Hyperhomocysteinemia and bone mineral density: a case - control study

To find out whether homocysteine has a direct effect on bone or it is an innocent bystander? The study was designed to investigate probable role of homocysteine on bone mineral density [BMD]. This a case-control study wherein, 30 patients with at Least one densitometry criterion of osteoporosis in femoral neck or Lumbar spine were enrolled as the case group along with another 30 normal subjects with normal BMD, as the control group. The patients of the two groups were matched for their ages and sex. In all eligible patients BMD was measured by DEXA and fasting serum homocysteine level were measured by Enzyme Immunoassay Kit. The mean of serum level of homocysteine were 11.67 +/- 4.38 and 11.97 +/- 3.09 imol/l in control and case groups respectively. The difference between two groups was not significant [P=0.761]. Serum homocysteine level and BMC of various areas in case and control groups had no significant correlation [lumbar spine in control group [r= 0.025, p=0.9], lumbar spine in case group [r=0.071, p=0.716], femoral neck in control group [r=0.276, p=0.147], femoral neck in case group [r=0.001, p=0.998fl. Despite numerous studies about direct effect of homocysteine on increase of osteoporotic fracture risk, our study did not show a correlation between serum Level of homocysteine and BMD. Due to multiplicity of factors affecting bone density, final conclusions need extensive investigations with attention to other confounding factors

Hyperhomocystinemia in patients with coronary artery disease

Hyperhomocystinemia has been related to an increased risk of cardiovascular disease in several studies. The C677T polymorphism for the gene that encodes the methylenetetrahydrofolate reductase enzyme (MTHFR) and low plasma folate levels are common causes of hyperhomocystinemia. Due to differences in nutritional patterns and genetic background among different countries, we evaluated the role of hyperhomocystinemia as a coronary artery disease (CAD) risk factor in a Brazilian population. The relation between homocysteine (Hcy) and the extent of CAD, measured by an angiographic score, was determined. A total of 236 patients referred for coronary angiography for clinical reasons were included. CAD was found in 148 (62.7 percent) patients and 88 subjects had normal or near normal arteries. Patients with CAD had higher Hcy levels [mean (SD)] than those without disease (14 (6.8) vs 12.5 (4.0) æM; P = 0.04). Hyperhomocystinemia (Hcy >17.8 æM) prevalence was higher in the CAD group: 31.1 vs 12.2 percent (P = 0.01). After adjustment for major risk factors, we found an independent association between hyperhomocystinemia and CAD (OR = 2.48; 95 percent CI = 1.02-6.14). Patients with a more advanced coronary score had a higher frequency of hyperhomocystinemia and tended to have higher mean Hcy levels. An inverse relation between plasma folate and Hcy levels was found (r = -0.14; P = 0.04). Individuals with the MTHFR C677T polymorphism had a higher prevalence of hyperhomocystinemia than those without the mutated allele. We conclude that hyperhomocystinemia is independently associated with CAD, with a positive association between Hcy level and disease severity.