Madhulika Kabra

AIIMS Bhopal All India Institute of Medical Sciences, Bhopal, Madhya Pradesh, India

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Publications (263)571.9 Total impact

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    ABSTRACT: Williams-Beuren syndrome (WBS) or Williams syndrome (OMIM 194050) is a multisystem disorder manifested by neurodevelopmental delay and is caused by a hemizygous deletion of ∼1.5-1.8 Mb in the 7q11.23 region. Clinical features include cardiovascular anomalies (mainly supravalvular aortic stenosis), peripheral pulmonary stenosis, distinctive facies, intellectual disability (usually mild), unique personality characteristics, and growth and endocrine abnormalities. Clinical diagnostic criteria are available for WBS; however, the mainstay of diagnosis is the detection of the contiguous gene deletion. Although FISH remains the most widely used laboratory test, the diagnosis can also be established by means of qPCR, MLPA, microsatellite marker analysis, and chromosomal microarray (CMA). We evaluated the utility of MLPA to detect deletion/duplication in the 7q11.23 region in 43 patients suspected to have WBS using MLPA kits for microdeletion syndromes. A hemizygous deletion in the 7q11.23 region was found in 41 (95.3%) patients using MLPA. One patient had an atypical deletion detected by CMA. During the initial period of this study, the results of 12 patients tested by MLPA were also confirmed by FISH. Compared to FISH and CMA, MLPA is a cheaper, high-throughput, less labor-intensive and less time-consuming technique for the diagnosis of WBS. Although CMA is expensive and labor-intensive, its effectiveness is demonstrated to detect an atypical deletion and to delineate the breakpoints.
    Cytogenetic and Genome Research 09/2015; DOI:10.1159/000439205 · 1.56 Impact Factor
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    ABSTRACT: Chanarin Dorfman Syndrome (CDS) is a very rare neutral lipid metabolism disorder with multisystem involvement. It is inherited as an autosomal recessive manner. It is characterized with congenital ichthyosiform erythroderma and involvement of liver, muscle, and central nervous system. Demonstration of lipid vacuoles in neutrophils from peripheral blood smears in patients with ichthyosiform erythroderma leads to the diagnosis. We report a novel ABHD5 truncating variant in a twenty nine month old female child, who presented with icthyosiform erythroderma.
    Gene 09/2015; DOI:10.1016/j.gene.2015.09.004 · 2.14 Impact Factor
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    American Journal of Medical Genetics Part A 05/2015; 167(10). DOI:10.1002/ajmg.a.37164 · 2.16 Impact Factor
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    ABSTRACT: GM1 gangliosidosis is a lysosomal storage disorder caused by mutations in the GLB1 gene, leading to the deficiency of the enzyme β-D-galactosidase. In this study, we report molecular findings in 50 Asian Indian families with GM1 gangliosidosis. We sequenced all the exons and flanking intronic sequences of GLB1 gene. We identified 33 different mutations (20 novel and 13 previously reported). The novel mutations include 12 missense (p.M1?, p.E129Q, p.G134R, p.L236P, p.G262E, p.L297F, p.Y331C, p.G414V, p.K493N, p.L514P, p.P597L, p.T600I), four splicing (c.246-2A>G, c.397-2A>G, c.552+1G>T, c.956-2A>G), three indels (p.R22Qfs*8, p.L24Cfs*47, p.I489Qfs*4) and one nonsense mutation (p.Q452*). Most common mutations identified in this study were c.75+2InsT (14%) and p.L337P (10%). Known mutations accounted for 67% of alleles frequency in our cohort of patients, suggesting these mutations in GLB1 are recurrent across different populations. Twenty three mutations were localized in the TIM barrel domain, β-domain 1 and β-domain 2. In silico sequence and structure analysis of GLB1 reveals that all the novel mutations affect the function and structure of the protein. We hereby report on the largest series of patients with GM1 gangliosidosis and the first from India. Copyright © 2015. Published by Elsevier B.V.
