Serum cystatin C concentration as an independent marker for hypertensive left ventricular hypertrophy

Background Serum cystatin C levels can be used to predict morbidity and mortality in patients with cardiovascular disease. However, the clinical relevance of serum cystatin C levels in patients with hypertensive left ventricular hypertrophy (LVH) has rarely been investigated. We designed the present study to investigate whether serum cystatin C levels are associated with cardiac structural and functional alterations in hypertensive patients. Methods We enrolled 823 hypertensive patients and classified them into two groups: those with LVH (n = 287) and those without LVH (n = 536). All patients underwent echocardiography and serum cystatin C testing. We analyzed the relationship between serum cystatin C levels and LVH. Results Serum cystatin C levels were higher in hypertensive patients with LVH than in those without LVH (P < 0.05). Using linear correlation analysis, we found a positive correlation between serum cystatin C levels and interventricular septal thickness (r = 0.247, P < 0.01), posterior wall thickness (r = 0.216, P < 0.01), and left ventricular weight index (r = 0.347, P < 0.01). When analyzed by multiple linear regression, the positive correlations remained between serum cystatin C and interventricular septal thickness (β = 0.167, P < 0.05), posterior wall thickness (β = 0.187, P < 0.05), and left ventricular weight index (β = 0.245, P < 0.01). Conclusion Serum cystatin C concentration is an independent marker for hypertensive LVH.     

Role of TGF-β1/Smads pathway in carotid artery remodeling in renovascular hypertensive rats and prevention by Enalapril and Amlodipine

Objective To investigate the role of transforming growth factor-β1 (TGF-β1), Smad2/3 and Smad7 expressions in carotid artery remodeling in renovascular hypertensive rats, and also the therapeutic effect of Enalapril and Amlodipine. Methods The renovascular hypertensive rat (RHR) models with “two-kidney and one-clip” were established, including model group (n = 6), sham-operated group (n = 6), Enalapril group (10 mg/kg per day, n = 6), Amlodipine group (5 mg/kg per day, n = 6) and combination group (Amlodipine 2.5 mg/kg per day + Enalapril 5mg/kg per day, n = 6). The medication were continuous administrated for six weeks. Carotid artery morphological and structural changes in the media were observed by HE staining, Masson staining and immuno histochemical staining. Media thickness (MT), MT and lumen diameter ratio (MT/LD), and the expression levels of media α-smooth muscle actin (α-actin), proliferating cell nuclear antigen (PCNA), TGF-β1, phosphorylated Smad2/3 (p-Smad2/3) and Smad7 in carotid arteries were measured. Results The media of carotid arteries in RHR model group was significantly thickened, the volume of smooth muscle cell was increased, and the array was in disorder; MT, MT/LD, the proliferation index of smooth muscle cell and collagen fiber area percentage of carotid arteries in the model group were significantly higher than those in the sham-operated group (P < 0.01). Compared to sham-operated group, the model group had significantly higher expressions of TGF-β1 and p-Smad2/3 (P < 0.05) and lower Smad7 expression. Both Enalapril and Amlodipine improved smooth muscle hypertrophy and collagen deposition, reduced RHR carotid MT, MT/LD, proliferation index of smooth muscle cell, collagen fiber area percentage and the expressions of TGF-β1 and p-Smad2/3 (P < 0.05), increased Smad7 expression (P < 0.05). Moreover, the combination treatment of Enalapril and Amlodipine had significantly better effects than single Amlodipine group (P < 0.05), but not single Enalapril group. Conclusions TGF-β1/Smads pathway may participate in the mechanism of carotid artery remodeling in RHR; the role of Amlodipine and Enalapril in inversing carotid artery remodeling may be related to the change of TGF-β1/Smads pathway, the combination treatment of Amlodipine and Enalapril had better effects than single administration of Amlodipine.     

Blast-derived microvesicles in sera from patients with acute myeloid leukemia suppress natural killer cell function via membrane-associated transforming growth factor-beta1

Background

Natural killer cell cytotoxicity is decreased in patients with acute myeloid leukemia in comparison to that in normal controls. Tumor-derived microvesicles present in patients’ sera exert detrimental effects on immune cells and may influence tumor progression.

Design and Methods

We investigated the microvesicle protein level, molecular profile and suppression of natural killer cell activity in patients with newly diagnosed acute myeloid leukemia.

