Lead poisoning, fairly common in the 20th century, has decreased drastically in the last decade. Severe lead poisoning in the form of encephalopathy has a fatality rate of 28% to 45% and neurological sequelae in about 82%. We present the management of a case of lead encephalopathy that recovered without any significant neurological sequelae in a resource-limited setting. A previously healthy seven-year-old boy presented with complaints of falling unconscious on the ground while playing, followed by multiple episodes of seizures, vomiting, and altered sensorium. The patient had pallor, Glasgow coma score of E2V3M3, with features of raised intracranial pressure. Lead poisoning was suspected as the patient had four months of exposure to a battery recycling factory. Management of seizures and raised intracranial pressure was done. X-ray long bones showed lead lines at the metaphysis. Blood lead levels were highly elevated (139.96 mcg/dL). Investigations revealed iron deficiency anemia, vitamin D deficiency, and renal tubular injury in the form of proteinuria. D-penicillamine with supplements was started due to unavailability of other chelating agents. Encephalopathy improved, but patient had psychiatric symptoms of hallucinations and delusions. On the 12th day, CaNa 2 EDTA was started, which resulted in significant improvement in the psychiatric symptoms.The patient had near-complete recovery in another one month, the patient being able to read, write, recite and speak as the pre-illness state. In conclusion, lead poisoning remains a significant health problem even today. Early recognition and management are of paramount importance in its outcome.

There is high incidence of hypertension in NS children during remission. Though significant positive correlation was found with positive family history of hypertension and deranged lipid profile highlighting possibility of essential hypertension in them, there is need for close active monitoring and management of hypertension in them as untreated cases may have significant target organ damage.

No abstract

Pseudo-Bartter's (PB) syndrome is characterized by hypokalemic metabolic alkalosis and failure to thrive which constitutes a rare but typical presentation of cystic fibrosis (CF) in children. The most common mutation of CF is F508del, due to loss of 3 base pairs, causing deletion of phenylalanine, at position 508. We present a case of CF presenting with failure to thrive, dehydration, PB syndrome associated with urosepsis and primo-colonization with Escherichia coli suggesting the role of epigenetic factors. The heterozygous state for Phe508del mutation in Exon 11 combination with Glu92Ala in Exon 4 resulted in epigenetic effect on atypical phenotype as PBS, a novel mutation identified in our case.