The interferon status in helminthiases. 1. Human unilocular hydatid disease]

In 51 patients with Echinococcus granulosus infection, blood IF alpha and IF gamma levels were measured using vesicular stomatitis virus culture. In patients with progressing disease, the IF alpha and IF gamma levels were significantly lower than in the benign form of the disease--144 +/- 28.8 and 51.6 +/- 10.1 U/ml, respectively (in healthy controls the levels were 1024 +/- 28.8 and 187.7 +/- 16.9 U/ml). The lowest levels of IF alpha and IF gamma were found in patients with primary localization of cysts in the lungs and multiorgan damages affecting the lungs--160 +/- 38.5 and 44.4 +/- 13.5 U/ml; 146.7 +/- 80.1 and 89.5 +/- 19.2 U/ml, respectively. After 5-6 thirty-day courses of mebendazole therapy (50 mg/kg body weight) at 30-day intervals, the average levels of IF alpha and IF gamma were 4 and 5 times higher. Measurement of IF levels in echinococcosis may be of prognostic value for the estimation of the efficacy of surgical and/or specific treatment.     

Elevated serum TNF-alpha level as a link between endothelial dysfunction and insulin resistance in normotensive obese patients.

AIMS: The aim of the study was to analyse the role of tumour necrosis factor-alpha (TNF-alpha) in insulin resistance and endothelial dysfunction in patients with different types of obesity. PATIENTS AND METHODS: Fasting serum TNF-alpha immunoreactive concentration (enzyme-linked immunosorbent assay, ELISA) and bioactivity (L929 cell cytotoxicity assay), endothelin-1 and C-peptide levels (radioimmunoassay, RIA) were measured in 15 patients with android- and 13 patients with gynoid-type obesity and 15 lean healthy controls with normal glucose tolerance and blood pressure. RESULTS: Significantly (P<0.01) higher TNF-alpha concentration (8.92 +/- 0.44 pg/ml) and bioactivity (3.12 +/- 0.48 U/ml) were found in patients with android obesity as compared to patients with gynoid obesity (7.01 +/- 0.30 pg/ml, 0.97 +/- 0.11 U/ml) and to the lean controls (6.88 +/- 0.26 pg/ml, 0.88 +/- 0.08 U/ml). Serum endothelin-1 (5.38 +/- 0.30 pg/ml) and C-peptide levels (4.82 +/- 0.71 ng/ml) were also significantly higher (P < 0.01) in patients with android-type obesity than in controls (3.89 +/- 0.43 pg/ml, 1.46 +/- 0.25 ng/ml, respectively). In patients with gynoid-type obesity, only the C-peptide levels proved to be significantly higher (2.84 +/- 0.29 ng/ ml). Endothelin-1 levels, although were found to be slightly higher, did not differ statistically from in controls (4.56 +/- 0.31 pg/ml). There were significant positive linear correlations only in patients with android-type obesity between TNF-alpha, body mass index (BMI), serum endothelin-1 and C-peptide levels. CONCLUSIONS: TNF-alpha may be one of the factors contributing to insulin resistance and vascular dysfunction in patients with android obesity.     

Clinical significance of serum CA125 in patients with tuberculous pleurisy

We measured CA125 levels of the sera and pleural effusions in both patients with tuberculous pleurisy (TB) and with benign non-tuberculous pleurisy (non-TB). In all the TB patients, serum CA125 levels were increased (78 to 370 U/ml, mean +/- SD = 167.3 +/- 96.8 U/ml, n = 8), and were significantly higher than those in non-TB patients (167.3 +/- 96.8 U/ml v.s. 36.9 +/- 18.4 U/ml, p less than 0.01). Neoplastic diseases or gynecological disorders were not found in these patients. On the other hand, either CA125 or LDH levels of pleural effusions were not significantly different between these two groups. Although adenosine deaminase (ADA) levels in pleural effusions were also significantly higher in the TB patients (p less than 0.05), there were no correlation between serum CA125 and ADA levels in pleural effusions. Serial measurement of serum CA125 levels in the TB patients revealed that serum CA125 levels were markedly decreased one to two months after anti-tuberculous therapy (172.6 +/- 103.3 U/ml to 23.3 +/- 9.9 U/ml, p less than 0.01). It is suggested that the measurement of serum CA125 in patients with tuberculous pleurisy is useful as an indicator of disease activity.     