Results

The patients’ sera contained higher levels of microvesicles compared to the levels in controls (P<0.001). Isolated microvesicles had a distinct molecular profile: in addition to conventional microvesicle markers, they contained membrane-associated transforming growth factor-β1, MICA/MICB and myeloid blasts markers, CD34, CD33 and CD117. These microvesicles decreased natural killer cell cytotoxicity (P<0.002) and down-regulated expression of NKG2D in normal natural killer cells (P<0.001). Sera from patients with acute myeloid leukemia contained elevated levels of transforming growth factor-β, and urea-mediated dissociation of microvesicles further increased the levels of this protein. Neutralizing anti-transforming growth factor-β1 antibodies inhibited microvesicle-mediated suppression of natural killer cell activity and NKG2D down-regulation. Interleukin-15 protected natural killer cells from adverse effects of tumor-derived microvesicles.

Conclusions

We provide evidence for the existence in acute myeloid leukemia of a novel mechanism of natural killer cell suppression mediated by tumor-derived microvesicles and for the ability of interleukin-15 to counteract this suppression.     

Serum Paraoxonase 1 Activity Status in Patients with Liver Disorders

Background/Aim:

Paraoxonase 1 (PON1) is an esterase, exclusively synthesized by liver. The present study has two objectives: to determine the PON1 activity status in various disorders associated with hepatocellular damage and to correlate the changes of PON1 activity with the standard liver function and fasting lipid profile tests in these disorders.

Patients and Methods:

The study groups consisted of 95 patients with liver diseases including acute viral hepatitis (14), cirrhosis with portal hypertension (33), leptospirosis (14), sepsis and multi organ failure (15), left ventricular failure (9), and falciparum malaria (10); and 53 healthy controls. Serum PON1 activity was measured manually using spectrophotometer. Liver function test parameters and fasting lipid profile were performed in clinical chemistry auto analyzer (Hitachi 912).

Results:

The serum PON1 activity in patients with acute viral hepatitis and sepsis decreased significantly (P<0.001) and moderately in falciparum malaria (P<0.05). However, in patients with cirrhosis, leptospirosis and left ventricular patients, its activity did not change significantly. On applying Pearson correlation, serum PON1 activity correlated positively with high-density lipoprotein-cholesterol (HDL-C) in patients with sepsis (r=0.633, P<0.05), left ventricular failure patients (r=0.814, P<0.05) and negatively with acute viral hepatitis patients (r=– 0.528, P<0.05).

Conclusion:

PON1 activity has decreased significantly in acute viral hepatitis, sepsis with multi organ failure and falciparum malaria patients. Determination of PON1 activity may serve as a useful additional test in assessing these conditions.     

Age and outcomes of primary percutaneous intervention for ST elevation myocardial infarction in a tertiary center—are we there yet?

Background Primary percutaneous intervention (PPCI) is the treatment of choice for ST elevation myocardial infarction (STEMI) but robust evidence in the very elderly is lacking. We compared PPCI outcomes between different age quartiles (quartile 1 < 60 years, quartile 2 ≥ 60 to < 70 years, quartile 3 ≥ 70 to < 80 years, quartile 4 ≥ 80 years). Methods Retrospective observational analysis of our Morriston Tertiary Cardiac Centre (Abertawe Bro Morgannwg University Health Board) patients from 2005 to 2010 with STEMI who underwent PPCI. Results Of 434 patients, 57 (13%) were in quartile 4 (≥ 80 years). In older age quartiles, patients were less likely to receive a drug eluting stent (DES, P = 0.001) or glycoprotein IIb/IIIa inhibitor (GPI, P < 0.0001). Increase in age was associated with reduced time to survival (β-coefficient: -0.192, t: -3.70, 95%CI: -4.91 to -1.50, P < 0.0001) as was the presence of cardiogenic shock (β-coefficient: -0.194, t = 3.77, 95%CI: -5.26 to -1.65, P < 0.0001). Use of GPI was associated with increased time to survival (β-coefficient: 0.138, t = 2.82, 95%CI: 1.58–8.58, P = 0.005) but older age quartiles were less likely to receive GPI (P < 0.0001). In-hospital mortality (1.8% quartile 1, 3.6% quartile 2, 10.9% quartile 3 and 12.3% quartile 4, P = 0.002) and 1-year mortality (5.4% quartile 1, 5.5% quartile 2, 16.8% quartile 3 and 24.6% quartile 4, P < 0.0001, respectively) was significantly higher in older age quartiles. Conclusions Increased short term and intermediate term mortality is seen in the very elderly after PPCI. Age and cardiogenic shock were prognostic factors. Intervention should not be based on age alone and awareness regarding prognostic factors can help improve management.     

