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      The association of smoking and risk of diabetic retinopathy in patients with type 1 and type 2 diabetes: a meta-analysis

      , , , , ,
      Endocrine
      Springer Nature

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          Hyperglycemia and microvascular and macrovascular disease in diabetes.

          John Klein (1995)
          In summary, over the past 16 years, since the publication of Kelly West's book, epidemiological study has provided better insight into the relation of hyperglycemia and diabetic complications. Data from the WESDR demonstrate a strong consistent relationship between hyperglycemia and the incidence and progression of microvascular (diabetic retinopathy, loss of vision, and nephropathy) and macrovascular (amputation and cardiovascular disease mortality) complications in people with IDDM and NIDDM (Figs. 19 and 20). The DCCT has demonstrated that intensive insulin therapy will reduce the incidence and progression of microvascular complications in people with IDDM (22). A number of further challenges await laboratory scientists and epidemiologists regarding hyperglycemia in people with diabetes. There is a need to understand the relation of hyperglycemia to pathogenetic mechanisms that lead to the development of specific complications, to develop new methods to detect and physiologically treat hyperglycemia, and to develop better methods of primary and secondary prevention of diabetic complications in people with IDDM and NIDDM.
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            Enhanced glucose control for preventing and treating diabetic neuropathy.

            There are two types of diabetes. Type 1 diabetes affects younger people and needs treatment with insulin injections. Type 2 diabetes affects older people and can usually be treated by diet and oral drugs. Diabetic neuropathy affects 10% of patients with diabetes mellitus at diagnosis and 40% to 50% after 10 years. Enhanced glucose control is the best studied intervention for the prevention of this disabling condition but there have been no systematic reviews of the evidence. To examine the evidence for enhanced glucose control in the prevention of distal symmetric polyneuropathy in people with type 1 and type 2 diabetes. We searched the Cochrane Neuromuscular Disease Group Specialized Register (30 January 2012), CENTRAL (2012, Issue 1), MEDLINE (1966 to January 2012) and EMBASE (1980 to January 2012) for randomized controlled trials of enhanced glucose control in diabetes mellitus. We included all randomized, controlled studies investigating enhanced glycemic control that reported neuropathy outcomes after at least one year of intervention. Our primary outcome measure was annual development of clinical neuropathy defined by a clinical scale. Secondary outcomes included motor nerve conduction velocity and quantitative vibration testing.  Two authors independently reviewed all titles and abstracts identified by the database searches for inclusion. Two authors abstracted data from all included studies with a standardized form. A third author mediated conflicts. We analyzed the presence of clinical neuropathy with annualized risk differences (RDs), and conduction velocity and quantitative velocity measurements with mean differences per year.  This review identified 17 randomized studies that addressed whether enhanced glucose control prevents the development of neuropathy. Seven of these studies were conducted in people with type 1 diabetes, eight in type 2 diabetes, and two in both types. A meta-analysis of the two studies that reported the primary outcome (incidence of clinical neuropathy) with a total of 1228 participants with type 1 diabetes revealed a significantly reduced risk of developing clinical neuropathy in those with enhanced glucose control, an annualized RD of -1.84% (95% confidence interval (CI) -1.11 to -2.56). In a similar analysis of four studies that reported the primary outcome, involving 6669 participants with type 2 diabetes, the annualized RD of developing clinical neuropathy was -0.58% (95% CI 0.01 to -1.17). Most secondary outcomes were significantly in favor of intensive treatment in both populations. However, both types of diabetic participants also had a significant increase in severe adverse events including hypoglycemic events. According to high-quality evidence, enhanced glucose control significantly prevents the development of clinical neuropathy and reduces nerve conduction and vibration threshold abnormalities in type 1 diabetes mellitus. In type 2 diabetes mellitus, enhanced glucose control reduces the incidence of clinical neuropathy, although this was not formally statistically significant (P = 0.06). However, enhanced glucose control does significantly reduce nerve conduction and vibration threshold abnormalities. Importantly, enhanced glucose control significantly increases the risk of severe hypoglycemic episodes, which needs to be taken into account when evaluating its risk/benefit ratio.
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              10. Microvascular Complications and Foot Care: Standards of Medical Care in Diabetes—2018

              (2017)
              The American Diabetes Association (ADA) "Standards of Medical Care in Diabetes" includes ADA's current clinical practice recommendations and is intended to provide the components of diabetes care, general treatment goals and guidelines, and tools to evaluate quality of care. Members of the ADA Professional Practice Committee, a multidisciplinary expert committee, are responsible for updating the Standards of Care annually, or more frequently as warranted. For a detailed description of ADA standards, statements, and reports, as well as the evidence-grading system for ADA's clinical practice recommendations, please refer to the Standards of Care Introduction Readers who wish to comment on the Standards of Care are invited to do so at professional.diabetes.org/SOC.
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                Author and article information

                Journal
                Endocrine
                Endocrine
                Springer Nature
                1355-008X
                1559-0100
                November 2018
                August 20 2018
                November 2018
                : 62
                : 2
                : 299-306
                Article
                10.1007/s12020-018-1697-y
                30128962
                3ac1bce4-8bc6-4e7e-af44-fa4da31420c9
                © 2018

                http://www.springer.com/tdm

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