Spectrum of esophagitis in children with cerebral palsy - A clinical, endoscopic, and histopathological correlation

Background: Gastrointestinal disease is frequent in children with severe neurological impairment and developmental disability. Dysphagia may worsen due to concurrent gastroesophageal reflux disease (GERD) and non-GERD esophagitis in children. Objective: The aim of our study was to study the spectrum of causes of esophagitis in cerebral palsy (CP) children with feeding difficulty. Methods: Children of CP with feeding difficulties in the age group of 1–18 years were included after written consent. Dysphagia in these childrenwas categorized according to the dysphagia disorder survey (DDS) score. Children who were unfit for endoscopy or having profound dysphagia were excluded from the study. UGI endoscopy and histopathological evaluation of esophagus was done in all the children. Results: Children of CP had a mean DDS score of 4.02±2.50. Endoscopic evidence of esophagitis was seen in 22 children (24.4%). Histological evidence was seen in 15 children; out of them, 11 had GERD-related esophagitis and 2 each had eosinophilic and fungalesophagitis. The mean DDS score and weight significantly improved in children with GERD after they were given specific treatment. Conclusion: Esophagitis whether GERD or non-GERD is an important and treatable cause of dysphagia in children with CP. Effort should be made to recognize and treat these causes for effective nutritional rehabilitation of this subset of children

Acute leukemia after cytotoxic treatment in a child with nephrotic syndrome

Renal involvement in acute lymphoblastic leukemia (ALL) occurs due to several factors including leukemic infiltration of the kidneys, therapy-related side effects such as tumor lysis syndrome, nephrotoxic drugs, and septicemias. A 3-year-old boy with nephrotic syndrome (NS) who was previously treated with prednisolone and cyclosporine A for 14 months after the initial diagnosis of NS, presented to the emergency department with fever, breathing difficulty, generalized edema, and body pain with pallor, without evidence of lymphadenopathy, hepatosplenomegaly, petechiae, or purpura. On investigation, peripheral blood smear showed blast cells >80% and bone marrow aspiration showed complete replacement of the marrow with L1 lymphoblasts, consistent with a diagnosis of ALL. The exact mechanism of developing acute leukemia after cytotoxic treatment has not been established; the possibility must be considered that the incidence of this malignant disease is increased after cytotoxic treatment for nonmalignant diseases