DOI: 10.4103/ipcares.ipcares_114_26 ISSN: 2772-5170

Intrafamilial Phenotypic Variability among Siblings with an Identical Variant in the ANK1 gene Causing Hereditary Spherocytosis – A Report of Two Siblings

C. Hari Prasath, P. Indira, P. Anil Kumar, Pentala Sripooja

Abstract

Background:

Hereditary spherocytosis (HS) shows considerable phenotypic variability even among individuals harboring identical pathogenic variants, with intrafamilial differences remaining under-recognized in clinical practice. We report two siblings with an identical heterozygous ANK1 frameshift variant presenting with markedly different clinical severity.

Clinical Description:

A 9-year-old, previously asymptomatic girl, born out of a third-degree consanguineous marriage, presented with an abrupt onset of yellowish discoloration of skin and urine, following a transient febrile illness. Family history was unremarkable. Examination revealed normal anthropometry and stable vitals, with severe pallor, icterus, and hepatosplenomegaly.

Management and Outcome:

Investigations showed hemoglobin 5.5 g/dL, reticulocyte count 15%, total bilirubin 4.2 mg/dL, with Coombs-negative hemolysis and microspherocytosis on peripheral smear. Liver enzymes, infective work-up for hepatitis, hemoglobin electrophoresis, and glucose-6-phosphate dehydrogenase were within normal limits. Osmotic fragility was increased. Investigations on the 7-year-old asymptomatic younger sibling showed hemoglobin 10.8 g/dL, borderline reticulocytosis, and mildly increased osmotic fragility. On whole exome sequencing, both siblings were found to have a heterozygous, likely pathogenic frameshift variant (NM_020476.3:c. 617del; p.Gly206AspfsTer47) in the ANK1 gene, absent from all major population databases, not previously reported in the literature. Parental Sanger sequencing was negative, consistent with germline mosaicism. The index child received transfusion support and folic acid; the sibling was managed conservatively. Both remained transfusion-independent till follow-up of 12 months.

Conclusion:

Children with HS may remain asymptomatic for years, and members within the same family with identical variant may present with varying phenotypes. A high degree of suspicion and systematic work-up for unexplained anemia, along with genetic analysis, can help reach a diagnosis.

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