Is β-cell failure in type 2 diabetes mellitus reversible?

BACKGROUND:

In the UK Prospective Diabetes Study (UKPDS), many subjects maintained glycemic goal (HbA_1c < 7.0%) at 9 years, showing that β-cell function was preserved and that the initial decline in β-cell function recovered with sulphonylureas. Moreover, obese subjects using high daily doses of insulin for several years rarely require insulin or oral hypoglycemic agents to maintain their glycemic goal following weight loss achieved by gastric bypass surgery. Thus, declining β-cell function during the course of type 2 diabetes mellitus (T2DM) is neither universal nor permanent.

OBJECTIVE:

To assess β-cell function in morbidly obese subjects before insulin withdrawal and on attaining the glycemic goal with weight loss and oral agents.

MATERIALS AND METHODS:

Serum C-peptide (CPEP) and glucose (G) concentrations were determined up to 180 min during an oral glucose tolerance test (OGTT) with 75 glucose in 10 obese men with T2DM, before insulin withdrawal, and on achieving the glycemic goal with metformin, glimepiride, and weight loss. Ten age-matched healthy men participated as controls. Cumulative responses (CR) of CPEP and G were calculated by adding differences between the level at each time-period during OGTT and fasting (F) concentration. β-Cell function was expressed as the FCPEP as well as the insulinogenic index (CRCPEP/CRG). Insulin sensitivity was determined as FCEP × FG.

RESULTS:

FCPEP was decreased, though still present, prior to insulin withdrawal. Moreover, on attaining the glycemic goal over 6-9 months, FCPEP, CRPEP/CRG, and FCPEP × FG improved markedly (P < 0.001).

CONCLUSION:

Decline in β-cell function in morbidly obese T2DM may not be progressive and is reversible on improving insulin sensitivity and on eliminating the inhibition by exogenous insulin.     

Low density lipoprotein cholesterol level inversely correlated with coronary flow velocity reserve in patients with Type 2 Diabetes

Objectives To evaluate the association of coronary artery endothelial function and plasma levels of low density lipoprotein cholesterol (LDL-C) and high density lipoprotein cholesterol (HDL-C) in patients with Type 2 Diabetes Mellitus (DM). Methods We investigated 90 participants from our institution between October 2007 to March 2010: non-DM (n = 60) and DM (n = 30). As an indicator of coronary endothelial dysfunction, we used non-invasive Doppler echocardiography to quantify coronary flow velocity reserve (CFVR) in the distal part of the left descending artery after rest and after intravenous adenosine administration. Results Plasma level of LDL-C was significantly higher in patients with DM than in non-DM (3.21±0.64 vs. 2.86±0.72 mmo/L, P < 0.05), but HDL-C level did not differ between the groups (1.01 ± 0.17 vs. 1.05 ± 0.19 mmo/L). Furthermore, the CFVR value was lower in DM patients than non-diabetics (2.45 ± 0.62 vs. 2.98 ± 0.68, P < 0.001). Plasma levels of LDL-C were negatively correlated with CFVR in all subjects (r = -0.35, P < 0.001; 95% confidence interval (CI): -0.52 - -0.15) and in the non-DM (r = -0.29, P < 0.05; 95% CI:-0.51 - -0.05), with an even stronger negative correlation in the DM group (r = -0.42, P < 0.05; 95% CI:-0.68 - -0.06). Age (β = 0.019, s = 0.007, sβ = -0435, 95% CI: -0.033 - -0.055, P = 0.008), LDL-C (β = -0.217, s = 0.105,sβ= -0.282, 95% CI: -0.428 - -0.005, P = 0.045) remained independently correlated with CFVR in the DM group. However, we found no correlation between HDL-C level and CFVR in any group. Conclusions Diabetes may contribute to coronary artery disease (CAD) by inducing dysfunction of the coronary artery endothelium. Increased LDL-C level may adversely impair coronary endothelial function in DM. HDL-C may lose its endothelial-protective effects, in part as a result of pathological conditions, especially under abnormal glucose metabolism.     

