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19 March 2023: Articles  Indonesia

Abdominal Pain Due to Eosinophilic Gastroenteritis Diagnosed in 25-Year-Old and 27-Year-Old Sisters with a Family History of Asthma

Challenging differential diagnosis, Diagnostic / therapeutic accidents, Unusual setting of medical care, Rare disease, Clinical situation which can not be reproduced for ethical reasons

Deshinta Putri Mulya1ABCDEFG*, Nuklear Adiwena1ABCDEFG, Neneng Ratnasari2EF, Muhammad Juffrie3EF

DOI: 10.12659/AJCR.938232

Am J Case Rep 2023; 24:e938232

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Abstract

BACKGROUND: Eosinophilic gastroenteritis (EG) can be associated with parasitic infections, atopic drug reactions, or atopic diseases, such as asthma. This report describes 25-year-old and 27-year-old sisters with a family history of asthma who presented with abdominal pain due to EG.

CASE REPORT: Case 1: A 25-year-old woman presented with a 4-month history of chronic left upper quadrant abdominal pain that did not improve with proton pump inhibitor and sucralfate therapy. She has a history of asthma and allergic rhinitis. Endoscopic pathology revealed pangastritis, with eosinophilic infiltration >25 per 1 high power field. Case 2: Her 27-year-old sister was admitted with chronic abdominal discomfort in the form of vomiting and recurrent abdominal pain for the past 2 years. Treatment with proton pump inhibitors and sucralfate did not lead to improvement. She also had intermittent asthma. Pathological findings on her endoscopy showed chronic inflammation of the fundus and antrum, with eosinophilic infiltration >40 per 1 high power field. Association of eosinophilic gastrointestinal diseases in siblings has not been reported previously.

CONCLUSIONS: This report has highlighted that atopic disease, such as asthma, is often familial, and can be associated with generalized eosinophilia, including EG. In these 2 sisters, the clinical history and histological findings on colonic biopsy were important to confirm the diagnosis.

Keywords: Allergy and Immunology, Gastrointestinal Diseases, Siblings, Female, Humans, Adult, Gastroenteritis, sucralfate, Eosinophilia, Asthma, Endoscopy, Gastrointestinal, proton pump inhibitors, Abdominal Pain

Background

Eosinophilic gastrointestinal diseases (EGIDs) are a group of rare diseases characterized by an increased presence of eosinophils in the gastrointestinal tract [1,2]. The prevalence of EGID in the world is unknown, but its incidence has increased in the last 3 decades, associated with increased clinician awareness of this disease [3,4]. A study from the United States showed the prevalence of eosinophilic gastroenteritis (EG) ranges between 8.4 and 28 per 100 000, with an incidence that has increased slightly over the last 50 years [5].

The prevalence of atopy in patients with EG and gastroenteritis appears to be high, at 38.5% and 45.6%, respectively [6]. Although the etiology and pathogenesis of EGID remain unclear, EG or gastroenteritis are associated with asthma and other allergic conditions, such as allergic rhinitis, drug or food allergies; eczema; or other autoimmune conditions, such as HIV infection or systemic lupus erythematosus [7]; however, strong evidence for a comparison with eosinophilic esophagitis is lacking [6]. Despite this, self-reported rates of allergic rhinitis and asthma were still found to be associated, as high as 63% and 39%, respectively [6].

Diagnosis is commonly described in the White population but is reported to occur in all races and ethnic backgrounds; up to 70% of patients with EGID have a personal or family history of atopic disorders (asthma, eczema, or hay fever) [8], and more than 50% of patients have blood eosinophilia [9]. It also predominantly affects female more than male patients [8]. Notably, up to 10% of patients with EGID have an immediate family member with a history of EGID [2], and most patients have a personal or family history of the atopic disorder [10,11]. Clinical manifestations can run chronically and vary depending on the bowel segment involved, and often there are no specific symptoms to diagnose EGID [3,12]. Variations in symptoms include abdominal discomfort, nausea, failure to thrive, abdominal pain, irritability, gastric dysmotility, vomiting, dysphagia, and diarrhea [8,13].

