Determinants of motor, language, cognitive, and global developmental delay in children with complicated severe acute malnutrition at the time of discharge: An observational study from Central India.

BACKGROUND: Undernutrition leads to impaired psychosocial and cognitive development. This study explored the developmental status of children with complicated severe acute malnutrition (SAM) and correlated it with various risk factors for SAM. METHODS AND FINDINGS: We recruited 100 children with SAM and no other associated significant health issues during the recovery phase of treatment using the Bayley Scales of Infant and Toddler Development III prior to discharge from the nutritional rehabilitation unit in R D Gardi Medical College, Ujjain, Central India. We also assessed composite developmental scores, developmental age equivalents, and average differences in developmental age. Risk factors for developmental delay were identified in children with complicated SAM. The results revealed that 75%, 75%, and 63% of children with SAM exhibited delay in motor (mean score: 78.22), language (mean score: 83.97), and cognitive (mean score: 78.06) domains, respectively. A total of 63% children exhibited delay by an average of 4-7 months in the total developmental age. The proportion of children with delay in motor, language, and cognitive domains was determined. An increased risk of global developmental delay was observedin children with a low birth weight (adjusted odds ratio [aOR]: 18.06, 95%CI: 2.08-156.56; P = 0.009), having working mothers (aOR: 17.54, 95%CI: 3.02-102.59; P = 0.001), weight-for-age less than three standard deviations (aOR: 6.09, 95%CI: 1.08-34.10; P = 0.04), and presence of severe anemia (aOR: 16.34, 95%CI: 2.94-90.73; P = 0.001). CONCLUSIONS: The results indicated that children with SAM exhibit developmental delay across all domains. Identifying multiple modifiable risk factors for developmental delay in children with SAM will be helpful in devising early interventional strategies in low-middle income countries; however, the exact timing of such interventions should be investigated.

Reversible Cerebral Atrophy in Infantile Tremor Syndrome.

BACKGROUND: We report changes in MRI brain of children with Infantile Tremor Syndrome (ITS) at the onset of illness and following treatment. CASE CHARACTERISTICS: Three children with infantile tremor syndrome were assessed for changes in brain neuroimaging at admission and at follow-up visit. On MRI, all children had mild to severe diffuse cerebral atrophy, which reverted back to normal on follow-up visits. OUTCOME: Children with infantile tremor syndrome have reversible diffuse cerebral atrophy on neuroimaging.

Infantile tremor syndrome: Role of Vitamin B12 revisited.

OBJECTIVE: To study the role of Vitamin B12 as an etiological factor in patients of infantile tremor syndrome (ITS). METHODS: Twelve consecutive admissions of children diagnosed clinically as ITS were assessed. Assessment was done using a predefined pro forma to document patient demographic factors, general examination, systemic examination as well as relevant hematological and biochemical investigations. RESULTS: Out of the 12 cases of ITS, 6 were males and 6 were females. Two cases had serum B12 levels below reference values, five had levels in low normal range, and remaining five had normal values. CONCLUSIONS: Role of Vitamin B12 deficiency as an etiological factor in the patients of ITS is inconclusive.

Characterization of drug resistance associated genetic polymorphisms among Plasmodium falciparum field isolates in Ujjain, Madhya Pradesh, India.

BACKGROUND: Since 2011, artesunate + sulphadoxine-pyrimethamine (ASP), instead of chloroquine, has been recommended for treatment of uncomplicated malaria in India. In Ujjain, central India, with an annual parasite index <0.1, the prevalence of drug-resistant Plasmodium falciparum is unknown. In other parts of India chloroquine and sulphadoxine-pyrimethamine-resistant P. falciparum is prevalent. The aim of this study was to determine the prevalence of anti-malarial drug resistance-associated genetic polymorphisms in P. falciparum collected in Ujjain in 2009 and 2010, prior to the introduction of ASP. METHODS: Blood samples from 87 patients with P. falciparum mono-infection verified by microscopy were collected on filter-paper at all nine major pathology laboratories in Ujjain city. Codons Pfcrt 72-76, pfmdr1 1034-1246, pfdhfr 16-185, pfdhps 436-632 and pfnhe1 ms4760 haplotypes were identified by sequencing. Pfcrt K76T and pfmdr1 N86Y were identified by restriction fragment length polymorphism, and pfmdr1 gene copy number by real-time PCR. RESULTS: Sulphadoxine-pyrimethamine resistance-associated pfdhfr 108 N and 59R alleles were found in 75/78 (96%) and 70/78 (90%) samples, respectively, and pfdhps 437G was found in 7/77 (9%) samples. Double mutant pfdhfr 59R + 108 N were found in 62/76 (82%) samples. Triple mutant pfdhfr 59R + 108 N and pfdhps 437G were found in 6/76 (8%) samples. Chloroquine-resistance-associated pfcrt 76 T was found in 82/87 (94%). The pfcrt 72-76 haplotypes found were: 80/84 (95%) SVMNT, 3/84 (4%) CVMNK and 1/84 (1%) CVMNT. Pfmdr1 N86 and 86Y were identified in 70/83 (84%) and 13/83 (16%) samples, respectively. Pfmdr1 S1034 + N1042 + D1246 were identified together in 70/72 (97%) of successfully sequenced samples. One pfmdr1 gene copy was found in 74/75 (99%) successfully amplified samples. CONCLUSION: This is the first characterization of key anti-malarial drug resistance-associated genetic markers among P. falciparum collected in Ujjain, Madhya Pradesh, India. The results indicate that the efficacy of standard dose chloroquine at the time of the study was likely to be poor, whereas ASP was likely to be efficacious, supporting the changed drug treatment policy. However, P. falciparum with reduced susceptibility to sulphadoxine-pyrimethamine is highly prevalent, highlighting the need for continuous surveillance of ASP efficacy in the study area.

Abernethy malformation: a case report.

BACKGROUND: Abernethy malformation is a very rare congenital vascular malformation defined by diversion of portal blood away from liver. It is commonly associated with multiple congenital anomalies. We present a case of Abernethy malformation, without associated congenital anomalies from India. CASE PRESENTATION: A 5-year-old female child presented with short history of jaundice. A provisional diagnosis of acute viral hepatitis was made in view of clinical presentation and local endemicity of viral hepatitis A. Persistence of jaundice on follow up after 4 weeks led to detailed investigations. Ultrasound and doppler study of abdomen revealed drainage of portal vein into inferior vena cava. CT angiography was performed which confirmed the diagnosis of Type 1 b Abernethy malformation without associated major anomalies. We discuss the common clinical presentations, associated anomalies, diagnostic workup and treatment options of this disorder. CONCLUSION: The treatment of the patients with congenital porto-systemic shunts depends on the site of the shunt, associated congenital anomalies and the extent of liver damage but the prognosis depends on the complications irrespective of anatomical type. However, the extent of associated abnormalities should not deter paediatricians to refer patients for treatment. Whenever possible closure of the shunt should be advised for cure or to prevent complications. Only symptomatic type I patients with absence of possibility to close the shunt may require liver transplant. Long-term follow-up is indicated for all patients.