High sensitivity C-reactive protein, tumor necrosis factor-α, interleukin-6, and vascular cell adhesion molecule-1 levels in Asian Indians with metabolic syndrome and insulin resistance (CURES-105)

Aim

The aim of this study was to assess levels of high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and vascular cell adhesion molecule-1 (VCAM-1) in South Indian subjects with and without MS and among MS subjects with and without insulin resistance (IR).

Methodology

From the population-based Chennai Urban Rural Epidemiology Study, 334 subjects with MS and 342 subjects without MS were selected. Metabolic syndrome was diagnosed based on modified National Cholesterol Education Program criteria. High-sensitivity C-reactive protein, TNF-α, IL-6, and VCAM-1 were measured by enzyme-linked immunosorbent assay. Insulin resistance was calculated using the homeostasis model assessment (HOMA-IR) using the following formula: fasting insulin (µIU/ml) × fasting glucose (mmol/liter)/22.5.

Results

Subjects with MS had significantly higher levels of all four inflammatory markers compared to those without MS: hs-CRP (2.57 vs 2.19 mg/liter) (p < .05), TNF-α (4.47 vs 3.89 pg/ml) (p < .05), IL-6 (16.22 vs 10.96 pg/ml) (p < .05), and VCAM-1 (13.8 vs 7.94 pg/ml) (p < .05). In the total study subjects, hs-CRP (r = 0.089, p = .047), TNF-α (r = 0.113, p = .040), IL-6 (r = 0.176, p = .042), and VCAM-1 (r = 0.230, p = .06) were significantly correlated with MS. With increasing quartiles of IR, mean levels of hs-CRP (p for trend <.001) and TNF-α (p for trend <.05) increased linearly. MS subjects with IR had higher levels of hs-CRP (p < .001) and TNF-α (p < .05) compared to MS subjects without IR.

Conclusion

In Asian Indians, inflammatory cytokines hs-CRP, TNF-α, IL-6, and VCAM-1 are elevated in subjects with MS while hs-CRP and TNF-α are further elevated in those with MS and IR.     

Evaluation of cardiovascular risk in patients with Parkinson disease under levodopa treatment

Background Levodopa is the indispensable choice of medial therapy in patients with Parkinson disease (PD). Since L-dopa treatment was shown to increase serum homocysteine levels, a well-known risk factor for cardiovascular disorders, the patients with PD under L-dopa treatment will be at increased risk for future cardiovascular events. The objective of this study is to evaluate cardiovascular risk in patients with PD under levodopa treatment. Methods The study population consisted of 65 patients with idiopathic PD under L-dopa treatment. The control group included 32 age and gender matched individuals who had no cognitive decline. Echocardiographic measurements, serum homocysteine levels and elastic parameters of the aorta were compared between the patients with PD and controls. Results As an expected feature of L-dopa therapy, the Parkinson group had significantly higher homocystein levels (15.1 ± 3.9 μmol/L vs. 11.5 ± 3.2 μmol/L, P = 0.02). Aortic distensibility was significantly lower in the patients with PD when compared to controls (4.8 ± 1.5 dyn/cm² vs. 6.2 ± 1.9 dyn/cm², P = 0.016). Additionally, the patients with PD had higher aortic strain and aortic stiffness index (13.4% ± 6.4% vs. 7.4% ± 3.6%, P < 0.001 and 7.3 ± 1.5 vs. 4.9 ± 1.9, P < 0.001, respectively). Furthermore, serum homocysteine levels were found to be positively correlated with aortic stiffness index and there was a negative correlation between aortic distensibility and levels of serum homocysteine (r = 0.674, P < 0.001; r = -0.602, P < 0.001, respectively). Conclusions The patients with PD under L-dopa treatment have increased aortic stiffness and impaired diastolic function compared to healthy individuals. Elevated serum homocysteine levels may be a possible pathophysiological mechanism.     

A comparative evaluation of safety and efficacy of rosuvastatin, simvastatin, and atorvastatin in patients of type 2 diabetes mellitus with dyslipidemia

AIM:

To evaluate and compare the safety and efficacy of rosuvastatin, simvastatin, and atorvastatin in patients of type 2 diabetes mellitus with dyslipidemia.

MATERIALS AND METHODS:

This open-label, randomized, parallel group, comparative, prospective study of 12-weeks duration included 60 patients of type-2 diabetes with dyslipidemia having good glycemic control with fixed dose combination of tablet glimepiride + metformin and divided into three groups of twenty each. Group-1 patients have received tablet rosuvastatin 10 mg once daily, group-2 received tablet atorvastatin 10 mg once daily, and group-3 received tablet simvastatin 10 mg once daily for 12 weeks each. The levels of serum cholesterol, serum triglyceride, LDL, VLDL, and HDL were assessed at baseline and at the end of 12 weeks.

