Intestinal effects of iron deficiency anemia in children.

A group of 11 children with iron deficiency anemia were studied with respect to intestinal structure and function. In six cases there were histological abnormalities of intestinal mucosa in varying degrees consisting of villous damage, increased activity in the crypts, increased lymphoplasmocytic infiltration and changes in the surface epithelium. Ultrastructurally, microvilli lesions, mitochondrial changes and an increase in lysosomes were observed. Relative malabsorption of iron and d-xylose malabsorption were present in a minority of patients. Functional and structural changes were correlated. Our results suggest that these changes are due to impairment of cell metabolism.     

In vitro activity of caspofungin compared to amphotericin B, fluconazole, and itraconazole against Candida strains isolated in a Turkish University Hospital.

We investigated the in vitro activity of caspofungin compared to amphotericin B, fluconazole, and itraconazole against clinical strains of Candida spp. (n =239). Antifungal susceptibility tests were done in accordance with NCCLS M27-A2 microdilution method and the results were read after 24 and 48 h. In general, 24 h MIC readings were similar to those at 48 h for most isolates and all antifungal agents. Caspofungin was active against all species tested. Caspofungin MICs of Candida parapsilosis were slightly higher than those for other Candida spp. Caspofungin MIC (microg/ml) ranges at 24 h for C. albicans, C. glabrata, C tropicalis, C. parapsilosis, C kefyr, C krusei, C. lusitaniae, C. norvegensis, C. guilliermondii and C. lipolytica were 0.06-2, 0.125-2, 0.125-2, 1-4, 0.125-2, 1-2, 0.5-2, 0.5-1, 0.5-2 and 1-2, respectively. Eagle (paradoxical) effect was observed in 31 and 8% of the isolates at highest concentrations of caspofungin and itraconazole, respectively. The activity of caspofungin against fluconazole- and/or itraconazole-resistant isolates was similar to that detected for the susceptible ones. We conclude that caspofungin appears as a promising antifungal agent with enhanced activity against Candida, including the azole-resistant strains.     

The prevalence of hereditary thrombophilia in the Trakya region of Turkey

The prevalences of deficiencies in antithrombin III (AT III), protein C (PC), protein S (PS) and in the activated protein C (APC) resistance in the thrombotic population of the Trakya region, Turkey were investigated. 37 patients with venous thrombosis (VT) and 17 patients with arterial thrombosis (ArT) were included in this study. The mean ages of the patients with VT and ArT were 46 years (range 20-70) and 38 years (range 32-40), respectively. The activity of AT III was measured by commercially available immuno-turbidimetric assay. The activities of PC and PS were determined by coagulometric assay. The APC resistance was measured using a modified APTT-based clotting assay. Among the VT patients, there were 2 cases (5.4%) with AT III, 5 (13.51%) with PC deficiency, 5 (13.51%) with PS deficiency and 2 (5.4%) with APC resistance. In the ArT patient group, there was 1 patient (5.88%) with AT III, 3 (17.64%) with PC deficiency, 1 (5.88%) with PS deficiency and no APC resistant patients, while there was one (2.08%) with PC deficiency and one (2.08%) with APC resistance in the control group (49 persons, mean age 41 years). The relative risk of thrombosis (odds ratio) was 1.7 in the deficiency of PC and 5.6 in the deficiency of PS. The data presented suggests that the prevalences of AT III, PC and PS deficiencies causing thrombophilia in the Trakya region of Turkey are higher than in other reported studies while the APC resistance is lower than in others. Further studies including more patients would be required to clarify these discrepancies.     

Calciphylaxis: A condition mimicking necrotizing vasculitis

Summary A patient with end stage renal disease developed ischaemic skin necrosis and digital gangrene. He had diffuse arterial calcification associated with hyperparathyroidism secondary to renal failure. The patient received inappropriate cyclophosphamide therapy as he had been misdiagnosed as having an inflammatory vasculitis. This clinical picture, previously named calciphylaxis should come into the differential diagnosis of systemic vasculitis in a uraemic patient with hyperparathyroidism.     

A cluster of nosocomial Klebsiella oxytoca bloodstream infections in a university hospital.

