in white-coat hypertensive or normotensive patients, others (12, 13) suggest that the changes in IMT that occur with white-coat and sustained hypertension are equivalent. If so, then white-coat hypertension may not be a benign condition. Unfortunately, in those earlier studies there was a lack of BP comparability between groups (9-12), which is key to resolving the true nature of white-coat hypertension. In the present study, therefore, we examined the progression of carotid arteriosclerosis in Japanese patients with white-coat hypertension whose clinical BPs were matched to those of untreated sustained hypertensives, and whose ambulatory BPs (ABPs) were matched to those of normotensives.

We examined whether hypertrophy of the carotid artery in patients with untreated essential hypertension is associated with compensatory carotid artery enlargement as these patients age. Carotid ultrasonography was evaluated in 163 patients with untreated essential hypertension (74 males and 89 females) and in 76 normotensive subjects. Intima-media end-diastolic thickness (IMT) and outer vessel diameter (VD) were measured, and relative wall thickness (IMT/R, R VD/2) and vascular mass (VM) were calculated. Determinants of vascular hypertrophy in patients with untreated essential hypertension were also investigated. VD, VM, and IMT were significantly correlated with age in both the normotensive and hypertensive groups. Additionally, IMT was significantly correlated with VD in both groups. There was no correlation between increasing age and IMT/R in either group. IMT, VD and VM were significantly higher in the hypertensive group 50 years than in age-matched normotensive controls. However, IMT/R was significantly higher in the 50-59 years hypertensive group than in normotensive controls of the same age group. In addition to age, VM was ing process of compensatory enlargement that preserves the luminal diameter despite the increase in the size of the plaque (2, 3). Glagov et al. (2) and Zarins et al. (3) found a highly significant association of artery size and plaque area in left human coronary arteries, which delayed the decrease in the vascular lumen until the lesion occupied about 40% of the internal elastic lamina. Similar investigations have been made in pathoanatomic studies of postmortem specimens (4), epicardial ultrasound imaging (5), and intravascular ultrasound of the coronary arteries (6). These studies examined arterial sites with moderate and large atherosclerotic plaques.

Objective To clarify the extent of asymptomatic cerebrovascular involvement in systemic lupus erythematosus (SLE). Patients and methods Cerebral magnetic resonance imaging (MRI) findings and ultrasonography findings of 100 patients with SLE lacking present or past clinical neurologic deficits were compared with 66 age-matched volunteers to determine the combined intima-media thickness (IMT) of the commoncarotid artery, and tests for anti-cardiolipin antibodies (aCL). Results Thirty-eight patients, but only 2 controls, showed imaging abnormalities. Among23 SLE patients with cerebrovascular lesions by MRI who underwent single-photon emission computed tomography (SPECT), 14 showed hypoperfusion of the lesion. The IMTvalue and prevalence of aCL did not differ between the 55 SLE patients tested and controls. SLE disease activity index (SLEDAI)as assessed by a quantitative clinical index was significantly greater in patients with brain lesions than in those without. Conclusion The prevalence of asymptomatic brain lesions in SLE patients is high, and shows a relationship to disease activity.

We studied the association of endothelin (ET)-1 with carotid atherosclerosis and asymptomatic cerebrovascular lesions in patients with essential hypertension. Neurologically normal patients with essential hypertension (n=293; 138 male, 155 female; mean age, 65 years) and age-matched control subjects (n=242) were studied with B-mode ultrasonography of the common and internal carotid arteries and magnetic resonance imaging of the brain. Plasma ET-1 was measured by enzyme immunoassay. Hypertensive patients were divided into groups with carotid plaques and low ET-1 concentrations (< 0.75 pg/ml; PL group); carotid plaques and mid-range ET-1 (0.75 to 1.55 pg/ml; PM group); carotid plaques and high ET-1 (> or = 1.55 pg/ml; PH group); no plaques and low ET-1 (NPL); no plaques and mid-range ET-1 (NPM); and no plaques and high ET-1 (NPH). Overall, ET-1 concentrations were significantly higher in patients than in control subjects. Carotid plaque prevalence was significantly related to ET-1 in hypertensive patients. ET-1 showed a significant positive relationship with the number of asymptomatic lacunar infarcts of the brain in hypertensive patients with carotid plaques (rho=0.48, p<0.001). No significant relationship was seen between ET-1 and periventricular hyperintensity scores in patients with plaques. ET-1 did not show a relationship to either brain lesion type in patients without carotid plaques. Thus, ET-1 may foster asymptomatic lacunar cerebral infarcts by promoting carotid atherosclerosis in patients with essential hypertension.

The effects of erythrosine (Red 3), rose bengal B (Red 105) and thyroidectomy on the development of thyroid tumor were examined in male Wistar rats treated with N‐bis(2‐hydroxypropyl)nitrosamine (DHPN). Red 3 and Red 105 were used at 4% in the basal diet and were administered for 19 weeks from week 2 to 20. Thyroidectomy was performed by resection of the left lobe at week 4. Single injection of DHPN was performed intraperitoneally at 280 mg per 100 g body weight at the beginning of the experiment. Red 3 and Red 105 significantly promoted the development of thyroid tumors in thyroidectomized rats given DHPN, but had no significant effect in non‐thyroidectomized rats. The incidence of thyroid tumors was 91% in rats with partial thyroidectomy, Red 3 and DHPN, 100% in rats with partial thyroidectomy, Red 105 and DHPN, and 64% in rats with partial thyroidectomy and DHPN. Serum TSH was 5.5±3.1 ng/ml in rats with partial thyroidectomy, Red 3 and DHPN, 2.1 ± 2.2 ng/ml in rats with partial thyroidectomy, Red 105 and DHPN, and 1.5±0.5 ng/ml in rats with partial thyroidectomy and DHPN.