Lipid profile as a strong indicator of coronary plaques: noninvasive assessment by multislice computerized tomography.

BACKGROUND: Most acute coronary syndrome disorders occur as a consequence of atherosclerotic plaque rupture. Lipids are involved in atherosclerotic plaque buildup. Advances in image quality of coronary computed tomography have enabled improved characterization of coronary plaques. The aim of our study was to evaluate the association between lipid profile and coronary plaque presence in general and soft plaques in particular. METHODS: In this cross-sectional survey, 258 consecutive patients presenting with chest pain either or both with low-to-moderate risk for coronary artery disease, were included. All patients were tested for lipid profile prior to cardiac imaging on a 64-slice computer tomography. Multivariate logistic regression models were used to assess the odds ratios (ORs) and 95% confidence interval (CI) for the relationship between blood lipid levels and prevalence of coronary plaques. RESULTS: Age, total cholesterol levels, hypertension, hyperlipidemia (dichotomous) and risk factor index, all were independently associated with prevalence all kind of plaques, especially with soft plaques. No significant relationships were detected among BMI, current smoking, diabetes or triglycerides levels. In a multivariate logistic regression, hyperlipidemia was associated with presence of coronary plaque risk with adjusted OR of 2.28 (95% CI 1.30-4.01), total cholesterol with adjusted OR = 1.05 (95% CI 1.01-1.06), and risk factor index (1-6) with adjusted OR = 2.23 (95% CI 1.40-3.55). CONCLUSION: Hyperlipidemia is strongly associated with prevalence of coronary plaques (P < 0.001) in individuals with low-to-intermediate risk for coronary artery disease, based on cardiac CT. Cardiac CT may serve as a noninvasive alternative for the early diagnosis of CAD in such individuals.

Real-World Outcomes with Lomitapide Use in Paediatric Patients with Homozygous Familial Hypercholesterolaemia.

INTRODUCTION: Homozygous familial hypercholesterolaemia (HoFH) is a rare, autosomal disease affecting the clearance of low-density lipoprotein cholesterol (LDL-C) from circulation, and leading to early-onset atherosclerotic cardiovascular disease (ASCVD). Treatment consists mainly of statins, lipoprotein apheresis (LA) and, more recently, the microsomal triglyceride transfer protein inhibitor lomitapide. Lomitapide is not licensed for use in children, but has been made available through an expanded access programme or on a named patient basis. METHODS: This case series includes 11 HoFH patients in 10 different centres in eight countries, less than 18 years of age (mean 11.6 ± 1.1 years, 64% male), with signs of ASCVD, and who have received treatment with lomitapide (mean dose 24.5 ± 4.3 mg/day; mean exposure 20.0 ± 2.9 months). Background lipid-lowering therapy was given according to local protocols. Lomitapide was commenced with a stepwise dose escalation from 2.5 mg or 5 mg/day; dietary advice and vitamin supplements were provided as per the product label for adults. Laboratory analysis was conducted as part of regular clinical care. RESULTS: In the 11 cases, mean baseline LDL-C was 419 ± 74.6 mg/dL and was markedly reduced by lomitapide to a nadir of 176.7 ± 46.3 mg/dL (58.4 ± 6.8% decrease). Six patients achieved recommended target levels for children below 135 mg/dL, five of whom had LA frequency reduced. In one case, LDL-C levels were close to target when lomitapide was started but remained stable despite 75% reduction in LA frequency (from twice weekly to biweekly). Adverse events were mainly gastrointestinal in nature, occurred early in the treatment course and were well managed. Three patients with excursions in liver function tests were managed chiefly without intervention; two patients had decreases in lomitapide dose. CONCLUSIONS: Lomitapide demonstrated promising effectiveness in paediatric HoFH patients. Adverse events were manageable, and the clinical profile of the drug is apparently similar to that in adult patients. FUNDING: Amryt Pharma.