    Gene 04/2015; 567(2). DOI:10.1016/j.gene.2015.04.078 · 2.14 Impact Factor
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    ABSTRACT: Hydatidiform mole (HM) is an aberrant human pregnancy with abnormal embryonic development and excessive proliferation of the trophoblast. Recessive mutations in NLRP7 are responsible for recurrent HM (RHM). Women with recessive NLRP7 mutations fail to have normal pregnancies from spontaneous conceptions with the exception of three out of 131 reported patients. Because there is no treatment for RHM and maternal-effect genes are needed in the oocytes to sustain normal embryonic development until the activation of the embryonic genome, one patient with recessive NLRP7 mutations tried ovum donation and achieved a successful pregnancy. This study reports three additional live births from donated ova to two patients with recessive NLRP7 mutations. The occurrence of two live births from spontaneous conceptions to two other patients is also reported. The reproductive outcomes and mutations of all reported patients were reviewed and it was found that live births are associated with some missense mutations expected to have mild functional consequences on the protein. The data support a previous observation that ovum donation appears the best management option for these patients to achieve normal pregnancies and provide an explanation for the rare occurrence of live births from natural spontaneous conceptions in patients with two NLRP7 mutations. Copyright © 2015 Reproductive Healthcare Ltd. Published by Elsevier Ltd. All rights reserved.
    Reproductive biomedicine online 04/2015; 31(1). DOI:10.1016/j.rbmo.2015.03.011 · 3.02 Impact Factor
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    ABSTRACT: The aim of our study was to examine the association of low pregnancy-associated plasma protein-A (PAPP-A) with adverse pregnancy outcome. A total of 1640 consecutive pregnant women between 9(+5) and 13(+6) weeks of pregnancy were recruited. One hundred and thirty women with PAPP-A levels < 0.4 multiple of median were followed till delivery and the outcome information was obtained for fetal loss, birthweight, growth restriction, preterm birth, reduced liquor and development of pre-eclampsia. During the study period, 130 (7.92%) women had low PAPP-A and were considered as cases and 200 women with normal PAPP-A were controls. Intrauterine growth restriction was observed in 28 (21.54%) cases as compared to 10 (5%) controls. Pre-eclampsia presented in 24 (18.46%) cases and in 18 (9%) controls. Twenty (15.38%) cases had preterm delivery compared to 12 (6%) controls. Fifty-six (43.08%) cases delivered low-birthweight babies compared to 22 (11%) controls. Thus, the incidence of intrauterine growth restriction, preterm birth and low birthweight was significantly more in the cases as compared to the control group. PAPP-A is a valuable analyte for predicting risk of adverse pregnancy outcome and women with low serum PAPP-A levels would benefit from closer surveillance. © 2015 The Authors. Journal of Obstetrics and Gynaecology Research © 2015 Japan Society of Obstetrics and Gynecology.
    Journal of Obstetrics and Gynaecology Research 03/2015; 41(7). DOI:10.1111/jog.12662 · 0.93 Impact Factor
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    ABSTRACT: Glutaric acidemia I (GA I, #231670) is one of the treatable, autosomal recessively inherited metabolic disorders. Macrocephaly, acute encephalitis-like crises, dystonia and characteristic frontotemporal atrophy are the hallmarks of this disease. In this communication, we present the clinical, biochemical and molecular profile of seventeen GA I patients from 15 unrelated families from India and report seven novel mutations in GCDH gene (c.281G>A (p.Arg94Gln), c.401A>G (p.Asp134Gly), c.662T>C (p.Leu221Pro), c.881G>C (p.Arg294Pro), c.1173dupG (p.Asn392Glufs*5), c.1238A>G (p.Tyr413Cys) and c.1241A>C (p.Glu414Ala)). Out of these, c.662T>C (p.Leu221Pro) in exon 8 and c.281G>A (p.Arg94Gln) allele in exon 4 were low excretor alleles, whereas c.1241A>C (p.Glu414Ala), c.1173dupG and c.1207C>T (p.His403Tyr) in exon 11 were high excretor alleles. We conclude that c.1204C>T (p.Arg402Trp) is probably the most common mutant allele. Exons 11 and 8 are the hot spot regions of GCDH gene in Indian patients with GA I. An early diagnosis and timely intervention can improve the underlying prognosis. Molecular confirmation is helpful in providing genetic counselling and prenatal diagnosis in subsequent pregnancy.
