Evaluating laboratory key performance using quality indicators in alexandria university hospital clinical chemistry laboratories

The performance of clinical laboratories plays a fundamental role in the quality and effectiveness of healthcare. To evaluate the laboratory performance in Alexandria University Hospital Clinical Laboratories using key quality indicators and to compare the performance before and after an improvement plan based on ISO 15189 standards. The study was carried out on inpatient samples for a period of 7 months that was divided into three phases: phase I included data collection for evaluation of the existing process before improvement [March-May 2012]; an intermediate phase, which included corrective, preventive action, quality initiative and steps for improvement [June 2012]; and phase II, which included data collection for evaluation of the process after improvement [July 2012-September 2012]. In terms of the preanalytical indicators, incomplete request forms in phase I showed that the total number of received requests were 31 944, with a percentage of defected request of 33.66%; whereas in phase II, there was a significant reduction in all defected request items [P< 0.001] with a percentage of defected requests of 9.64%. As for the analytical indicators, the proficiency testing accuracy score in phase I showed poor performance of 10 analytes in which total error [TE] exceeded total error allowable [Tea], with a corresponding sigma value of less than 3, which indicates test problems and an unreliable method. The remaining analytes showed an acceptable performance in which TE did not exceed the TEa, with a sigma value of more than 6. Following an intervention of 3 months, the performance showed marked improvement. Error tracking in phase I showed a TE of [5.11%], whereas in phase II it was reduced to 2.48% [P<0.001]. For the postanalytical indicators, our results in phase I showed that the percentage of nonreported critical results was 26.07%. In phase II, there was a significant improvement [P< 0,001]. The percentage of nonreported results was 11.37%, the reasons were either inability to contact the authorized doctor [8.24%], wrong patient identification [1.0%], lack of reporting by lab doctor [1.11%], and finally, lack of reporting by the lab technician [1.03%]. Standardization and monitoring of each step in the total testing process is very important and is associated with the most efficient and well-organized laboratories

Noninvasive serum markers: liver fibrosis staging among hepatitis C virus infected patients

Accurate monitoring of changes in fibrosis would be helpful in defining the need for intervention, and the response to treatment. In this case control study we aimed to evaluate the diagnostic utility of different serum markers and indices in detecting the stage of fibrosis in order to recommend the most accurate and efficient serum marker to be used in routine clinical practice to replace or minimize the use of liver biopsy. A written informed consent was collected from all patients and the study was approved by the ethical committee; thirty FICV infected patients admitted to Alexandria University hospital were enrolled together with fifteen healthy adults as controls. Initial liver biopsy was done to assess the degree of liver fibrosis. Laboratory work up included all routine liver tests, estimation of Hyaluronic acid level, Matrix metalloproteinase[MMP-1], Aminoterminal propeptide type III procollagen [PIIINP]. Marker Algorithms based on common laboratory tests included AST-to-platelet ratio [APRI score], AST-to-ALT ratio, Fibro test, Actitest. Forn's index, Shasta index and hepascore were calculated together with PIIINP/MMP-iscore. A statistically significant increase in ALT, AST, Hyaluronic acid and PIIINP, as well as APRI score, Hepascore and Shasta score was found among HCV patients compared to controls p<0.05; while MMP-1, Forn's score, fibrotest were not significantly different between both groups. Comparing serum markers with METAVIR fibrosis stage we found that PIIINP, APRI score, Forn's score and ALT/AST ratio were significantly correlated to Metavair fibrosis stage in groups with no or early fibrosis while MMP-l, Shasta score, 1-lepascore and Fibrotest were significantly correlated to late stages of fibrosis P<0.05. When using a calculated stepwise logistic regression analysis; a manual score equation for fibrosis has emerged; where F0F1 vs F2F3F4 score=-0.60 log MMP-l+ 0.936 log PIIINP and F0F1F2 vs. F3F4 score=-0.421 log MMP-l-0.272 log PHINP. These equations yielded different cut off scores which were applied in order to estimate two clinically relevant fibrosis stages in patients, FOFI versus F2F3F4 termed "significant fibrosis" and FOFIF2 versus F3F4 or "extensive fibrosis". A score below 0.2 observed in 23 patients [76.7%] excluded the presence of extensive fibrosis [F3F4] with negative predictive values of 99% and 86% respectively. A combination of markers as well as indices is an emerging tool for differentiating early from advanced fibrosis. PIIINP, APRI, Forn's score and ALT/AST ratio were significantly correlated to Metavair fibrosis stage in no or early fibrosis group. While Shasta score, HA, Hepascore, Fibrotest and MMP were significantly correlated to late stages. Fibrotest was of significant value for detecting early as well as significant fibrosis, but poor at predicting intermediate levels of fibrosis. Shasta score, APRI score and Forn's score showed AUC 1.0 with a sensitivity of 100% and specificity of 100% to exclude the presence of significant fibrosis. Liver biopsy may still be needed for chronic HCV cases to correctly stage liver fibrosis

