Anaemia during pregnancy: impact on birth outcome and infant haemoglobin level during the first 18 months of life

To determine the effect of maternal anaemia on pregnancy outcome and describe its impact on infant haemoglobin level in the first 18 months of life, we conducted a prospective study of 617 pregnant women and their children in Benin. Prevalence of maternal anaemia at delivery was 39.5%, and 61.1% of newborns were anaemic at birth. Maternal anaemia was not associated with low birth weight [OR = 1.2 (0.6-2.2)] or preterm birth [OR = 1.3 (0.7-2.4)], whereas the newborn's anaemia was related to maternal anaemia [OR = 1.8 (1.2-2.5)]. There was no association between an infant's haemoglobin level until 18 months and maternal anaemia. However, malaria attacks during follow-up, male gender and sickle cell trait were all associated with a lower infant haemoglobin level until 18 months, whereas good infant feeding practices and a polygamous family were positively associated with a higher haemoglobin level during the first 18 months of life.     

Update on the Role of Quantitative HBsAg and HBeAg Monitoring during Peginterferon Therapy

Pegylated Interferon alfa (PEG-IFN) is the only licensed agent that allows a sustained virologic response in a subset group of patients with chronic hepatitis B, both e antigen (HBeAg)-positive and negative, after a finite course of therapy. Despite this major advantage, its use is limited because of its lack of efficacy in a large proportion of patients and a high relapse rate especially in HBeAg-negative patients. Baseline host and viral factors have been largely used to identify candidates for PEG-IFN therapy in the pre-treatment phase, but they have failed to translate into a clear therapeutic choice because of their low predictability. Recently, the use of HBeAg and especially hepatitis B surface antigen (HBsAg) as quantitative serological markers, has led to a revolution in the management of this disease by introducing a new concept of on-treatment prediction of response and stopping rules as early as week 12 of therapy.     

Stigma as a barrier to health care utilization among female sex workers and men who have sex with men in Burkina Faso

Purpose

The aim of this study is to examine the prevalence and correlates of perceived health care stigma among female sex workers (FSWs) and men who have sex with men (MSM), including other stigma types, suicidal ideation, and participation in social activities.

Staging Fibrosis in Chronic Viral Hepatitis

Staging fibrosis accurately has always been a challenge in viral hepatitis and other liver diseases. Liver biopsy is an imperfect gold standard due to its intra and interobserver agreement limitations and additional characteristics such as its safety and cost. Hence, non-invasive tests have been developed to stage liver fibrosis. In addition to serological biomarkers, physical tests with reasonable accuracy are available and adopted in the daily clinic regarding viral hepatitis fibrosis staging. In this review, we discuss the published data regarding the staging of liver fibrosis in chronic hepatitis B and C, emphasizing non-invasive markers of fibrosis, both serological and physical. Moreover, we also discuss a persistent central gap, the evaluation of liver fibrosis after HCV cure.     

Simultaneous development of lymphoma in recipients of renal transplants from a single donor: donor origin confirmed by human leukocyte antigen staining and microsatellite analysis

BACKGROUND: Posttransplant lymphoproliferative disorders (PTLD) occur in 0.5% to 2.5% of cases in renal-transplant recipients. Epstein-Barr virus (EBV) is usually detected in the tumor cells, suggesting a role for this virus as an agent of B-cell proliferation. It is unusual for patients receiving allografts from the same donor to develop PTLD simultaneously. METHODS: we describe two patients who received renal allografts from the same donor and developed PTLD simultaneously. The presence of EBV in both tumors was confirmed. In this report, the origin of tumor cells was determined by immunohistochemical human leukocyte antigen (HLA) typing and microsatellite analysis. Clonality was studied by immunoglobulin gene rearrangement analysis. RESULTS: Our results suggest that the tumor originated from donor cells in both patients but, because immunoglobulin gene rearrangements were different, this could mean that lymphoid cells proliferate independently in each recipient. CONCLUSIONS: We propose the following pathogenesis: immortalization of passenger B lymphocytes by EBV, proliferation of these cells, and development of PTLD by means of immunosuppression, antigenic stimulation, and HLA mismatch.     

Trisomy 7 mosaicism, maternal uniparental heterodisomy 7 and Hirschsprung's disease in a child with Silver-Russell syndrome

Prenatal trisomy 7 is usually a cell culture artifact in amniocytes with normal diploid karyotype at birth and normal fetal outcome. In the same way, true prenatal trisomy 7 mosaicism usually results in a normal child except when trisomic cells persist after birth or when trisomy rescue leads to maternal uniparental disomy, which is responsible for 5.5-7% of patients with Silver-Russell syndrome (SRS). We report here on the unusual association of SRS and Hirschsprung's disease (HSCR) in a patient with maternal uniparental heterodisomy 7 and trisomy 7 mosaicism in intestine and skin fibroblasts. HSCR may be fortuitous given its frequency, multifactorial inheritance and genetic heterogeneity. However, the presence of the trisomy 7 mosaicism in intestine as well as in skin fibroblasts suggests that SRS and HSCR might possibly be related. Such an association might result from either an increased dosage of a nonimprinted gene due to trisomy 7 mosaicism in skin fibroblasts (leading to SRS) and in intestine (leading to HSCR), or from an overexpression, through genomic imprinting, of maternally expressed imprinted allele(s) in skin fibroblasts and intestine or from a combination of trisomy 7 mosaicism and genomic imprinting. This report suggests that the SRS phenotype observed in maternal uniparental disomy 7 (mUPD(7)) patients might also result from an undetected low level of trisomy 7 mosaicism. In order to validate this hypothesis, we propose to perform a conventional and molecular cytogenetic analysis in different tissues every time mUPD7 is displayed.     

