RESUMEN
Patients with liver cirrhosis present an increased susceptibility to the systemic inflammatory response syndrome [SIRS], which is considered the cause of hospital admission in about 10% of patients and is present in about 40% of those admitted for ongoing complications. We tried to assess the prevalence of the SIRS with the possible effects on the course of the disease during hospital stay. Two hundred and three patients with liver cirrhosis were examined and investigated with close monitoring during hospital stay. The main clinical endpoints were death and the development of portal hypertension-related complications. Eighty-one patients met the criteria of SIRS [39.9%]. We found significant correlations between SIRS and jaundice [p = 0.005], bacterial infection [p = 0.008], white blood cell count [p < 0.001], low haemoglobin concentration [p = 0.004], high serum creatinine levels [p < 0.001], high alanine aminotransferase levels [p < 0.001], serum bilirubin levels [p < 0.001], international normalised ratio [p < 0.001], serum albumin levels [p = 0.033], high Child-Pugh score [p < 0.001]. During the follow-up period, 26 patients died [12.8%], 15 developed portal hypertension-related bleeding [7.3%], 30 developed hepatic encephalopathy [14.7%], and 9 developed hepatorenal syndrome type-1 [4.4%]. SIRS showed significant correlations both to death [p < 0.001] and to portal hypertension-related complications [p < 0.001]. The systemic inflammatory response syndrome occurs in patients with advanced cirrhosis and is associated with a bad prognosis
RESUMEN
Background: Viral infection has been implicated in the pathogenesis of bone marrow failure. We designed this study to explore the influence of chronic HCV infection on the bone marrow status in patients withliver cirrhosis presenting with peripheral blood cytopenias
Patients and Methods: The present study was conducted on 70 patients with different grades of liver cirrhosis based on Child-Pugh scoringsystem . They were categorized into those positive for HCV infection [50patients] and those without [20 patients]based on assay of anti-HCV anti-bodies and qualitative PCR for HCV-RNA. Complete blood count and bonemarrow examination have been performed to all studied patients
Results: Normal bone marrow cellularity was more evident in pa-tients without HCV infection. However, hypercellular bone marrow wasmore evident in patients with positive HCV infection .Furthermore, no significant changes in different bone marrow elements in patients with posi-tive HCV infection were demonstrated when compared to patients withnegative HCV infection [P<0.05]
Conclusion: HCV infection has no evident direct suppressive effecton bone marrow elements in cirrhotic patients presenting with mono, biorpancytopenia. Understanding the pathogenetic mechanism of cytopeniasin cirrhotic patients is important to improve the management strategy andoutcome
RESUMEN
Diabetes mellitus imposes a tremendous burden on health economies mainly because of its devastating complications. A long duration of metabolic disturbances can cause vascular damage leading to both macro and micro vascular complications. There is an increasing evidence that atherosclerosis is accompanied by inflammation. Our aim in this study is to prove that a low grade inflammation accompany the diabetes mellitus and this inflammatory process is correlated to diabetic control and diabetic complications. Our study was done on 100 elderly diabetic patients whose total white blood cell count was in the normal range. Their age ranged from 65-85years with mean age of them is 68.1 years, half of them were males and the other half were females. They undergo full clinical examination and laboratory investigations including total white blood cell count, serum Creatine protein level, albumin level in urine. glycosylated haemoglobin in addition to other routine laboratory investigations. The patients were divided into 5 quintiles according to the distribution of the total white blood cell count and serum C-reactive protein level. We found a highly significant positive correlation [P value <0.0001] of the total white blood cell count and serum C-reactive protein level to the diabetes duration, body mass index, systolic and diastolic blood pressure, fasting and post prandial blood glucose levels, glycosylated haemoglobin, total cholesterol, low density lipoprotein-cholesterol, serum creatinine and albuminuria and a highly significant negative Correlation with the high density Iipoprotein-cholesterol [P value<0.0001]. We found also a highly significant positive correlation of the total white blood cell Count and serum C-reactive protein level with diabetic micro and macro vascular complications [P value<0.0001]. Moreover, there is an increased risk of macro and micro vascular complications with progressive quintiles of both white blood cell count and serum C-reactive protein level. The odds ratio for the group 5 of the