Hepatic dysfunction in patients with extrahepatic portal venous obstruction

Background: Extrahepatic portal venous obstruction (EHPVO) developing due to thrombotic occlusion of the portal vein in children is generally considered a benign disease. Whether hepatic dysfunction develops in these patients in the absence of a gastrointestinal bleed has not been well studied. Materials and methods: Forty‐three patients with EHPVO who had not bled in the last 3 months were studied. Patients were divided into those with (group I) or without ascites (group II). Matched cirrhotic patients with ascites (group III) served as controls. Clinical, biochemical, ultrasonographic, and histopathological evaluation was carried out. Portal biliopathy was assessed in five patients in group I and in 12 patients in group II by cholangiography. Results: Of 43 EHPVO patients, ascites was seen in nine (21%) patients (group I). Thirty‐four patients had no ascites (group II). Serum ALT (54±24 vs. 34±10 IU/l, P<0.01), albumin (3.2±0.3 vs. 3.7±0.4 g/dl, P<0.01), and prothrombin time difference (9.0±4.5 vs. 2.4±1.9 s, P<0.05) were deranged in patients in group I compared with group II. Patients in group I were 4 years older, and the duration of portal hypertension was longer than in group II (11.5 vs. 5.6 year, P<0.05). Portal biliopathy changes were significantly more severe in group I than in group II patients. Ascites was high gradient in all the patients in group I and the serum‐ascitic albumin gradient was comparable between groups I and III. None of the EHPVO patients, but four cirrhotic patients, developed spontaneous bacterial peritonitis during a follow‐up of 11±4 months. Conclusions: Hepatic dysfunction in the form of ascites and deranged liver functions is not uncommon in patients with EHPVO, more so in patients with prolonged portal hypertension. Based on our data it would be worthwhile to study whether prolonged portal vein thrombosis in EHPVO patients could lead to progressive liver disease.     

Iron stores,response to α-interferon therapy,and effects of iron depletion in chronic hepatitis C

Abstract: We studied 81 patients with chronic hepatitis C to investigate the relationship between iron and α-interferon response. Sixty-one patients (group A) were given α-interferon irrespective of iron status, whereas 20 (group B) with iron overload, were iron depleted before α-interferon therapy. In group A, 21 patients responded to α-interferon and 40 were non-responders. Increased iron indices were significantly more frequent in non-responders than responders. Multivariate analysis showed that among the independent variables evaluated, only γ-GT and liver iron concentration predicted therapy outcome. After phlebotomy treatment, serum alanine aminotransferase fell significantly both in patients of group B (196±122 IU/1 vs 82±37 IU/1, p<10^-6) and in 12 non-responders of group A (198±89 IU/1 vs 107±81 IU/1, p<10^-6). In 16 iron depleted patients, eight from each group, subsequent treatment with α-interferon produced a response in only one patient. These results suggest that increased liver iron is a negative prognostic factor for a-interferon response in chronic hepatitis C. Iron depletion had a beneficial effect on serum alanine aminotransferase in all the patients treated, but did not improve the response to α-interferon.     

Cardiac catheterization in patients with end‐stage liver disease: Safety and outcomes

Introduction : Patients with end‐stage liver disease (ESLD) awaiting transplant are at increased risk of bleeding. Nevertheless, these patients routinely undergo cardiac catheterization for various indications. Safety and outcomes of cardiac catheterization in these patients are not well reported. Methods : In a case–control study 43 patients with ESLD who underwent angiography for liver transplant work‐up were compared to 43 age and gender‐matched controls with no liver dysfunction. In‐hospital outcomes and procedural variables were compared. Results : Patients with ESLD had a lower baseline hemoglobin (12.1 ± 2.1 vs. 13.7 ± 1.8, P < 0.0005), lower platelet counts (86.8 ± 66 vs. 247 ± 80, P < 0.0001) and higher international normalized ratio (INR) (1.4 ± 0.2 vs. 1.1 ± 0.2, P < 0.0001) than controls. Among ESLD group, five (11.6%) patients received platelet transfusions, one received blood transfusion, and three patients (7%) with INR > 1.6 received fresh frozen plasma (FFP) compared with none in the control group. Smaller size (four French) vascular sheaths were used more frequently in the group with ESLD (16% vs. 4%, P = 0.04). There were no significant vascular or bleeding complications in either group. Conclusions : Elective cardiac catheterization can be safely performed in patients with ESLD with outcomes (vascular and bleeding complications, length of hospital stay and in‐hospital mortality) similar to patients without liver disease despite significant thrombocytopenia and elevated INR in patients with ESLD. Practices such as platelet transfusion for platelets <60,000 μL, prophylactic FFP transfusion for INR ≥≥ 1.6, less frequent use of antiplatelet therapy and more frequent use of smaller vascular sheaths may have contributed to the safety of cardiac catheterization in ESLD patients. © 2010 Wiley‐Liss, Inc.     