RESULTS:

The mean serum cholesterol, serum triglyceride, LDLc, and VLDLc levels were significantly reduced on therapy (P<0.001). Simultaneously, the mean levels of HDL were highly significantly increased (P<0.001) after therapy for 12 weeks with rosuvastatin, atorvastatin, and simvastatin. Reduction of LDL levels in rosuvastatin group was statistically significant when compared with those of simvastatin group (P< 0.05) but was statistically nonsignificant when compared with atorvastatin group (P> 0.05). Conclusion: 10 mg of rosuvastatin was comparable to 10 mg of atorvastatin and more efficacious than 10 mg simvastatin in reducing LDL levels after 12 weeks of therapy in patients of type 2 diabetes mellitus with dyslipidemia.     

Clinical Relevance of Serum Vascular Endothelial Growth Factor and Interleukin-6 in Patients With Colorectal Cancer

Background/Aim:

Some biological factors play a role in stimulation of malignant growth, metastasis and angiogenesis; however, their clinical relevance has not yet been well established for most of them. This work was aimed at studying the clinical relevance of serum vascular endothelial growth factor (VEGF) and interleukin -6 (IL-6), in patients with colorectal cancer (CRC).

Materials and Methods:

Preoperative serum levels of VEGF and IL-6 were measured by enzyme -linked immuno -assay in 35 CRC patients and in 30 healthy controls.

Results:

CRC patients with or without metastasis had significantly higher VEGF and IL-6 levels than healthy controls (all P < 0.001). Patients with advanced clinical stage had significantly higher levels of VEGF and IL-6 than those with early clinical stage (all P < 0.001). Also, patients with metastatic disease had significantly higher VEGF and IL-6 levels than those with localized disease (all P < 0.001). The diagnostic accuracy for invasiveness was 83% for VEGF (cut off value = 240 pg/ml) and 66% for IL-6 (cut off value = 6.7 pg/ml), with sensitivity 79% and 74% and specificity 68% and 59%, respectively.

Conclusion:

In CRC patients, preoperative measurement of serum VEGF and Il-6 may prove useful non-invasive diagnostic indicators associated with advanced clinical stage and tumor metastasis that warrants further investigations.     

Continued improvement in myocardial T2* over two years of deferasirox therapy in β-thalassemia major patients with cardiac iron overload

Background

The efficacy of cardiac iron chelation in transfusion-dependent patients has been demonstrated in one-year prospective trials. Since normalization of cardiac T2* takes several years, the efficacy and safety of deferasirox was assessed for two years in patients with β-thalassemia major in the cardiac sub-study of the EPIC trial.

Design and Methods

Eligible patients with myocardial T2* greater than 5 to less than 20 ms received deferasirox, with the primary endpoint being the change in T2* from baseline to two years.

Results

Baseline myocardial T2* was severe (>5 to <10 ms) in 39 patients, and moderate-to-mild (10 to <20 ms) in 62 patients. Mean deferasirox dose was 33.1±3.7 mg/kg/d in the one-year core study increasing to 36.1±7.7 mg/kg/d during the second year of treatment. Geometric mean myocardial T2* increased from a baseline of 11.2 to 14.8 ms at two years (P<0.001). In patients with moderate-to-mild baseline T2*, an increase was seen from 14.7 to 20.1 ms, with normalization (≥20 ms) in 56.7% of patients. In those with severe cardiac iron overload at baseline, 42.9% improved to the moderate-to-mild group. The incidence of drug-related adverse events did not increase during the extension relative to the core study and included (≥5%) increased serum creatinine, rash and increased alanine aminotransferase.

Conclusions

Continuous treatment with deferasirox for two years with a target dose of 40 mg/kg/d continued to remove iron from the heart in patients with β-thalassemia major and mild, moderate and severe cardiac siderosis. (Clinicaltrials.gov identifier: {"type":"clinical-trial","attrs":{"text":"NCT 00171821","term_id":"NCT00171821"}}NCT 00171821)     

Serum levels of homocysteine in mice with malignant tumours

BACKGROUND:

Oxygen radicals and malondialdehyde (MDA) are tumourigenic. Homocysteine generates oxygen radicals. The possibility exists that hyperhomocysteinemia is a risk factor for cancer.

