[Abstract unavailable

Overt hypothyroidism may result in accelerated atherosclerosis and coronary heart disease (CHD) presumably because of the associated hypertension, hypercholesterolemia, and hyperhomocysteinemia. As many as 10%-15% of older women have subclinical hypothyroidism (SH) and thyroid autoimmunity. Whether SH is associated with risk for CHD is controversial. We examined 57 women with SH and 34 healthy controls. SH was defined as an elevated thyrotropin (TSH) (>4.5 mU/L) and normal free thyroxine (FT(4)) level (8.7-22.6 nmol/L). None of the patients had been previously treated with thyroxine. In all participants we determined blood pressure, body mass index (BMI), and fasting TSH, FT(4), antibodies to thyroid peroxidase and thyroglobulin, total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), triglycerides, folic acid, vitamin B(12), creatinine, and total plasma homocysteine levels. The SH and control groups did not differ in their total homocysteine values. Mean diastolic blood pressure was increased in SH patients versus controls (82 vs. 75 mm Hg; p < 0.01). Mean values of TC, HDL-C, LDL-C, triglycerides, TC/HDL-C, and LDL-C/HDL-C were not different in patients with SH compared with controls. Individual analysis revealed that the percentage of patients with SH having hypertension (20%), hypertriglyceridemia (26.9%), elevated TC/HDL-C (11.5%), and LDL-C/HDL-C (4%) ratios were higher than the percentages in controls. Hyperhomocysteinemia (> or = 10.98 micromol/L) was observed in 29.4% of SH and was not significantly different from the percentage in controls (21.4%). No significant correlation between TSH and biochemical parameters was detected. We conclude that subclinical hypothyroidism in middle-aged women is associated with hypertension, hypertriglyceridemia, and elevated TC/HDL-C ratio. This may increase the risk of accelerated atherosclerosis and premature coronary artery disease in some patients.

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By selective dissociation of histones with the ionic detergent sodium deoxycholate, we have demonstrated that these basic chromosomal polypeptides, which are effective inhibitors of transcription, are more tenaciously bound to DNA in mitotic than in S-phase chromatin. Evidence is presented which suggests that cell-cycle-stage-specific non-histone chromosomal proteins can account for such variations in the association of histones with DNA. When chromatin is reconstituted with DNA and histones are pooled from S-phase and mitotic cells and either S-phase or mitotic non-histone chromosomal proteins, a preferential extraction of histones with sodium deoxycholate from chromatin reconstituted with S-phase rather than mitotic non-histone chromosomal proteins is observed. In contrast, the extractability of histones with sodium deoxycholate from nucleohistone complexes reconstituted with DNA pooled from S-phase and mitotic cells and either S-phase or mitotic histones is identical. Since non-histone chromosomal proteins rather than histones are responsible for the differences in chromatin template activity during S-phase and mitosis, we propose that non-histone chromosomal proteins may modify gene expression during the cell cycle by mediating the binding of histones to DNA.

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