CA 125 levels in patients with non-Hodgkin lymphoma and other hematologic malignancies

Cancer antigen (CA 125) is a glycoprotein commonly used as a tumor marker. In this study, CA 125 levels were measured in 149 patients and 26 healthy control subjects. The study group included 69 non-Hodgkin lymphomas (NHL), 25 Hodgkin disease (HD), 20 acute myelocytic leukemia (AML), 14 chronic lymphocytic leukemia (CLL), 12 chronic myelocytic leukemia (CML), and nine multiple myeloma (MM) patients. CA 125 was elevated in 37 of the patients and in none of the control subjects. Average CA 125 level in NHL patients was significantly higher than the controls (56.2 +/- 9.2 U/ml, 7.99 +/- 1.05 U/ml respectively) (P < 0.05). CA 125 levels were significantly higher in NHL patients with abdominal involvement (113.6 +/- 23.4 U/ml), with B-symptoms (72.3 +/- 13.2 U/ml), higher stage of the disease (stages III and IV -75.3 +/- 14.9 U/ml), bulky disease (99.9 +/- 30.4 U/ml) and in those with serosal involvement (103.1 +/- 18.5 U/ml) (P < 0.05 for all). CA 125 levels were also elevated in seven patients with HD and in a patient with CLL with pleural effusion. In conclusion, for patients with NHL, high levels of CA 125 were associated with B-symptoms, advanced stage, bulky disease, abdominal, and serosal involvement. Therefore, CA 125 might be used as a marker to predict prognosis and to detect advanced disease in NHL.     

Gastric juice immunoreactive epidermal growth factor levels in patients with peptic ulcer disease

Immunoreactive epidermal growth factor (IR-EGF) was measured by a highly sensitive and specific radioimmunoassay in gastric juice samples obtained during endoscopy from 26 control subjects, 44 patients with duodenal ulcers, and 18 with benign gastric ulcers. In the active stage, the concentrations of the peptide were consistently reduced, compared with those found in control subjects (592.7 +/- 55.8 pg/ml), in both duodenal (262.6 +/- 21.4 pg/ml) and gastric ulcer patients (320.2 +/- 34.1 pg/ml) (p less than 0.001 and 0.01, respectively). Mean IR-EGF values distinctly lower than in the controls were still present in the gastric juice of patients with inactive duodenal ulcers (349.7 +/- 35.9 pg/ml; p less than 0.001), whereas no difference was observed in patients with healed gastric ulcers (502.2 +/- 132.3 pg/ml). Although these findings suggest a possible role for EGF deficiency in the pathogenesis of peptic ulcer disease, the pathophysiological significance of our results (if any) remains to be elucidated.     

Serum ghrelin concentrations in patients with chronic renal failure undergoing dialysis

BACKGROUND: Ghrelin is a recently discovered protein hormone mainly synthesized in the gastric endocrine cells. This hormone not only is a potent growth hormone secretagogue but also is involved in the regulation of food ingestion and energy metabolism. Derangements in ghrelin secretion in patients with chronic renal failure (CRF) have not been fully evaluated. OBJECTIVE: Our aim has been to quantify serum concentrations of total ghrelin in a group of patients with CRF on chronic therapy with both haemodialysis (HD) and peritoneal dialysis (PD) in comparison with a group of patients on conservative management (predialysis). PATIENTS AND MEASUREMENTS: We studied 68 CRF patients treated by HD (n = 30, 16 men, age 61.2 +/- 1.8 years) and PD groups (n = 38, 21 men, age 54.4 +/- 1.7 years). A group of 19 uraemic patients on conservative management served as the control. Serum concentrations of ghrelin, leptin, insulin, IGF I and GH were measured in all subjects. RESULTS: Patients undergoing HD showed similar concentrations of ghrelin in comparison with the control group (9491 +/- 787 vs 9280 +/- 918 pg/ml, NS). However, PD patients exhibited baseline ghrelin concentrations significantly lower than those found in patients on conservative management (3230 +/- 216 pg/ml, P < 0.0001). Men and women showed similar serum ghrelin levels in both HD (9845.9 +/- 1071 vs 9085 +/- 1194 pg/ml) and PD patients (3214 +/- 297 vs 3250 +/- 324 pg/ml). Hypertension and diabetes mellitus did not influence ghrelin levels. Serum GH levels were positively correlated with serum ghrelin concentrations in both HD (r = 0.46, P < 0.05) and PD (r = 0.53, P < 0.001) patients; however, no relationships between ghrelin, leptin, insulin and IGF I were found. CONCLUSIONS: These results suggest that PD is accompanied by a striking decrement in baseline ghrelin concentrations in comparison with values found both in HD and control patients. Further studies are necessary to determine mechanisms involved in ghrelin regulation in uraemic patients.     

