Complications of obesity in children and adolescents

Is there a causal relationship between obesity and puberty

Nutritional rickets and osteomalacia are common in dark-skinned and migrant populations. Their global incidence is rising due to changing population demographics, failing prevention policies and missing implementation strategies. The calcium deprivation spectrum has hypocalcaemic (seizures, tetany and dilated cardiomyopathy) and late hypophosphataemic (rickets, osteomalacia and muscle weakness) complications. This article reviews sustainable prevention strategies and identifies areas for future research. The global rickets consensus recognises the equal contribution of vitamin D and dietary calcium in the causation of calcium deprivation and provides a three stage categorisation for sufficiency, insufficiency and deficiency. For rickets prevention, 400 IU daily is recommended for all infants from birth and 600 IU in pregnancy, alongside monitoring in antenatal and child health surveillance programmes. High-risk populations require lifelong supplementation and food fortification with vitamin D or calcium. Future research should identify the true prevalence of rickets and osteomalacia, their role in bone fragility and infant mortality, and best screening and public health prevention tools.

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Nutritional Rickets and Osteomalacia in the Twenty-first Century: Revised Concepts, Public Health, and Prevention Strategies.

Langerhans cell histiocytosis (LCH) is a group of diseases characterized by the proliferation and accumulation of Langerhans cells. Clinical presentations of LCH vary widely. A PubMed search was conducted using Clinical Queries with the key term “Langerhans cell histiocytosis”. The search strategy included meta-analyses, randomized controlled trials, clinical trials, observational studies, and reviews. This paper is based on, but not limited to, the search results. Generally, patients with LCH can be divided into two groups based on the extent of involvement at diagnosis, namely, single-system LCH and multisystem LCH. The involvement may be unifocal or multifocal. Patients with isolated bone lesions typically present between 5 and 15 years of age, whereas those with multisystem LCH tend to present before 5 years of age. The clinical spectrum is broad, ranging from an asymptomatic isolated skin or bone lesion to a life-threatening multisystem condition. Clinical manifestations include, among others, "punched out" lytic bone lesion, seborrheic dermatitis-like eruption, erythematous/reddish-brown crusted/scaly papules/maculopapules/plaques/patches, and eczematous lesions, diabetes insipidus, hepatosplenomegaly, cytopenias, lymphadenopathy, and an acute fulminant disseminated multisystem condition presenting with fever, skin rash, anemia, thrombocytopenia, lymphadenopathy, and hepatosplenomegaly. The diagnosis is clinicopathologic, based on typical clinical findings and histologic/immunohistochemical examination of a biopsy of lesional tissue. Positive CD1a, S100, and/or CD207 (Langerin) immunohistochemical staining of lesional cells is required for a definitive diagnosis. Watchful waiting is recommended for patients with skin-only LCH. Patients with symptomatic or refractory skin-only LCH may be treated with topical tacrolimus/corticosteroids, topical nitrogen mustard, oral methotrexate, or oral hydroxyurea. The current recommended first-line therapy for patients with multisystem LCH is 12 months therapy with prednisone and vinblastine. Mercaptopurine is added for patients with risk organ involvements. Because of the broad spectrum of clinical manifestations and the extreme diversity of disease, LCH remains a diagnostic dilemma. Morphological identification of LCH cells and positive immunochemical staining with CD1a, S100, and/or CD207 (Langerin) of lesional cells are necessary for a definitive diagnosis.

Childhood Langerhans cell histiocytosis: a disease with many faces.

CONTEXT Inactivating germline mutations in the aryl hydrocarbon receptor interacting protein (AIP) gene are linked to pituitary adenoma predisposition. Here, we present the youngest known patient with AIP-related pituitary adenoma. CASE DESCRIPTION The patient presented at the age of 4 years with pituitary apoplexy and left ptosis with severe visual loss following a 1-year history of abdominal pain, headaches, and rapid growth. His IGF-1 level was 5× the upper limit of normal, and his random GH level was 1200 ng/mL. MRI showed a 43 × 24 × 35‒mm adenoma with suprasellar extension invading the left cavernous sinus (Knosp grade 4). After transsphenoidal surgery, histology showed a grade 2A sparsely granulated somatotropinoma with negative O6-methylguanine-DNA methyltransferase and positive vascular endothelial growth factor staining. Genetic testing identified a heterozygous germline nonsense AIP mutation (p.Arg81Ter). Exome sequencing of the tumor revealed that it had lost the entire maternal chromosome-11, rendering it hemizygous for chromosome-11 and therefore lacking functional copies of AIP in the tumor. He was started on octreotide, but because the tumor rapidly regrew and IGF-1 levels were unchanged, temozolomide was initiated, and intensity-modulated radiotherapy was administered 5 months after surgery. Two months later, bevacizumab was added, resulting in excellent tumor response. Although these treatments stabilized tumor growth over 4 years, IGF-1 was normalized only after pegvisomant treatment, although access to this medication was intermittent. At 3.5 years of follow-up, gamma knife treatment was administered, and pegvisomant dose increase was indicated. CONCLUSION Multimodal treatment with surgery, long-acting octreotide, radiotherapy, temozolomide, bevacizumab, and pegvisomant can control genetically driven, aggressive, childhood-onset somatotropinomas.

Surgery, Octreotide, Temozolomide, Bevacizumab, Radiotherapy, and Pegvisomant Treatment of an AIP Mutation‒Positive Child.