"Normal" liver stiffness values differ between men and women: a prospective study for healthy living liver and kidney donors in a native Korean population

Background and Aim: Liver stiffness (LS) measurement can distinguish individuals with potential liver disease (LD) from the general population. However, if LS is sex‐sensitive, prevalence of LD may be incorrectly estimated when the same reference LS value is applied irrespective of sex. Here, we evaluated whether normal ranges of LS differ between healthy men and women. Methods: LS was measured in a cohort of healthy living liver and kidney donors, none of whom suffered from diabetes mellitus, hypertension, hepatitis B or C virus infection, heart or liver dysfunction, or metabolic syndrome. Patients with abnormal laboratory findings related to potential LD (platelet count < 150 × 10³/µL; aspartate aminotransferase > 40 IU/L; alanine aminotransferase [ALT] > 40 IU/L; albumin < 3.3 g/dL; total bilirubin > 1.2 mg/dL; gamma‐glutamyl transpeptidase > 54 IU/L; alkaline phosphatase > 115 IU/L) were excluded. Results: Among 242 patients analyzed, the mean age was 34.1 for men (n = 121) and 40.5 years for women (n = 121) (P < 0.001). Men had a higher mean LS value than women (5.2 ± 1.2 vs 4.8 ± 1.1 kPa/P < 0.001). Multivariate‐linear regression analysis identified sex as the only independent factor for LS values (β = 0.361/P = 0.021). Using the 5th–95th percentiles, we determined normal LS ranges of 3.7–7.0 kPa in men and 3.3–6.8 kPa in women. In subgroups with ALT < 30 IU/L (subgroup‐1, n = 216) and ALT < 20 IU/L (subgroup‐2, n = 163), men had significantly higher LS values than women (5.2 ± 1.3 vs 4.7 ± 1.1 kPa/P = 0.003 and 5.1 ± 1.2 vs 4.7 ± 1.1 kPa/P = 0.030, respectively), demonstrating an independent sex effect (β = 0.483/P = 0.003 and β = 0.389/P = 0.030, respectively). Conclusions: An independent sex effect on LS values was confirmed. Thus, sex‐specific references should be used for effective screening based on LS measurements.     

Long-term Follow-up of Patients Undergoing Postconditioning During ST-Elevation Myocardial Infarction

Reperfusion injury may offset the optimal salvage of myocardium achieved during primary coronary angioplasty. Thus, coronary reperfusion must be combined with cardioprotective adjunctive therapies in order to optimize myocardial salvage and minimize infarct size. Forty-three patients with their first ST-elevation myocardial infarction were randomized to myocardial postconditioning or standard of care at the time of primary coronary angioplasty. Postconditioning was performed immediately upon crossing the lesion with the guide wire and consisted of four cycles of 30 s occlusion followed by 30 s of reperfusion. End-points included infarct size, myocardial perfusion grade (MPG), left-ventricular ejection fraction (LVEF), and long-term clinical events (death and heart failure). Despite similar ischemic times (≅4.5 h) (p = 0.9) a reduction in infarct size was observed among patients treated with the postconditioning protocol. Peak creatine phosphokinase (CPK), as well as its myocardial band (MB) fraction, was significantly lower in the postconditioning group when compared with the control group (CPK—control, 2,444 ± 1,928 IU/L vs. PC, 2,182 ± 1,717 IU/L; CPK-MB—control, 242 ± 40 IU/L vs. PC, 195 ± 33 IU/L; p = 0.64 and p < 0.01, respectively). EF in the postconditioning group was improved when compared with the control group (control, 43% ± 15 vs. PC, 52% ± 9; p = 0.05). After a mean follow-up of 3.4 years, a 6-point absolute difference in LVEF was still evident in the postconditioning group (p = 0.18). MPG was better among patients treated with the postconditioning protocol compared with control (2.5 ± 0.5 vs. 2.1 ± 0.6; p = 0.02). Due to the small sample size no significant differences in clinical events were detected (p value for death = 0.9; p value for heart failure = 0.2). A simple postconditioning protocol applied at the onset of mechanical reperfusion, resulted in reduction of infarct size, better epicardial and myocardial flow, and improvement in left ventricular function. The beneficial effects of postconditioning on cardiac function persist beyond 3 years.     

