Canan et al.[
Firstly, the authors performed upper gastrointestinal endoscopy with the presumptive diagnosis
of protein losing enteropathy since no proteinuria was detected. Before the endoscopic analysis,
however, fecal protein loss might have been shown easily and noninvasively by the measurement
of fecal alpha-1 antitrypsin level, which is not normally excreted from feces[
Secondly, their patient had hypoproteinemia (albumin 3.1 g/dl and total protein 4.3 g/dl,
respectively), which is characteristic for Ménétrier’s disease. Although the expected finding was
hypogammaglobulinemia, they noted hypergammaglobulinemia (IgG: 2210 mg/dl, IgA 220 mg/dl,
and IgM 300 mg/dl, respectively). Indeed, protein level other than albumin (total protein minus
albumin) should not exceed 1.2 g/dl. Hypergammaglobulinemia or hypoproteinemia therefore
requires further explanation. If the blood samples for gammaglobulin and protein analysis were
taken on two different occasions, this discrepancy might be explained.
Thirdly, multiple gastric ulcers were proposed to be related with CMV infection since their
patient did not have other risk factors for ulcer formation such as concurrent steroid use, higher
NSAID (nonsteroidal anti inflammatory drug) dose, multiple NSAID use, etc. The authors were
less inclined to consider NSAID-induced gastric ulcer since the patient ingested only two doses
of naproxen. Indeed, the gastric ulcers are probably related with CMV infection. However, it
is well known that even a single low dose of NSAID may be enough to cause gastric ulcer in
susceptible individuals[
In summary, fecal alpha-1 antitrypsin measurement is an easy and noninvasive way to demonstrate
protein loss from the gastrointestinal tract. Hypogammaglobulinemia is an expected finding
in case of hypoproteinemia, which is observed in due course of Ménétrier’s disease. Finally,
NSAIDs per se are drugs that may cause hemorrhagic gastritis and ulcer formation even with
a single dose.