    03/2015; 21. DOI:10.1007/8904_2014_377
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    ABSTRACT: Background: Valproate is a commonly used anticonvulsant drug. Uridine 5΄-diphospho (UDP)-glucuronosyltransferase (UGT) contributes to around 50% of valproate metabolism and its polymorphisms may be important for explaining the considerable variation in valproate levels in patients with epilepsy. Aim: This study was aimed to analyze the genetic polymorphisms of UGT1A6 in Indian children with epilepsy and their potential influence on the pharmacokinetics of valproate. Setting and Design: This cross-sectional study was carried out in the Department of Pediatrics, All India Institutes of Medical Sciences (AIIMS), New Delhi, between March 2011 and July 2012. Materials and Methods: Children aged 3-12 years diagnosed with epilepsy on valproate monotherapy for at least 1 month were enrolled. They underwent a detailed clinical examination. The UGT1A6 polymorphisms were detected by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Random samples were checked by genetic sequencing. The steady-state plasma concentrations of valproate were measured by High Performance Liquid Chromatography (HPLC) and associated with UGT1A6 polymorphisms. Results: A total of 80 children were studied. The prevalence of UGT1A6 T19G was as follows: TT (45%), TG (38.8%), and GG (16.3%); that of UGT1A6 A541G was: AA (48.8%), AG (38.8%), and GG (12.5%); and that of UGT1A6 A552C was: AA (43.8%), AC (40%), and CC (16.3%). The association between valproate doses or standardized serum valproate concentration and the various UGT1A6 genotypes could not be studied reliably in this small study population. Conclusions: The frequencies of UGT1A6 geneotypes and alleles were reported in the study population.
    Neurology India 03/2015; 63(1):35-39. DOI:10.4103/0028-3886.152631 · 1.23 Impact Factor
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    ABSTRACT: Type 1 Gaucher disease is an inherited lysosomal enzyme deficiency with variable age of symptom onset. Common presenting signs include thrombocytopenia, anemia, hepatosplenomegaly, bone abnormalities and, additionally in children, growth failure. Fifty-seven patients aged 3-62 years at the baseline of two phase III trials for velaglucerase alfa treatment were enrolled in the single extension study. In the extension, they received every-other-week velaglucerase alfa intravenous infusions for 1.2-4.8 years at 60 U/kg, although 10 patients experienced dose reduction. No patient experienced a drug-related serious adverse event or withdrew due to an adverse event. One patient died following a convulsion that was reported as unrelated to the study drug. Only one patient tested positive for anti-velaglucerase alfa antibodies. Combining the experience of the initial phase III trials and the extension study, significant improvements were observed in the first 24 months from baseline in hematology variables, organ volumes, plasma biomarkers and, in adults, the lumbar spine bone mineral density Z-score. Improvements were maintained over longer-term treatment. Velaglucerase alfa had a good long-term safety and tolerability profile and patients continued to respond clinically, which is consistent with the results of the extension study to the phase I/II trial of velaglucerase alfa. EudraCT number 2008-001965-27; identifier NCT00635427. This article is protected by copyright. All rights reserved. © 2015 Wiley Periodicals, Inc.
    American Journal of Hematology 03/2015; 90(7). DOI:10.1002/ajh.24012 · 3.80 Impact Factor
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    ABSTRACT: To the Editor: Acrodermatitis enteropathica (AE) is a rare disorder of zinc metabolism [1]. Deficiency of essential amino acids and fatty acids may also induce acrodermatitis enteropathica like lesions. The proposed name for such lesions is acrodermatitis acidemia/acrodermatitis dysmetabolica [2]. We report two rare cases of organic-acidemias who developed these lesions.Case 1:A 35-d-old-boy, born to a non-consanguinous-couple, presented with refractory seizures, poor-feeding and lethargy since day-5-of-life. Neurological evaluation showed microcephaly, lethargy and central hypotonia. Magnetic Resonance Imaging (MRI) of the brain showed bilateral diffusely swollen, hyperintense cerebral white matter with T2-weighted hyperintensities in dorsal pons, cerebellar peduncles, cerebellar white matter, globus pallidus and posterior limb of internal capsule. The blood spot tandem mass spectroscopy (TMS) showed highly elevated leucine/ isoleucine and valine levels with low alanine levels which c ...