The effect of preoperative aspirin administration on postoperative level of von Willebrand factor in off-pump coronary artery bypass surgery

The effect of preoperative administration of aspirin on endothelial function in the patients undergoing off-pump coronary artery bypass (OPCAB) surgery is still unclear. Fifty consecutive patients undergoing OPCAB between May 2006 and May 2007 were equally divided into two groups — one without preoperative aspirin (group A; the first 25 patients) and the other with preoperative aspirin (group B; the next 25 patients). We investigated the degree of postoperative endothelial dysfunction by measuring the von Willebrand factor activity, which is a possible indicator of endothelial damage. The level of von Willebrand factor was not different between groups before surgery (group A 166% ± 53% vs group B 181% ± 62%; P = 0.39). Immediately after surgery it was significantly higher than before surgery in group A (231% ± 79%; rate of increase 1.24 ± 0.58), but not in group B (183% ± 77%; rate of increase 1.03 ± 0.55) (P < 0.02). The level was still significantly higher in group A than in group B on postoperative day 1 (group A 294 ± 66 vs 254 ± 51; P = 0.03), but there was no difference between groups on postoperative day 6. Although the frequency of blood transfusion was higher in group B, there was no difference in the amount of intraoperative bleeding between the groups. Preoperative use of aspirin before OPCAB could suppress the postoperative increase in von Willebrand factor, a possible indicator of endothelial damage, only in the early postoperative phase.     

大剂量阿托伐他汀对急性冠状动脉综合征患者血清抗氧化能力的影响

目的探讨大剂量阿托伐他汀对急性冠状动脉综合征患者血清抗氧化能力的影响。方法168例急性冠状动脉综合征患者随机分为大剂量阿托伐他汀治疗组和小剂量阿托伐他汀治疗组,分别检测治疗前、治疗1周和治疗2周后血清超氧化物歧化酶、谷胱甘肽过氧化物酶和丙二醛的含量;同时选择健康体检者50例作为正常对照组。结果急性冠状动脉综合征患者血清超氧化物歧化酶和谷胱甘肽过氧化物酶含量明显低于正常对照组(P<0.01),血清丙二醛含量明显高于对照组(P<0.01)。小剂量阿托伐他汀治疗组血清超氧化物歧化酶、谷胱甘肽过氧化物酶和丙二醛含量在阿托伐他汀治疗1周后无明显变化(P>0.05),治疗2周后血清超氧化物歧化酶和谷胱甘肽过氧化物酶含量开始升高(P<0.05),丙二醛开始下降(P<0.01)。大剂量阿托伐他汀治疗组在阿托伐他汀治疗1周时血清超氧化物歧化酶和谷胱甘肽过氧化物酶含量升高(P<0.05)、丙二醛含量明显降低(P<0.01),治疗2周后超氧化物歧化酶和谷胱甘肽过氧化物酶继续升高(P<0.05),丙二醛继续下降(P<0.01);且其血清超氧化物歧化酶和谷胱甘肽过氧化物酶含量升高幅度和丙二醛下降幅度均大于小剂量阿托伐他汀治疗组。结论短期大剂量阿托伐他汀能提高急性冠状动脉综合征患者血清的抗氧化能力。     

Autonomic dysfunction in non-diabetic continuous ambulatory peritoneal dialysis patients as measured by sympathetic skin response