Increased serum levels of eotaxin in patients with inflammatory bowel disease

BACKGROUND: The CC-chemokines eotaxin and eotaxin-2, produced by epithelial and phagocytic cells, are potent and selective chemoattractants for eosinophils and basophils. The eosinophil is a potent inflammatory cell thought to play an important role in the pathogenesis of inflammatory bowel disease (IBD). In this study we investigated the serum concentrations of eotaxin and eotaxin-2 in patients with Crohn disease and ulcerative colitis. METHODS: Thirty-one patients with Crohn disease, 35 patients with ulcerative colitis and 41 control patients were studied. Eotaxin and eotaxin-2 serum levels were measured with solid phase sandwich enzyme-linked immunosorbent assays. RESULTS: Significantly increased serum eotaxin levels were observed in both patients with Crohn disease (289.4+/-591.5 pg/ml) and ulcerative colitis (207.0+/-243.4 pg/ml) when compared with controls (138.0+/-107.8 pg/ml) (P < 0.01). Moreover, patients with active Crohn disease and ulcerative colitis showed significantly higher serum eotaxin levels than patients with quiescent disease (434.0+/-776.8 pg/ml versus 113.8+/-65.4 pg/ml in Crohn disease and 295.7+/-337.1 versus 121.2+/-91.9 pg/ml in ulcerative colitis, P < 0.05). In contrast, there was no significant difference in eotaxin-2 serum levels among patients with Crohn disease (863.5+/-448.2 pg/ml), ulcerative colitis (1028.3+/-431.4 pg/ml) and controls (981.4+/-539.4 pg/ml). CONCLUSIONS: Eotaxin is significantly increased in serum of patients with active Crohn disease and ulcerative colitis, suggesting that this cytokine may play a role in the pathogenesis of IBD.     

The extraction of circulating catecholamines by the lungs in normal man and in patients with pulmonary hypertension.

We directly measured the net pulmonary extraction of circulating norepinephrine, epinephrine and dopamine in control patients and patients with primary or secondary pulmonary hypertension. Mixed pulmonary artery norepinephrine, epinephrine and dopamine were 314 +/- 13 pg/ml, 102 +/- 9 pg/ml, 51 +/- 5 pg/ml, respectively, for the control group; values were similar in patients with pulmonary hypertension. The pulmonary extraction of norepinephrine was 25.4 +/- 2.6% (clearance 266 +/- 62 ng/min) in control patients; epinephrine and dopamine were not extracted. There was no net extraction or production of any of the three catecholamines by the lungs in any of the patients with pulmonary hypertension. We conclude that the lungs play a significant role in the inactivation of circulating norepinephrine in man. This metabolic function of the lungs appear to be lost in pulmonary hypertension.     

Plasma level of mitochondrial coupling factor 6 increases in patients with coronary heart disease.