Physiological inhibitors of coagulation in fulminant hepatic failure.

To study the effect of the severe loss of hepatic synthetic function on the inhibitors of coagulation we have measured protein S (total and free), protein C, heparin cofactor II and antithrombin III in 30 patients with fulminant hepatic failure. The results showed severe reduction in all inhibitor levels with mean (+/- SE) values of: protein S, 0.26 +/- 0.03 U/ml; protein C, 0.26 +/- 0.03 U/ml; heparin cofactor II, 0.12 +/- 0.02 U/ml and antithrombin III, 0.21 +/- 0.02 U/ml. Heparin cofactor II was significantly lower than the other inhibitors (P less than 0.01). Although the reduction in free protein S was significant in fulminant hepatic failure as compared to normal subjects (0.40 +/- 0.05 U/ml compared to 1.02 +/- 0.08 U/ml, P less than 0.001), the ratio of free to total protein S was significantly increased (0.67 +/- 0.02 compared to 0.40 +/- 0.04, P less than 0.01). Prothrombin time (INR) was significantly inversely correlated with total protein S (r = -0.56, P less than 0.001) and free protein S (r = -0.48, P less than 0.01), but not with the ratio of free to total protein S. No significant correlation between the different coagulation inhibitors and other measures of hepatic function could be detected. Although the loss of hepatic synthetic function appears to be the major cause of the loss of coagulation inhibitors, other effects such as increased consumption and rate of clearance may play a role. The balance of these will be reflected in the circulating levels of the coagulation inhibitors.     

Interleukin 6 activity in pleural effusion. Its diagnostic value and thrombopoietic activity.

We measured interleukin 6 (IL-6) concentrations in the pleural fluid of various patients to determine its role in pathophysiology and diagnosis by using specific functional bioassay. IL-6 levels were significantly higher in exudate than in transudate (79.3 +/- 176.2 U/ml [n = 55] vs 1.7 +/- 1.8 U/ml [n = 12]; p < 0.01). Tuberculous effusion contained a significantly higher amount of IL-6 than malignant effusion (181.3 +/- 176.2 U/ml [n = 13] vs 29.4 +/- 71.5 U/ml [n = 29]; p < 0.005). Pleural IL-6 levels were invariably higher than serum IL-6 levels, and both were significantly correlated (n = 21, r = 0.632; p < 0.02). Pleural IL-6 levels were significantly correlated with lactate dehydrogenase (LDH) in pleural fluid (r = 0.392; p < 0.01), ratio of pleural/serum LDH (r = 0.571; p < 0.01), pleural adenosine deaminase activity (r = 0.599; p < 0.01), and serum C-reactive protein (r = 0.494; p < 0.01). Furthermore, IL-6 levels were significantly correlated with peripheral blood platelet counts (r = 0.447; p < 0.001). These results suggest that (1) IL-6 is produced locally in pleural space, (2) pleural IL-6 level is helpful for differential diagnosis, and (3) locally produced IL-6 could leak to circulation and cause systemic effects such as the induction of C-reactive protein and thrombocytosis.     

Soluble interleukin-2 receptor in sera of patients with pulmonary tuberculosis

Interleukin-2 receptor, the complex of IL-2R-alpha and/or IL-2R-beta, is expressed mainly on T-lymphocytes, and the soluble form of IL-2R-alpha (sIL-2R-alpha) has been reported to be detected in the serum of patients with lymphoproliferative disorders or disease characterized by the cellular immune reaction. We measured serum sIL-2R-alpha levels among patients with pulmonary diseases and found that sIL-2R-alpha levels were significantly elevated in patients with active pulmonary tuberculosis (1,327 +/- 209 U/ml) and sarcoidosis (1,037 +/- 115 U/ml) when compared with healthy volunteers (468 +/- 49 U/ml, p less than 0.01). Among patients with pulmonary tuberculosis, the sIL-2R-alpha levels were high in sera from patients with extensive parenchymal lesions on the roentgenogram (2,745 +/- 705 U/ml) and patients with tuberculous pleurisy (2,111 +/- 679 U/ml). In contrast, the sIL-2R-alpha levels in tuberculous patients with minimal lesion (455 +/- 92 U/ml) or moderate lesion (1,082 +/- 189 U/ml) were not significantly elevated when compared with healthy volunteers. After the treatment with antituberculosis agents, serum sIL-2R-alpha levels decreased in accordance with improvement of roentgenographic findings and laboratory data. These results suggest that serum sIL-2R-alpha level may be useful as a monitor for the disease activity in patients with pulmonary tuberculosis.     

