|LETTER TO THE EDITOR
|Year : 2017 | Volume
| Issue : 6 | Page : 608-609
Acute respiratory distress syndrome and erosive gastritis with hepatitis A in children
Anirban Mandal1, Puneet Kaur Sahi2
1 Department of Pediatrics, Sitaram Bhartia Institute of Science and Research, India
2 Department of Pediatrics, Kalawati Saran Children’s Hospital, New Delhi, India
|Date of Web Publication||17-Jan-2018|
Dr. Anirban Mandal
B-16 Qutub Institutional Area, New Delhi - 110 016
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Mandal A, Sahi PK. Acute respiratory distress syndrome and erosive gastritis with hepatitis A in children. Med J DY Patil Univ 2017;10:608-9
|How to cite this URL:|
Mandal A, Sahi PK. Acute respiratory distress syndrome and erosive gastritis with hepatitis A in children. Med J DY Patil Univ [serial online] 2017 [cited 2020 Feb 19];10:608-9. Available from: http://www.mjdrdypu.org/text.asp?2017/10/6/608/223354
We read with much interest the case report by Parikh et al., published in the recent issue of your journal  but at the same time would like to make the following comments, clarification to which would benefit the general readers of MJDPU.
The second case presented by the authors describes a 5-year-old boy with fever for 8 days, abdominal pain for 4 days, 4 episodes of vomiting and puffiness of the face with breathlessness for 2 days. This child subsequently developed acute respiratory distress syndrome (ARDS) and also tested positive for hepatitis A IgM. The diagnosis of acute hepatitis A virus (HAV) infection in this case raises many questions. First, though the symptoms at the onset were consistent with acute HAV infection, one would be very surprised looking at the serum transaminases (serum glutamic-oxaloacetic transaminase 83 IU/L and serum glutamic-pyruvic transaminase 29 IU/L) of the child. The transaminases are expected to be raised many folds above the normal in acute HAV infection except in cases of massive hepatocellular necrosis, which does not seem to be the case here with a prothrombin time of 16 s (though the child had received fresh frozen plasma at another center). The authors also have not provided serum albumin values which could have given a fair idea about the severity or the chronicity of the liver failure. Elevation of the transaminases has been found to be a very good marker of acute HAV infection, and on the other hand, false-positive hepatitis IgM results are also known., Second, the child had puffiness of the face with breathlessness along with edema, ascites, and pleural effusion (probably only on the right side as per clinical findings) on examination. The diagnosis of ARDS required exclusion of a cardiogenic pulmonary edema, which may have all the above-mentioned clinical features. Although hypoalbuminemia along with ARDS can also lead to the above manifestations, in the absence of serum albumin value, one would be really cautious, especially because ARDS is extremely rare with HAV infection. Third, the authors conclude that HAV was the cause of ARDS in this child as “All other coinfections were ruled out in the child”. However, actually, they mention ruling out hepatitis B, hepatitis C, HIV (Human immunodeficiency virus), leptospira, dengue and “blood culture-positive septicemia.” Knowing the long list of possible etiologies of ARDS, this will be quite a bold statement as many other possible infectious tropical diseases such as atypical pneumonia, scrub typhus, and malaria  can actually have presented in a manner similar to this case to cause ARDS.
In the first case, the authors report a 4½-year-old girl with acute HAV infection and erosive gastritis. It has a very important clinical lesson that in cases of hematemesis with acute viral hepatitis, apart from variceal bleeding, one should always think of gastritis; especially when coagulation parameters and platelet count are within normal limits. In this, one should consider drug-induced gastritis as one of the possibilities. As the child was symptomatic for 15 days before hematemesis (which is also expected in a case of acute HAV infection), there is a possibility of the child being administered over-the-counter medicines or even alternate forms of therapy, both of which may lead to erosive gastritis. In this context, a drug history becomes very important.
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| References|| |
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