BACKGROUND: The aim of the present study was to investigate alterations in the plasma level of coupling factor 6 (CF6), a novel endogenous inhibitor of prostacyclin, in patients with coronary heart disease. METHODS AND RESULTS: In total, 35 patients with coronary heart disease and 20 age-matched healthy subjects were examined. Plasma levels of CF6 and 6-keto-prostaglandin (PG)F(1a) (a stable metabolite of prostacyclin) were measured using radioimmunoassay. The plasma level of CF6 was significantly increased in patients (254.1+/-29.8 pg/ml vs 219.4 +/-36.7 pg/ml in controls, p<0.0001), whereas that of 6-keto-PGF(1a) was significantly decreased (23.4 +/-2.3 pg/ml vs 26.1+/-4.5 pg/ml in controls, p=0.001). Moreover, after percutaneous transluminal coronary angioplasty (PTCA) and stent therapy, the level of CF6 was further increased by 30% to 330.4+/-26.0 pg/ml, and that of 6-keto-PGF (1a) was decreased by 42% to 13.5+/-2.0 pg/ml, compared with baseline (all p<0.01). Univariate analysis showed a significant result that the plasma level of CF6 was inversely correlated with that of 6-keto-PGF(1a) in the patients. The plasma ratio of CF6 to 6-keto-PGF(1a) was 8.4 in the control group and that in patients with coronary heart disease was increased to 24.4 after the therapy from 10.9 before therapy. CONCLUSIONS: The results suggest that an increased CF6 level may be responsible in part for the decreased prostacyclin level observed in patients with coronary heart disease, in particular after PTCA and stent therapy. As a potential risk factor for coronary heart disease, CF6 might have important clinical significance.     

Circulating nerve growth factor levels are increased in humans with allergic diseases and asthma.

Nerve growth factor (NGF) serum levels were measured in 49 patients with asthma and/or rhinoconjunctivitis and/or urticaria-angioedema. Clinical and biochemical parameters, such as bronchial reactivity, total and specific serum IgE levels, and circulating eosinophil cationic protein levels, were evaluated in relation to NGF values in asthma patients. NGF was significantly increased in the 42 allergic (skin-test- or radioallergosorbent-test-positive) subjects (49.7 +/- 28.8 pg/ml) versus the 18 matched controls (3.8 +/- 1.7 pg/ml; P < 0.001). NGF levels in allergic patients with asthma, rhinoconjunctivitis, and urticaria-angioedema were 132.1 +/- 90.8, 17.6 +/- 6.1, and 7.6 +/- 1.8 pg/ml (P < 0.001, P < 0.002, and P < 0.05 versus controls), respectively. Patients with more than one allergic disease had higher NGF serum values than those with a single disease. When asthma patients were considered as a group, NGF serum values (87.6 +/- 59.8 pg/ml) were still significantly higher than those of control groups (P < 0.001), but allergic asthma patients had elevated NGF serum levels compared with nonallergic asthma patients (132.1 +/- 90.8 versus 4.9 +/- 2.9 pg/ml; P < 0.001). NGF serum levels correlate to total IgE serum values (rho = 0.43; P < 0.02). The highest NGF values were found in patients with severe allergic asthma, a high degree of bronchial hyperreactivity, and high total IgE and eosinophil cationic protein serum levels. This study represents the first observation (that we know of) that NGF is increased in human allergic inflammatory diseases and asthma.     

The selected pro- and anti-inflammatory cytokines in the patients with coronary heart disease: preliminary communication

Recent findings suggest that inflammation and cytokines regulation may play a role in the pathogenesis of atherosclerosis and coronary heart disease. The aim of this study was to assess serum concentrations of selected pro- (TNF alpha) and antiinflammatory (IL-10) cytokines in patients with coronary heart disease. We studied 29 patients with coronary heart disease: 14 with stable angina (group I) and 15 with unstable angina (group II). The control group (group K) consisted of 10 healthy subjects. Patients with inflammatory diseases, previous myocardial infarction (last 6 months) and with ECG abnormalities, that would invalidate ST-segment analysis, were excluded from examined groups. We evaluated: clinical state of patients and results of some diagnostic examinations (lipids, ECG, echocardiography, coronary angiography, concomitant diseases). In each patients serum levels of TNF alpha and IL-10 were measured according to the special protocol by ELISA. The mean serum concentrations of TNF alpha and IL-10 were significantly higher in group I (respectively: 18.75 +/- 11.7 pg/ml, 89.0 +/- 114.9 pg/ml) and II (14.21 +/- 5.9 pg/ml, 49.38 +/- 72.9 pg/ml) in comparison to the healthy subjects (9.41 +/- 1.7 pg/ml, 9.69 +/- 4.5 pg/ml). We found positive correlations between mean TNF alpha and IL-10 concentrations in group II (48 hours after last symptom) and between mean TNF alpha concentration and LVM (left ventricular mass), LVMI (left ventricular mass index) in group I. The concentrations of TNF alpha and IL-10 did not correlate with other clinical parameters. The results of our study suggest that serum concentrations of pro- (TNF alpha) and antiinflammatory (IL-10) cytokines may be increased in patients with stable and unstable angina. These increased concentrations do not reflect the clinical state of patients.     