[EFFECT OF YOUNG AGE ON CLINICAL, PATHOLOGICAL FEATURES AND SURVIVAL OF PATIENTS WITH COLORECTAL CANCER].

BACKGROUND: Colorectal cancer is one of the most common malignancies in the Western World and in Israel. Most patients with colon cancer are older than 50 years of age. There is no consensus in the literature regarding the behavior of this disease in young patients. AIM: The aim of the present study is to compare clinical and ic pathological features of colon cancer between young and sold patients. METHODS: All clinical and pathological characteristics of 200 patients with colon cancer treated at our center during the period 2001-2006 were retrospectively reviewed. RESULTS: Twenty five patients (12.5%) were <50 years age (young patients) at diagnosis (mean age 41 years) and 175 were >50 years (mean age 68 years). Males were 56% of the young group and 60.1% of the old one. Arab patients were 52% of the young group, although their total number was 35 of the 200 patients. No significant difference was found in the stage of tumor at diagnosis between the two groups. Histopathological grade 3 tumors were found in 33.3% of young versus 7.7% in old patients. Surgery and chemotherapy were performed in 96% and 88% versus 95.4% and 69.7% in the two groups respectively. In a median follow-up period of 96 months, 35% of young patients died of their disease compared to 33.1% of the old patients. CONCLUSIONS: Other than histological grade, no difference was found in colon cancer features and survival of young compared to old patients. Further studies with higher numbers of patients are suggested to clarify our findings.

Anti-atherogenic properties of high-density lipoproteins in psychiatric patients before and after two months of atypical anti-psychotic therapy.

Some of the medications used for the management of schizophrenia are associated with clinically significant increases in weight and adverse alterations in serum lipid levels. The aim of the study was to investigate the effect of short-term (two months) treatment with atypical anti-psychotics on coronary heart disease risk factors, including the functional properties of high-density lipoprotein (HDL), in psychiatric patients. Nineteen patients diagnosed with schizophrenia, schizoaffective, and bipolar disorder and ten healthy volunteers were enrolled in the study. In the present study blood was drawn at baseline and after two months of atypical anti-psychotic treatment. Wilcoxon non-parametric-test was used to examine differences in the psychotic group before and two months after treatment.Waist circumference and oxidative stress in psychiatric patients were higher compared with the control group. Serum-mediated cholesterol efflux capacity was lower in psychotic patients compared to controls. Two months of anti-psychotic therapy was associated with increased abdominal obesity, decreased paraoxonase lactonase activity, but with no further change in serum-mediated cholesterol efflux from macrophages. Psychotic patients have low serum-mediated cholesterol efflux from macrophages as a parameter of HDL functionality. Atypical anti-psychotic treatment for two months increased metabolic derangements in these patients but without further decrement in serum-mediated cholesterol efflux.

Effects of phosphodiesterase-5 inhibitor on ischemic kidney injury during nephron sparing surgery: quantitative assessment by NGAL and KIM-1.

PURPOSE: Interruption of renal blood flow is often necessary during nephron sparing surgery (NSS) and can induce renal injury. This study examines whether tadalafil, a phosphodiesterase-5 (PDE-5) inhibitor and well-known vasodilator, exerts nephroprotective effects in patients undergoing NSS. METHODS: This non-randomized study included 49 patients with enhancing solid renal mass. All patients were subjected to open NSS during which clamping the renal artery was performed. Twenty-two patients were pretreated with tadalafil 1 day prior NSS and 2 days following surgery. The other 27 patients underwent the same surgical procedure but did not receive tadalafil (controls). Urine samples were collected before surgery and following renal pedicle clamp removal. Urine levels of NGAL and KIM-1, two novel biomarkers for acute kidney injury (AKI), were determined. RESULTS: Clamping the renal artery induced kidney dysfunction as reflected by increases in urinary NGAL and KIM-1 in all participants. These increases in urinary NGAL and KIM-1 excretion were evident 1 h after renal ischemia and lasted for 72 and 24 h, respectively. Pretreatment with tadalafil reduced the absolute urinary excretion of KIM-1, but not of NGAL. Although the incidence of AKI was comparable between tadalafil-treated and untreated NSS subjects, the elevation in serum creatinine (SCr) was significantly attenuated in tadalafil-treated group as compared with NSS controls. CONCLUSIONS: Tadalafil exerts nephroprotective effects in AKI following NSS, as was evident by reduced urinary excretion of KIM-1 and attenuation of SCr elevation. Carefully controlled large clinical studies are needed before defining the role of PDE-5 inhibition therapy in these patients.