OBJECTIVE:

To investigate if serum levels of homocysteine and MDA are elevated in mice with malignant tumours.

METHODS:

Levels of serum homocysteine and MDA were estimated in 22 control and 22 tumour-bearing Balb/c mice.

RESULTS:

Serum homocysteine levels in control and tumour-bearing mice were 3.01±0.26 μmol/L and 4.05±0.46 μmol/L, respectively. The serum levels of MDA were 6.23±0.72 nmol/mL and 11.60±1.72 nmol/mL, respectively, in control and tumour-bearing mice.

CONCLUSION:

These results suggest that cancer in mice is associated with an increase in serum levels of homocysteine and the lipid peroxidation product MDA. It is, however, not known if this rise in homocysteine and MDA is due to cancer or if this rise causes cancer.     

Effect of Interferon Treatment on Hearing of Patients with Chronic Hepatitis C

Background/Aim:

Some reports in the literature have linked interferon therapy for the treatment of hepatitis C (HCV) with hearing loss. The aim of this study has been to examine the effects of interferon therapy on hearing of patients treated for HCV.

Patients and Methods:

Patients were recruited according to preset inclusion criteria from two centers. All patients received standard dose pegylated interferon (PEG-IFN α-2b or α-2a) plus ribavirin (RBV). All patients had pure-tone audiometry (PTA), tympanogram and distortion-product otoacoustic emission (DPOAE) before treatment, three months after initiation of treatment, and three months after completion of treatment.

Results:

Twenty one patients were prospectively recruited. The mean age was 45.7 years. The male to female ratio was 1.1:1. The mean PTA was 15.9 ± 5.3 before treatment, 17.4 ± 6.1 during treatment and 16.5 ± 5.1 after treatment. The differences between pre and mid, pre and post, as well as mid and post were not significantly different (P>0.05) in all audiological assessments.

Conclusions:

Our results indicate that PEG-IFN\RBV therapy does not have any impact on the hearing thresholds of patients with HCV.     

Protective effect of intermittent clamping of the portal triad in the rat liver on liver ischemia-reperfusion injury

Background

Intermittent clamping (IC) of the portal triad is an effective method of protecting the liver from ischemia-reperfusion injury (IR). In clinical practice, this method is employed during a resection, but its mechanism is still not clear.

Objectives

To evaluate the effect of IC on rat liver and determine its mechanisms.

Materials and Methods

Wistar rats were submitted to 60-min IC (cycles of 12-min clamping followed by 4-min reperfusion), and the samples were collected after 1, 6, and 72 hrs of reperfusion. We determined the serum activity of alanine aminotransferase (ALT), and measured the concentration of TNF-α, malondialdehyde (MDA) and myeloperoxidase (MPO) in liver homogenates. The apoptosis of hepatocytes was evaluated immunohistochemically.

Results

When compared to the IR rats, the activity of ALT decreased in the IC group in all periods of observation (the highest decrease of ~48% after 1 hr of reperfusion). When compared to the IR group, a statistically significant decrease (p < 0.05) in the TNF-α concentration (~33%) in the IC rats occurred only after 1 hr of reperfusion, and it was accompanied by a decrease in the MPO concentration after 1 and 6 hrs of reperfusion. IC reduces the effects of reactive oxygen species (ROS) activity, which has been confirmed by a statistically significant decrease in MDA concentration by 25%-35% in all studied periods. The limitation of hepatocytes apoptosis due to IC occurs in the early (~26%; p < 0.05) and late (~45%; p < 0.01) phases of reperfusion.

Conclusions

The use of IC in early phase of reperfusion brings about a decrease in TNF-α release, which can be related to liver injury due to neutrophil infiltration and apoptotic cell reduction. It seems that the reduction of lipid peroxidation may also limit the liver injury.     

Use of the Platelet Count/Spleen Diameter Ratio for the Noninvasive Diagnosis of Esophageal Varices in Patients with Schistosomiasis

Background/Aim:

In patients with liver cirrhosis, the platelet count/spleen diameter ratio has been validated as a parameter for the noninvasive diagnosis of esophageal varices. Schistosoma infection is a frequent cause of portal hypertension in Middle Eastern countries, and is associated with the development of esophageal varices. In this study we aimed to evaluate the platelet count/spleen diameter ratio as a noninvasive tool for the prediction of the presence of esophageal varices in patients with schistosoma-related chronic liver disease.