The relationship of clinical and inflammatory markers to outcome in stable patients with cystic fibrosis

Decreased survival in patients with cystic fibrosis has been related to FEV1, BMI, and infection with Burkholderia cepacia complex (BCC). We have assessed the relationship of blood, sputum, and urine inflammatory markers to lung function, BMI, colonization with B cenocepacia (Bc), and patient survival. Thirty-nine stable cystic fibrosis (CF) patients (10 with Bc) were enrolled in a study to determine the effect of alpha-1-antitrypsin on airways inflammation. Pre-treatment measurements were used in this study. Demographics, sputum microbiology, heart rate, oxygen saturation, lung function were recorded. Blood samples were obtained for white blood count (WBC), C-Reactive Protein (CRP), and plasma neutrophil elastase/AAT complexes (pNEC). Neutrophil elastase (NE), neutrophil elastase/AAT complexes (sNEC), interleukin-8 (IL-8), TNF-receptor 1 (sTNFr), and myeloperoxidase (MPO) were measured in sputum and urinary desmosine concentration determined. Patients with Bc had significantly higher levels of pNEC, 332 +/- 91.4 ng/ml (mean +/- SEM) versus 106 +/- 18.2 ng/ml (P = 0.0005) and sNEC, 369 +/- 76.6 ng/ml versus 197 +/- 36.0 ng/ml compared to those who were not. Five deaths were reported at the end of 1 year, (four with Bc) (P = 0.011). Patients who subsequently died had significantly lower lung function FEV1, 1.2 +/- 0.2 L versus 2.0 +/- 0.1 L (P = 0.03) and FVC, 2 +/- 0.3 L versus 3.1 +/- 0.2 L (P = 0.01), compared to those that survived. There was significantly higher NE activity, 3.6 +/- 1.6 U/ml versus 1.5 +/- 0.6 U/ml (P = 0.03), pNEC, 274 +/- 99 ng/ml versus 142 +/- 30 ng/ml (P = 0.05), MPO, 163 +/- 62 mcg/ml versus 54 +/- 6.9 mcg/ml (P = 0.03), and urinary desmosines 108 +/- 19.9 pM/mg creatinine versus 51.1 +/- 3.3 pM/mg creatinine (P = 0.001), in those patients who subsequently died compared to those that survived. These data suggest there is increased neutrophil degranulation in patients infected with Bc and these patients have a poor outcome.     

冠心病患者分泌型磷脂酶A2的变化及其与白细胞介素8、溶血磷脂酸的关系

目的了解冠心病患者分泌型磷脂酶 A2(sPLA2)的变化,并通过测定 IL-8、LPA 等相关细胞因子,对 sPLA2的作用机制进行初步探讨。方法冠状动脉造影确诊的262例患者,其中急性冠脉综合征(ACS)110例,稳定性冠心病(SCHD)63例,正常患者89例,分别测定 sPLA2、白细胞介素8(IL-8)、高敏 C 反应蛋白(hs-CRP)和溶血磷脂酸(LPA)水平,并进行对比分析。结果冠心病患者sPLA2[(68±17)U/ml]、IL-8[(182±80)pg/ml]以及 LPA[(2.85±0.36)μmol/L]均明显高于对照组[sPLA2:(55±12)U/ml,IL-8:(119±33)pg/ml,LPA:(2.34±0.36)μmol/L,均 P<0.01],其中ACS 组的 sPLA2[(71±18)U/ml]、IL-8[(195±78)pg/ml]也明显高于 SCHD 组[sPLA2:(63±12)U/ml],IL-8:[(159±79)pg/ml,均 P<0.01;sPLA2与 IL-8(r=0.203,P=0.007)、LPA(r=0.658,P<0.01)、hs-CRP(r=0.231,P=0.005)均呈正相关;sPLA2≥63.75 U/ml 时,患冠心病的相对危险度为6.248(P<0.01)。结论冠心病患者 sPLA2明显升高,它可能与 IL-8共同参与冠心病的炎症发展过程,并与下游相关产物 LPA 进一步加速其进展。提示 sPLA2升高是冠心病的独立危险因素之一。     