Contribution of cellular HIV-1 DNA quantification to the efficacy analysis of antiretroviral therapy: a randomized comparison of 2 regimens, including 3 drugs from 2 or 3 classes (TRIANON, ANRS 081)

Cellular HIV-1 DNA level was sequentially measured by quantitative polymerase chain reaction in 141 patients not previously treated with highly active antiretroviral therapy (HAART), who were enrolled in a 72-week randomized trial (ANRS 081 "Trianon") comparing 2 regimens, including 3 drugs from 2 classes (indinavir + stavudine + lamivudine, group 1) or 3 classes (indinavir + stavudine + nevirapine, group 2). The median decrease from baseline to week 72 in cellular HIV-1 DNA level was not significantly different between the 2 groups (0.54 and 0.45 log10 copies/10 peripheral blood mononuclear cells [PBMCs] in groups 1 and 2, respectively), whereas a higher proportion of patients maintained a plasma HIV-1 RNA level less than 20 copies/mL at week 72 in group 1 than in group 2 (79% and 52%; P = 0.0009). Furthermore, the difference in cellular HIV-1 DNA decrease from baseline to week 72 between patients who achieved a plasma HIV-1 RNA level less than 20 copies/mL at week 72 and those who did not was not statistically significant (0.54 and 0.45 log10 copies/10 PBMCs, respectively; P = 0.14). The decay in cellular HIV-1 DNA from baseline to week 72 was higher in antiretroviral-naive patients than in pretreated patients (0.55 and 0.23 log10 copies/10 PBMCs, respectively; P = 0.0008). The cellular HIV-1 DNA level change under therapy was best fitted to a 2-phase decay model with a junction point at week 16, from which its half-life was estimated at 18 weeks during the initial phase and at 104 weeks thereafter. In conclusion, the changes under therapy in cellular HIV-1 DNA level, which were mostly coincident to those of plasma HIV-1 RNA, did not add significant information to the comparison of the viral efficacy of the 2 studied regimens.     

Neutralizing antibodies to interferon-α and circulating interferon in patients with chronic hepatitis C non-responding to pegylated interferon plus ribavirin re-treated by pegylated interferon-α-2a and ribavirin (ANRS HC16 GAMMATRI substudy)

A lack of antiviral response in patients with chronic hepatitis C treated with pegylated (PEG)‐interferon (IFN)‐α‐2a + ribavirin (RIBA) may be explained by neutralizing antibodies to IFN‐α‐2a. The aim of this study was to assess neutralizing antibodies to IFN‐α‐2a and IFN levels in non‐responder patients who were re‐treated by PEG IFN‐α‐2a and RIBA for 12 weeks. Non‐responders to a first‐line treatment of PEG IFN‐α‐2a + RIBA were included for treatment with PEG IFN‐α‐2a (180 µg/week) + RIBA (1,000 mg/day if <75 kg, 1,200 mg otherwise) for 48 weeks. HCV RNA was measured at week 12. IFN levels and neutralizing antibodies to IFN‐α‐2a were measured retrospectively on stored sera at baseline and weeks 4 and 12, using a quantitative sandwich ELISA for neutralizing antibodies to IFN‐α‐2a. Twenty‐three patients were non‐responders and 19 patients were responders at week 12 of the initial phase of the second‐line treatment. Non‐responders and responders did not differ statistically: baseline age (median age 47 vs. 50 years), HCV RNA (median 6.8 vs. 6.4 log₁₀ copies/ml), gender (70% vs. 73% males), genotype (genotype 1: 91% vs. 80%). The median IFN‐α‐2a levels (pg/ml) at weeks 0, 4, and 12 (interquartile range) did not differ between the 19 responders to initial phase of second‐line treatment and the 23 non‐responders: <3.3 (<3.3–371.4), 1457.3 (106.8–3284.8), and 1,652 (90.8–5,000); 84.5 (3.3–277.4), 1407.4 (120.2–2443.4), and 1620.1 (120.2–2287.1), respectively. Among non‐selected consecutive non‐responder patients, re‐treatment with PEG IFN‐α‐2a + RIBA is associated with virological response regardless of the presence of antibody‐mediated resistance to conventional IFN treatment. J. Med. Virol. 82:2027–2031, 2010. © 2010 Wiley‐Liss, Inc.     

Prenatal diagnosis of a 12q22q23.2 interstitial deletion by array CGH in a malformed fetus

We report the prenatal diagnosis of a 12q22q23.2 de novo interstitial deletion performed by array based comparative genomic hybridization (array CGH) in a fetus with cystic hygroma colli, intrauterine growth retardation, microcephaly and micrognathism. Haploinsufficiency for insuline-like growth factor 1 gene (IGF1), which is mapped in the deleted region, is suggested because of its implication in prenatal and postnatal growth and in neuronal maturation. This case demonstrates the contribution of array CGH in prenatal diagnosis for detecting small unbalanced chromosomal abnormalities in malformed fetuses and, subsequently, for genetic counselling.