Making a case for hepatitis a vaccination in glucose -6 Phosphate dehydrogenase deficient subjects
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《美国医学杂志》
Indraprastha Apollo Hospital, Sarita Vihar, New Delhi, India
G6PD deficiency is the most common inherited enzyme deficiency worldwide.[1] Acute viral hepatitis A is widely prevalent in India.[2] A chance association of these two relatively common conditions is therefore to be expected and has been reported from India[3] and from other parts of the world.[4]
Of 481 hepatobiliary referrals over a period of 39 months seen at our centre fulminant hepatic failure (FHF) was present in 26 cases. Hepatitis A was etiologic agent in 12 cases and 3 children had both hepatitis A and hepatitis E infection. Nine patients with hepatitis A also had G6PD deficiency, out of which 5 developed FHF (55.6%). All of them were anemic and their G6PD levels were less than 100 mu / 10(9) RBC. The mean peak serum bilirubin was 56.8 mg/dl (range 24.7-87 mg/dl) and rate of rise was more than 10mg/dl in 24 hours. Three patients were ventilated electively because of worsening encephalopathy. Four developed renal dysfunction of which two required hemodialysis. One child underwent a living related liver transplant. There were four children with concomitant hepatitis A and G6PD deficiency who did not develop FHF. Mean serum bilirubin in this group was 28.1 mg/dl (range 18-42 mg/dl). Although the rise was not as much as in the patients who developed FHF, it was higher than that found in patients with hepatitis A infection 16 mg/dl (range 6 - 20 mg/dl ) without an associated G6PD deficiency.
HAV infection is considered to be a mild disease in majority of cases. This virus, however, in children with G6PD deficiency can cause hemolytic anemia, severe hyperbilirubinemia, renal failure and fulminant hepatic failure.[5] Given the serious manifestations, there is need for hospitalization and advanced medical intervention (dialysis, intensive care management or even liver transplantation). So, we believe that there is a case for vaccinating children with G6PD deficiency against hepatitis A virus infection to prevent the occurrence of severe hepatitis and fulminant hepatic failure.
References
1. Beutler F. G6PD Deficiency. Blood 1994; 84(11): 3612-3638.
2. Tandon BK, Gandhi RM, Joshi VK. Etiological spectrum of viral hepatitis and prevalence of markers of A and B virus infection in North India. Bull World Health Organisation 1984; 62: 87-92.
3. Sarkar S, Prakash D, Marwah RK. Acute intravascular hemolysis in G6PD deficiency. Ann Trop Pediatr 1993; 13: 391-394.
4. Chan TK, Todd D. Hemolysis complicating viral hepatitis in patients with G6PD deficiency. Br Med J 1975; 1: 131-133.
5. Mishra D, Singh R, Sibal A. Liver transplantation for fulminant hepatitis A infection. Indian Pediatr 2002 Feb; 39(2): 189-192.(Sharma Deepa, Sibal Anupa)
G6PD deficiency is the most common inherited enzyme deficiency worldwide.[1] Acute viral hepatitis A is widely prevalent in India.[2] A chance association of these two relatively common conditions is therefore to be expected and has been reported from India[3] and from other parts of the world.[4]
Of 481 hepatobiliary referrals over a period of 39 months seen at our centre fulminant hepatic failure (FHF) was present in 26 cases. Hepatitis A was etiologic agent in 12 cases and 3 children had both hepatitis A and hepatitis E infection. Nine patients with hepatitis A also had G6PD deficiency, out of which 5 developed FHF (55.6%). All of them were anemic and their G6PD levels were less than 100 mu / 10(9) RBC. The mean peak serum bilirubin was 56.8 mg/dl (range 24.7-87 mg/dl) and rate of rise was more than 10mg/dl in 24 hours. Three patients were ventilated electively because of worsening encephalopathy. Four developed renal dysfunction of which two required hemodialysis. One child underwent a living related liver transplant. There were four children with concomitant hepatitis A and G6PD deficiency who did not develop FHF. Mean serum bilirubin in this group was 28.1 mg/dl (range 18-42 mg/dl). Although the rise was not as much as in the patients who developed FHF, it was higher than that found in patients with hepatitis A infection 16 mg/dl (range 6 - 20 mg/dl ) without an associated G6PD deficiency.
HAV infection is considered to be a mild disease in majority of cases. This virus, however, in children with G6PD deficiency can cause hemolytic anemia, severe hyperbilirubinemia, renal failure and fulminant hepatic failure.[5] Given the serious manifestations, there is need for hospitalization and advanced medical intervention (dialysis, intensive care management or even liver transplantation). So, we believe that there is a case for vaccinating children with G6PD deficiency against hepatitis A virus infection to prevent the occurrence of severe hepatitis and fulminant hepatic failure.
References
1. Beutler F. G6PD Deficiency. Blood 1994; 84(11): 3612-3638.
2. Tandon BK, Gandhi RM, Joshi VK. Etiological spectrum of viral hepatitis and prevalence of markers of A and B virus infection in North India. Bull World Health Organisation 1984; 62: 87-92.
3. Sarkar S, Prakash D, Marwah RK. Acute intravascular hemolysis in G6PD deficiency. Ann Trop Pediatr 1993; 13: 391-394.
4. Chan TK, Todd D. Hemolysis complicating viral hepatitis in patients with G6PD deficiency. Br Med J 1975; 1: 131-133.
5. Mishra D, Singh R, Sibal A. Liver transplantation for fulminant hepatitis A infection. Indian Pediatr 2002 Feb; 39(2): 189-192.(Sharma Deepa, Sibal Anupa)