Decreased growth hormone (GH) response to oral clonidine in endemic cretinism: effect of L-T3 therapy

As GH secretion is dependent upon thyroid hormone availability, the GH responses to clonidine (150 micrograms/m2) and the TSH and PRL response to TRH were studied in eight endemic (EC) cretins (3 hypothyroid, 5 with a low thyroid reserve) before and after 4 days of 100 micrograms of L-T3. Five normal controls (N) were also treated in similar conditions. Both groups presented a marked increase in serum T3 after therapy (N = 515 +/- 89 ng/dl; EC = 647 +/- 149 ng/dl) followed by a decrease in basal and peak TSH response to TRH. However, in the EC patients an increase in serum T4 levels and in basal PRL and peak PRL response to TRH after L-T3 therapy was observed. One hypothyroid EC had a markedly elevated PRL peak response to TRH (330 ng/dl). There were no significant changes in basal or peak GH values to treatment with L-T3 in normal subjects. In the EC group the mean basal plasma GH (2.3 +/- 1.9 ng/ml) significantly rose to 8.8 +/- 3.2 ng/ml and the mean peak response to clonidine (12.7 +/- 7.7 ng/ml) increased to 36.9 +/- 3.1 ng/ml after L-T3. Plasma SM-C levels significantly increased in N from 1.79 +/- 0.50 U/ml to 2.42 +/- 0.40 U/ml after L-T3 (p less than 0.01) and this latter value was significantly higher (p less than 0.05) than mean Sm-C levels attained after L-T3 in the EC group (respectively: 1.14 +/- 0.59 and 1.78 +/- 0.68 U/ml). These data indicate that in EC the impaired GH response to a central nervous system mediated stimulus, the relatively low plasma Sm-C concentrations, and the presence of clinical or subclinical hypothyroidism may contribute to the severity of growth retardation present in this syndrome.     

Hydatid acute pancreatitis.

BACKGROUND/AIMS: Hydatid acute pancreatitis is a rare condition, mostly reported as case presentations. METHODS: A series of eight patients with hydatid acute pancreatitis, referred between January 1990 and January 2003, are reported. All patients presented acute pancreatitis confirmed with clinical presentation, radiologic examination and laboratory findings. All patients had elevated levels of blood amylase value (more than 500 U/L). Five patients (62%) had high bilirubin levels (2.1 to 3.4 mg/dl) during the initial hospitalization. Computed tomography findings revealed acute pancreatitis in four patients; two had associated pseudocyst formation. RESULTS: Endoscopic retrograde cholangiopancreatography was performed on all patients and revealed hydatid cystic material in the common bile duct secondary to cystobiliary rupture in all patients. All patients underwent endoscopic sphincterotomy that was performed after dilatation with extractor balloon, and hydatid material was removed in all. Six patients were operated on after the initial episode subsided. Drainage of the cyst, appropriate cavity management and T-tube drainage of the common bile duct was employed in all patients to control bile leakage after the operation. Scolices and hydatid membrane were detected during common bile duct exploration in all patients due to presentation of cystobiliary rupture. There was no mortality. Postoperative pulmonary infection and wound infection were encountered in one patient each. During two to 13 years' follow-up, one patient developed recurrent hydatid disease. Recurrent pancreatitis did not occur. CONCLUSIONS: Hydatid acute pancreatitis is a rare condition. However, it should be remembered in patients with abdominal pain, especially in endemic areas.     

