Association of autoimmune type atrophic corpus gastritis with Helicobacter pylori infection

AIM:To study the association between Helicobacter pylori(H.pylori)infection and autoimmune type atrophic gastritis. METHODS:Twenty-three patients with different grades of atrophic gastritis were analysed using enzyme immunoassay-based serology,immunoblot-based serology,and histology to reveal a past or a present H.pylori infection.In addition,serum markers for gastric atrophy(pepsinogenⅠ,pepsinogenⅠ/Ⅱand gastrin)and autoimmunity[parietal cell antibodies(PCA), and intrinsic factor(IF),antibodies]were determi...     

Early ileocolonoscopy with biopsy for the evaluation of persistent post-transplantation diarrhea

AIM: To investigate the signifi cance of ileocolonoscopy with histology in the evaluation of post-transplantation persistent diarrhea (PD). METHODS: We retrospectively reviewed all records of renal transplant patients with PD, over a 3-year period. All patients were referred for ileocolonoscopy with biopsy, following a negative initial diagnostic work up. Clinical and epidemiological data were compared between cases with infectious or drug-induced diarrhea. RESULTS: We identif ied 30 episodes of PD in 23 renaltransplant patients (1-3 cases per patient). There were 16 male patients and the mean age at the time of PD was 51.4 years. The average time from transplantation to a PD episode was 62.3 ± 53.2 mo (range 1-199 mo). Ileocolonoscopy detected mucosal abnormalities in 19 cases, whereas the intestinal mucosa appeared normal in 11 cases. Histological examination achieved a specific diagnosis in 19/30 cases (63.3%). In nine out of 11 cases (82%) with normal endoscopic appearance of the mucosa, histological examination of blinded biopsies provided a specif ic diagnosis. The etiology of PD was infectious in 11 cases (36.6%), drug-related in 10 (33.3%), of other causes in three (10%), and of unknown origin in six cases (20%). Infectious diarrhea occurred in significantly longer intervals from transplantation compared to drug-related PD (85.5 ± 47.6 mo vs 40.5 ± 44.8 mo, P < 0.05). Accordingly, PD due to drug-toxicity was rarely seen after the f irst year post-transplantation. Clinical improvement followed therapeutic intervention in 90% of cases. Modif ication of immunosuppressive regimen was avoided in 57% of patients. CONCLUSION: Early ileocolonoscopy with biopsies from both affected and normal mucosa is an important adjunctive tool for the etiological diagnosis of PD in renal transplant patients.     

Identification of poor households for premium exemptions in Ghana's National Health Insurance Scheme: empirical analysis of three strategies

Objectives To evaluate the effectiveness of three alternative strategies to identify poor households: means testing (MT), proxy means testing (PMT) and participatory wealth ranking (PWR) in urban, rural and semi‐urban settings in Ghana. The primary motivation was to inform implementation of the National Health Insurance policy of premium exemptions for the poorest households. Methods Survey of 145–147 households per setting to collect data on consumption expenditure to estimate MT measures and of household assets to estimate PMT measures. We organized focus group discussions to derive PWR measures. We compared errors of inclusion and exclusion of PMT and PWR relative to MT, the latter being considered the gold standard measure to identify poor households. Results Compared to MT, the errors of exclusion and inclusion of PMT ranged between 0.46–0.63 and 0.21–0.36, respectively, and of PWR between 0.03–0.73 and 0.17–0.60, respectively, depending on the setting. Conclusion Proxy means testing and PWR have considerable errors of exclusion and inclusion in comparison with MT. PWR is a subjective measure of poverty and has appeal because it reflects community’s perceptions on poverty. However, as its definition of the poor varies across settings, its acceptability as a uniform strategy to identify the poor in Ghana may be questionable. PMT and MT are potential strategies to identify the poor, and their relative societal attractiveness should be judged in a broader economic analysis. This study also holds relevance to other programmes that require identification of the poor in low‐income countries.     

Does cytogenetic evolution have any prognostic relevance in myelodysplastic syndromes? A study on 153 patients from a single institution

The present study was designed to establish the incidence of cytogenetic evolution (CE), defined as the acquisition of chromosomal defects during the course of MDS, in order to correlate it with the WHO classification and IPSS score, and to assess its impact on overall survival (OS) and risk of MDS/AML evolution (progression-free interval, PFI) by means of Cox models for time-dependent covariates. Adjustments for known risk factors were achieved by performing a bivariable analysis. The study was carried out in 153 MDS patients who were followed for a median period of 45.2 months. Disease progression occurred in 42.4% of patients after a 65.2-month median PFI, while CE occurred in 30.7% of patients. Our study shows that (1) CE was more common in advanced than in early MDS, and advanced MDS presented secondary chromosomal defects distinct from those of early MDS; (2) CE significantly affected OS and PFI independently of other prognostic variables; (3) del(7)(q31q34) was the only secondary chromosomal defect which significantly affected PFI; trisomy 8 had only a moderate influence.     

The clinical view through the Archives: the clinical notes of 2009

The Clinical Notes published in 2009 serve as a resource to reflect on clinical aspects relevant to different clinical entities. Through this review an attempt is likewise made to bring the reader closer to the clinical reality of our environment.     

Antithrombin Murcia (K241E) causing antithrombin deficiency: a possible role for altered glycosylation

Background

Identification of mutations in the SERPINC1 gene has revealed different mechanisms responsible for antithrombin deficiency. Deletions and nonsense mutations associate with type I deficiency. Certain missense mutations cause type II deficiency by affecting the heparin binding site or the reactive center loop, while others result in type I deficiency by intracellular retention or RNA instability.

Design and Methods

We studied the molecular, biochemical, proteomic and glycomic characterization of a new natural mutant (K241E) that may be classified as pleiotropic.

Results

The mutation caused a significant decrease in the anticoagulant activity mainly due to a reduced heparin affinity and a modification of the electrostatic potential that might explain the impaired ability of the mutant protein to form complexes with the target protease in the absence of heparin. Mass spectrometry and glycomic analyses confirmed an increased molecular weight of 800 Da in the mutant protein possibly due to core-fucosylation, provoking the loss of heparin affinity. Additionally, carriers of this mutation also have a minor mutant isoform that still followed normal glycosylation, retaining similar heparin affinity to wild-type α-antithrombin, and certain anticoagulant activity, which may explain the milder thrombotic risk of patients carrying this mutation. Similar results were observed using recombinant K241E antithrombin molecules.

Conclusions

Our data suggest a new mechanism involved in antithrombin type II deficiency by indirectly affecting the glycosylation of a natural variant. Additional studies are required to confirm this hypothesis.