ObjectivesThe purpose of this study was to evaluate the prevalence of autonomic dysfunction in non-diabetic continuous ambulatory peritoneal dialysis patients and to investigate its risk factors using the sympathetic skin response.MethodsWe performed a cross-sectional study on 113 non-diabetic continuous ambulatory peritoneal dialysis patients using the sympathetic skin response, a non-invasive test to detect sympathetic sudomotor deficit.ResultsSixty-six patients (58.4%) showed an abnormal sympathetic skin response suggesting a sympathetic sudomotor deficit. Patients were then categorized into two groups according to their sympathetic skin response result. The baseline clinical data, nutritional and dialysis adequacy indices of the two groups were compared. Patients with an abnormal sympathetic skin response are significantly older (54.9 ± 12.52 vs 61.79 ± 12.16 years, p=0.004), more malnourished with a lower albumin (35.79 ± 2.41 vs 33.98 ± 4.92 g/L, p=0.012) and normalized protein nitrogen appearance values (0.99 ± 0.17 vs 0.93 ± 0.16 g/kg/day, p=0.046). Further, they have a lower residual renal function as calculated by weekly renal Kt/V (0.63 ± 0.61 vs 0.29 ± 0.35, p=0.001) or renal creatinine clearance (41.35 ± 40.2 vs 21.96 ± 27.22 L/wk/1.73 m², p=0.006). Patients with an abnormal sympathetic skin response are also receiving a smaller dialysis dose as calculated by the total weekly Kt/V (2.13 ± 0.6 vs 1.83 ± 0.41, p=0.004) or the total creatinine clearance (82. 42 ± 37.34 vs 66.81 ± 25.38 L/wk/1.73 m², p=0.017).ConclusionBased on sympathetic skin response, autonomic dysfunction is common among non-diabetic continuous ambulatory peritoneal dialysis patients. Patients with autonomic dysfunction are significantly older, more malnourished, have low residual renal function and are receiving a smaller dialysis dose. A prospective study is warranted to investigate the reversibility of autonomic dysfunction after an increment in dialysis dose.     

Pentoxifylline for the treatment of non-alcoholic steatohepatitis: a randomized controlled trial

Introduction. The burden of non-alcoholic steatohepatitis (NASH) is growing and current pharmacologic treatments are limited by side effects and inconsistent efficacy. Pilot studies suggest that pentoxifylline (PTX) can reduce liver injury in patients with NASH.Objective. We sought to determine the tolerability of PTX and its effect on aminotransferases and liver histology in patients with NASH.Material and methods. Thirty patients with biopsy proven NASH were randomized in a 2:1 fashion to receive 1,200 mg PTX or placebo for 12 months. Metabolic parameters, aminotransferases, liver histology and hepatic gene expression changes were compared.Results. At baseline the groups were similar. Adverse events were mild, most frequently headache and abdominal cramps, and did not differ between groups (p = NS). After 12 months, ALT and AST decreased from 92 ± 12 IU/L to 67 ± 13 IU/L and 67 ± 6 IU/L to 47 ± 6 IU/L (p < 0.05), respectively in patients treated with PTX. No significant effect was seen with placebo. Steatosis and cellular ballooning improved in the PTX group (p < 0.05), whereas no histological feature of steatohepatitis improved with placebo. However, between groups comparison of both biochemical and histological features were nonsignificant.Conclusion. Pentoxifylline is safe, well tolerated and improves transaminases and histology in patients with NASH when compared to baseline and may be a reasonable therapeutic modality for the treatment of NASH. However PTX failed to reduce transaminases compared to placebo and did not positively affect any of the metabolic markers postulated to contribute to NASH. Although animal data and small pilot studies in humans have suggested that PTX may be effective as a treatment for NASH, translating this therapy to clinical practice may prove challenging.     

Undiagnosed cirrhosis occurs frequently in the elderly and requires periodic follow ups and medical treatments

Background: Autopsy examinations frequently reveal undiagnosed cirrhosis, but its characteristics have rarely been addressed in the elderly. Methods: From 1597 consecutive autopsies, those of patients with liver cirrhosis were selected and their clinicopathological findings were examined. Results: Seventy‐six patients had liver cirrhosis; 18 of these patients (23.7%) were classified as an “undiagnosed” group and in that they had not been diagnosed as having cirrhosis before death. The remaining 58 patients were classified as a “clinical” group. Compared to the clinical group, the undiagnosed group demonstrated a significantly lower Child–Pugh score (7.1 ± 1.9 vs 8.6 ± 2.1; P < 0.01) and infrequent hepatocellular carcinoma (72.4% vs 5.6%; P < 0.0001). The undiagnosed group also demonstrated significantly lower complication rates of hepatic encephalopathy and esophageal varix, and a volume of ascites. The patients in the undiagnosed group were significantly older (79.9 ± 8.1 vs 74.2 ± 8.5 years; P < 0.01), and fewer patients died of liver‐related causes (17% vs 67.2%; P < 0.0001). The etiology of cirrhosis was unknown in five patients in the undiagnosed group, and seven patients did not show any suggestive symptoms or imaging signs. Conclusion: Liver cirrhosis is often undiagnosed (23.7%) in the elderly. In the undiagnosed group, liver function was preserved and serious complications were infrequent. Because the diagnosis of cirrhosis leads to early identification of hepatocellular carcinoma and good prognosis, detailed examination and periodic follow ups should be performed when liver dysfunction is indicated, even in the elderly.     