Thrombocyte activity in dilatative cardiomyopathy and latent cardiomyopathy compared to coronary heart disease

In a comparative study on the pathomechanism of myocardial hypoxia we determined a parameter each of platelet activity and thrombin activity in 46 patients with angina pectoris, i.e., 15 patients with dilatative cardiomyopathy (DCM), 15 patients with latent cardiomyopathy (LCM) and 16 patients with coronary heart disease (CHD) compared to 15 normal subjects (N). beta-thromboglobulin (beta TG) and fibrinopeptide A (FPA) were measured both at rest (I) and after symptom-limited maximal exercise (II) in plasma. In N, beta TG was not increased in any case, neither at rest nor on exertion (I: 20.5 +/- 6.1 ng/ml, II: 22.4 +/- 6.7 ng/ml). Patients with LCM did not differ significantly from N (I: 20.9 +/- 6.1 ng/ml, II: 22.7 +/- 7.9 ng/ml). beta TG values of some patients with DCM and CHD were increased at rest and especially under exercise (DCM I: 27.9 +/- 9.6 ng/ml, vs. N p less than 0.025; II: 49.9 +/- 45.5 ng/ml, vs. N p less than 0.01; CHD I: 25.2 +/- 7.7 ng/ml, vs. N p less than 0.05; II: 38.6 +/- 34.3 ng/ml, vs. N p less than 0.01). Patients with DCM developing significant angina under exercise showed a higher beta TG under these exercise conditions than those with mild or no angina (p less than 0.01). In patients with coronary heart disease, this correlation was not to be found. With regard to FPA the four investigated groups differed in an analogous way, as they did with regard to beta TG; but only a weak correlation within both values was shown.(ABSTRACT TRUNCATED AT 250 WORDS)     

Increased serum levels of soluble IL-2 receptor, CD30 and CD8 molecules, and gamma-interferon in angioimmunoblastic lymphadenopathy: possible pathogenetic role of immunoactivation mechanisms

Abnormal immunoreaction associated with increased cell activation phenomena might play a role in the pathogenetic events leading to the development of angioimmunoblastic lymphadenopathy (AILD). In the present study we investigated the serum levels of some soluble molecules related to cell activation in 24 patients with AILD at presentation. In particular, we measured by immunoenzymatic or immunoradiometric techniques the levels of the Tac peptide (sIL-2R), soluble CD30 (sCD30) and CD8 (sCD8) antigens, and gamma-IFN (gIFN). The results show that all the above molecules are increased as compared to normal controls, with a different pattern of increase for the different molecules. The sIL-2R levels were very high in all cases with no overlap between AILD and control samples (mean 6315 +/- 3374 U/ml, controls 271 +/- 112 U/ml, P less than 0.001). Very high values of the sCD30 antigen (722 +/- 895 U/ml) were detected in all cases but five, as opposed to the lack of detectable levels in controls. A significant increase of sCD8 (978 +/- 646 U/ml, controls 334 +/- 95 U/ml, P less than 0.01) and gIFN (329 +/- 236 U/ml, controls 97 +/- 43 U/ml, P less than 0.01) was also observed with some overlap between AILD samples and controls. The above findings further support the view that a condition of abnormally enhanced cell activation is likely to play a central role in the pathogenetic events leading to the composite clinicopathological picture of AILD.     

Accelerated production of nucleosome in cultured human mononuclear cells in untreated Graves' disease

The apoptosis of lymphocytes, which occurs in autoimmune diseases, is usually induced by the Fas/Fas ligand system. As the assay of nucleosomes produced by apoptotic cells can be used to quantitate apoptosis, we evaluated nucleosome and soluble Fas ligand (sFasL) levels of cultured mononuclear cells to clarify the apoptosis of mononuclear cells in patients with autoimmune thyroid diseases by enzyme-linked immunosorbent assay. Nucleosome levels of cultured mononuclear cells in patients with untreated Graves' disease were significantly higher (3.27+/-2.90 U/ml) than those of control subjects (1.39+/-0.24 U/ml) and euthyroid patients with treated Graves' disease (1.53+/-0.33 U/ml). Nucleosome levels of cultured mononuclear cells were positively correlated with sFasL levels (r=0.544, p<0.01). It is therefore likely that increased sFasL levels elicit apoptosis of these cells in untreated Graves' disease.     