Increased serum levels of interleukin-15 in rheumatoid arthritis with long- term disease

OBJECTIVE: To study the serum levels of IL-15 in patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), seronegative spondyloarthropathies (SSd) and healthy donors. METHODS: The IL-15 serum levels were measured by ELISA in sera from 50 RA patients, 30 patients with SLE, 30 patients with SSd and 30 healthy donors. In RA patients, several clinical and demographic parameters were also obtained at the time of sample collection. IL-15 levels were compared in different RA subpopulations (positive or negative rheumatoid factor [RF], long term or recent onset disease, high or low disease activity). In addition, the possible association with other demographic and clinical parameters (gender, age, disease duration, etc) was also analysed. RESULTS: RA patients had significantly higher serum levels of IL-15 (102.4 +/- 150 pg/ml; p = 0.0001) than SLE patients (9.8 +/- 15.3 pg/ml), SSd patients (7.9 +/- 14.6 pg/ml) and healthy donors' (5.2 +/- 11.6 pg/ml). RA patients with a disease evolution less than 2 years showed lower IL-15 levels (33.7 +/- 62.2 pg/ml) than those with long-term disease (152.4 +/- 64.6 pg/ml; p = 0.004). In addition, a significant correlation between IL15 in serum and the number of disease-modifying antirheumatic drugs (DMARDs) prescribed was detected in RA patients (r = 0.42; p = 0.002). No association between IL-15 levels and age, gender, RF or disease activity was observed in this group. CONCLUSION: IL-15 is elevated in RA patients, specially in those with long term disease, compared to other rheumatic disorders. This finding supports that IL-15 is involved in the perpetuation of RA synovitis.     

B-type natriuretic peptide and extent of lesion on coronary angiography in stable coronary artery disease

OBJECTIVE: Although it is well established that plasma B-type natriuretic peptide (BNP) levels are higher in patients with acute coronary syndromes, the relationship between plasma BNP level and stable coronary artery disease is not clear. The aim of this study was to examine the relationship between plasma BNP levels and the extent of obstructive lesions on coronary angiography in stable coronary artery patients. METHODS: Plasma BNP concentrations were measured in 62 patients with a diagnosis of stable angina pectoris who had a left ventricular ejection fraction (LVEF) >or=45% on echocardiographic evaluation. Coronary angiography was performed for all patients, who were than divided into two groups according to the results of the angiography. Group I consisted of the patients who had a lesion leading to an obstruction of the lumen in any coronary artery by less than 50% or those who had normal coronary arteries. All other patients constituted group II. RESULTS: In group I (n=26), the mean plasma BNP level was 64.8+/-29.5 pg/ml. In group II (n=36), it was 99.7+/-55.4 pg/ml. BNP was significantly higher in group II (P=0.007) than group I. The BNP concentration of the patients with one-vessel disease (n=12), two-vessel disease (n=16), and three-vessel disease (n=8) were 77.9+/-34.9 pg/ml, 109.3+/-67.9 pg/ml, 113.3+/-48.1 pg/ml consecutively. In this respect, the plasma BNP was significantly higher in the groups with more extended vessel disease (P=0.02). When we compared the patients according to involvement of left anterior descending artery (LAD), BNP levels were significantly higher in this group, (116.1+/-55.8 pg/ml versus 64.1+/-30.2 pg/ml; P=0.001). CONCLUSION: Plasma levels of BNP were higher in patients who have stable coronary artery disease with preserved left ventricular systolic function. The level of increase in plasma BNP concentration was positively correlated with the extent of lesion and LAD involvement on coronary angiography.     

