Plasma homocysteine concentrations and serum lipid profile as atherosclerotic risk factors in subclinical hypothyroidism.

BACKGROUND AND OBJECTIVES: Because subclinical thyroid dysfunction may be a risk factor for cardiovascular disease, we evaluated the atherosclerosis tendency in subclinical hypothyroid (SCH) patients. PATIENTS AND METHODS: Fifty-three subclinical hypothyroid patients (serum thyrotropin [TSH] concentrations >4.12 mU/L) were compared with a control group of 50 euthyroid subjects whose age, sex and body mass indices were similar to the patient group. We tested whether serum TSH concentrations were correlated with plasma total homocysteine concentration (tHcy), low-density lipoprotein cholesterol (LDL-C), very low-density lipoprotein cholesterol (VLDL-C), high-density lipoprotein cholesterol (HDL-C), total cholesterol (TC) and triglycerides (TG). RESULTS: There was a significant statistical difference between the patient and control groups for normal free T4 (1.02+/-0.17 vs. 0.86+/-0.13, P<.001), TSH (1.64+/-1.02 vs. 6.62+/-2.61, P<.001), TC (185+/-39 vs. 206 +/- 42, P=.01), TG (103+/-54 vs. 132+/-85, P=.04), LDL-C (114+/-33 vs. 127+/-36, P=.04), and TC/HDL-C (3.81+/-106 vs. 4.19+/-1.02, P=.04), respectively. No statistically significant difference was found between the two groups for HDL-C, VLDLC, LDL-C/HDL-C, and tHcy. Serum TSH was significantly correlated with plasma tHcy (r=0.55; P=.001), TC (r=0.52; P=.001), LDL-C (r=0.49; P=.001), TC/HDL-C (r=0.38; P=.002) and LDL-C/HDL-C (r=0.36; P=.004) across all participants. CONCLUSION: Our study suggests that the atherogenicity of SCH is not mediated by hyperhomocysteinemia. Associated hyperlipidemia may explain the observed increased risk of coronary artery disease in patients with SCH.

Central diabetes insipidus following intracranial hemorrhage due to vitamin K deficiency in a neonate.

A previously healthy 30-day-old girl presented with seizures, irritability and inability to sleep for three days. Vitamin K was not given just after birth. She was lethargic. A multifocal clonic seizure was evident during examination. Anisocoria was diagnosed on eye examination. Brain magnetic resonance imaging showed intracerebral hemorrhage, ventricular dilatation, and hematoma in the left temporofrontal region extending to the hypothalamus. Central diabetes insipidus was diagnosed by water deprivation due to dehydration and hypernatremia, and then desmopressin was added to phenobarbital. The possible mechanism of central diabetes insipidus in our patient is damage of vasopressin pathway resulting from compression of hemorrhage. An operation of ventriculoperitoneal shunt was also performed due to hydrocephalus. While she was symptom-free except for neurological sequel during routine control examinations after discharging from hospital, the parents said that she died, most probably from bronchopneumonia, at the age of 7.5 months. In conclusion, we emphasize that prophylactic vitamin K should be administrated to all babies just after birth, and infants with intracranial hemorrhage should carefully be monitored for central diabetes insipidus.