    The Indian Journal of Pediatrics 02/2015; 82(9). DOI:10.1007/s12098-015-1715-5 · 0.87 Impact Factor
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    ABSTRACT: Hereditary fructose intolerance (HFI) is a difficult-to-confirm diagnosis, requiring either invasive liver biopsy-enzyme assay or potentially hazardous fructose challenge test or expensive molecular genetic analysis. Therefore, worldwide there has been a trend towards finding "common mutations" in distinct ethnic groups to simplify the process of diagnosis. The nonspecific presentation of the disease often leads to diagnostic confusion with other metabolic liver disorders such as glycogenoses, galactosemia, and tyrosinemia. This leads to much delay in diagnosis with consequent harm to the patient.We report mutations in the ALDOB gene, from eleven Indian patients, seven of whom belong to the Agarwal community. Six patients from the Agarwal community and two non-Agarwal patients harbored one novel mutation, c.324+1G>A (five homozygous and one heterozygous), in the ALDOB gene. Haplotyping performed in families confirmed a founder effect. The community has been known to harbor founder mutations in other genes such as the MLC1, PANK2, and CAPN3 genes, thus providing another evidence for a founder effect in the community in case of HFI. This may pave the path for a simpler and quicker test at least for this community in India. In addition to the founder mutation, we report four other novel mutations, c.112+1delG, c.380-1G>A, c.677G>A, and c.689delA, and a previously reported mutation, c.1013C>T, in the cohort from India.
    01/2015; 19. DOI:10.1007/8904_2014_374
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    ABSTRACT: Xeroderma pigmentosum (XP) is an autosomal recessive genetic disorder characterized by cutaneous and ocular photosensitivity and an increased risk of developing cutaneous neoplasms. Progressive neurological abnormalities develop in a quarter of XP patients. To study the clinical profile and perform a mutation analysis in Indian patients with xeroderma pigmentosum. Ten families with 13 patients with XP were referred to our clinic over 2 years. The genes XPA, XPB and XPC were sequentially analyzed till a pathogenic mutation was identified. Homozygous mutations in the XPA gene were seen in patients with moderate to severe mental retardation (6/10 families) but not in those without neurological features. Two unrelated families with a common family name and belonging to the same community from Maharashtra were found to have an identical mutation in the XPA gene, namely c.335_338delTTATinsCATAAGAAA (p.F112SfsX2). Testing of the XPC gene in two families with four affected children led to the identification of the novel mutations c.1243C>T or p.R415X and c.1677C>A or p.Y559X. In two families, mutations could not be identified in XPA, XPB and XPC genes. The sample size is small. Indian patients who have neurological abnormalities associated with XP should be screened for mutations in the XPA gene.
    Indian Journal of Dermatology Venereology and Leprology 01/2015; 81(1):16-22. DOI:10.4103/0378-6323.148559 · 1.39 Impact Factor
  • Seema Kapoor · Sangeeta Gupta · Madhulika Kabra
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    ABSTRACT: Pediatricians are the first contact of a child with genetic disorders such as Down Syndrome. After diagnosis, parents often express and wish that if it was possible to detect it during pregnancy and could it be avoided in the future pregnancy. This makes it essential that pediatricians should have some idea about the basic screening methods and strategy used during pregnancy.