All-trans retinoic acid suppresses liver injury induced by Propionibacterium acnes and lipopolysaccharide in rats

All-trans retinoic acid (ATRA) has been reported to exert major effects on the immune system, including monocytes/macrophages. The present study was designed to determine whether ATRA would modulate macrophage-associated liver injury induced by Propionibacterium acnes and lipopolysaccharide (LPS) in rats. All-trans retinoic acid administration alleviated the liver injury and reduced the incidence of death following hepatic failure. Serum alanine aminotransferase (ALT) levels 5 h after, and survival rates within 12 h after the administration of LPS were significantly lower in the ATRA-treated group (134 ± 119 IU/L and 72.7%) compared with the control group (713 ± 411 IU/L and 18.2%; P < 0.05). Histological findings supported these results. These effects may be due to suppression of tumour necrosis factor-α (TNF-α) and superoxide anions produced by activated macrophages. Serum levels of TNF-α 1 h after LPS administration were significantly lower in the ATRA-treated group (60.5 ± 7.0 ng/mL) as compared with the control group (105.2 ± 39.3 ng/mL; P < 0.05). Formazan deposition that was generated by the perfusion of the liver with nitroblue tetrazolium, also suggested suppression of the release of superoxide anions from hepatic macrophages. These results suggest that ATRA acts as an immunomodulator in liver injury by suppressing the activation of liver macrophages.     

End-stage renal disease and hepatitis C infection: comparison of alanine aminotransferase levels and liver histology in patients with and without renal damage

Background and aim: To what extent the serum levels of alanine aminotransferase (ALT) are related to histological characteristics of liver damage caused by hepatitis C virus (HCV) infection among patients with end-stage renal disease (ESRD) remains unclear.Methods: Patients with a positive anti-HCV antibody titer confirmed by supplemental tests were evaluated by liver biopsy. We compared ALT levels in patients with and without renal damage, with similar histological grades and stages of inflammation and fibrosis. Patients were divided into two groups: patients with ESRD (n = 25) and patients without renal damage (n = 39).Results: The ALT level was 42.1 ± 24.3 IU/L for the ESRD group, compared with 109.9 ± 55.8 IU/L for the non-ESRD group (P < 0.001). Liver inflammation (modified Knodell grade) was 4.0 ± 2.1 in the ESRD group versus 5.2 ± 2.4 in the non-ESRD group; fibrosis (6-point scale) was 1.1 ± 1.2 versus 1.7 ± 1.5, respectively.Conclusions: Despite histological evidence of liver inflammation, ALT levels in the ESRD group were normal, while ALT levels were significantly higher in the non-ESRD group with similar levels of liver inflammation. In conclusion, ALT levels are not a useful indicator of HCV infection in patients with ESRD and liver biopsies should be recommended for kidney transplant candidates.     

Serum cholinesterase is an early and sensitive marker of graft-versus host-disease (GVHD) and transplant-related mortality (TRM).

Serum cholinesterase (CHE) has been reported to be a significant indicator of liver function and prognosis in patients with cirrhosis. On the other hand, liver complications are frequent following allogeneic stem cell transplantation (HSCT). We therefore tested whether CHE was predictive of graft-versus-host disease and outcome in HSCT recipients. We studied 689 patients receiving a HSCT from an HLA-identical sibling (SIB) (n = 511), an alternative donor (n = 173) or a syngeneic twin (n = 5). Acute graft-versus-host disease (GVHD) was scored as 0-I, II, III-IV in 325 (47%), 279 (41%), and 85 patients (12%) respectively; 190 (28%) patients died of transplant-related complications (TRM). On day -7 the median CHE serum level was comparable in patients who either survived or died of TRM (5900 IU/l). On day 0, serum CHE levels were respectively 2310 and 2120 IU/l (P = NS) indicating the impact of the conditioning regimen. On day +7 after HSCT, the median level for surviving patients was 2598 IU/l vs 2309 IU/l for patients who subsequently died (P = 0.0002), on day +21 CHE levels were respectively 3348 vs 2528 IU/l (P < 0.00001), on day +50, 3575 vs 2358 IU/l (P < 0.00001) and on day +100 4193 vs 2729 IU/l (P < 0.00001). CHE levels on day +50 strongly correlated with aGVHD (3803 vs 3070 vs 1933 IU/l for patients with GVHD grade 0-I, II, and III-IV, respectively (P < 0.00001) and relapse (3569 for patients relapsing vs 3115 IU/l for patients not relapsing, P = 0.0006). In conclusion, (1) serum cholinesterase is a simple and reliable marker of acute GVHD and transplant-related complications; and (2) high CHE levels on day +50 predict relapse. If confirmed, the latter patients may be eligible for early reduction of immunosuppressive therapy.     