total white blood cell count in comparison to group 1and2 equals 7.35 [confidence Interval= 3.12-9.31] for macro vascular complications and it equals 7.19 [confidence interval= 4.12-9.19] for micro vascular complications. The odds ratio for groups 3,4and 5 of the serum C-reactive protein level equals 9.31[confidence interval= 6.19-18.1] in comparison to groups 1 and 2 for macro vascular complications and it equals 7.31 [confidence interval= 5.19-15.9] for micro vascular complications. We found also an increased risk for smokers to develop both macro and micro vascular complications of diabetes mellitus , odds ratio equals 6.87[confidence interval= 2.14-22.06] and 3 [confidence interval=1.07-8.38] respectively compared with non smokers in the lowest quintile
RESUMEN
Background: The development of cachexia is a particular predictor of adverse prognosis in chronic heart failure [CHF]. Less is known about anabolic metabolism in CHF. Leptin -the hormone product of obesity gene has been shown to inhibit food intake, increase energy expenditure and fat oxidation. Insulin sensitivity and secretion is related to leptin. Leptin has been reported also to stimulate proliferation of CD4 T cells and increases cytokine production. The study aimed to investigate leptin. Insulin sensitivity and tumor necrosis factor-alpha [TNF-alpha] in chronic heart failure with and without cachexia
Methods: We studied 31 male patients with CHF, mean age [59.87 +/- 6.91 years], mean New York Heart Association Functional Class [2.52 +/- 0.81], mean left ventricular ejection fraction [LVEF] [0.33+0.08] and 13 male healthy control subjects, mean age [59.87 +/- 6.91]. Of the CHF patients, 14 were cachectic [cCHF] with non-oedematous weight loss >7.5% over at least6 months and 17 non-cachectic. Serum insulin was measured by enzyme immunoassay, insulin sensitivity was assessed by intravenous glucose tolerance. Serum leptin and TNF were meas ured using commercially available ELISA kit
Results: Compared with the healthy control subjects, patients had elevated levels of leptin, fasting insulin and TNF-alpha [P<0.001], with reduced insulin sensitivity [P<0.001]. Both ncCHF and cCHF subgroups had higher leptin and TNF levels than the control group [P<0.001]. The cCHF subgroup-compared with ncCHF subgroup-showed reduced leptin and fasting insulin levels [P<0.001 and P<0.01] respectively and elevated TNF-alpha levels [P<0.001]. In both patients and control subjects there was a positive correlation between leptin and fasting insulin levels [r=0.59, P<0.001 and r=0.54, P<0.05] respectively. The relative risk of incidence of cCHF in NYHA Functional class [I and II] versus NYHA Functional class [III and IV] was 0.427 [P<0.05]
Conclusion: CHF is hyperleptinaemic state and is associated with decreased insulin sensitivity and elevated fasting plasma insulin levels. The state of cardiac cachexia is associated with higher TNF-alpha levels and more worse NYHA Functional Class. Leptin and TNF-alpha may be valid targets for novel therapeutic interventions in patients with CHF
RESUMEN
Background: Repolarization and ischemic-like electrocardiographic [ECG] changes observed during acute phase of stroke may cause diagnostic and management dilemmas for the clinician. Some of these changes have been thought to be due either to the stroke state itself or pre-existing heart disease
Objective: The aim of this study is to assess the effect of acute phase of stroke on QT dispersion [QTd]
Patients and Methods: The study consisted of 42 patients [24] males and [18] females [test group], hospitalized for acute cerebrovascular stroke within 24 hours of symptom onset. A control group of 38 healthy presons were submitted to the study. They were age and sex matched. All test and control groups were subjected to history taking, clinical examination especially cardiac and neurological examination, routine laboratory tests, echocardiography. Twelve leads ECG was done for both test group and control group during the first 24 hours after symptom onset then after one week for test group. Norepinephrine level was done for both test and control groups
Results: QT dispersion and corrected QT dispersion [QTcd] were significantly greater in 24h-ECG than in 1 week [1w] ECG and the control ECG [P < 0.001]. In 24h-ECG QTd and QTcd were significantly greater in patients with larger lesions [mean +/- SD [0.048+/-0.009 and 0.053 +/- 0.009] vs small lesions [0.04 +/- 0.009 and 0.041+0.004] seconds, P < 0.001]. In 1w-ECG patients with right sided lesions were found to have significantly greater QTd and QTcd values [[0.034+0.008 and 0.039+0.005] vs left sided lesions [0.025+0.007 and 0.03+0.004] seconds, P< 0.001]
Conclusion: Acute stroke increases QTd and QTcd in patients without any known cardiac diseases. In the first 24hour, QTd and QTcd seem to be more prominent and related to humoral effects of acute insult. However, within one week, stroke localization may also play a role