Patients and Methods:

Forty-three patients with hepatosplenic schistosomiasis underwent upper digestive endoscopy to check for the presence of esophageal varices. Furthermore, all patients underwent abdominal ultrasonography, and maximum spleen diameter (in mm) was measured. The platelet count/spleen diameter ratio was calculated in all patients.

Results:

Esophageal varices were found in 31 patients (72%). Age and gender were not significantly different between patients with and without varices. In patients with varices, median platelet count (82,000/μL versus 172,000/μL, P < 0.0001) and platelet count/spleen diameter ratio (571 versus 1651, P < 0.0001) were significantly lower, while spleen diameter (147 mm versus 109 mm, P = 0.0006) was significantly larger. In multivariate analysis, the platelet count/spleen diameter ratio was the only parameter independently associated with the presence of varices (P < 0.0001).

Conclusions:

In this study we have validated the use of the platelet count/spleen diameter ratio for the noninvasive diagnosis of esophageal varices in patients with portal hypertension caused by schistosoma infection. In these patients, the platelet count/spleen diameter ratio might be used to allow better rationalization of medical resources and use of endoscopy.     

Association between serum adipocytokine levels and microangiopathies in patients with type 2 diabetes mellitus

Aims/Introduction

It is thought that adipocytokines contribute to the increased risk of vascular complications in type 2 diabetes. However, there is still limited information on the relationship between microangiopathies and adipocytokines, such as adiponectin, leptin and tumor necrosis factor‐α (TNF‐α) in patients with type 2 diabetes.

Materials and Methods

The present study examined the relationship between fasting serum adiponectin, leptin, and TNF‐α levels and microangiopathies in Korean type 2 diabetes. A total of 153 patients were recruited and evaluated for diabetic nephropathy, retinopathy and neuropathy. Serum adiponectin, TNF‐α and leptin levels were measured.

Results

Serum adiponectin levels were significantly lower in patients with nephropathy than in those without nephropathy (P = 0.017), and were significantly higher in patients with retinopathy or neuropathy than those without retinopathy or neuropathy (P = 0.01 and P = 0.002, respectively). The mean levels of leptin were significantly higher in patients with neuropathy than in those without neuropathy (P = 0.002). The mean levels of TNF‐α were not significantly different according to any of the three microangiopathies. Multivariate logistic regression analysis showed that the odds ratio for the presence of neuropathy in the highest tertile of adiponectin was 4.3 (95% confidence interval 1.59–11.62), as compared with the patients in the lowest tertile of adiponectin level.

Conclusions

Levels of adipocytokines were significantly different according to the presence of each microangiopathy. In particular, higher serum adiponectin was independently associated with increased odds for the presence of neuropathy. Future prospective studies with larger numbers of patients are required to establish a direct relationship between plasma adipocytokine concentrations and the development or severity of diabetic microangiopathies.     

Comparison of adverse effects related to pegylated interferon-based therapy for patients with chronic hepatitis B and chronic hepatitis C in Taiwan

Purpose

Pegylated interferon (Peg-IFN)-based therapy is effective in treating chronic hepatitis B (CHB) and C (CHC) but frequently induces adverse events (AEs). This study was conducted to compare the incidence of Peg-IFN-based therapy-associated AEs in Taiwanese patients with CHB and CHC.

Methods

Fifty-six patients with CHB and 103 age-, sex- and treatment duration-matched patients with CHC were enrolled. Patients with CHB were treated with Peg-IFN-α-2a 180 μg/week for 24 weeks (HBeAg⁺, n = 31) or 48 weeks (HBeAg⁻, n = 25); patients with CHC were treated with Peg-IFN-α-2a 180 μg/week plus ribavirin 1,000–1,200 mg/day for 24 weeks (genotype 2/3, n = 57) or 48 weeks (genotype 1, n = 46).

Results

Significantly higher incidences of Peg-IFN-related AEs, especially neuropsychiatric symptoms, and ribavirin-associated skin manifestations were observed in patients with CHC compared with those with CHB, with either the 24- or 48-week regimen. Frequencies of laboratory abnormalities, except for anemia, were comparable in both groups. Neither group showed overt hepatic decompensation. Frequency of dose reduction was similar between the groups. Substantially higher rates of early termination and severe AEs were observed in patients with CHC.

Conclusions

Patients with CHB treated with Peg-IFN had fewer AEs than patients with CHC treated with Peg-IFN/ribavirin. All patients were treated safely.