Asymmetric dimethylarginine in homocystinuria due to cystathionine β-synthase deficiency: Relevance of renal function

Summary Objective Vascular disease is associated with increased plasma asymmetric dimethylarginine (ADMA) and homocysteine, and both are increased in renal failure. In cystathionine β-synthase deficiency (CBS) there is severe hyperhomocysteinaemia, precocious vascular disease, and endothelial dysfunction. We investigated whether ADMA levels are elevated in CBS patients with and without renal impairment, and whether lowering plasma homocysteine also lowers ADMA. Methods We measured plasma homocysteine, arginine, asymmetric and symmetric dimethylarginines, nitrate + nitrite, creatinine and cystatin C in 23 CBS-deficient patients and 24 age-matched controls. Results In the patients, nitrate + nitrite and the ratio L-arginine/ADMA were markedly reduced (21.6 ± 6.1 vs 57.7 ± 7.5 μmol/L and 132.9 ± 24.7 vs 181.9 ± 56.1, respectively, p < 0.001 for both), reflecting endothelial dysfunction. Plasma ADMA for the group was moderately increased (0.55 ± 0.08 vs 0.49 ± 0.07 μmol/L, p = 0.018), but this was due to significantly higher levels than controls in only those 7 of the 23 patients who had elevated cystatin C levels (0.59 ± 0.08 vs 0.49 ± 0.07 mg/L, p = 0.007). Posttreatment total homocysteine in patients varied widely (15–285, median 92 μmol/L), but was not correlated with ADMA or other measured variables. In three newly-diagnosed patients, marked reduction of total homocysteine during treatment produced minimal changes in ADMA. Conclusions ADMA levels were significantly increased only in the CBS-deficient patients with elevated cystatin C levels, and not in those with normal renal function. The reported relationship between hyperhomocysteinaemia and ADMA may not be direct, but could be secondary to reduced renal function. Communicating editor: Guy Besley Competing interests: None declared     

Safety and Efficacy of Citrate Anti‐Coagulation Continuous Renal Replacement Therapies in Post‐Cardiac Surgery Patients With Liver Dysfunction

The study's aim was to examine safety and efficiency of citrate anticoagulated continuous renal replacement therapies (CRRT) in cardiac surgery patients with acute kidney injury and associated liver dysfunction. The study was conducted on critical ICU patients, hospitalized after cardiac surgery, who developed renal and liver acute failures due to low‐flow syndrome. CRRT in continuous veno‐venous hemodiafiltration with regional citrate anticoagulation (RCA) was prescribed to address renal failure and avoid bleeding‐risk. Patient Ca⁺⁺ was measured to monitor RCA safety, while thromboelastography (TEG) and circuit Ca⁺⁺ were used to verify efficacy. CRRT effectiveness was evaluated through creatinine and urea levels, while liver function was monitored through bilirubin, aspartate aminotransferase, glutamic oxaloacetic transaminase (AST GOT) and gamma glutamyl transferase (GT) levels. The study did not require ethical approval. Hepatic and renal failures were confirmed by baseline levels (total bilirubin = 3.1 ± 3.37 mg/dL, AST GOT = 153 ± 147 U/L and gamma GT = 93.3 ± 86 IU/L, creatinine = 1.97 ± 0.88 and blood urea nitrogen [BUN] 98.13 ± 71.34) assessed in 15 patients. During treatment, Ca⁺⁺ (patient and circuit) remained stable and within range for the whole therapy thanks to low citrate dose (2.8 ± 0.3 mmol/L of blood), while hepatic markers did not show any significant changes the therapy, although treatment with citrate is contraindicated in patients with hepatic failure. RCA quality was confirmed by TEG values, which showed an anticoagulated circuit with no effects on patients. These results involved a high filter lifespan (49.76 ± 22.10 h) and with an effective creatinine and BUN clearance. No episodes of citrate intoxication were reported (total/ionized calcium ratio remained stable and physiologic). RCA during CRRT with dilute solutions proved both effective and safe, even in patients with acute liver failure.     

