ABSTRACT
BACKGROUND: Nosocomial acquisition of spontaneous bacterial peritonitis (SBP) is debated as having a different microbial etiology and prognosis. Identification of clinical, laboratory predictors of mortality and appropriate empirical antimicrobial selection is necessary to prevent early mortality and morbidity. We aimed to find the clinical and bacteriological profile in nosocomial and community acquired SBP and its variants, and the predictors of mortality. MATERIAL AND METHODS: One hundred and fifty patients with 162 discrete episodes of different types of SBP were analyzed. Relevant clinical and laboratory data were analyzed. SBP was diagnosed according to standard criteria and classified as community acquired if the infection detected within 48 h of admission and as nosocomial after 48 h of admission to the hospital. RESULTS: Eighty seven percent had community acquired SBP (CSBP), 13% had nosocomial SBP (NSBP). Patients of NSBP were older, had more episodes of GI bleed and higher previous episodes of encephalopathy. Patients who died were older, had worse encephalopathy. NSBP had higher one month mortality. Age, serum sodium, encephalopathy and NSBP predicted mortality. Culture positivity was 22.22%. Escherichia coli was the commonest organism isolated. There was no difference in the bacteriological profile between CSBP and NSBP. E. coli showed up to 48% resistance to third generation cephalosporins. Overall sensitivity to aminoglycosides was more than 75%. CONCLUSIONS: Overall mortality was 59%. NSBP had significantly high one month mortality. Age, serum sodium, encephalopathy and NSBP were predictors of mortality. Bacteriological profile was similar between CSBP and NSBP.
ABSTRACT
Wilson disease is a rare, inherited autosomal recessive disease of copper metabolism and may be more common where consanguinity is prevalent. Much has been known about the disease after it was first described by Kinnier Wilson as 'progressive lenticular degeneration in 1912. Over 500 mutations of the ATP7B gene has been identified with no clear genotype to phenotype correlation. Loss of ATP7B function leads various grades of reduced biliary excretion of copper and reduced incorporation of copper into ceruloplasmin; accumulation and toxicity of copper in the liver, brain and other tissues results in liver toxicity and other myriad manifestations of the disease. The clinical features may vary from asymptomatic state to chronic liver disease, acute liver failure, neuropsychiatric manifestations and hemolytic anemia. Diagnosis is based on the combination of clinical sign's, biochemical features, histologic findings and mutation analysis of ATP7B gene. Subtle geographical differences exist with a disproportionate proportion of children presenting with acute liver failure. A high index of suspicion is needed for an early diagnosis. Ratios of biochemical indices for early diagnosis need validation across geographical regions and may not be particularly applicable in children. Better biomarkers or the need for tests for early detection of ALF persists. Drugs used in the treatment of Wilson disease include copper chelating agents such as d-Penicillamine, trientine and zinc salt. Untreated Wilson disease uniformly leads to death from liver disease or severe neurological disability. Early recognition and treatment has excellent prognosis. Liver transplantation is indicated in acute liver failure and end stage liver disease. Family screening in order to detect the disorder in the first-degree relatives is warranted. This review provides an overview of different aspects of Wilson disease including geographical differences in presentations and clinical management and the limitations of currently available tests.
