The occurrence of nephrotic syndrome following a bee sting is rarely reported in the literature. Hypersensitivity is believed to be the precipitating factor for the renal disease. We report a two-year-old boy, who developed generalized edema and decreased urine output, seven days after a bee sting. Physical examination and laboratory findings were consistent with nephrotic syndrome; and corticosteroid treatment induced prompt remission with resolution of clinical symptoms and normalization of laboratory findings. There was no relapse of the disease during a one-year follow up.

Primary ovarian lymphoma is rare, with ovary more commonly involved secondarily in generalized disease. Primary ovarian lymphoma presents as mass in the ovary with chronic symptoms; an acute presentation has not been described previously. A 75-year-old female presented with acute abdomen and features of peritonism. Computed tomography and magnetic resonance imaging demonstrated large mass in left ovary along with infiltration of adjacent sigmoid colon causing perforation and pneumoperitoneum. Few jejunal loops were also involved. Intraoperatively, there was left ovarian mass infiltrating the sigmoid colon with perforation and fecal peritonitis. Distal jejunal loops were adherent to the tumor. The involved sigmoid colon was resected with total abdominal hysterectomy, bilateral salpingo-oophorectomy and resection of adherent jejunal loops. Histopathology revealed ovarian tissue with necrotic neoplasm composed of small-to medium-sized round cells exhibiting nuclear irregularity and scanty cytoplasm, forming discohesive sheets with the neoplasm infiltrating the retroperitoneal remnant tissue and resected bowel. This case highlights an unusual presentation of primary ovarian lymphoma.

Recessive hereditary methemoglobinemia (RCM) associated with severe neurological abnormalities is a very rare disorder caused by NADH- cytochrome b5 reductase (cb5r) deficiency (Type II). We report a case of 11 month old male child who had severe mental retardation, microcephaly and gross global developmental delay with methemoglobin level of 61.1%. The diagnosis of NADH-CYB5R3 deficiency was made by the demonstration of significantly reduced NADH-CYB5R3 activity in the patient and intermediate enzyme activity in both the parents. Mutation analysis of the CYB5R gene revealed a novel nine nucleotide deletion in exon 6 leading to the elimination of 3 amino acid residues (Lys173, Ser174 and Val 175). To confirm that this mutation was not an artifact, we performed PCR-RFLP analysis using the restriction enzyme Drd I. As the normal sequence has a restriction recognition site for Drd I which was eliminated by the deletion, a single band of 603-bp was seen in the presence of the homozygous mutation. Molecular modeling analysis showed a significant effect of these 3 amino acids deletion on the protein structure and stability leading to a severe clinical presentation. A novel homozygous 9 nucleotide deletion (p.K173–p.V175del3) is shown to be segregated with the disease in this family. Knowing the profile of mutations would allow us to offer prenatal diagnosis in families with severe neurological disorders associated with RCM — Type II.

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