Magnesium efficacy in magnesium deficient and nondeficient patients with rapid ventricular response atrial fibrillation.

We assessed the effect of magnesium sulphate (MgSO4) on lowering the rate in ventricular atrial fibrillation (AF), and evaluated the effect of this therapy in magnesium (Mg) deficient and nondeficient patients. This experimental clinical study was performed on 34 patients with rapid AF (ventricular rate [VR] > 120/minute) presenting to the emergency department of a tertiary care university hospital. Patients with systolic blood pressure < or = 100 mmHg, Hb level < or = 11.8, saO2 of < or = 96%, BUN > or = 40 or creatine > or = 1.8 were excluded (n = 15). Nineteen patients were given an initial 2 g MgSO4 bolus i.v. and a 1 g/hour continuous infusion over 6 hours. To evaluate the presence of Mg deficiency, urine was collected from the onset of treatment and continued for the next 24 hours, and the excretion rate of administered Mg was calculated. Ventricular rates were obtained at baseline, after MgSO4 bolus, and every 15 minutes for the first hour. The decrease in the VR was statistically significant at 15, 30 and 60 minutes after Mg therapy (p = 0.0025, p < 0.001, p > 0.001). There was no difference in the response to Mg therapy between Mg deficient and nondeficient patients at 15, 30 or 60 minutes after therapy (p = 0.41, p = 0.28, p = 0.08). It is concluded that i.v. MgSO4 has a statistically significant but clinically limited effect on VR and this effect did not differ between patients with and without Mg deficiency.     

Postinfarction ventricular septal rupture: surgical intervention and risk factors influencing hospital mortality

Postinfarction rupture of the interventricular septum is usually fatal without surgical intervention and requires urgent closure. Between 1989 and 2003 twenty consecutive patients (15 male, 5 female), underwent postinfarction ventricular septal rupture (VSR) repair. Mean age of the patients was 62.05 +/- 7.51 years. Fifteen patients were operated within 48 hours after myocardial infarction. Patch reconstruction was performed in all patients. Infarct locations were anterior in 65%, posterior in 35%. Coronary artery surgery was performed in 14 patients (70%). Hospital mortality was 30% (6 patients). Four patients were presented for surgical therapy with frank cardiogenic shock or low cardiac output syndrome. A residual shunt was detected in 4 patients and three of these patients were reoperated. One of them, who has been reoperated on the first day of the postoperative period, did not survive. The statistical analysis of the patients' records demonstrated that time period between MI and surgery, applied additional CABG procedure, the sex of the patients and the site of the rupture are significant factors influencing in-hospital mortality. Preoperative condition, age of the patients and the number of the affected coronary vessels do not have an important effect on the mortality. Postinfarction ventricular septal rupture is a fatal complication of the myocardial infarction and must be treated surgically. The time interval between septal rupture independent from the preoperative haemodynamic condition, the location of the defect and additional myocardial revascularization procedure are the factors influencing the early outcome.     

Up-regulated eotaxin plasma levels in chronic liver disease patients indicate hepatic inflammation, advanced fibrosis and adverse clinical course

BACKGROUND AND AIMS: Recent studies highlight the role of chemokines for the attraction of inflammatory cells in liver injury and fibrogenesis. The CC chemokine ligand 11, eotaxin (CCL11), is up-regulated in senescent human hepatic stellate cells and crucial in animal models of T-cell mediated hepatitis. The aim of this study was to analyze the role of eotaxin in chronic liver disease. METHODS: Plasma eotaxin levels of 111 patients with chronic liver disease were correlated with clinical presentation, laboratory parameters, liver histology and clinical course in a 6-year follow-up. RESULTS: Eotaxin concentrations were significantly up-regulated in patients with liver cirrhosis and increased according to Child-Pugh and model of end-stage liver disease (MELD) score. Eotaxin correlated with the hepatic biosynthetic capacity and other inflammatory cytokines. High eotaxin was associated with hepatic necroinflammation and fibrosis in liver histology. In patients with typical clinical complications of cirrhosis, eotaxin was found to be increased. High eotaxin indicated an unfavorable prognosis in 6-year follow-up. CONCLUSIONS: High eotaxin expression may be involved in the pathogenesis of chronic liver diseases. Plasma eotaxin levels correlate with the degree of liver cirrhosis and could serve as an additional biomarker indicating histological hepatic necroinflammation and fibrosis as well as an adverse clinical course.     