急性冠状动脉综合征患者血液凝固性加强

目的通过研究急性冠状动脉综合征患者凝血状态的变化,探讨急性冠状动脉综合征患者的发病与血栓前状态的关系,以期对危重冠心病患者及早作出诊断和治疗。方法选择急性冠状动脉综合征患者86例,对照组为稳定型心绞痛患者75例,以酶联免疫吸附法测定两组患者血浆凝血酶原片段1和2、可溶性纤维蛋白单体复合物等凝血分子标志物的含量并进行比较。结果急性冠状动脉综合征患者血浆凝血酶原片段1和2及可溶性纤维蛋白单体复合物较稳定型心绞痛患者均显著升高(1.21±0.23nmolL比0.76±0.20nmolL;85.4±12.4mgL比68.7±13.8mgL,P均<0.001)。急性冠状动脉综合征合并2型糖尿病时血浆凝血酶原片段1和2及可溶性纤维蛋白单体复合物较不伴有2型糖尿病时显著升高(1.28±0.19nmolL比1.16±0.20nmolL;89.8±12.4mgL比82.7±13.7mgL,P均<0.05)。急性冠状动脉综合征合并原发性高血压时血浆凝血酶原片段1和2及可溶性纤维蛋白单体复合物较不伴有原发性高血压时显著升高(1.26±0.24nmolL比1.16±0.20nmolL;90.0±12.8mgL比82.7±13.7mgL,P均<0.05)。结论稳定型心绞痛患者的凝血系统处于稳定状态,而急性冠状动脉综合征患者处于高凝状态,合并2型糖尿病或原发性高血压的急性冠状动脉综合征患者高凝状态更显著,提示高凝状态与急性冠状动脉综合征的发病密切相关。     

Abnormal Q waves on the admission electrocardiogram of patients with first acute myocardial infarction: Prognostic implications

Background: Q waves developed in the subacute and persisting into the chronic phase of myocardial infarction (MI) usually signify myocardial necrosis. However, the mechanism and significance of Q waves that appear very early in the course of acute MI (<6 h from onset of symptoms), especially if accompanied by ST elevation, are probably different. Hypothesis: This study assesses the prognostic implications of abnormal Q waves on admission in 2,370 patients with first acute MI treated with thrombolytic therapy <6 h of onset of symptoms. Results: Patients with abnormal Q waves in ≥2 leads with ST-segment elevation (n = 923) were older than patients without early Q waves (n = 1,447) (60.6 ±11.9 vs. 58.8 ±11.9 years, respectively; p = 0.0003), and had a greater incidence of hypertension (34.3 vs. 30.5% p = 0.05) and anterior MI (60.6 vs. 41.1 % p<0.0001). Time from onset of symptoms to therapy was longer in patients with Q waves upon admission (208 ± 196 vs. 183 ± 230 min; p = 0.01). Peak serum creatine kinase (2235 ± 1544 vs. 1622 ± 1536 IU; p<0.0001), prevalence of heart failure during hospitalization (13.8 vs. 7.0%, p<0.0002), hospital mortality (8.0 vs. 4.6% p = 0.02), and cardiac mortality (6.6 vs. 4.5%, p = 0.11) were higher in patients with anterior MI and with abnormal Q waves than in those without abnormal Q waves upon admission. There was no difference in peak creatine kinase, prevalence of heart failure, in-hospital mortality, and cardiac mortality between patients with and without abnormal Q waves in inferior MI. Multivariate regression analysis confirmed that mortality is independently associated with presence of Q waves on admission (odds ratio 1.61; 95% CI 1.04–2.49; p = 0.04 for all patients; odds ratio 1.65; 95% CI 0.97–2.83; p=0.09 for anterior wall MI. Conclusion: Abnormal Q waves on the admission electrocardiogram (ECG) are associated with higher peak creatine kinase, higher prevalence of heart failure, and increased mortality in patients with anterior MI. Abnormal Q waves on the admission ECG of patients with inferior MI are not associated with adverse prognosis.     

