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Severe acute malnutrition (SAM) not only increases risk of mortality, but it also increases the risk of impaired motor, cognitive, and psychosocial development. Across the globe, 43% of all children younger than five years of age are at risk of not achieving their developmental potential. The World Health Organization management guidelines for SAM has included the integration of early childhood development (ECD) directed sensory and psychosocial stimulation and structured play therapy in the medico-nutritional care process. Despite this, management still largely focuses on nutrition rehabilitation, while these interventions take a backseat. Most countries are moving towards home-based management of uncomplicated SAM children. Hence, it is equally important to have a strong ECD component in the community-based management programs. Strengthening the support of sensory and psychosocial stimulation and structured play support in both facility and community-based care of SAM children will not only help them to survive, but also thrive and transform. With this background, we briefly describe the experiences of a pilot study aiming at strengthening of these interventions support in 10 nutritional rehabilitation centers across India.

Objective To study the various comorbidities and their impact on outcome of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infected children. Methodology Review of medical records of 120 children (58.4% males), aged 1 month to 18 years, admitted between 1 March and 31 December, 2020 with at least one positive RT-PCR test for SARS-CoV-2. Clinical and demographic variables were compared between children with and without co-morbidities. Results 62 (51.7%) children had comorbidities. The most common comorbidity was tuberculosis (32.3%) followed by other infections (27.4%) and hematological (19.4%) conditions. Fever (89.2%) was the most common clinical feature followed by respiratory (52.5%) and gastrointestinal (32.5%) manifestations. There was no significant difference in the severity of COVID illness, length of hospital stay and adverse outcomes (ventilation and mortality) among children with and without comorbidities. Conclusions The presence of a comorbid illness in pediatric inpatients with COVID-19 did not impact the illness severity, length of hospitalization, ventilation requirement and mortality.

Objectives To assess pubertal development and its determinants in adolescents with transfusion-dependent thalassemia (TDT). Methods In this cross-sectional study from a tertiary teaching hospital in Delhi, records of adolescents aged 17-19 years with TDT on regular transfusion at thalassemia day-care centre were reviewed. Pubertal development and its determinants were assessed. Results Records of 58 (33 male) adolescents with TDT were reviewed. Among them, 42 (72.4%) had normal/delayed onset with spontaneous progression of puberty, while 16 (27.6%) had pubertal arrest/failure and received hormonal replacement therapy (HRT). Short stature was observed in all adolescents on HRT. Amongst other endocrinopathies, only hypoparathyroidism was found to be significantly higher in the HRT group. On multivariate analysis, serum ferritin (OR-1.005, 95% CI 1.002, 1.009) was observed to be the only significant determinant of pubertal arrest/failure. Conclusions A significant proportion of adolescents with TDT continue to have pubertal arrest/failure. High systemic iron load is the key determinant for this.

Objective To compare the effect of the application of three growth references (Agarwal, 1992; Indian Academy of Paediatrics (IAP), 2015; and World Health Organisation (WHO), 2007) on interpretation of anthropometric parameters in schoolchildren. Setting Cross-sectional school-based study. Participants Children 8-15 years studying in one government school and one private school of Delhi. Procedure The age- and gender-specific standard deviation scores of height-for-age and BMI-for-age were estimated for each student enrolled, using the three growth references independently. Main outcome measure The proportion of children with short stature, thinness and overweight/ obesity determined by each growth reference were compared. Results A total of 1237 students participated in the study. A significantly higher proportion of children (both sexes) were classified to have short stature using WHO 2007 reference (8.8%) as compared to the Agarwal (3.3%) charts and IAP, 2015 references (3.6%). The combined prevalence of overweight and obesity was highest (34.8%) by the IAP, 2015 reference as against 32% by Agarwal charts and 29.1% by WHO, 2007 reference. Good agreement existed between the IAP, 2015 reference and Agarwal charts in classifying subjects into different BMI categories (Kappa=0.82) and short stature (Kappa=0.99). Conclusions In view of differences noted, use of national population derived reference data is suggested to correctly define growth trajectories in children.

