Menetriers disease is ruled in due to its prevalence between ages 30 60 years old, with

peak incidence of 55 years old. According to two studies1 , Menetrier disease has an insidious
onset and progressive clinical course. A retrospective study of 48 cases diagnosed as Menetriers
disease showed that symptoms were refractory to other medical therapy, such as proton pump
inhibitors, anti-cholinergic medications or anti-emetics for at least 6 months. As to the case, the
patient had recurrent epigastric pain four years ago which was managed by PPI therapy for a
month, however it recurred which may support the diagnosis of Menetriers disease.
Patients with Menetriers disease most often present four classic symptoms such as nausea,
vomiting, epigastric pain and edema. Among the four classic symptoms, the patient manifested
recurrent epigastric pain and edema. According to one study of Rich et al15, 44% of cases present
these two symptoms that are present to the patient. Gastointestinal hemorrhage in a form of
hematemesis and melena may be present; case reports showed its rarity, however it may lead to
death if not managed well, qualifying this case to be one of such rare events in Menetrier disease.
Hypoalbunemia is considered as a cornerstone in the diagnosis; this is also present in her
laboratory results and manifested as grade 1+ peripheral edema. It is 20-100% prevalent in cases
of Menetriers disease which is an indication of protein-losing enteropathy.
The endoscopic findings of Menetriers disease show thickened and enlarged gastric folds
which are seen as multiple large polyps, as to the case, the patient has an endoscopic finding of
6x4 cm polypoid, irregular, edematous mass pointing to its similarity. An enlarged gastric fold is
defined by Bjork et al. as a fold measuring greater than 1.0 cm on endoscopy. On contrastenhanced CT images, they appear as areas of thickened mucosa that project into gastric lumen
that may resemble convolution of brain, our case revealed multiple filling defects on the gastric
lumen, with consideration between mass lesion versus blood clots. This further strongly
supported our diagnosis of Menetrier disease.
Rich et al. proposed an algorithm for the diagnosis of MD that rely on
clinicohistopathological analysis of the following criteria: upper GIT endoscopy with gastric pH,
appropriate laboratory tests (CBC, serum albumin, serum gastrin, H. pylori and CMV) and full
thickness mucosal biopsy. This is to be correlated with classic clinical features of epigastric pain,
nausea and vomiting due to the local effect of the huge gastric folds, in addition to peripheral
edema due to the protein losing nature of the disease that leads to hypoalbuminemia.
With the above criteria, our case have met some of the variables, with its variant clinical
presentations as presented by case reports, we still quantify this as essential in the diagnosis of
Menetriers disease.
Menetriers disease could not be fully ruled out due to the prevalence among men over
women. In one study, 8% of reported cases had none of the classic findings (abdominal pain,
nausea, vomiting and edema). Fifty percent of patient with Menetrierscdisease have a
microcytic, hypochromic type of anemia, our case did not show this, instead, the laboratory
result revealed normocytic, normochromic anemia which is secondary to her acute
gastrointestinal bleeding.

Our case doesnt show any association to H. pylori infection as per laboratory results.
Despite many literatures proposing this as an essential part in the pathogenesis, many case
reports still show without infection leading to weak causal relation.
To date, Menetriers disease lack diagnostic criteria, however, with the hallmarks of such
disease and clinicopathologic manifestations present in the patient we have concluded that this is
a case of Menetriers disease. Menetriers disease is listed by the Office of Rare Disease of the
National Institutes of Health as a rare disease, a designation that means it has a prevalence of less
than 1 in 200,000 people.