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。     

HCV infection in haemodialysed patients: A role for serum IL-10 and TGF-β1 in liver damage?

BACKGROUND: Hepatitis C virus (HCV) infection is often clinically silent in haemodialysed (HD) patients and their immune response may modulate liver damage in HCV infection. IL-10 and TGF-beta1 could play a role in this setting as, IL-10 down-regulates hepatic fibrosis, while TGF-beta1 is a pro-fibrotic cytokine. AIM: To evaluate the role of IL-10 and TGF-beta1 in HD/HCV+ patients. PATIENTS: 71 HD/HCV+ patients (58 with normal [HD/HCV-N] and 13 with high serum transaminases [HD/HCV-H]), 40 non-uremic patients with chronic hepatitis C (HCV+), 56 HD anti-HCV- patients and 20 healthy volunteers (H). METHODS: IL-10 and TGF-beta1 serum levels were assessed using ELISA tests. Liver histology was assessed by Ishak's score. RESULTS: IL-10 serum levels were significantly higher in HD patients, both HCV+ (3.7+/-0.4 pg/ml; p<0.01) and HCV- (3.8+/-0.8 pg/ml; p<0.05) than in non-uremic HCV patients (2.3+/-0.4 pg/ml). Among the HD/HCV+ patients, IL-10 serum levels were similar in HD/HCV-N and in HD/HCV-H patients. Among the HD/HCV+ patients, IL-10 serum levels were similar in those with moderate histological damage compared to those with mild damage. TGF-beta1 serum levels were significantly lower in HD patients, both HCV+ (4.6+/-0.9 ng/ml) and HCV- (6.0+/-0.9 ng/ml) than in non-uremic HCV+ patients (8.1+/-1.1 ng/ml; p<0.001 and p<0.01, respectively), but similar to the values found in H (5.3+/-0.9 ng/ml; p=n.s.). No correlation was seen between IL-10 and TGF-beta1 serum levels in any of the groups considered. CONCLUSIONS: Patients on haemodialysis treatment to have high levels of IL-10, which remain high even when patients are anti-HCV+, whereas the opposite is true of TGF-beta1. The cytokine pattern observed in HD patients is compatible with the hypothesis explaining the relatively benign evolution of HCV-related liver disease in HD patients, and has a pathophysiological role.     

Atrial natriuretic peptide during pacing in controls and patients with coronary arterial disease

At rest, during cardiac catheterization, aortic plasma levels of immunoreactive atrial natriuretic peptide did not differ between 10 controls with atypical chest pains and normal coronary arteries and 9 patients with stable angina pectoris and coronary arterial disease (55.2 +/- 19.8 vs. 64.8 +/- 19.8 pg/ml, NS). Nor did atrial natriuretic peptide values differ between the two groups during or after atrial pacing (150 beats/minute), which induced electrocardiographic and metabolic signs of acute myocardial ischaemia in the patients with coronary arterial disease but in none of the controls. Pacing, when carried out for more than 300 seconds, induced an increase of plasma atrial natriuretic peptide that correlated with duration of pacing (r = 0.80, P less than 0.001), and similarly in controls and patients with coronary arterial disease. In a second part of the study, which included 2 controls and 2 patients with coronary arterial disease, post-pacing coronary sinus concentrations of atrial natriuretic peptide were 10-20 times higher than peripheral levels (415- greater than 890 pg/ml). The concentration of atrial natriuretic peptide rose as blood from the caval veins (34 +/- 7 pg/ml) entered the right atrium (56 +/- 24 pg/ml), but thereafter was unchanged in the pulmonary artery (51 +/- 3 pg/ml) and the aorta (46 +/- 9 pg/ml). In conclusion, the results gave no evidence for ischaemic heart disease without congestive cardiac failure to be associated with altered levels of atrial natriuretic peptide. It was confirmed that atrial pacing stimulates the secretion of atrial natriuretic peptide which is produced by the heart and released via the coronary sinus into the circulation.     