Congenital adrenal hyperplasia (CAH) is an autosomal recessive endocrine disorder which can manifest after birth with ambiguous genitalia and salt-wasting crisis. However, genital ambiguity is not seen in male babies and may be mild in female babies, leading to a missed diagnosis of classical CAH at birth. In this review, we provide a standard operating protocol for routine newborn screening for CAH in Indian settings. A standardization of first tier screening tests with a single consistent set of cut-off values stratified by gestational age is also suggested. The protocol also recommends a two-tier protocol of initial immunoassay/time resolved fluoroimmunoassay followed by liquid chromatography tandem mass spectrometry for confirmation of screen positive babies, wherever feasible. Routine molecular and genetic testing is not essential for establishing the diagnosis in all screen positive babies, but has significant utility in prenatal diagnosis and genetic counseling for future pregnancy.

Treatment of congenital adrenal hyperplasia (CAH) requires lifelong replacement of glucocorticoids with regular follow up to manage associated morbidities. The current review focuses on follow-up and management of infants diagnosed with classical CAH pertinent to Indian context. Early initiation of oral hydrocortisone in divided doses is recommended after diagnosis in newborn period, infancy and childhood. Fludrocortisone is recommended for all infants with classical CAH. All infants should be monitored as per protocol for disease and treatment related complications. The role of prenatal steroids to pregnant women with previous history of CAH affected infant for prevention of virilization of female fetus is controversial.

The bacteriological study of the nasopharyngeal, throat, per nasal tracheal aspirate, and percutaneous lung aspirate was non-contributory, and virological examinations failed to yield a viral agent. Meanwhile the child received treatment with penicillin and streptomycin for 8 days. She became afebrile on 7th day of hospitalization, and her respiratory findings, adenopathy and splenomegaly disappeared while the liver receded to 2 cm below costal margin. The throat swab specimen after being stored at –20 oC to –70 oC for 27 days was examined for M. pneumoniae by inoculating on agar plates and diphasic medium, and its growth was confirmed on the 7th day of first agar subculture. On day 14 of incubation in diphasic medium, a drop in pH (glucose fermentation) and spherular colonies were observed floating in the media. The colonies demonstrated guinea pig erythrocyte hemolysis (within 48 hours) and sheep cell haemadsorption, properties peculiar to M. pneumoniae. Isolation of M. pneumoniae from throat and tracheal aspirates of this child with pneumonia – whose extensive bacterial and viral investigations were non-contributory – indicated etiological role of M. pneumoniae. The child was treated with demethyl-chlortetracycline. A repeat X-ray 3 month later showed persisting middle lobe infiltrates, although child was asymptomatic.

We continue our expedition into the past while reviewing an article from the September 1965 issue data due to less severe forms associated with females or the gender bias in healthcare seeking behavior. In both of the cases, calcium, phosphorus and serum alkaline phosphatase levels in serum were normal. The only salient diagnostic findings were radiological (described later). Biopsies demonstrated proliferative chondroid tissue. The fungating mass in the second case was infectious, not malignant. The discussion of this article dwelt on various nomenclature, demographic characteristics, hereditary pattern (64% familial, remaining unknown or due to a new mutation), and clinical and radiological features (bony projections of various size and contour with the apex pointing towards the shaft and away from the nearest epiphysis, heterogeneously radio-opaque with interspersed areas of translucency). Historical background and past knowledge: A patient with multiple exostoses was presented in a lecture by Hunteras as early as 1786, while another with familial involvement was reported in 1814 [2,3]. Various terms based on the typical clinical and histopathological features (i.e. multiple osteochondromas, cartilaginous exostosis, deforming chondrodysplasia, diaphyseal aclasis) were in use. The prefix ‘hereditary’was added once the familial nature was recognized. HME remained an enigma till the 1950s when some groundbreaking research emerged. Solomon, et al. [4] delineated the clinical, radiological, pathological and genetic characteristics of HME in 1963. In this paper, it was stated that exostoses were cartilage-capped bony outgrowths from the juxta-ephipyseal regions of rapidly growing ends of bones originating in cartilage. Long bones and less commonly flat bones were described to be involved with sparing of face and skull. It was described that lesions appear by the end of the first decade, increase during puberty, and become dormant with cessation of growth. The number, size and location of exostoses were reported to vary between and within families. of Indian Pediatrics. This comprised of 41 pages with four research papers (ECG changes in progressive muscular dystrophy, a mathematical method to estimate gene frequencies, antenatal illnesses in villages of Punjab and a case series), two case records (pulmonary agenesis, polyarteritis nodosa), book reviews, current literature and news. We selected the case series of Hereditary multiple exostoses (HME), primarily to showcase the meticulousness with which the authors attempted to trace back the pedigree [1]. After briefly discussing the scientific knowledge that existed then, we will touch upon the recent advances that have evolved in understanding this disorder at the molecular and genetic levels.

