ENDOCRINE AND METABOLIC ALTERATIONS MAY UNDERLIE MORTALITY OF SEVERE SEPSIS AND SEPTIC SHOCK PATIENTS ADMITTED TO ICU.

The study evaluated endocrinal and metabolic response to sepsis and its applicability for the prediction of outcome of septic patients. Patients were 39 adult with severe infections and within 24 h after onset or suspected clinical tissue hypoperfusion. At enrollment patients were evaluated for acute physiology and chronic health evaluation II score (APACHE II) and Glasgow Coma Scale (GCS). Global hemodynamic parameters including systolic blood pressure (SBP), heart rate (HR) and central venous pressure (CVP) were recorded and monitored. All patients were managed at ICU due to Surviving Sepsis Campaign guidelines. ELISA estimated serum copeptin, macrophage migration inhibitory factor (MIF) and total cortisol (TC) and blood lactate levels. Study outcome was survival rate via 28 days (28-D SR) and best predictor for it. The results showed that 22 patients passed total hospital stay uneventfully for a total survival rate of 56.4%. Seventeen patients died; 10 during ICU stay and 7 during word stay. At admission serum markers levels were significantly higher in survivors and non-survivors compared to controls and in non-survivors compared to survivors. Survival showed negative significant correlation with age, high blood lactate and serum copeptin, TC and MIF levels. Survival showed positive significant correlation with SBP, CVP and urine output. ROC curve and Regression analyses defined high at admission serum copeptin and blood lactate levels as significant predictors for mortality of septic patients.

Interferon therapy shifts natural killer subsets among Egyptian patients with chronic hepatitis C.

Natural killer cells can be divided into five subpopulations based on the relative expression of CD16 and CD56 markers. The majority of natural killer cells are CD56(dim), which are considered to be the main cytotoxic effectors. A minority of the natural killer cells are CD56(bright), and function as an important source of immune-regulatory cytokines. Shifts of these subsets have been reported in patients with chronic hepatitis C virus infection. We sought to investigate the shift of natural killer subsets among Egyptian patients with chronic HCV and to analyze the influence of interferon therapy on this shift. We applied a flow cytometric analysis of peripheral blood natural killer subsets for 12 interferon-untreated and 12 interferon-treated patients with chronic HCV, in comparison to 10 control subjects. Among interferon-untreated patients, there was a significant reduction of CD56⁻16(+) (immature natural killer) cells. Among interferon-treated patients, the absolute count of natural killer cells was reduced, with expansion of the CD56(bright) subset and reduction of the CD56(dim)16(+) subset. Natural killer subset counts were not significantly correlated to HCV viral load and were not significantly different among interferon responders and non-responders. In conclusion, HCV infection in Egyptian patients has been observed to be statistically and significantly associated with reduction of the CD56⁻16(+)NK subset, while a statistically significant expansion of CD56(bright) and reduction of CD56(dim)16(+) subsets were observed after interferon therapy. Further studies are required to delineate the molecular basis of interferon-induced shift of natural killer subsets among patients with HCV.

Interferon therapy shifts natural killer subsets among egyptian patients with chronic hepatitis C

Natural killer cells can be divided into five subpopulations based on the relative expression of CD16 and CD56 markers. The majority of natural killer cells are CD56dim, which are considered to be the main cytotoxic effectors. A minority of the natural killer cells are CD56bright, and function as an important source of immune-regulatory cytokines. Shifts of these subsets have been reported in patients with chronic hepatitis C virus infection. We sought to investigate the shift of natural killer subsets among Egyptian patients with chronic HCV and to analyze the influence of interferon therapy on this shift. We applied a flow cytometric analysis of peripheral blood natural killer subsets for 12 interferon-untreated and 12 interferon-treated patients with chronic HCV, in comparison to 10 control subjects. Among interferon-untreated patients, there was a significant reduction of CD56-16+ (immature natural killer) cells. Among interferon-treated patients, the absolute count of natural killer cells was reduced, with expansion of the CD56bright subset and reduction of the CD56dim16+ subset. Natural killer subset counts were not significantly correlated to HCV viral load and were not significantly different among interferon responders and non-responders. In conclusion, HCV infection in Egyptian patients has been observed to be statistically and significantly associated with reduction of the CD56-16+NK subset, while a statistically significant expansion of CD56bright and reduction of CD56dim16+ subsets were observed after interferon therapy. Further studies are required to delineate the molecular basis of interferon-induced shift of natural killer subsets among patients with HCV.

Diminished absolute counts of CD56dim and CD56bright natural killer cells in peripheral blood from Egyptian patients with hepatocellular carcinoma.

Natural killer cells (NK) as components of the innate immunity substantially contribute to anti-tumor immune responses, NK cell subpopulations can be defined on the basis of the relative expression of CD16 and CD56 markers. Earlier research demonstrated a dramatic reduction in the frequency of peripheral blood CD56dimCD16+ NK subsets in hepatocellular carcinoma (HCC) patients compared with healthy subjects. We aim to assess the relative and absolute counts of natural killer cells subsets in hepatitis C-related HCC among Egyptian patients. Flowcytometric analysis of peripheral blood NK subsets was performed for HCV with HCC patients (n=20) and HCV without HCC patients (n=14) as compared to healthy control subjects (n=152). We found that HCC patients displayed a marked reduction in the relative frequency of peripheral CD56im subsets compared with healthy subjects. Moreover, there was a significant reduction in the absolute counts of CD56dim16+, CD56dim16- and CD56bright. In conclusion, this study demonstrated that the absolute counts of dim and bright NK cell subsets were decreased in different proportions in patients with HCV-related HCC that refers to a possible role for these cells, particularly CD 56 bright cells, in the immune response to HCC. This might aid in developing new therapeutic strategies targeting both NK subsets for HCC.

Applications and limitations of blood eosinophilia for the diagnosis of acute cellular rejection in liver transplantation.

This study evaluates the predictive value of the blood eosinophil count in the diagnosis of acute cellular rejection, its value as a marker of response to treatment, the diagnostic use in a subgroup of patients with normal transaminases and compares blood eosinophilia in patients with and without hepatitis C virus infection. A consecutive cohort of 101 liver transplant patients, 275 liver biopsies, and blood eosinophils recorded on the day or one day before biopsy were analyzed. An elevated eosinophil count has a positive predictive value for acute cellular rejection of 82%. A normal eosinophil count excludes moderate/severe rejection with a predictive value of 86%. The eosinophil count decreases in 69% of patients following treatment of acute cellular rejection with corticosteroids irrespective of treatment outcome. Acute cellular rejection in the presence of an elevated eosinophil count occurs significantly less often (p = 0.007) in patients with hepatitis C virus. An elevated eosinophil count is a valuable marker of acute cellular rejection. However, blood eosinophil levels should not be used to predict acute cellular rejection following treatment with corticosteroids. Blood eosinophilia, seen less often in patients with hepatitis C virus, may reflect an over-diagnosis of acute cellular rejection in these patients.