Effects of octreotide and propranolol on colonic mucosa in rats with portal hypertensive colopathy

BACKGROUND/AIMS: The aim of the study is to clarify the effects of octreotide and propranolol, agents used in the treatment of portal hypertension, on mucosal changes in portal hypertensive colopathy. METHODOLOGY: Portal hypertension was induced in all rats by partial portal vein ligation, and after the operation all rats were caged for a 10-week period. Then, animals were divided into three groups and for two weeks medical treatment were administered to the individual groups as follows: Control group, saline 0.5 mL/day, intraperitoneally. Octreotide group, octreotide 100 micrograms/kg/12 hours, subcutaneously. Propranolol group, propranolol 20 mg/kg/day, intraperitoneally. In order to assess the portal hypertensive colopathy, criteria such as mean diameters of dilated vessels in colonic mucosa, and the existence of mucosal edema, capillary ectasia, hyperemia and hemorrhage, inflammation were used. RESULTS: When parameters were compared for the control versus propranolol groups, mucosal edema and hyperemia and hemorrhage criteria were found to be significant for the propranolol group; control versus octreotide groups, mucosal edema, capillary ectasia, and hyperemia and hemorrhage criteria were found to be significant for the octreotide group; octreotide versus propranolol groups, capillary ectasia and mucosal edema criteria were found to be significant for the octreotide group. CONCLUSIONS: The mucosal changes in portal hypertensive colopathy could be corrected by drugs modifying portal blood flow, octreotide may find a place in the treatment of portal hypertensive colopathy.     

Comparison of SPECT findings and neuropsychological sequelae in carbon monoxide and organophosphate poisoning

Abnormal regional cerebral blood flow in patients with acute carbon monoxide (CO) and organophosphate (OP) poisoning was examined using (99m)Tc-hexamethylpropylene amine oxime (HMPAO) brain single photon emission computed tomography (SPECT) in fourteen patients. We evaluated the predictive significance of acute phase brain SPECT findings for long-term neuropsychological sequelae. Changes were found in the frontal, temporal, parietal lobes within the first week after both types of poisoning. The distribution of the hypoperfused cerebral areas as demonstrated by (99m)Tc-HMPAO imaging was similar in the two groups during the acute phase. Neuropsychological sequelae developed in five patients poisoned with OP and six with CO. Patients who had SPECT findings heterogeneously or in the temporal or frontal lobes displayed disorientation. Those with fronto-parietal and frontal lobe changes displayed mental confusion. Parkinsonism also was observed in patients with parieto-occipital, parietal and frontal lobe lesions. The distribution of these lesions appears to predict the long term sequelae of these poisonings, though additional studies with larger numbers of patients are needed to confirm the role of SPECT imaging in both OP and CO poisonings.     

Resistin serum levels are associated with insulin resistance, disease severity, clinical complications, and prognosis in patients with chronic liver diseases

OBJECTIVES: Hyperinsulinemia and insulin resistance are present in nearly all patients with liver cirrhosis. Resistin, a mainly adipose-derived peptide hormone, reduces insulin sensitivity in adipocytes, skeletal muscles, and hepatocytes. In experimental cirrhosis models, resistin expression is upregulated. We aimed to evaluate the potential clinical value of resistin in chronic liver diseases (CLD). METHODS: Serum resistin was measured in 82 non-diabetic CLD patients during evaluation for potential liver transplantation and 76 age- and sex-matched healthy controls. Patients were followed for 6 yr. RESULTS: Resistin serum levels were significantly elevated in patients with liver cirrhosis compared with healthy controls (p<0.001). Resistin increased with stage of liver cirrhosis as defined by Child-Pugh or model for end-stage liver disease (MELD) score. Serum resistin correlated with insulin secretion (C-peptide, p<0.001) and inversely with insulin sensitivity (HOMA-index, p=0.008) in CLD patients. Resistin also correlated inversely with markers of hepatic biosynthetic capacity and positively with markers of inflammation such as tumor necrosis factor alpha (TNF-alpha) or C-reactive protein (CRP), as well as with clinical complications, e.g., portal hypertension. Patients with elevated resistin had increased mortality in 6-yr-survival (p=0.005, Cox regression model). CONCLUSION: Resistin offers novel application potential as a clinical biomarker in the assessment of liver cirrhosis. Elevated resistin may contribute to insulin resistance in advanced liver dysfunction.     