Elevated BAL fluid histamine levels and parenchymal pulmonary disease in rheumatoid arthritis

To determine the amount of histamine in BAL fluid in subjects with RA and to ascertain if elevated histamine levels were associated with parameters of active pulmonary disease, we measured BAL fluid histamine levels in 31 subjects with RA and 36 normal subjects. The subjects with RA had a significantly greater mean BAL histamine level than the normal subjects, (313 +/- 154 pg/ml vs 18 +/- 8 pg/ml; p less than 0.05). When the subjects with RA were divided into three groups based on chest radiograms (1 = normal; 2 = pleural disease only; 3 = interstitial or nodular disease), we found that subjects in group 3 had significantly lower values for TLC and D. Subjects in group 3 also had higher percentages of BAL neutrophils and eosinophils and higher BAL histamine levels (group 1, 115 +/- 52 pg/ml; group 2, 30 +/- 30 pg/ml; and group 3, 1,182 +/- 709 pg of histamine per milliliter). Moreover, BAL histamine levels were negatively correlated with TLC (r = -0.46; p = 0.01) and FVC (r = -0.45; p = 0.01) and positively correlated with BAL neutrophils (r = 0.6; p = 0.0003) and BAL eosinophils (r = 0.89; p = 0.0001). These data suggest that the BAL histamine level may be a useful marker to determine the activity of pulmonary disease in RA.     

Serum levels of soluble CD30 molecule (Ki-1 antigen) in Hodgkin''s disease: relationship with disease activity and clinical stage

In all cases of Hodgkin's disease (HD) Reed-Sternberg (RS) cells express the CD30 antigen. It has been recently demonstrated that this molecule can be released from the cell membrane of CD30+ neoplastic cells in a soluble form (sCD30), detectable in culture supernatants and body fluids. In this paper we investigated by an immunoassay the serum levels of sCD30 in 58 patients with HD, in order to define the possible relationship of this molecule to the clinical and pathological findings. sCD30 molecule was found at detectable levels in 24 out of 50 patients (48%) with active disease, whereas it was always absent in control sera and in cases in complete remission. Among the patients with active HD, the incidence and mean values of detectable levels (+/- SEM) of sCD30 were higher in cases with progressive or relapsing disease (61.5%, mean 458 +/- 190 U/ml) as compared to those at presentation (43.2%, mean 116 +/- 33 U/ml). Among the cases at presentation, detectable levels were observed more often in patients with advanced stages (III + IV: 61%) and constitutional symptoms ('B': 61.5%) than in early stages (I + II: 26%) and without symptoms ('A': 33.3%). In addition, higher mean values were found in stages III + IV (182 +/- 60 U/ml) and in 'B' cases (208 +/- 73 U/ml) than in stages I + II (65 +/- 30 U/ml) or 'A' patients (64 +/- 26 U/ml). The above findings suggest a possible role for the sCD30 as a tumour marker in HD.     

Plasma levels of interleukin 2, 6, 10 and phenotypic characterization of circulating T lymphocytes in ischemic heart disease.