老年脑梗死患者血清对氧磷酶1活性与氧化应激的关系及其在动脉粥样硬化中的作用

目的 探讨老年脑梗死患者血清对氧磷酶1活性与氧化应激的关系及其在动脉粥样硬化中的作用.方法 通过DSA检查确诊颈动脉狭窄的老年脑梗死患者72例作为研究对象(其中轻度狭窄33例,中度狭窄24例,重度狭窄15例),以非脑血管病健康体检者38例作为对照组,用分光光度计法、黄嘌呤氧化酶法和硫代巴比妥酸反应物质法分别测定血清对氧磷酶1活性、超氧化物歧化酶和丙二醛含量,分析对氧磷酶1活性与超氧化物歧化酶、丙二醛之间的关系.结果 脑梗死组患者血清对氧磷酶1活性(95.62±18.26 ku/L)和超氧化物歧化酶含量(69.59±10.56 ku/L)显著低于对照组(分别为168.36±27.82 ku/L和98.34±13.42 ku/L,P<0.01],而丙二醛含量(24.46±5.68nmol/L)显著高于对照组(15.64±8.26 nmol/L,P<0.01).轻度、中度和重度狭窄组患者对氧磷酶1活性(分别为112.48±19.32、98.64±10.84和81.95±13.42 ku/L)、超氧化物歧化酶(分别为80.62±13.26、70.26±14.09和58.82±10.06ku/L)和丙二醛含量(分别为19.52±8.48、23.56±9.81和27.28±9.89nmol/L)差异均有显著性(均P<0.01),并且对氧磷酶1活性和超氧化物歧化酶含量随颈动脉狭窄程度加重,呈逐渐下降的趋势,而丙二醛含量随颈动脉狭窄程度加重呈上升趋势.相关分析表明,对氧磷酶1活性与超氧化物歧化酶含量正相关(r=0.628,P<0.01),而与丙二醛含量负相关(r=－0.541,P<0.01).结论 老年脑梗死患者血清对氧磷酶1活性降低及氧化应激增强,对氧磷酶1活性和氧化应激及其复杂的相互作用参与动脉粥样硬化发生和发展.     

梗死前心绞痛对合并糖尿病的急性心肌梗死患者左心室功能的影响

目的　探讨梗死前心绞痛对合并糖尿病的急性心肌梗死 (AMI)患者左心室功能的近期影响。方法　首次AMI并行急诊PCI患者 15 6例 ,在糖尿病和非糖尿病患者中分别比较有梗死前心绞痛和无梗死前心绞痛组血清肌酸激酶MB(CKMB)峰值和左心室功能的变化。结果　非糖尿病患者中有梗死前心绞痛组血清CKMB峰值低于 ,左室EF高于无梗死前心绞痛组 (CKMB :10 8± 79IU/Lvs 15 6± 10 1IU/L ;EF∶5 8± 13%vs 5 0±11% ,P <0. 0 5 ;糖尿病患者中有梗死前心绞痛组和无梗死前心绞痛组血清CKMB峰值和左心室EF无显著性差异。结论　梗死前心绞痛可在非糖尿病合并AMI患者中限制梗死面积 ,保护左心功能 ,而在糖尿病合并AMI患者中无保护作用。     

The Serum Endothelın-1 Level in Steatosıs and NASH, and Its Relatıon wıth Severıty of Lıver Fıbrosıs

Endothelin-1 (ET-1) is known to play an important role in hepatic fibrosis. ET-1 is also a mediator that is elevated in conditions such as insulin resistance, hyperglycemia, oxidative stress, and endothelial cell dysfunction. In this study, we investigated whether ET-1 has a role in determining the severity of liver fibrosis in NASH. Also, the relation between ALT levels, obesity, diabetes, and AST/ALT ratio and fibrosis and ET-1 level was sought. A total of 92 patients were enrolled in the study. The patients were categorized into three groups: group 1, patients with elevated transaminase levels who were diagnosed as NASH by liver biopsy (n=40); group II, patients with only hepatosteatosis determined by biopsy but having elevated transaminase levels (n=12); and group III, patients with hepatosteatosis observed by ultrasonography, having normal transaminase levels (n=40). The serum ET-1 level was measured by an appropriate ELISA kit for all patients. Mean serum ET-1 level was statistically significantly higher in the NASH group compared to the other two groups (15.56±4.63 vs 6.75±2.46 and 5.74±2.34 μmol/L; P < 0.01). Mean serum ET-1 levels in NASH patients with grade I, grade II, and grade IV fibrosis were 14.06±0.92, 17.70±2.32, and 20.40±1.40 μmol/L, respectively. None of the patients were identified as grade III fibrosis. It was found that the serum ET-1 level showed a statistically significant increase as fibrosis severity increased in NASH patients (P < 0.05). In conclusion, the serum ET-1 level is higher in NASH patients compared to patients having only steatosis. There appears to be a correlation between severity of fibrosis and serum ET-1 level in NASH patients. It has been found that NASH patients having a twofold increase in their ALT levels had higher ET-1 levels and a more severe grade of fibrosis.