Whyth in 1768 for his treatise ‘Dropsy in the brain’ [2]. The patho-physiology of TBM was unravelled by Arnold Rich and McCordock in 1933 [3]. Before the mid-20th century, childhood TB was uniformly fatal. The introduction of isoniazid in early 1950’s revolutionized the treatment of TB. For nearly two decades, the standard treatment comprised of combination of isoniazid and streptomycin, following which rifampicin was introduced. Still, the mortality was very high, and significant proportions were left with physical and mental disabilities due to delay in treatment initiation and poor compliance. To strengthen the fight against TB, the Government of India launched “District Tuberculosis Control Programme” in 1962 which focussed on prevention, control and management of the disease in both urban as well as rural areas. At the time of publication of this article [1], there existed wide disparity in the reported incidence (0.5-13%) of TBM in India, and its true situation was difficult to determine because of diagnostic uncertainties and poor case notification. In most cases, the diagnosis was presumptive, based on clinical suspicion and circumstantial evidence as bacteriological confirmation was often not possible.

elicited in both families as complete family history was not available, but a strong familial tendency of the disease was suggested. The cardinal triad (blue sclera, deafness and brittle bones) was not seen in all cases, while the blue sclera was reported as consistent finding. The combination of blue sclera and fracture was more common as compared to deafness. Among the 7 cases reported, 2 fitted into the more severe congenital variety and the rest into the milder tarda form, as per the accepted classification of OI at that time. The family tree revealed that the incidence of deep blue sclera and fractures increased with subsequent pregnancies. The outcome of the congenital variety was poor as mortality occurred early, while the tarda type did well later in life. Historical background and past knowledge: OI is a clinical entity known since 1000 BC, evident through an Egyptian mummy of an infant kept in London’s museum. The medical literature on this disorder can be recognized ever since the seventeenth century, when various alternative terms – like osteomalacia congenita, mollities ossium, fragilitas ossium, and osteopsathyrosis idiopathica – were used to describe it. The term ‘osteogenesis imperfecta’ was first coined by Lobstein in 1835. In 1906, Looser categorized OI into congenital (Vrolik) and tarda (Lobstein) varieties based on clinical severity [2]. The congenital variety was a more severe form that presented with intrauterine fractures, while the tarda variety followed a milder course, often complicated by otosclerosis with advancing age. The tarda variety was subsequently further divided into gravis (fractures occurring in infancy) and levis (fractures in late childhood) type by Seedorff in 1949 [3]. The characteristic triad of blue sclera, hearing loss and brittle bones was established as distinguishing diagnostic feature of OI by this time. The most accepted hypothesis regarding pathogenesis of OI was impaired maturation of collagen and a defect in osteoblastic activity transmitted by autosomal dominance. The December 1965 issue of Indian Pediatrics had three original articles related to psychoneurosis in the young, osteogenesis imperfecta, and disorders of anomalous fusion of skeleton. Amongst these, we decided to review the article on osteogenesis imperfecta (OI) for this series. Much progress has occurred in understanding of various aspects of OI and its management since the publication of this article fifty years ago.