The purpose of this study was to assess lymphocyte receptors expression in patients with ischemic heart diseases, as well as to measure the plasma levels of interleukin (IL) 2, 6 and 10. T Lymphocytes are found in large numbers in human atherosclerotic plaques, indicating that immune and inflammatory mechanisms are important factors in the pathogenesis of atherosclerosis. Recent data have also implicated T lymphocytes in the pathogenetic mechanism of unstable angina and ischemic heart disease. Three groups of patients were studied: 42 with an acute ischemic syndrome (AIS), 36 with stable angina (SA) and 39 healthy controls. To characterize lymphocyte phenotype, flow cytometry was performed in whole-blood samples. IL-2, IL-6 and IL-10 were measured using the ELISA method. Double fluorescence evaluation showed an increase in CD8+/CD11b+ cells (cytotoxic T lymphocytes) and in CD11b+/CD16+CD56+ cells (NK lymphocytes) in the AIS group and in SA group as compared to the control group (P < 0.05 and P < 0.001, respectively). IL-2 was increased in the AIS and SA groups compared to the control group (AIS 4.5 +/- 0.5 pg/ml; SA 6.3 +/- 0.6 pg/ml; controls 2.4 +/- 0.8 pg/ml, P < 0.05), whereas IL-6 was higher in the AIS group than in the other two groups (AIS 10.8 +/- 1.8 pg/ml; SA 1.8 +/- 0.8 pg/ml; controls 1.2 +/- 0.6 pg/ml, P < 0.0001). These data show that patients with ischemic heart disease have an increase in circulating cytotoxic T lymphocytes and in IL-2 plasma levels, irrespective of their clinical presentation, compared to normal control subjects, whereas IL-6 is elevated only in patients with AIS.     

Circulating and cerebrospinal fluid ghrelin and leptin: potential role in altered body weight in Huntington's disease

OBJECTIVE: In addition to neurological impairment, weight loss is a prominent characteristic of Huntington's disease (HD). Neuropathologically, the disease affects the caudate nucleus and the cerebral cortex, and also the hypothalamus. The recently discovered orexigenic hormone of gastric origin, ghrelin and the adipocyte hormone leptin, are two peripherally produced hormones exerting opposite effects on specific populations of hypothalamic neurons that play a key role in regulating energy intake and energy output. The aim of this study was to investigate the possible involvement of cerebrospinal fluid (CSF) and circulating ghrelin and leptin in the regulation of energy balance in patients with HD. METHODS: Twenty healthy normal-weight subjects undergoing orthopedic surgery, and fifteen patients with genetically verified HD, were enrolled in this study. The unified Huntington's disease rating scale (UHDRS) was used to assess clinical course of the disease. Blood samples for hormonal measurements were obtained by venipuncture and in-parallel CSF samples for leptin/ghrelin determination were obtained by lumbar puncture. RESULTS: Patients with HD had increased concentrations of ghrelin in plasma compared with healthy subjects (4523.7+/-563.9 vs 2781.1+/-306.2 pg/ml, P<0.01). On the other hand, patients with HD had decreased concentrations of leptin in plasma compared with healthy subjects (4.8+/-1.6 vs 10.9+/-2.4 ng/ml, P<0.01). The concentrations of CSF ghrelin and CSF leptin were equivalent to values in healthy subjects. No correlation was found between disease duration--and other clinical features of HD--and plasma or CSF leptin/ghrelin levels. In patients with HD, baseline levels of GH, IGF-I, insulin and glucose did not differ from those in healthy subjects. CONCLUSION: High circulating ghrelin and low leptin levels in patients with HD suggest a state of negative energy balance. Early nutritional support of patients with HD is advocated since patients with HD and higher body mass index at presentation have slower progression of the disease.     

Circulating immunoreactive somatostatin in man. Effect of age, pregnancy, growth hormone deficiency and achlorhydria