T-cell activation in Crohn's disease. Increased levels of soluble interleukin-2 receptor in serum and in supernatants of stimulated peripheral blood mononuclear cells

Serum levels of soluble interleukin-2 receptor were determined in 29 patients with active and quiescent Crohn's disease. In addition, the ability of peripheral blood mononuclear cells of 23 of these patients to generate soluble interleukin-2 receptor following mitogenic stimulation was studied in vitro. Serum soluble interleukin-2 receptor concentrations of patients with active Crohn's disease (n = 19) were significantly elevated (757 +/- 438 U/ml) compared with levels in patients with inactive disease (n = 10; 412 +/- 120 U/ml) and healthy control individuals (n = 40; 375 +/- 102 U/ml; p less than 0.003 and p less than 0.0005, respectively). Serial determinations of serum soluble interleukin-2 receptor concentration in a follow-up of 11 hospitalized patients treated for highly active disease showed a decrease from 1252 +/- 494 U/ml to 527 +/- 193 U/ml (p less than 0.004) that corresponded to clinical improvement, as assessed by Crohn's disease activity index and a reduction of inflammatory parameters. In vitro phytohemagglutinin stimulation of peripheral blood mononuclear cells derived from patients with Crohn's disease resulted in elevated soluble interleukin-2 receptor production not only in patients with active disease (3987 +/- 2439 U/ml), but also in patients with inactive disease (3297 +/- 2282 U/ml), compared with the amount of soluble interleukin-2 receptor produced by mononuclear cells of healthy individuals (1523 +/- 1152 U/ml; p less than 0.005 and p less than 0.02, respectively). In addition, cultivation of mononuclear cells without mitogen resulted in higher soluble interleukin-2 receptor production in patients with active disease than in patients with inactive disease (p less than 0.02). However, patients suffering from active ulcerative colitis also had significantly increased serum levels of soluble interleukin-2 receptor (1080 +/- 400 U/ml) compared with the levels in patients with chronic disease (455 +/- 140 U/ml; p less than 0.0025). In addition, peripheral blood mononuclear cells derived from patients with ulcerative colitis produced significantly more soluble interleukin-2 receptor upon mitogenic stimulation with phytohemagglutinin (2314 +/- 936 U/ml), than cells from healthy controls (1523 +/- 1152 U/ml; p less than 0.05). The finding of elevated soluble interleukin-2 receptor serum levels in patients with active Crohn's disease and its increased production by mononuclear cells of patients with both active and inactive disease is a further example of an alteration of the immune system in this condition; however, this alteration can also be found in other inflammatory bowel diseases.     

Mononuclear cell activation in Crohn's disease. Evaluation using serum assay of neopterin and interleukin-2 soluble receptors

To determine the degree of mononuclear blood cell activation in Crohn's disease (CD), 65 patients were prospectively investigated (22 with mild, 26 with moderate and 17 with severe disease). Serum levels of soluble receptors for interleukin-2 (SR-IL-2) were measured by ELISA. In CD patients SR-IL-2 levels were significantly higher (m = 707 +/- 326 U/ml) than in three other groups: 70 controls (m = 258 +/- 87 U/ml, p less than 0.0001); 8 patients with acute infectious colitis (m = 405 +/- 216 U/ml, p less than 0.0001); 101 HIV seropositive subjects (m = 564 +/- 216 U/ml, p less than 0.002). There was a positive correlation between SR-IL-2 level and the Van Hees activity index (r = 0.595, p less than 0.0001). On the other hand, the numbers of activated T cells (CD 3+, HLA DR+), CD 4+, CD 8+ and NK cells did not differ according to the CD activity groups. Furthermore, CD patients treated with steroids (n = 39) did not differ from those without any medication. As a marker of monocyte activation, serum neopterin level was determined by RIA. All CD patients considered as a group, serum neopterin level was 2.89 +/- 1.44 ng/l (n less than 2.5 ng/l). Neopterin level increased with disease activity (1.97 +/- 0.92 vs 3.10 +/- 1.46 vs 3.74 +/- 1.36, p less than 0.01), and was positively correlated with SR-IL-2 (r = 0.609, p less than 0.0001). These results suggest a monocyte-macrophage activation in CD, which parallels disease activity.(ABSTRACT TRUNCATED AT 250 WORDS)     

Regression of structural vascular changes in hypertensives after captopril treatment.