Frequency of functional gastrointestinal disorders in children with familial Mediterranean fever

Clinical Rheumatology - Familial Mediterranean fever (FMF) is characterized by self-limiting fever episodes usually accompanied by serositis, arthralgia, and arthritis. Functional gastrointestinal...     

Longitudinal monocyte Human leukocyte antigen‐DR expression is a prognostic marker in critically ill patients with decompensated liver cirrhosis

Background: Critical illness in cirrhotic patients is associated with a poor prognosis and increased susceptibility to infections. Monocyte HLA‐DR expression is decreased in cirrhotic patients, but its prognostic value has not been investigated prospectively. Methods: Thirty‐eight critically ill patients with decompensated liver cirrhosis were included in this prospective study. On admission to the intensive care unit (ICU), inflammatory parameters (C‐reactive protein, procalcitonin and lipopolysaccharide‐binding protein), interleukin (IL)‐10, interferon (IFN)‐γ serum levels, tumour necrosis factor (TNF)‐αex vivo stimulation (whole blood assay) and HLA‐DR expression on monocytes (FACS analysis) were determined. Immune parameters were furthermore measured every third day until discharge from the ICU or death of the patients. Results: Intensive care unit mortality of the cirrhotic patients was 34.2%. During admission, TNF ex vivo, IFN‐γ and HLA‐DR expression were lower in non‐survivors (all P<0.05), while IL‐10 levels were increased in non‐survivors compared with survivors (P=0.001). However, individual values clearly overlapped between groups. Prospective analysis revealed that monocyte HLA‐DR expression remained stable or increased in survivors, but decreased in non‐survivors (P=0.002). A decrease in HLA‐DR expression between admission and day 3 was strongly associated with decreased IFN‐γ levels and increased ICU mortality (hazard ratio 3.36, P=0.008), mostly owing to late sepsis. This association was independent of the sequential organ failure assessment and model for end‐stage liver disease score. Conclusions: Here we establish the relative HLA‐DR expression (admission/day 3) as a prognostic marker for ICU mortality in critically ill cirrhotic patients. These results may guide the evaluation of immune‐modulating therapies in these patients.     

Circulating levels of cytokines are increased in restless legs syndrome

Background

Restless legs syndrome [RLS] is known as a disease of iron and dopaminergic dysregulation but inflammatory processes might also have a role in the pathogenesis. In this study, we compared the circulating levels of hsCRP, IL-1β, IL-6, and TNF-α in patients with primary restless legs syndrome [RLS] and healthy control subjects.

Methods

We prospectively included 29 patients with primary RLS and 65 healthy controls [HC], all age-sex matched. The diagnosis of RLS was established using international guidelines. IRLSSG Severity Scale was used to evaluate the severity of RLS. Plasma levels of hsCRP, IL-1β, IL-6, and TNF-α were measured in all participants.

Results

The mean age of patients was 37.8?±?11.3 and 52% of RLS group were women. Serum IL-1β, IL-6, and TNF-α levels of the patient group were statistically significantly higher compared to HC [p?<?0.001 for all variables]. Plasma levels of hsCRP did not differ between groups. There were 8 patients with mild RLS [28%], 13 patients with moderate RLS [45%], and 8 patients with severe RLS [28%]. Only IL-6 values were significantly different between the groups. In the severe group, the value of IL-6 was significantly higher than in the other groups [p: 0.03].

Conclusion

These results showing higher circulating levels of inflammatory cytokines in patients with RLS support the notion that inflammation may be involved in the pathogenesis of primary RLS. However, it is necessary to perform further studies to determine if this finding is a cause or an effect.