Arterial elasticity in obese subjects with coronary slow flow phenomenon.

BACKGROUND: Coronary slow flow phenomenon (CSFP) is a functional and structural disease that is diagnosed by coronary angiogram. OBJECTIVES: To evaluate the possible association between CSFP and small artery elasticity in an effort to understand the pathogenesis of CSFP. METHODS: The study population comprised 12 patients with normal coronary arteries and CSFP and 12 with normal coronary arteries without CSFP. We measured conjugated diene formation at 234 nm during low density lipoprotein (LDL) oxidation, as well as platelet aggregation. We estimated, noninvasively, arterial elasticity parameters. Mann-Whitney nonparametric test was used to compare differences between the groups. Data are presented as mean +/- standard deviation. RESULTS: Waist circumference was 99.2 +/- 8.8 cm and 114.9 +/- 10.5 cm in the normal flow and CSFP groups, respectively (P = 0.003). Four patients in the CSFP group and one in the normal flow group had type 2 diabetes. Area under the curve in the oral glucose tolerance test was 22% higher in the CSFP than in the normal group (P = 0.04). There was no difference in systolic and diastolic blood pressure, plasma concentrations of total cholesterol, triglycerides, high density lipoprotein, LDL and platelet aggregation parameters between the groups. Lag time required until initiation of LDL oxidation in the presence of CuSO4 was 17% longer (P = 0.02) and homocysteine fasting plasma concentration was 81% lower (P = 0.05) in the normal flow group. Large artery elasticity was the same in both groups. Small artery elasticity was 5 +/- 1.5 ml/mmHg x 100 in normal flow subjects and 6.1 +/- 1.9 ml/mmHg x 100 in the CSFP patients (P = 0.02). CONCLUSIONS: Patients with CSFP had more metabolic derangements. Arterial stiffness was not increased in CSFP.

Effect of letrozole on plasma lipids, triglycerides, and estradiol in postmenopausal women with metastatic breast cancer.

PURPOSE: The aromatase inhibitor letrozole effectively treats breast cancer by decreasing estrogen levels in postmenopausal women. The aim of this prospective study was to evaluate the effect of letrozole on plasma lipids, triglyceride lipase (TGL), and estradiol levels in women with metastatic breast cancer (MBC). MATERIALS AND METHODS: Fifty-two postmenopausal women with MBC received letrozole, 2.5 mg/day. Blood samples for assessment of plasma levels of total cholesterol (TC), low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol, TGL, and estradiol were taken at baseline and after 3, 6, and 12 months of treatment. RESULTS: A nonsignificant increase was found in TC and HDL cholesterol levels after 3 months, which returned to baseline levels after 6 months (p = .794 and p = .444, respectively). LDL cholesterol increased nonsignificantly after 6 months and returned to baseline thereafter (p = .886). The mean estradiol level was suppressed from 44 pmol/l before treatment to <18 pmol/l after 6 months (p = .014). No difference was found in the estradiol suppression rate whether baseline levels were >40 or <40 pmol/l. CONCLUSION: Letrozole has a safe effect on the lipid and TGL profiles of postmenopausal women with MBC. Estradiol levels were maximally suppressed within 6 months of treatment. The increased levels of TC during treatment were reversible and returned to normal levels after 3 months.

