PubMed · 13132818
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H HORNBOSTEL. 1953-10-23. [Hypoglycemic death].. https://pubmed.ncbi.nlm.nih.gov/13132818/
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Homocysteine is a sulphur aminoacid with a free thiol group which is not present in dietary protein. This aminoacid is a secondary f methionine by-product from cysteine metabolism. The pathogenic mechanisms of homocysteine in vascular damage have not been clarified. At present, it is no possible to develop an atherogenic and thrombogenic hypothesis. Yet high levels of homocysteine can cause endothelial damage, with increased thrombosis and atherosclerosis. Hyperhomocysteinemia has been reported in patients with diabetes mellitus type 1 and type 2; the prevalence and secondary cardiovascular risk is higher in patients with diabetes type 2 than those with diabetes type 1. In patients with diabetes mellitus type 1, microvascular and macrovascular complications and neuropathy are found to be increased in those with hyperhomocysteinemia. In patients with diabetes mellitus type 2, the relationship between hyperhomocysteinemia, macrovascular complications and renal disease is unclear; however, a higher prevalence of macrovascular complications in diabetic patients with hyperhomocisteinemia is associated with a higher prevalence of renal disease. Moreover, patients with hyperhomocysteinemia have hypertension and dyslipemia. Multivariate regression analyses have shown an independent relationship between homocysteine and macrovascular complications. The relationship between retinopathy and homocysteine has not been clarified. In summary, hyperhomocysteinemia could be a risk factor accounting for chronic complications in diabetic patients. Nevertheless, it is necesary to perform more prospective and intervention studies to clarify the independent risk of homocysteine and thus assay alternative treatments.
Infections of the tissue surrounding the teeth (periodontitis) are usually caused by anaerobic gram-negative microorganisms. This infection causes destruction of the supporting alveolar bone and can lead to tooth loss. Removal of these microorganisms can slow or arrest the progression of periodontitis. Diabetes patients are at greater risk of developing periodontitis, may not respond as well to periodontal therapy as nondiabetic patients, and may require more aggressive treatment to manage periodontitis. Microorganisms that cause periodontitis and the host response to these may increase insulin resistance in diabetic patients. Treatment of periodontitis could improve glycemic control. A model is presented in which periodontal pathogens may cause increases in proinflammatory cytokines that mediate increases in insulin resistance, resulting in an increase in blood glucose. Following periodontal therapy, this process may be reversed.