In order to investigate whether hypertension-related structural vascular changes may be influenced by antihypertensive treatment, 10 patients were studied suffering from essential arterial hypertension, five males and five females, aged between 34 and 61 years (mean age: 46.9 +/- 8.13 years). All patients received a placebo for 1 week and then captopril, 75 mg b.i.d. for 3 months. After placebo and captopril treatments, the following parameters were evaluated: SBP, DBP, mean blood pressure (MBP), by the formula 1/3 (SBP + 2 x DBP) and basal and minimal vascular resistances, respectively obtained by the ratios MBP/rest flow and MBP/peak flow. Blood flows have been obtained by strain gauge plethysmography. A significant decrease in systolic (P less than 0.025), diastolic (P less than 0.01) and mean blood pressure (P less than 0.01), basal vascular resistances (52 +/- 19 vs 28 +/- 12 A.U., P less than 0.01) and minimal vascular resistances (6.3 +/- 2.2 vs 3.9 +/- 2.8 A.U., P less than 0.025) has been observed after captopril treatment in comparison to placebo, whereas rest (2.9 +/- 0.7 vs 4.1 +/- 0.9 ml.min-1.100 g-1, P less than 0.01) and peak blood flows (21.3 +/- 5.8 vs 29.7 +/- 9.4 ml.min-1.100 g-1) significantly increased. These data seem to indicate that antihypertensive treatment with the angiotensin-converting enzyme inhibitor, captopril, is not only efficacious in inducing a significant blood pressure decrease, consequent to the reduction of basal vascular resistance (due to the vasodilating effects of the drug), but is also able to reduce minimal vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)     

Serum levels of carbohydrate antigen 125 in patients with chronic heart failure: relation to clinical severity,hemodynamic and Doppler echocardiographic abnormalities,and short-term prognosis

OBJECTIVES: The aim of this study was to evaluate the serum levels of carbohydrate antigen 125 (CA125) in patients with congestive heart failure (CHF). BACKGROUND: CA125 is a glycoprotein produced by serosal epithelium, found to be increased in ovarian cancer. METHODS: Serum levels of CA125 were obtained in 286 patients (122 males and 164 females; age 69 +/- 13 years) with CHF (left ventricular ejection fraction 30 +/- 11%). A non-invasive evaluation was obtained by Doppler echocardiography; right heart catheterization was performed in 88 patients. An attempt to adjust medical therapy to maximally tolerated doses was done, and CA125 was repeated after 18 days (range 7 to 40) in 80 patients. The mean follow-up duration was 6 +/- 3 months in 240 patients. RESULTS: The mean value of CA125 was 68 +/- 83 U/ml (range 3 to 537): 71 +/- 85 in men and 56 +/- 64 U/ml in women (p = NS). CA125 above the normal value (<35 U/ml) was found in 152 (53%) of 286 patients; it was higher in patients with advanced New York Heart Association (NYHA) functional class (n = 140 in class I/II: 15 +/- 9 U/ml; n = 63 in class III: 57 +/- 18 U/ml; n = 83 in class IV: 167 +/- 94 U/ml; p < 0.005). CA125 was related to the deceleration time of early filling on transmitral Doppler (r = -0.63, p < 0.05) and to pulmonary artery wedge pressure (r = 0.66, p < 0.05) and right atrial pressure (r = 0.69, p < 0.05). During 6 +/- 3 months of follow-up, a combined end point of mortality and CHF hospitalization was observed in 16 of 127 patients with CA125 <35 U/ml, compared with 70 of 113 patients with CA125 >35 U/ml (p < 0.01). After medical treatment optimization, NYHA class decreased by more than one grade in 56 of 80 patients and was unchanged or increased in 24 patients: CA125 decreased from 125 +/- 98 to 53 +/- 61 U/ml (p < 0.001) in the former and changed from 130 +/- 81 to 153 +/- 61 U/ml (p = NS) in the latter. CONCLUSIONS: Our data suggest that CA125 is related to CHF severity and short-term prognosis. Furthermore, fluctuations of CA125 serum levels over time may reflect changes induced by therapy. Therefore, measurements of CA 125 serum levels might be proposed for the serial assessment of CHF patients.     