Ezetimibe's effect on platelet aggregation and LDL tendency to peroxidation in hypercholesterolaemia as monotherapy or in addition to simvastatin.

WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT: Statins demonstrate a pleiotropic effect which contributes beyond the hypocholesterolaemic effect to prevent atherosclerosis. WHAT THIS STUDY ADDS: Ezetimibe has an antioxidative effect when given as monotherapy or as an add-on to the statin, simvastatin. AIMS To investigate the effect of lowering low-density lipoprotein-cholesterol (LDL-C) on platelet aggregation and LDL tendency to peroxidation by ezetimibe alone or with simvastatin in hypercholesterolaemia. METHODS: Sixteen patients with LDL-C >3.4 mmol l(-1) received ezetimibe for 3 months (Part I). Twenty-two patients on fixed simvastatin dose with LDL-C >2.6 mmol l(-1) were enrolled (Part II). Part II patients continued simvastatin treatment 20 mg day(-1) for 6 weeks, then received 20 mg day(-1) simvastatin combined with ezetimibe 10 mg day(-1) for another 6 weeks. The tendency of LDL to peroxidation measured by lag time in minutes required for initiation of LDL oxidation and by LDL oxidation at maximal point (plateau) was measured before and after ezetimibe treatment. RESULTS: Part I: Ezetimibe 10 mg daily for 3 months decreased plasma LDL-C level 16% (P = 0.002), prolonged lag time to LDL oxidation from 144 +/- 18 min to 195 +/- 16 min (P < 0.001), decreasing maximal aggregation from 83 +/- 15% to 60 +/- 36% (P = 0.04). Part II: Serum level LDL-C decreased 23% (P = 0.02) and lag time in minutes to LDL oxidation was prolonged from 55.9 +/- 16.5 to 82.7 +/- 11.6 (P < 0.0001) using combined simvastatin-ezetimibe therapy. There were no differences in platelet aggregation. CONCLUSIONS: Ezetimibe was associated with decreased platelet aggregation and LDL tendency to peroxidation. Treatment with ezetimibe in addition to simvastatin has an additive antioxidative effect on LDL.

Orlistat reverse fatty infiltration and improves hepatic fibrosis in obese patients with nonalcoholic steatohepatitis (NASH).

Nonalcoholic steatohepatitis (NASH) may cause progressive hepatic fibrosis, cirrhosis, and hepatocellular carcinoma. Treatment, thus far, has been restricted to diet and weight loss, but without compelling results. In this study we aimed to evaluate the efficacy of orlistat therapy in obese patients with NASH. Fourteen obese patients with NASH underwent liver biopsy prior to and subsequent to 6 months treatment with orlistat (120 mg tid). Hepatic fat extension was graded as normal, mild, moderate, or severe. Hepatic fibrosis was scored on a scale from 0 to 4, with 0 denoting no fibrosis and 4, cirrhosis. Portal inflammation was scored as 0-3, with 0 = normal, 1 = mild, 2 = moderate, and 3 = severe inflammation. Fourteen patients had NASH associated with diabetes, hyperlipidemia, or obesity. Orlistat reduced fatty infiltration in 10 patients (70%; P<0.01), 3 of whom had normal liver fat content after treatment. Orlistat improved inflammatory activity by 2 grades in 28% and by 1 grade in 50% of patients and effected no change in 22% of patients. Five patients (35%) returned to normal inflammatory activity. Orlistat improved hepatic fibrosis by 2 grades in three patients (21%) and by 1 grade in seven patients (50%). There was no change in four patients (28%). Orlistat lowered aminotransferases levels, total cholesterol, triglycerides and low-density lipoprotein, respectively. Insulin resistance index and malonyl dialdehyde levels improved significantly after orlistat therapy, whereas HbAic remained unchanged. In conclusion, in obese patients with NASH, liver fibrosis and inflammation improved after therapy with orlistat.