BACKGROUND: On February 19, 2003, four patients (patients 1-4) in the neurology ward underwent cranial magnetic resonance angiography (MRA) and developed fever within 1 hour afterward. Klebsiella oxytoca was isolated from blood cultures of patients 1 through 3. OBJECTIVE: To identify the source of this cluster of nosocomial K. oxytoca bloodstream infections. DESIGN: Outbreak investigation. SETTING: A 1,000-bed university hospital. METHODS: The infection control team reviewed patient charts and interviewed nursing staff about the preparation and administration of parenteral fluids. The procedure of cranial MRA was observed. Arbitrarily primed polymerase chain reaction (AP-PCR) was performed to show the clonal relationship among these three strains. RESULTS: AP-PCR revealed that three K. oxytoca isolates had the same molecular profile. Cranial MRA was found to be the only common source among these patients. During MRA, before injection of the contrast medium, normal saline solution was infused to check the functioning of the intravenous catheter. Use of the solution for multiple patients was routine, but the access diaphragm of the bottle was not cleansed. The bottle of normal saline solution used on February 19 had already been discarded and the culture sample taken from the solution on the day of observation was sterile. CONCLUSIONS: We speculate that normal saline solution became contaminated during manipulation and that successive uses might have been responsible for this cluster. Poor aseptic techniques employed during successive uses appear to be the most likely route of contamination. Use of parenteral solutions for multiple patients was discontinued.     

Increased immunoglobulin E response in acute coronary syndromes

The role of inflammation and mast cell activation has been implicated in atherosclerotic plaque destabilization and rupture. To investigate the role of immunoglobulin E (IgE) in acute coronary syndrome, a prospective clinical study was conducted in patients with acute myocardial infarction (AMI), unstable angina pectoris (UAP), stable angina pectoris (SAP), and healthy controls. IgE levels were serially measured and compared in consecutive patients with AMI (n = 16) and UAP (n = 14) on days 1, 3, 7, 21 after admission and 3 months later and only once in stable angina pectoris (n = 15) and healthy controls (n = 14). In addition, blood eosinophil and basophil levels on admission were measured in all groups and compared. Initial IgE levels determined at admission in patients with AMI, UAP, and SAP were significantly higher than levels in the control group (p = 0.002). Initial high IgE level in AMI on day 1 increased to a peak by day 7 (p = 0.024), then gradually decreased by day 21 and at 3 months (p = 0.052). High IgE level in UAP persisted by day 7 and gradually decreased by day 21 and 3 months (p = 0.037 and p = 0.018, respectively). Blood eosinophil count on admission was significantly higher in UAP than in the control group (p = 0.005). Basophil levels of both AMI and UAP groups on admission were found to be elevated as opposed to control group (p = 0.02 and p = 0.012, respectively). This study demonstrates that the level of IgE significantly increased during the acute phase of acute coronary syndromes and gradually decreased, supporting the role of acute inflammatory response and mast cell involvement in plaque rupture.     

Chronic hepatitis C responds poorly to combination therapy in chronic hepatis B carriers

BACKGROUND: The effect of conventional interferon-based therapy of hepatitis B virus (HBV) and hepatitis C virus (HCV) dual infection is controversial. Yet, no studies have been carried out into pegylated interferon treatment for chronic HBV/HCV coinfection. We aimed to evaluate the response rate and side effects of conventional or pegylated interferon combined with ribavirin on chronic HBV/HCV coinfection therapy. METHODS: The study included 36 chronic hepatitis patients (M/F: 28/8, mean age 47+/-12 years) who were positive for HBsAg and anti-HCV. They were tested for the presence of HBV-DNA by hybridisation assay, and the samples giving negative results were retested by polymerase chain reaction (PCR). All patients were tested for HCV-RNA using PCR, and the HCV genotype was determined. RESULTS: Nineteen patients were given standard interferon either alone or in combination with ribavirin, whereas 17 were given pegylated interferon and ribavirin combination therapy. None of the patients had HBV-DNA positivity; however, all had HCV-RNA detectable by PCR. All the patients had HCV genotype 1b. The mean alanine aminotransferase and aspartate aminotransferase levels were 118+/-65 U/l and 90+/-95 U/l respectively. Five patients in each group discontinued the treatment due to side effects. Only two patients (one from each group) reached sustained virological response. CONCLUSION: Neither pegylated nor conventional interferon based regimes were effective for HBV/HCV coinfection, in which the dominant virus was HCV. Pegylated interferon and ribavirin therapy was not superior to conventional interferon based regimes in the treatment of HBV/HCV coinfection.