Clinical significance of serum soluble interleukin-2 receptor level in patients with non-Hodgkin's lymphoma]

The aim of this study was to assess the clinical significance of serum soluble interleukin-2 receptors (sIL-2R) in non-Hodgkin's lymphoma (NHL). Using a sandwich ELISA method, serum sIL-2R levels were measured in 720 samples from 87 patients with NHL (including 65 untreated patients) and 36 patients with other diseases such as infectious mononucleosis. The mean serum sIL-2R level in NHL was 4,017 U/ml (mean +/- SD, 4017 +/- 6352 U/ml). Patients in clinical stages III/IV (5116 +/- 6629) had significantly higher sIL-2R levels than those in clinical stages I/II (813 +/- 611). Patients with sIL-2R levels exceeding 8,000 U/ml had significantly lower survival rates (2-year survival: 12.3%) than those with sIL-2R levels below 8,000 U/ml (2-year survival: 76.0%) (P < 0.01). Multivariate analysis of variables including age, clinical stage, LDH, CRP, performance status, number of extranodal diseases, and sIL-2R demonstrated that sIL-2R and LDH were significant prognostic indicators of overall survival. The upper limit of the 95% confidence interval for maximum sIL-2R level in follow-up of patients with complete remission was 2,014 U/ml. Although an increased sIL-2R level of around 2,000 U/ml in the remission stage did not necessarily suggest relapse of NHL, it did seem to warrant careful follow-up. The serum sIL-2R level appears to reflect tumor activity and may prove to be a useful prognostic indicator in patients with NHL.     

Serum soluble Fas in patients with Schistosomal cor pulmonale

BACKGROUND: Schistosomal cor pulmonale is considered an important pathological condition in endemic areas. Few recent studies have reported the role of apoptosis in pulmonary hypertension. OBJECTIVES: The aim of this study was to assess serum levels of soluble Fas (sFas), an inhibitor of apoptosis, in patients with schistosomal cor pulmonale as compared to patients with cor pulmonale due to chronic obstructive pulmonary disease (COPD) and normal subjects. METHODS: Serum sFas was assessed in 15 men with schistosomal cor pulmonale (age 32 +/- 10 years), 15 men with chronic cor pulmonale secondary to COPD and 20 healthy men, matched for age. RESULTS: Serum levels of sFas were significantly higher in patients with schistosomal cor pulmonale (74 +/- 80 U/ml) than in patients with cor pulmonale due to COPD (15 +/- 10 U/ml) and normal subjects (19 +/- 11 U/ml, p < 0.001 in both). In patients with schistosomal cor pulmonale, sFas was significantly higher in patients with mean pulmonary artery pressure > 30 mm Hg as compared to patients with pressure < or = 30 mm Hg (109 +/- 97 vs. 34 +/- 20 U/ml, p = 0.01). There was a significant correlation between serum sFas and the mean pulmonary artery pressure in patients with bilharzial cor pulmonale (r = 0.4, p < 0.01), but not in patients with COPD (r = 0.1, p = NS). CONCLUSIONS: Serum sFas levels are elevated in patients with schistosomal cor pulmonale and they are related to the severity of pulmonary hypertension. These findings suggest a role of apoptosis in schistosomal cor pulmonale.     

Serum insulin-like growth factor I levels in adult diabetic patients: the effect of age

Despite reports of reduced serum insulin-like growth factor (IGF) levels in experimentally diabetic animals, human diabetic patients have been reported to have decreased, normal, or even elevated levels. This study was a cross-sectional examination of the effect of age on immunoreactive IGF-I levels in adult patients with insulin-dependent or noninsulin-dependent diabetes mellitus (IDDM and NIDDM) attending a diabetes out-patient clinic. The patients and normal subjects studied were divided into the age ranges 21-30, 31-40, 41-50, 51-60, and over 60 yr. For all ages combined, the mean IGF-I level (+/- SD) was 0.84 +/- 0.26 U/ml (202 +/- 62 ng/ml) in 133 normal subjects, significantly reduced to 0.41 +/- 0.17 U/ml in 121 IDDM patients, and 0.49 +/- 0.19 U/ml in 46 NIDDM patients (both P less than 0.001). In both groups there was a marked decline in IGF-I with increasing age (P less than 0.01). Except for NIDDM patients aged 21-30 yr (only two patients), IGF-I levels in both IDDM and NIDDM patients were significantly lower in every age range than those in age-matched normal subjects, but did not differ between the two diabetic groups. Glycosylated hemoglobin levels correlated inversely with IGF-I levels only in younger patients with IDDM (r = -0.486; P less than 0.05 for patients aged 21-40 yr). We conclude that factors common to IDDM and NIDDM, perhaps related to relative nutritional deficiency at the cellular level, cause a reduction in serum IGF-I levels, and that this reduction occurs independently of age-related changes in IGF-I.