The beneficial effect of aspirin and enoxaparin on fibrosis progression and regenerative activity in a rat model of cirrhosis.

The aim of this study was to examine the effect of the antithrombotic drugs aspirin and enoxaparin on fibrosis progression and regenerative activity in a rat model of liver cirrhosis and to determine if these two drugs are beneficial in animals with advanced fibrosis or with established cirrhosis undergoing partial hepatectomy. Thioacetamide-induced cirrhotic rats received saline (N=10), aspirin (N=7), or enoxaparin (N=11) for a 5-week treatment period. Hepatic fibrosis was assessed according to METAVIR score. Liver regeneration was monitored using PCNA immunostaining. Compared to untreated cirrhotic controls, a significant improvement in fibrosis grade was observed in the aspirin (43%; chi(2)=54, P<0.001) and enoxaparin (36%; chi(2)=43, P<0.001) treated groups. Postoperatively, total serum bilirubin levels were lower in the aspirin (1.4+/-0.18 mg/dl; P<0.01) and enoxaparin (1.8+/-0.35 mg/dl; P<0.05)-treated groups compared to untreated cirrhotic controls (3.2+/-0.6 mg/dl). Hepatic regenerative activity was significantly improved in the aspirin group (57.3%+/-6.8%, versus 34.2%+/-7.2% in untreated cirrhotic controls; P<0.01) but unchanged in the enoxaparin group. We conclude that aspirin and enoxaparin hold promise as a useful therapy for patients with extensive fibrosis.

Monounsaturated fat decreases hepatic lipid content in non-alcoholic fatty liver disease in rats.

AIM: To evaluate the effects of different types of dietary fats on the hepatic lipid content and oxidative stress parameters in rat liver with experimental non-alcoholic fatty liver disease (NAFLD). METHODS: A total of 32 Sprague-Dawley rats were randomly divided into five groups. The rats in the control group (n = 8) were on chow diet (Group 1), rats (n = 6) on methionine choline-deficient diet (MCDD) (Group 2), rats (n = 6) on MCDD enriched with olive oil (Group 3), rats (n = 6) on MCDD with fish oil (Group 4) and rats (n = 6) on MCDD with butter fat (Group 5). After 2 mo, blood and liver sections were examined for lipids composition and oxidative stress parameters. RESULTS: The liver weight/rat weight ratio increased in all treatment groups as compared with the control group. Severe fatty liver was seen in MCDD + fish oil and in MCDD + butter fat groups, but not in MCDD and MCDD + olive oil groups. The increase in hepatic triglycerides (TG) levels was blunted by 30% in MCDD + olive oil group (0.59 +/- 0.09) compared with MCDD group (0.85 +/- 0.04, P < 0.004), by 37% compared with MCDD + fish oil group (0.95 +/- 0.07, P < 0.001), and by 33% compared with MCDD + butter group (0.09 +/- 0.1, P < 0.01). The increase in serum TG was lowered by 10% in MCDD + olive oil group (0.9 +/- 0.07) compared with MCDD group (1.05 +/- 0.06). Hepatic cholesterol increased by 15-fold in MCDD group [(0.08 +/- 0.02, this increment was blunted by 21% in MCDD + fish oil group (0.09 +/- 0.02)]. In comparison with the control group, ratio of long-chain polyunsaturated fatty acids omega-6/omega-3 increased in MCDD + olive oil, MCDD + fish oil and MCDD + butter fat groups by 345-, 30- and 397-fold, respectively. In comparison to MCDD group (1.58 +/- 0.08), hepatic MDA contents in MCDD + olive oil (3.3 +/- 0.6), MCDD + fish oil (3.0 +/- 0.4), and MCDD + butter group (2.9 +/- 0.36) were increased by 108%, 91% and 87%, respectively (P < 0.004). Hepatic paraoxonase activity decreased significantly in all treatment groups, mostly with MCDD + olive oil group (-68%). CONCLUSION: Olive oil decreases the accumulation of triglyceride in the liver of rats with NAFLD, but does not provide the greatest antioxidant activity.

