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Hypertrophic Pyloric Stenosis commonly presents with non-bilious progressive vomiting usually after a feed. The vomiting usually starts after third week with a range of symptoms onset from first week to fifth month of life. Less commonly it is associated with hyperbilirubinemia (unconjugated > conjugated) which subsides after surgical correction. We report a case of Hypertrophic Pyloric Stenosis who presented early in fifth day of life with repeated vomiting after each feed and unconjugated hyperbilirubinemia. Ultrasonography revealed Hypertrophic Pyloric Stenosis without any evidence of other cause of jaundice. Patient was treated conservatively, prepared for surgery, surgical correction done with Ramstedt’s Pyloromyotomy following that vomiting and jaundice both subsided. Early presentation of HPS may suggest congenital etiology and association of unconjugated hyperbilirubinemia should alert clinician for future Gilbert Syndrome.

The article ''Acute Liver Failure in a Sickle Cell Patient'' by Rizvi Ahsan et al made an interesting read where the authors presented a case of acute sickle cell intrahepatic cholestasis (SCIC) managed with exchange transfusion (1). There are a few important concerns about the article.First, in acute hepatic sequestration of sickle cell disease, patients usually present with acute severe right upper quadrant pain, rapidly evolving hepatomegaly, worsening anaemia leading to shock and death (2). The authors did not discuss in detail about evidence of haemolysis which results in extreme hyperbilirubinemia in SCIC (3). Moreover, severe SCIC cases are usually accompanied by renal impairment (2-4), which was left aside by authors. Furthermore, before concluding SCIC as the cause of liver failure, a targeted search for other causes of hepatic dysfunction (hepatotropic, non-hepatotropic viruses, malaria, dengue, metabolic liver diseases) is justified. Table 1 provided scant information regarding etiological evaluation.Additionally, liver biopsy is a relative contraindication in SCIC with coagulopathy due to a high risk of bleeding and rupture of the liver. It is only recommended when results are expected to modify diagnosis and management (5). Moreover, haemoglobin S (HbS) percentage before and after exchange transfusion (recommendation to decrease HbS <20-30% of total haemoglobin) are not mentioned (5).Finally, we observe a limited literature review of SCIC as only 17 published cases are suggested; however, 44 cases of SCIC have been reviewed in detail by Ahn et al (4). Subsequently, several cases of SCIC have been published (6). We recently published a case of sickle cell disease presenting with acute liver failure and acute kidney injury requiring exchange transfusion and haemodialysis (7). To conclude, a concise description of the present case, recommended line of management, comprehensive latest literature review and finally a new message would have been more interesting.