    Indian pediatrics 12/2014; 51(12):959-62. DOI:10.1007/s13312-014-0540-7 · 1.04 Impact Factor
  • Genetics in medicine: official journal of the American College of Medical Genetics 10/2014; 17(1). DOI:10.1038/gim.2014.149 · 7.33 Impact Factor
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    ABSTRACT: Mucopolysaccharidosis IV A (Morquio syndrome A, MPS IVA) is a lysosomal storage disease caused by the deficiency of N-acetylgalactosamine-6-sulfatase (GALNS). The mutation spectrum in this condition is yet to be determined in Indians. We aimed to analyze the mutations in the GALNS gene in Asian Indians with MPS IVA. All the exons and the adjacent intronic regions of the gene were amplified and sequenced in sixty-eight unrelated Indian families. We identified 136 mutant alleles comprising of 40 different mutations. We report twenty-two novel mutations that comprise of seventeen missense (p.Asn32Thr, p.Leu36Arg, p.Pro52Leu, p.Pro77Ser, p.Cys79Arg, p.His142Pro, p.Tyr191Asp, p.Asn204Thr, p.Gly188Ser, p.Phe216Ser, p.Trp230Cys, p.Ala291Ser, p.Gly317Arg, p.His329Pro, p.Arg386Ser, p.Glu450Gly, p.Cys501Ser), three splice-site variants (c.120 + 1G > C, c.1003-3C > G, c.1139 + 1G > A), one nonsense mutation (p.Gln414*) and one frameshift mutation (p.Pro420Leufs*440). Eighteen mutations have been reported earlier. Among these p.Ser287Leu (8.82%), p.Phe216Ser (7.35%), p.Asn32Thr (6.61%) and p.Ala291Ser (5.88%) were the most frequent mutations in Indian patients but were rare in the mutational profiles reported in other populations. These results indicate that the Indian patients may have a distinct mutation spectrum compared to those of other populations. Mutant alleles in exon 1, 7 and 8 accounted for 44.8% of the mutations, and sequencing of these exons initially may be a cost-effective approach in Asian Indian patients. This is the largest study on molecular analysis of patients with MPS IVA reported in the literature, and the first report from India
    American Journal of Medical Genetics Part A 09/2014; 164A(11). DOI:10.1002/ajmg.a.36735 · 2.16 Impact Factor
  • Neerja Gupta · Madhulika Kabra · Seema Kapoor
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    ABSTRACT: Early detection and prevention of birth defects is necessary to further reduce neonatal morbidity and mortality. A birth defect registry or surveillance system is necessary to assess the exact magnitude, profile and modifiable risk factors for birth defects. We review the existing efforts and suggest possible options for addressing this important issue. Connecting birth defects registry with the pre-existing programs such as National Neonatal Perinatal Database could be one of the option.
    Indian pediatrics 09/2014; 51(9):693-6. DOI:10.1007/s13312-014-0483-z · 1.04 Impact Factor
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    ABSTRACT: Background: Post licensure studies have identified an increased risk of intussusception following vaccination with currently licensed rotavirus vaccines, raising safety concerns generic to all rotavirus vaccines. We describe the surveillance for intussusception in a phase III clinical trial with an oral monovalent rotavirus vaccine developed from the neonatal 116E strain. Methods: Using broad screening criteria and active surveillance, the incidence of intussusception between 6 weeks and 2 years of age was measured in 4532 children who received three doses of vaccine and 2267 children who received a placebo in the clinical trial. Possible intussusceptions were evaluated with a screening ultrasonogram. An independent intussusception case adjudication committee reviewed all intussusceptions and graded them on Brighton Collaboration criteria for diagnostic certainty. Results: We identified twenty-three intussusceptions on ultrasound from 1361 evaluated sentinel events. Eleven were of level 1 diagnostic certainty as determined by the independent intussusception case adjudication committee. None required surgical intervention, and the earliest identified intussusception was at 36 days following the third dose in a placebo recipient. Among vaccine recipients the first event of intussusception occurred 112 days after the third dose. The incidence of ultrasound-diagnosed intussusception was 200/100,000 child-years (95% CI, 120, 320) among those receiving the vaccine and 141/100,000 child-years (95% CI, 50, 310) among those receiving the placebo. The incidence rate of confirmed intussusception among vaccine recipients was 94/100,000 child-years (95% CI, 41, 185) and 71/100,000 child-years (95% CI, 15, 206) among those receiving the placebo. Conclusion: In this licensure study, 23 cases of intussusception were identified through an active surveillance system, but there was no temporal association with rotavirus vaccination. The use of active surveillance with broad criteria intended for ensuring safety of children participating in a trial, identified several transient intussusceptions that were of doubtful clinical significance.
