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עמוד בית
Tue, 23.07.24

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July 2006
H. Liss
 Background: A publication bias exists towards positive results in studies funded by pharmaceutical companies.

Objectives: To determine whether drug studies in the pulmonary/allergy literature also demonstrate a publication bias towards more favorable results when a pharmaceutical company funds the study.

Methods: We reviewed all original articles published in seven pulmonary and allergy journals between October 2002 and September 2003. Included in the review were studies of inhaled corticosteroids (oral or nasal), long- or short-acting bronchodilators, or leukotriene receptor antagonists. Articles with funding from a pharmaceutical company and/or one or more authors employed by a pharmaceutical company were considered pharmaceutical company-sponsored studies. The remaining studies were considered not sponsored by a pharmaceutical company. Results were compared to ascertain whether positive results were obtained more frequently in the company-sponsored studies.

Results: Of the 100 articles included in this review 63 were considered pharmaceutical company-sponsored research. Results favorable for the drugs studies were significantly more common in those funded by a pharmaceutical company (98% vs. 32%).

Conclusions: In the pulmonary and allergy literature, as in other fields, there is a publication bias towards positive results in pharmaceutical company-sponsored research.

Y. Turgeman, P. Levahar, I. Lavi, A. Shneor, R. Colodner, Z. Samra, L. Bloch and T. Rosenfeld
 Background: Adult calcific aortic stenosis is a well-known clinical entity but its pathophysiology and cellular mechanism have yet to be defined.

Objectives: To determine whether there is an association between the presence and severity of adult calcific aortic stenosis and Chlamydia pneumoniae seropositivity

Methods: Forty adult patients (23 women, 17 men) were divided into three groups according to echocardiographic aortic valve area: Group A – 7 symptomatic subjects (age 67 ± 7 years) with normal aortic valve and normal coronary angiogram, Group B – 16 patients (age 73 ± 6) with moderate ACAS[1] (AVA[2]> 0.8 £ 1.5 cm2), and Group C – 17 patients (age 76 ± 7) with severe ACAS (AVA £ 0.8 cm2). We tested for immunoglobulins M, G and A as retrospective evidence of C. pneumoniae infection using the micro-immunofluorescence method. Past C. pneumoniae infection was defined by IgG titer > 16 £ 512.

Results: No patients in Group A showed positive Ig[3] for C. pneumoniae. IgM was not detected in any of the patients with ACAS (groups B and C) while 2 of 17 patients (12%) in group C showed IgA for the pathogen. High titers of IgG were found in 14 of 33 (42%) of the patients with moderate or severe ACAS: 5 of 16 (31%) in group B and 9 of 17 (53%) in group C (P = 0.2). Both groups had the same prevalence of coronary artery disease (66%). AVA was lower in IgG-seropositive patients than in the seronegative group (0.88 ± 0.3 cm2 vs. 1.22 ± 0.4 cm2, respectively, P = 0.02).

Conclusions: Past C. pneumoniae infection may be associated with a higher prevalence and greater severity of ACAS.


 





[1] ACAS = adult calcific aortic stenosis

[2] AVA = aortic valve area

[3] Ig = immunoglobulin


I. Arad, M. Baras, B. Bar-Oz and R. Gofin
 Background: Maternal transport, rather than neonatal transport, to tertiary care centers is generally advocated. Since a substantial number of premature deliveries still occur in hospitals with level I and level II nurseries, it is imperative to find means to improve their outcome.

Objectives: To compare the neonatal outcome (survival, intraventricular hemorrhage and bronchopulmonary dysplasia) of inborn and outborn very low birth weight infants, accounting for sociodemographic, obstetric and perinatal variables, with reference to earlier published data.

Methods: We compared 129 premature infants with birth weights of 750–1250 g delivered between 1996 and 2000 in a hospital providing neonatal intensive care to 99 premature babies delivered in a referring hospital. In the statistical analysis, variables with a statistical significant association with the outcome variables and dissimilar distribution in the two hospitals were identified and entered together with the hospital of birth as explanatory variables in a logistic regression.

Results: Accounting for the covariates, the odds ratios (outborns relative to inborns) were 0.31 (95% confidence interval = 0.11–0.86, P = 0.03) for mortality, 1.37 (95%CI[1] = 0.64–2.96, P = 0.42) for severe intraventricular hemorrhage, and 0.86 (95%CI = 0.38–1.97, P = 0.78) for bronchopulmonary dysplasia. The odds ratio for survival without severe intraventricular hemorrhage was 1.10 (95%CI = 0.55–2.20, P = 0.78). Comparing the current results with earlier (1990–94) published data from the same institution showed that mortality decreased in both the outborn and inborn infants (OR[2] = 0.23, 95%CI = 0.09–0.58, P = 0.002 and 0.46; 95%CI = 0.20–1.04, P = 0.06, respectively), but no significant change in the incidence of severe intraventricular hemorrhage or brochopulmonary dysplasia was observed. Increased survival was observed also in these infants receiving surfactant, more so among the outborn. The latter finding could be attributed to the early, pre-transport surfactant administration, implemented only during the current study.

Conclusions: Our data suggest that very low birth weight outborn infants may share an outcome comparable with that of inborn babies, if adequate perinatal care including surfactant administration is provided prior to transportation to a tertiary center.


 





[1] CI = confidence interval

[2] OR = odds ratio


S.W. Moses, M. David, E. Goldhammer, A. Tal and S. Sukenik
D. Rimar, Y. Rimar and Y. Keynan
 Today, more than 10 years and 2000 articles since human herpesvirus 8 was first described by Chang et al., novel insights into the transmission and molecular biology of HHV-8[1] have unveiled a new spectrum of diseases attributed to the virus. The association of HHV-8 with proliferative disorders – including Kaposi's sarcoma, multicentric Castleman disease and primary effusion lymphoma – is well established. Other aspects of HHV-8 infection are currently the subject of accelerated research. Primary HHV-8 infection may manifest as a mononucleosis-like syndrome in the immunocompetent host, or in various forms in the immunocompromised host. The association of HHV-8 with primary pulmonary hypertension was observed by Cool et al. in 2003, but six clinical trials evaluating the role of HHV-8 in pulmonary hypertension have not been able to replicate this intriguing observation. It has been speculated that HHV-8 may secondarily infect proliferating endothelium in patients with pulmonary hypertension. HHV-8 epidemiology, modes of transmission, new spectrum of disease and treatment are presented and discussed.







[1] HHV-8 = human herpesvirus 8


T. Hershcovici, T. Chajek-Shaul, T. Hasin, S. Aamar, N. Hiller, D. Prus and H. Peleg
J.A. Gómez-Puerta, G. Espinosa, J.M. Miró, O. Sued, J.M. Llibre, R. Cervera and J. Font
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