LDL oxidation is associated with increased blood hemoglobin A1c levels in diabetic patients.

AIM: To investigate whether levels of blood HbA1c in diabetic patients are associated with susceptibility of LDL to oxidation. METHODS: LDL was separated from blood of 40 diabetic patients with known blood glucose and HbA1c levels. The tendency to undergo lipid peroxidation was assessed via lag time required for initiation of LDL oxidation. HbA1c formation was measured in vitro following incubation of red blood cell (RBC) hemolysate for 3 months with increasing concentrations of glucose in the absence or presence of LDL or oxidized LDL. RESULTS: Lag time for copper-induced LDL oxidation was twice as long in normal subjects compared to diabetic patients. Correlation analyses between LDL oxidation lag time and HbA1c blood levels revealed an R value of 0.74. Incubation of RBC hemolysate with high glucose concentration (up to 400 mg/dl) resulted in increased blood HbA1c concentration by up to 107%. Addition of LDL to this hemolysate over a period of 3 months resulted in LDL oxidation and an increase in HbA1c levels by up to 168%. Similarly, addition of oxidized LDL to the hemolysate increased HbA1c by up to 240%. CONCLUSIONS: Increased tendency of LDL to undergo lipid peroxidation in diabetic patients contributes to increased levels of blood HbA1c, mainly in those with HbA1c<7.3.

The changes in renal function after a single dose of intravenous furosemide in patients with compensated liver cirrhosis.

BACKGROUND: Patients with compensated Child-A cirrhosis have sub clinical hypovolemia and diuretic treatment could result in renal impairment. AIM: To evaluate the changes in renal functional mass as reflected by DMSA uptake after single injection of intravenous furosemide in patients with compensated liver cirrhosis. METHODS: Eighteen cirrhotic patients were divided in two groups; eight patients (group 1, age 56 +/- 9.6 yrs, Gender 5M/3F, 3 alcoholic and 5 non alcoholic) were given low intravenous 40 mg furosemide and ten other patients (group 2, age 54 +/- 9.9, Gender 6M/4F, 4 alcoholic and 6 non alcoholic) were given high 120 mg furosemide respectively. Renoscintigraphy with 100MBq Of Tc 99 DMSA was given intravenously before and 90 minutes after furosemide administration and SPECT imaging was determined 3 hours later. All patients were kept under low sodium diet (80mEq/d) and all diuretics were withdrawn for 3 days. 8-hours UNa exertion, Calculated and measured Creatinine clearance (CCT) were performed for all patients. RESULTS: Intravenous furosemide increased the mean renal DMSA uptake in 55% of patients with compensated cirrhosis and these changes persist up to three hours after injection. This increase was at the same extent in either low or high doses of furosemide. (From 12.8% +/- 3.8 to 15.2% +/- 2.2, p < 0.001 in Gr I as compared to 10.6% +/- 4.6 to 13.5% +/- 3.6 in Gr 2, p < 0.001). In 8 patients (45%, 3 pts from Gr 1 and 5 pts from Gr 2) DMSA uptake remain unchanged. The mean 8 hrs UNa excretion after intravenous furosemide was above 80 meq/l and was higher in Gr 2 as compared to Gr 1 respectively (136 +/- 37 meq/l) VS 100 +/- 36.6 meq/l, P = 0.05). Finally, basal global renal DMSA uptake was decreased in 80% of patients; 22.5 +/- 7.5% (NL > 40%), as compared to normal calculated creatinine clearance (CCT 101 +/- 26), and measured CCT of 87 +/- 30 cc/min (P < 0.001). CONCLUSION: A single furosemide injection increases renal functional mass as reflected by DMSA in 55% of patients with compensated cirrhosis and identify 45% of patients with reduced uptake and who could develop renal impairment under diuretics. Whether or not albumin infusion exerts beneficial effect in those patients with reduced DMSA uptake remains to be determined.

