Anganwadi based nutritional survey of children in Attappadi

Background: Malnutrition and anaemia form major public health problems among the school age children, particularly in the developing countries.Methods: A cross sectional study was conducted among children between 6 months and 18 years, in randomly selected 25 Anganwadis of Attappadi area. Objective of the study was to estimate the prevalence of anaemia and malnutrition among the children of Attappadi. Children were divided in to tribal and nontribal. Anthropometric measurements, haemoglobin estimation by cyanmethemoglobin method and peripheral smear examination were done.Results: 65.5% tribal and 54.1% non-tribal were anaemic. Among males 65.9% tribal and 56.4% non-tribal were anaemic. Among females 65.1% tribal and 52.6% nontribal were anaemic. In the age group less than 6 years, 9% tribal females, 8.9% nontribal females, 12% tribal males and 5.8% nontribal males were severely stunted. Above 6yrs it was 3.3% tribal females, 2.7% nontribal females, 2.4% tribal males and 7.4% nontribal males. In the age group less than 6 years, 12.5% tribal females, 3.9% nontribal females, 15.9% tribal males and 4.3% nontribal males had severe underweight. Above 6 years it was 8.3% tribal females, 0% non-tribal females, 19% tribal males and 3% non-tribal males.Conclusions: Anaemia and malnutrition are common among children of Attappadi. Tribal children are more affected than non-tribal children. Anaemia is more common among two age groups, less than 5 years and more than 11 years. Among females’ adolescent girls are more affected. Periodic assessment of growth parameters and early detection and treatment of anaemia are needed.</jats:p

Clinical and Genetic Spectrum of a Large Cohort of Patients With Leukocyte Adhesion Deficiency Type 1 and 3: A Multicentric Study From India

Leukocyte adhesion deficiency (LAD) syndrome is a group of inborn errors of immunity characterized by a defect in the cascade of the activation and adhesion leading to the failure of leukocyte to migrate to the site of tissue injury. Three different types of LAD have been described. The most common subtype is LAD type 1 (LAD1) caused due to defects in theITGβ2gene. LAD type 2 (LAD2) is caused by mutations in theSLC35C1gene leading to a generalized loss of expression of fucosylated glycans on the cell surface and LAD type 3 (LAD3) is caused by mutations in theFERMT3gene resulting in platelet function defects along with immunodeficiency. There is a paucity of data available from India on LAD syndromes. The present study is a retrospective analysis of patients with LAD collated from 28 different centers across India. For LAD1, the diagnosis was based on clinical features and flow cytometric expression of CD18 on peripheral blood leukocytes and molecular confirmation by Sanger sequencing. For patients with LAD3 diagnosis was largely based on clinical manifestations and identification of the pathogenic mutation in theFERMT3gene by next-generation Sequencing. Of the total 132 cases diagnosed with LAD, 127 were LAD1 and 5 were LAD3. The majority of our patients (83%) had CD18 expression less than 2% on neutrophils (LAD1°) and presented within the first three months of life with omphalitis, skin and soft tissue infections, delayed umbilical cord detachment, otitis media, and sepsis. The patients with CD18 expression of more than 30% (LAD1+) presented later in life with skin ulcers being the commonest manifestation. Bleeding manifestations were common in patients with LAD3. Persistent neutrophilic leukocytosis was the characteristic finding in all patients. 35 novel mutations were detected in theITGβ2gene, and 4 novel mutations were detected in theFERMT3gene. The study thus presents one of the largest cohorts of patients from India with LAD, focusing on clinical features, immunological characteristics, and molecular spectrum.</jats:p