Identification of some Helicobacter species in patients with hepatitis C virus-related liver cirrhosis with and without hepatocellular carcinoma; a retrospective study

The progression of hepatitis C virus [HCV] positive liver disease from hepatitis to cirrhosis and hepatocellular carcinoma [HCC] involves factors other than the virus itself. An etiologic agent capable of inducing chronic active hepatitis and hepatocellular tumors in mouse was discovered belonging to the genus Helicobacter, and was named Helicobacter Hepaticus. Several research have reported high seroprevalence of helicobacter pylori antibodies in patients with hepatitis C virus. Since then, the relation between helicobacter species and liver disease in human was investigated. The aim of the present work was to identify and study the prevalence of some helicobacter species [helicobacter pylori [HP] and helicobacter pullorum] in HCV positive liver cirrhosis with and without hepatocellular carcinoma [HCC] in humans. The study was carried out on liver biopsies of 45 patients classified into 3 equal groups; Group I [control group]: where the liver biopsy specimens were taken from grossly normal areas of 15 hepatectomy specimens resected for hepatic benign tumours/cysts or metastatic tumours; Group II: 15 liver biopsy specimens from patients with HCV positive liver cirrhosis; and Group III which included 15 liver biopsy specimens belonging to HCV positive patients diagnosed by histopathology as hepatocellular carcinoma [HCC]. Identification of Helicobacter species as well as detection of Cag A positive and glm M positive strains was done in liver biopsies using polymerase chain reaction. Staining of helicobacter pylori in liver biopsies with immune stain was carried out. Helicobacter genus DNA was detected in 15 cases out of 45 studied cases: 6 cases out of 15 [40%] in group II [liver cirrhosis group], 8 cases out of 15[53. 33%] in group III [HCC group], and only one case out of 15 [6.67%] in the control group. The prevalence of helicobacter positive cases were significantly higher in group II [liver cirrhosis group] and in group III [HCC group] than in group I [control group] [P=0.02].No significant difference between the three studied groups was found regarding the Cag A and the glmM gene status. Helicobacter pullorum was detected in only two cases; one in group II and the other in group III. Helicobacter pylori was detected by immune stain in 4 cases out of 15 cases positive for HP by PCR in group III [HCC]. Helicobacter DNA is present in liver tissue of HCV positive liver disease. Further research is recommended to explore the role of Helicobacter species in the progression of HCV positive liver disease to HCC

Transforming growth factor- beta 1 in patients with angiographically proven coronary heart disease

Transforming growth factor- beta 1 [TGF- beta 1] is a multifunctional cytokine that exhibits vasculoprotective properties. Production and plasma levels of TGF- beta 1 are influenced by polymorphisms in the TGF- beta 1 gene. A T-C transition at nucleotide 29 of the TGF- beta 1 gene results in a Leu-Pro substitution at amino acid 10 of the signal peptide. We investigated whether the T29-C polymorphism of TGF- beta 1 is associated with myocardial infarction among a sample of Egyptian coronary artery diseased males. The study population consisted of 90 patients with angiographically proven myocardial infarction and 30 control individuals without signs or symptoms of myocardial infarction. Polymorphism-related genotypes were determined with allele-specific PCR [polymerase chain reaction]. In this study; we found no differences between patients with MI and healthy subjects regarding the genotype and allele frequencies of codon 10 TGF- beta 1 polymorphism. Thus, our results indicate that this polymorphism does not appear to predispose to the development of MI. There was an agreement between genotypes observed and those predicted by the Hardy-Weinberg equilibrium in the control group [Codon 10, x[2] goodness of fit was not significant = 0.777, p; 0.87]. Negative association findings in this study did not exclude that TGF- beta 1 is a susceptibility locus for myocardial infarction, but further study on a larger scale is needed