Objective: Primary - to determine the age of pubertal onset in Indian boys. Secondary - (a) to assess the impact of obesity on pubertal timing, (b) to assess the relationship between gonadotropins and puberty. Design: Cross-sectional. Setting: General community-seven schools across New Delhi. Participants: Random sample of 1306 school boys, aged 6–17 years. Materials and Methods: Anthropometric measurement for weight and height and pubertal staging was performed for all subjects. Body mass index (BMI) was calculated to define overweight/obesity. Serum luteinizing hormone (LH), follicle stimulating hormone, and serum testosterone were measured in every sixth subject. Main Outcome Measure: Age at pubertal onset-testicular volume ≥4 mL (gonadarche) and pubic hair Stage II. Results: Median age of attaining gonadarche and pubarche was 10.41 years (95% confidence interval [CI]: 10.2–10.6 years) and 13.60 (95% CI: 13.3–14.0 years), respectively. No significant difference in the age of attainment of gonadarche was observed in boys with normal or raised BMI, though pubarche occurred 8 months earlier in the latter group. Serum gonadotropins and testosterone increased with increasing stages of puberty but were unaffected by BMI. Serum LH level of 1.02 mIU/mL and testosterone level of >0.14 ng/mL showed the best prediction for pubertal onset. Conclusion: The study establishes a secular trend of the age of onset of puberty in Indian boys. Pubarche occurred earlier in overweight/obese boys. The cutoff levels of serum LH and testosterone for prediction of pubertal onset have been established.

Pubertal onset in apparently healthy Indian boys and impact of obesity

Objective: Linear growth is best estimated by serial anthropometric data or height velocity (HV). In the absence of recent data on growth velocity, we undertook to establish normative data in apparently healthy North Indian children. Materials and Methods: Prospective longitudinal study in a representative sample of 7710 apparently healthy children, aged 3–17 years from different regions of Delhi. Height was measured at baseline and at 12 months while pubertal examination was performed at baseline in a subset of children. Results: The data on HV and puberty were available in 5635 participants (73.08%; 2341 boys and 3294 girls) and 1553 participants (622 boys; and 931 girls), respectively. The mean peak height velocity (PHV) was 7.82 ± 2.60 cm in boys seen at 12–12.9 years and 6.63 ± 1.81 cm in girls at 10–10.9 years Although late maturing boys had a greater HV than early or normal maturers, it did not vary with the age of pubertal maturation in girls. HV correlated with parental height in prepubertal boys, girls, and pubertal boys (P

Height Velocity in Apparently Healthy North Indian School Children.

Developing Indigenous Therapeutic Calcium Supplementation for Treating Nutritional Rickets

Objective: To evaluate for subclinical atherosclerosis and its risk factors in Indian obese children. Materials and Methods: A cross-sectional, case–control study was conducted to recruit 80 children aged 6–17 years with constitutional obesity as cases and 23 age- and gender-matched controls with normal body mass index (BMI). Anthropometric and clinical evaluation was followed by biochemical analysis and body fat estimation by dual-energy X-ray absorptiometry in cases. Similar evaluation was performed for controls except laboratory parameters. Carotid intima-media thickness (CIMT) was measured with B-mode ultrasonography in both cases and controls to evaluate subclinical atherosclerosis. Results: The mean age of cases was 12.8 ± 3 years, with mean BMI of 29.2 ± 4.8 kg/m2. The mean CIMT was significantly higher in cases than controls (0.54 ± 0.13 vs. 0.42 ± 0.08; P < 0.001 across all ages). CIMT was significantly higher in participants who were hypertensive than nonhypertensive (0.6 ± 0.11 vs. 0.53 ± 0.11 mm; P = 0.04). CIMT showed a positive correlation with BMI (r = 0.23, P = 0.02), percentage body fat and fat mass index (r = 0.28 and 0.3 respectively; P < 0.001), but not with waist: hip ratio. CIMT showed significant positive correlation with blood glucose at 60 min (r = 0.22; P = 0.04), serum insulin at 60 min (r = 0.28; P = 0.01) while negative correlation with whole body insulin sensitivity (r = −0.27; P = 0.01). Conclusion: CIMT correlated significantly to blood pressure, insulin sensitivity, and body fat in Indian obese children.

Carotid Intima-medial Thickness and Glucose Homeostasis in Indian Obese Children and Adolescents.

To ascertain the growth and endocrinal disturbances associated with Pediatric Langerhans Cell Histiocytosis (LCH). Retrospective analysis of hospital records of subjects with LCH, aged 1 mo to 18 y was performed. The diagnosis of LCH was made as per Histiocyte Society criteria. Subjects were classified as group A: multifocal bone disease; B: soft tissue involvement without organ dysfunction; and C: organ dysfunction and treated as per DAL-HX-83 protocol of the Histiocyte Society LCH treatment guidelines. Paired t-test was used to compare the baseline and follow-up data. Total 62 records (group A- 18, B-32 and C-12) were identified with median follow-up of 5.3 ± 3.3 y. Growth failure [measured as weight/ height Standard deviation score (SDS) ≤−2] was the commonest disorder seen in 27 (44 %) subjects. Central Diabetes Insipidus (DI) was seen in 12 (19 %) subjects. Subjects with group C of LCH had poorer weight and height at baseline and follow-up than subjects with group A or B. Height SDS were lower in subjects with concomitant DI than those without DI at baseline (−2.35 ± 1.9 and −1.69 ± 1.4; P 0.18). Subjects with DI did not show significant catch-up in their height (P 0.12) unlike those without DI who showed a catch-up in height (P 0.03) on follow-up. Growth monitoring and screening for DI should be essential part of follow-up in all subjects with LCH.

Growth and Endocrinal Abnormalities in Pediatric Langerhans Cell Histiocytosis.

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