Predictive factors of catch-up growth in term, small for gestational age infants: a two-year prospective observational study in Algeria.

OBJECTIVES: Most small for gestational age (SGA) infants show catch-up growth but the minority who do not may benefit from growth-promoting treatment. We determined the prevalence of, and risk factors for, failure to show catch-up growth in term SGA infants. METHODS: Prospective observational study of infants born at 37-42 weeks gestation between December 2012 and March 2014 with birth weight <10th percentile. Length, weight and head circumference were measured from birth to 2 years. RESULTS: Of 457 (3.9 %) term infants with SGA, 446 (97.6 %) were followed up until 2 years. At 24 months, supine length, weight and head circumference were ≥-2 standard deviation score (SDS) in 87.9 , 96.4 and 97.1 % subjects, with persistent short stature in 12.1 %. In a multivariate analysis, the independent predictors of failure to show catch-up growth at 24 months were: maternal height <150 cm, difference between mid-parental height and birth length of ≥2.2 SDS, height at 24 months <-2 SDS below mid-parental height SDS, history of SGA, ponderal index <3rd centile and duration of breast feeding <3 months. CONCLUSIONS: This study provides data concerning the epidemiology of SGA in Algeria and the factors associated with post-natal growth. Establishing which children remain short at 2 years has identified a cohort of patients requiring continuing follow up, with a view to instituting growth hormone therapy in selected cases. These results favour the setting up of an integrated national program to register SGA infants at birth, with re-evaluation at 2 years. (250 words).

Prevalence of BTK mutations in male Algerian patterns with agammaglobulinemia and severe B cell lymphopenia.

X linked agammaglobulinemia (XLA) is the first described primary immunodeficiency and the most common form of agammaglobulinemia. It is characterized by susceptibility to recurrent infections, profound decrease of all immunoglobulin isotypes and very low level of B lymphocytes in peripheral blood. The disorder is caused by mutations in the Bruton's Tyrosine Kinase (BTK). Nine male patients suspected to have XLA from nine unrelated families were enrolled in this study. We performed sequencing of the BTK gene in all nine patients, and in the patients' relatives when possible. The XLA diagnosis was confirmed for six patients with six different mutations; we identified a novel mutation (c.1522G>A) and five known mutations. One third of nine unrelated patients do not have mutations in BTK and thus likely suffer from autosomal recessive agammaglobulinemia in the setting of consanguinity. Our results support that the autosomal recessive agammaglobulinemia can be more common in Algeria.

Clinical, immunological and genetic features in eleven Algerian patients with major histocompatibility complex class II expression deficiency.

Presenting processed antigens to CD4+ lymphocytes during the immune response involves major histocompatibility complex class II molecules. MHC class II genes transcription is regulated by four transcription factors: CIITA, RFXANK, RFX5 and RFXAP. Defects in these factors result in major histocompatibility complex class II expression deficiency, a primary combined immunodeficiency frequent in North Africa. Autosomal recessive mutations in the RFXANK gene have been reported as being the principal defect found in North African patients with this disorder. In this paper, we describe clinical, immunological and genetic features of 11 unrelated Algerian patients whose monocytes display a total absence of MHC class II molecules. They shared mainly the same clinical picture which included protracted diarrhoea and respiratory tract recurrent infections. Genetic analysis revealed that 9 of the 11 patients had the same RFXANK founder mutation, a 26 bp deletion (named I5E6-25_I5E6+1, also known as 752delG26). Immunological and genetic findings in our series may facilitate genetic counselling implementation for Algerian consanguineous families. Further studies need to be conducted to determine 752delG26 heterozygous mutation frequency in Algerian population.