    Vaccine 08/2014; 32, Supplement 1:A104-A109. DOI:10.1016/j.vaccine.2014.03.036 · 3.62 Impact Factor
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    ABSTRACT: This cross sectional study assessed the prevalence of behavioral comorbidity and its association with epilepsy-related factors in children and adolescents with epilepsy. One hundred consecutive patients with active epilepsy, aged 6–16 years, were screened for behavioral comorbidity using the Child Behavior Checklist and those who qualified as having behavioral comorbidity were compared with those who did not have it. Behavioral comorbidity was found in 43 of 100 participants. Being treated with antiepileptic drug polytherapy (odds ratio 6.3, 95% confidence interval 1.4–17.3, p = 0.01) independently predicted behavioral comorbidity in the patients studied. The demonstrated high frequency of behavioral comorbidity in children with epilepsy suggests that pediatrician and pediatric neurologists should be sensitive to this fact in order to identify behavioral comorbidity in children with epilepsy.
    Journal of Clinical Neuroscience 08/2014; 21(8). DOI:10.1016/j.jocn.2013.11.023 · 1.38 Impact Factor
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    ABSTRACT: This study was undertaken in view of the paucity of data regarding the profile of prothrombotic factors in children with ischemic stroke. Sixty-four children with ischemic stroke were prospectively evaluated for presence of prothrombotic factors over a 2 year period. The blood samples were analyzed for protein C (PC), protein S (PS), activated protein C resistance (APCR), factor V Leiden (FVL), anti-thrombin-III (AT-III), lipoprotein (a) [Lp(a)], lupus anticoagulant (LA), anti-cardiolipin antibodies (aCL) immunoglobulin (Ig) M and IgG, homocysteine, and methylenetetrahydrofolate reductase (MTHFR) at least 3 months after the onset of stroke. At least one prothrombotic factor was identified in 45.3% children (29/64). These included hyperhomocysteinemia (11/64), PC deficiency (9/64), aCL (8/64), PS deficiency (5/64), APCR (3/64), AT-III deficiency (2/64) and LA (1/64). Multiple factors were coexistent in 17.2% (11/64). The prevalence of PC deficiency, PS deficiency and co-existence of multiple abnormalities observed were similar to the published literature. Elevated Lp(a) and APCR were less prevalent. FVL and MTHFR were not seen in any of the study children. Forty-five percent of children had at least one prothrombotic abnormality. Hyperhomocysteinemia, PC deficiency, aCL and PS deficiency were the most frequent prothrombotic abnormalities.
    Journal of Clinical Neuroscience 08/2014; 21(8). DOI:10.1016/j.jocn.2013.10.030 · 1.38 Impact Factor
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    ABSTRACT: Iodine deficiency (ID) is an endemic health problem in Kangra District, Himachal Pradesh (HP) state. ID leads to mental retardation, deaf mutism, squint, dwarfism, spastic diplegia, neurological defects and congenital anomalies. Iodine nutrition status amongst neonates can be assessed by estimating Thyroid Stimulating Hormone (TSH). The present study was conducted with an objective to assess the iodine nutrition status amongst Neonates in Kangra district, HP. All of the hospitals in the district which provide obstetric services were enlisted, of which three were selected for this survey. A total of 613 umbilical cord blood samples of neonates were collected on filter paper and analyzed for TSH. WHO (2007) reported that that a < 3% frequency of TSH concentrations above 5mIU/L in samples collected 3-4 days after birth indicates iodine sufficiency in a population. In our study we found that 73.4% of the neonates had TSH levels of more than 5mlU/l, thus indicating ID in the population studied. Iodine deficiency continues to be a public health problem in Kangra district, Himachal Pradesh.
    Journal of Trace Elements in Medicine and Biology 07/2014; 28(3). DOI:10.1016/j.jtemb.2014.03.009 · 2.37 Impact Factor

Publication Stats

2k Citations
571.90 Total Impact Points


  • 2008–2015
    • AIIMS Bhopal All India Institute of Medical Sciences
      Bhopal, Madhya Pradesh, India
  • 1994–2015
    • All India Institute of Medical Sciences
      • Department of Paediatrics
      New Dilli, NCT, India
  • 2014
    • Maulana Azad Medical College
      New Dilli, NCT, India
    • Lok Nayak Hospital
      New Dilli, NCT, India
  • 2013
    • Tulane University
      • Hayward Genetics Center
      New Orleans, Louisiana, United States
  • 2006
    • Centre of Excellence in Molecular Biology
      Lāhaur, Punjab, Pakistan