Background — Although thyroid hormone (TH) exerts relevant effects on the cardiovascular system, it is unknown whether TH also regulates vascular reactivity in humans. Methods and Results — We studied 8 patients with hyperthyroidism, basally (H) and 6 months after euthyroidism was restored by methimazole (EU). Thirteen healthy subjects served as control subjects (C). We measured forearm blood flow (FBF) by strain-gauge plethysmography during intrabrachial graded infusion of acetylcholine, sodium nitroprusside (SNP), norepinephrine, and L-NMMA (inhibitor of NO synthesis). Basal FBF (in mL · dL −1 · min −1 ) was markedly higher in H than in C (5.8±1.2 and 1.9±0.1, respectively; P <0.001) and was close to normal in EU (2.6±0.3, P <0.01 versus H). During acetylcholine infusion, FBF increased much more in H (+33±5) than in C (+14±3, P <0.01 versus H) and in EU (+20±5, P =0.01 versus H and P =NS versus C). In contrast, the response to SNP infusion was comparable in the patients and control subjects. During norepinephrine infusion, the fall in FBF was much more pronounced in H (−6±1) than in C (−0.7±0.3, P <0.005 versus H) and in EU (−1.5±0.3, P <0.01 versus H). Finally, inhibition of NO synthesis by L-NMMA decreased FBF by 2.8±0.6, 0.61±0.7, and 1.4±0.3 in H, C, and EU, respectively (H versus C and EU, P <0.05). Conclusions — In hyperthyroidism, (1) the marked basal vasodilation is largely accounted for by excessive endothelial NO production, (2) vascular reactivity is exaggerated because of enhanced sensitivity of the endothelial component, (3) the vasoconstrictory response to norepinephrine is potentiated, and (4) this abnormal vascular profile is corrected when euthyroidism is restored by medical therapy. The data demonstrate that vascular endothelium is a specific target of TH.

Starting from the observation that a number of consecutive patients with non-Hodgkin's lymphoma (NHL) resulted positive for hepatitis C virus (HCV) antibodies on routine testing, we set up a survey for HCV contact prevalence in all patients with lymphoproliferative disorders (LPD) followed in our institution. We searched for HCV antibodies by a third-generation ELISA technique, followed by a confirmation test (RIBA III); serum viral RNA and HCV genotype were investigated by a RT-PCR technique. We screened a total of 315 patients suffering from B-NHL (91), multiple myeloma (56), MGUS (48), chronic lymphocytic leukemia (57), Waldentrom's macroglobulinemia (13), Hodgkin's disease (HD)(43), and T-NHL (9). While only 1 of 52 patients with a non-B-LPD (HD or T-NHL) had signs of HCV contact (i.e., 1.9%, which is in the range of the normal population in the South of Italy), 59 of 263 patients with a B-LPD (22.4%) had HCV antibodies or RNA, or both, with no major differences among the various types of disorders, except for WM, in which the rate was higher (61.5%). The same prevalence was found for patients tested at diagnosis or during the follow-up, and in transfused or never-transfused patients. Only a few patients were aware of having a liver disease; one-half of HCV-positive patients never had transaminase increase. A review of data from Central and Northern Italy is included, showing similar findings; a report from Japan has confirmed such an association, while limited surveys in England have not revealed any correlation. These findings may have important biological and clinical implications.

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Background-The reason why patients with growth hormone (GH) deficiency (GHD) are at increased risk for premature cardiovascular death is still unclear. Although a variety of vascular risk factors have been identified in GHD, little is known regarding vascular reactivity and its contribution to premature arteriosclerosis. Methods and Results-We assessed vascular function in 7 childhood-onset, GH-deficient nontreated patients (age 22Ϯ3 years, body mass index [BMI] 25Ϯ1 kg/m 2 ) and 10 healthy subjects (age 24Ϯ0.4 years, BMI 22Ϯ1 kg/m 2 ) by using strain gauge plethysmography to measure forearm blood flow in response to vasodilatory agents. The increase in forearm blood flow to intrabrachial infusion of the endothelium-dependent vasodilator acetylcholine was significantly lower in GH-deficient nontreated patients than in control subjects (PϽ0.05). Likewise, forearm release of nitrite and cGMP during acetylcholine stimulation was reduced in GH-deficient nontreated patients (PϽ0.05 and PϽ0.002 versus controls). The response to the endothelium-independent vasodilator sodium nitroprusside was also markedly blunted in GH-deficient patients compared with control subjects (PϽ0.005). To confirm that abnormal vascular reactivity was due to GHD, we also studied 8 patients with childhood-onset GHD (age 31Ϯ2 years, BMI 24Ϯ1 kg/m 2 ) who were receiving stable GH replacement therapy. In these patients, the response to both endothelium-dependent and -independent vasodilators, as well as forearm nitrite and cGMP, release was not different from that observed in normal subjects. Peak hyperemic response to 5-minute forearm ischemia was significantly reduced in GH-deficient nontreated patients (17.2Ϯ2.6 mL ⅐ dL Ϫ1 ⅐ min Ϫ1 , PϽ0.01) but not in GH-treated patients (24.8Ϯ3.3 mL ⅐ dL Ϫ1 ⅐ min Ϫ1 ) compared with normal subjects (29.5Ϯ3.2 mL ⅐ dL Ϫ1 ⅐ min Ϫ1 ). Conclusions-The

Background and Methods. The value of serum alpha‐L‐fucosidase activity in the diagnosis of hepatocellular carcinoma (HCC) was investigated by determining the enzyme activity levels in 21 patients with HCC, 76 patients with cirrhosis, 22 patients with other malignant neoplasms, and 23 healthy subjects. Results. The serum alpha‐L‐fucosidase activity level in patients with HCC (575.76 ± 212.86 nmol/ml/h) was significantly higher than that found in patients with cirrhosis (274.55 ± 138.97 nmol/ml/h; P < 0.001) or other neoplasms (257.91 ± 128.12 nmol/ml/h P < 0.001) and in controls (221.23 ± 114.45 nmol/ml/h; P < 0.001). No significant differences were found between controls and patients with cirrhosis and between controls and patients with other malignant neoplasms. When 443 nmol/ml/h is taken as the cutoff value (mean value of controls plus 2 standard deviations), alpha‐L‐fucosidase sensitivity and specificity were 76% and 90.9%, respectively. Conclusions. These results suggest that alpha‐L‐fucosidase is a useful marker for detecting HCC, in conjunction with alpha‐fetoprotein and ultrasonography.