inflammation contributes to the formation of an autoimmune reaction. Nicotine, as a component of cigarette smoke, reduces the activity of all clinical manifestations, by activating cholinergic anti-inflammatory way. Nicotine decreases innate immunity reactions, specifically the activity of phagocytes and NK cells, which increases the risk of infectious complications.Nicotine reduces the synthesis of pro-inflammatory cytokines, the expression of costimulatory molecules, which leads to the disturbance of the antigen presentation to T-cells. As a result, anergy of cellular and humoral immunity is observed. Perhaps the effect of nicotine on the immune system explains the flaccid, progressive course of chronic obstructive pulmonary disease associated with smoking (regaredless of infectious exacerbation). The participation of autoimmune reactions in the genesis of the disease makes the process irreversible. Keywords Smoking, immune system, nicotine, pathogenesis of chronic obstructive pulmonary disease
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