group with otorrhea (26.3%). The average incubation period – recorded in 78 cases where the information was available – was 13.4 days with maximum deaths observed in cases with incubation period 99 oF within 24 hours of admission were the factors associated with grave prognosis. Most (96.8%) deaths occurred within first week of admission. No significant difference in mortality was recorded with different dosage schedules of anti-tetanus serum (ATS) while the use of penicillin was associated with improved outcome. Historical background and past knowledge: After Hippocrates’ primeval description of tetanus in medical literature, no significant advancement in understanding occurred till the early 19th century [2]. The causative agent of tetanus was identified by Rossenbach [3] but isolation of Clostridium tetani is credited to Kitasato in 1889 [4]. This gram-positive, spore-forming, motile, anaerobic bacillus constitutes the normal intestinal flora of animals. As the spores are ubiquitous and persist for long time in the soil, these can easily contaminate wounds. Thus, any nonor partially-vaccinated individual is vulnerable to develop tetanus. In 1897, Edmond Nocard established the role of tetanus anti-toxin in inducing passive immunity in humans. Nearly three decades later, tetanus toxoid – developed by Descombey in 1924 – was widely used during World War II. The use of tetanus toxoid as a combined vaccine in the form of DPT (Diphtheria, Pertussis and Tetanus) was licensed in 1949. In the prevaccination era, the true burden of tetanus was largely unknown as most neonatal births and deaths occured at home without an account of the either event.

Historical background and past knowledge: The earliest reference to BHS, then referred to as infantile form of temper tantrums or infantile syncope, were made by Rillet and Barthezin in 1843, and by Meigsin in 1848. Subsequently in the 20th century, various authors published their clinical viewpoints on its pathophysiology and prognostic significance. Based on the color change demonstrated by the child during the spell, BHS were classified as cyanotic, pallid and mixed. Till the 1960’s, despite several hypotheses, the pathophysiology and etiology remained largely nebulous and uncertainities existed regarding the outcome. Multiple factors like disturbed parent-child relationship, hereditary autonomic instability, self asphyxiation, decreased cerebral blood flow secondary to increased intrathoracic pressure due to spontaneous valsalva manoeuvre and altered cerebral mechanism secondary to various stimuli were implicated for cyanotic BHS [1]. For the pallid form, circulatory failure secondary to asystole leading to cerebral anoxia was considered the most probable hypothesis [2].

The clinical features of severe acute malnutrition (SAM) often overlap with the common manifestations of celiac disease. In this observational pilot study, 76 children fulfilling the case definition of SAM were investigated for celiac disease, tuberculosis and HIV. Celiac disease was diagnosed in 13.1% of SAM children while tuberculosis and HIV were diagnosed in 9.3% and 4%, respectively.

A cross sectional survey was conducted in the year 2001, to establish the current status of iodine nutriture and level of salt iodisation in the state of Andhra Pradesh, India. All the 23 districts were included. The data was collected in each district through school approach. A total of 3706 salt samples and 1952 casual urine samples were collected. Nearly 45% of the population was found to be consuming iodised salt. All the districts had adequate iodine nutriture except Rangareddy and Cuddapah. The districts which were earlier found endemic to iodine deficiency namely Srikakulam, Vizianagaram, Visakhapatnam, Godavari, Khammam, Adilabad and Warrangal were found with adequate iodine nutriture as reflected by median UIE level of more than 100 microg/L. The study revealed success of salt iodisation program in the state.

Iodine deficiency disorders (IDD) is a public health problem in India. A ban on the sale of uniodised salt for household consumption has been introduced in Rajasthan State since 1992. The present study was conducted in the district of Bharatpur, Rajasthan with the objective to assess the prevalence of iodine disorders in school children as no data is available on this aspect. A total of 3072 children in the age group of 6-12 years were included in the study and were clinically examined. On the spot urine samples were collected randomly from 450 children. A total of 1064 salt samples were collected randomly from the families of the children. The total goiter prevalence was found to be 7.2% in the subjects studied. It was found that the percentage of children with urinary iodine excretion20.0; 20.0-49.9, 50.0-99.9 and 100 mcg/L and above was 1.1, 1.1, 7.8 and 90.0% respectively. The assessment of iodine content of salt revealed that 56% of the families were consuming iodised salt. The findings of the present study indicated that the population is in a transition phase from iodine deficient (as revealed by the TGR) to iodine sufficient (as revealed by the medium UIE of 200.0 mcg/L) nutriture.