Plasma immunoreactive somatostatin (IRS) levels were measured fasting at 09.00 h in groups of adult individuals and children of different ages, as well as in pregnant women, in patients with pernicious anaemia documented to be achlorhydric, and in children with growth hormone deficiency. There was a gradual rise in the mean level of IRS from the third decade (mean 35.8 +/- 3.8 pg/ml), which reached significance at the seventh (61.1 +/- 8.4 pg/ml), eighth (66.7 +/- 5 pg/ml) and ninth decade (82.6 +/- 13.8 pg/ml). No change was observed in the second 28.3 +/- 3.8 pg/ml) and third (31.1 +/- 3.2 pg/ml) trimester of pregnancy when compared with matched, non-pregnant controls (29.7 +/- 2.2 pg/ml); however, the children aged under 2 years (69.6 +/- 11.2 pg/ml) had significantly higher values than the eldest group (12 to 16 years old) (46.3 +/- 7.2 pg/ml) (P less than 0.05). In achlorhydric patients, basal (27.2 +/- 3.7 pg/ml; P less than 0.01) and postprandial IRS (42.8 +/- 7.7 pg/ml; P less than 0.001) was significantly lower than in a matched, normal control group (basal 59.4 +/- 7.2; postprandial 132.1 +/- 26.3 pg/ml). Growth hormone deficiency was not associated with any differences in circulating IRS, basally or after insulin hypoglycaemia, when compared with values in normal children.(ABSTRACT TRUNCATED AT 250 WORDS)     

Rise and fall of B-type natriuretic peptide levels in patients with coronary artery disease and normal left ventricular function after cardiac revascularization

BACKGROUND: Recently, it was shown that B-type natriuretic peptide levels are increased in patients with acute coronary syndromes. AIMS: To assess the relation between B-type natriuretic peptide and ischemia in patients with stable and unstable angina pectoris with normal left ventricular function in relation to the extent of ischemia and response to revascularization. METHODS: Fifty-nine consecutive patients were enrolled in the study, patients were divided into two groups: stable angina patients (group I, n=18), and unstable coronary patients (group II, n=41). Baseline characteristics were compared with 15 age-matched and sex-matched participants. B-type natriuretic peptide levels were measured at baseline and 3, 7 and 90 days after coronary revascularization in group I and II. RESULTS: Patients with unstable angina pectoris had increased B-type natriuretic peptide levels compared with stable angina pectoris patients (B-type natriuretic peptide levels: controls 15.5+/-13 pg/ml, stable angina pectoris group 28.4+/-19 pg/ml, unstable angina pectoris group 104+/-81 pg/ml; P<0.01). A relationship between the number of affected coronary vessels and B-type natriuretic peptide was assessed (one-vessel 29.9+/-21 pg/ml, two-vessel 93.8+/-87 pg/ml, three-vessel 119+/-88 pg/ml; P<0.01). After revascularization, B-type natriuretic peptide levels decreased in groups I and II (25+/-20 vs. 39+/-28 pg/ml) and were similar after 90 days in percutaneous transluminal coronary angiograghy and in coronary artery bypass grafting groups (percutaneous transluminal coronary angiography 26+/-22 pg/ml, coronary artery bypass grafting 36+/-26 pg/ml; NS). CONCLUSIONS: B-type natriuretic peptide levels increase in unstable angina pectoris patients and are linked to the extent of coronary disease in patients with normal left ventricular systolic function, and returned to baseline level after surgical or catheter revascularization.     

Atrial natriuretic peptide in Cushing's disease

Atrial Natriuretic Peptide (ANF), is secreted by atrial myocytes in response to atrial stretch. Its plasma levels have been found elevated in conditions leading to salt and fluid repletion and consequent atrial distention. Recently, it has been demonstrated that dexamethasone can enhance ANF secretion, by acting on ANF gene expression and mRNA synthesis. High plasma levels of ANF have been observed in normal man after administration of cortisol and ACTH. In the case of glucocorticoid excess, as in Cushing's disease, limited and conflicting data are available. Therefore, we measured ANF basal values and ANF response to postural changes and volume expansion in eight patients with Cushing's disease. In our patients ANF values were higher than normals. ANF responded to volume expansion, 47.8 +/- 5.1 pg/ml before sodium load and 69.9 +/- 7.0 pg/ml after sodium load, and changed minimally after postural manoeuvres, 47.3 +/- 3.2 pg/ml supine and 41.7 +/- 5.1 pg/ml upright. These data indicate that ANF secretion is enhanced in Cushing's disease, and its regulation is partially altered. Since in this condition hypervolemia has not been certainly demonstrated, a direct relationship between elevated ANF and glucocorticoid excess could be suggested.