Effect of insulin-sensitizing agents in combination with ezetimibe, and valsartan in rats with non-alcoholic fatty liver disease.

AIM: To assess whether treatment with insulin-sensitizing agents (ISAs) in combination with ezetimibe and valsartan have greater effect on hepatic fat content and lipid peroxidation compared to monotherapy in the methionine choline-deficient diet (MCDD) rat model of non-alcoholic fatty liver disease (NAFLD). METHODS: Rats (n = 6 per group) were treated with different drugs, including MCDD only, MCDD diet with either metformin (200 mg/kg), rosiglitazone (3 mg/kg), metformin plus rosiglitazone (M+R), ezetimibe (2 mg/kg), valsartan (2 mg/kg), or combination of all drugs for a total of 15 wk. Liver histology, lipids, parameters of oxidative stress and TNF-alpha were measured. RESULTS: Fatty liver (FL) rats demonstrated severe hepatic fatty infiltration (> 91% fat), with an increase in hepatic TG (+ 1263%, P < 0.001), hepatic cholesterol (+ 245%, P < 0.03), hepatic MDA levels (+ 225%, P < 0.001), serum TNF-alpha (17.8 +/- 10 vs 7.8 +/- 0.0, P < 0.001), but a decrease in hepatic alpha tocopherol (-74%, P<0.001) as compared to the control rats. Combination therapy with all drugs produced a significant decrease in liver steatosis (-54%), hepatic TG (-64%), hepatic cholesterol (-31%) and hepatic MDA (-70%), but increased hepatic alpha tocopherol (+ 443%) as compared to FL rats. Combination therapy with ISA alone produced a smaller decrease in liver steatosis (-32% vs -54%, P < 0.001) and in hepatic MDA levels (-55% vs -70%, P < 0.01), but a similar decrease in hepatic lipids when compared with the all drugs combination. TNF-alpha levels decreased significantly in all treatment groups except in ISA group. CONCLUSION: Combination therapies have a greater effect on liver fat content as compared to monotherapy. Rosiglitazone appears to improve hepatic steatosis to a greater extent than metformin.

Serum CA125: a tumor marker for monitoring response to treatment and follow-up in patients with non-Hodgkin's lymphoma.

PURPOSE: Serum CA125 is an important prognostic factor in patients with non-Hodgkin's lymphoma (NHL). Elevation of CA125 level correlates with advanced disease, poor response to treatment, and poor survival rates. The aim of the current study is to evaluate CA125 levels in patients with NHL and to investigate the correlations between high CA125 level and other presenting features. MATERIALS AND METHODS: Thirty-eight patients (14 with low-grade and 24 with aggressive histologically proven NHL) were studied prospectively. Serum CA125 assessment was done at diagnosis, during treatment, and at follow-up. The associations between CA125 levels and other presenting features were examined. RESULTS: CA125 levels were elevated in 43% of patients with low-grade NHL and in 46% of patients with aggressive NHL (i.e., 45% of all patients). A higher CA125 level was associated with advanced disease, bone marrow involvement, extranodal involvement, poor performance status, the presence of B symptoms, and high serum lactate dehydrogenase level. Complete responses occurred in 86% of patients with normal CA125 levels and in 59% of patients with elevated CA125 levels. In both low-grade and aggressive NHL, the estimated 5-year overall survival rate was higher in patients with normal CA125 levels than in patients with elevated CA125 levels (88% versus 50% and 70% versus 27%, respectively). CONCLUSION: High serum CA125 is an important prognostic factor in NHL and correlates with more advanced disease, low response rates, and worse survival. CA125 measurements may be used for staging, monitoring response to treatment, and follow-up of patients with NHL.