Primary EGID is categorized based upon the site in the gastrointestinal tract, such as eosinophilic esophagitis, eosinophilic gastritis, eosinophilic gastroenteritis, eosinophilic enteritis, and eosinophilic colitis [14]. EGID diagnosis requires the presence of a gastrointestinal symptom, gastrointestinal eosinophilia by biopsy, and exclusion of other known causes of tissue eosinophilia [3,4,15].

This report describes 25-year-old and 27-year-old sisters with a family history of asthma who presented with abdominal pain due to EG.

Case Reports

CASE 1:

A 25-year-old woman was referred to our Gastroenterology Clinic with chief concerns of abdominal pain in the upper left quadrant of the abdomen, nausea, and bloating for 4 months. The patient had previously been treated at a general clinic, with a diagnosis of functional dyspepsia, but did not improve with proton pump inhibitors and sucralfate therapy. Symptoms of pain felt dominant and relapsed, with a visual analog score of 6–7. The patient denied a history of diarrhea, melena, or weight loss. Abdominal pain often occurred even though the patient did not consume any spicy or sour foods.

Further questioning revealed that she had a history of atopy in the form of intermittent asthma and allergic rhinitis. There was a family history of asthma atopy in the mother’s line but no history of EGID.

There was tenderness in the left upper abdomen on physical examination, but no mass or organ enlargement was found in the abdomen. Laboratory findings were as follows: leukocyte count of 7800/mm3 (reference range, 3600–11 000/mm3; neutrophil, 54.4%; lymphocyte, 35.9%; eosinophil, 2%), total eosinophil count of 35/mm3, hemoglobin level of 11.4 g/dL (reference range, 11.7–15.5 g/dL), erythrocyte sedimentation rate of 5 mm/h (reference range, 0–20 mm/h), and immunoglobulin E total (total IgE) of 387 IU/mL (reference range, 0–120 IU/mL). The abdominal ultrasound examination was unremarkable. The patient then underwent esophagogastroduodenoscopy (EGD) and colonoscopy as well as a biopsy. The EGD imaging (Olympus Ltd) showed a mild edematous mucosa, with scattered erythematous points accompanied by multiple linear erosions in the distal body and the antrum to the pylorus, which matched the appearance of pangastritis. Meanwhile, on colonoscopy, edema of the mucosa with circular erythematous patches scattered was found from the caecum to the rectum region, which matched the appearance of pancolitis.

Multiple gastric biopsies were taken from 3 different stomach segments. They reported markedly increased eosinophils infiltration (>25 per 1 high power field [HPF]) in the mucosal tissue, and there was no parasite or helicobacter pylori seen. Also, multiple random colonic biopsies were taken in several spots in every segment of the colon and showed diffuse infiltration of eosinophils in the lamina propria (>30 per 1 HPF; Figure 1).

The skin prick test showed positive results for dust mite, shrimp, soy, chicken, quill, wheat, and banana. The antinuclear antibody (ANA) immunofluorescence was 1: 100, and the ANA-profile test showed strong positive results for the dense fine speckled, 70kDa molecular weight antibodies (DFS70) antigen (+3). The parasitological examination and bacterial stool culture were un-remarkable. An additional feces evaluation measurement with a Nanodrop DNA sequencing ratio of 260/230 nm and 260/280 nm were 1.695 and 2.055, respectively (reference range, 1.8–2.00), providing information that no organism was involved.

For 4 weeks, the patient was treated with oral desloratadine once daily (q.d), lansoprazole 30 mg q.d, and methylprednisolone 4 mg q.d. Upon follow-up review, the patient noted the complete resolution of symptoms. At the time of this writing, she had no abdominal pain after avoiding her allergens identified by the skin prick test result.

CASE 2:

Her older sister, a 27-year-old woman, was also referred to our Gastroenterology Clinic with a chief concern of abdominal discomfort. The patient had nausea and vomiting accompanied by abdominal pain, with a visual analog score of 5. Her symptoms had been felt for the last 5 months and had not improved despite treatment with proton pump inhibitors and sucralfate therapy. Previously, the patient had also felt similar symptoms in the last 2 years. The previous clinician established the diagnosis of dyspepsia, and she was given oral lansoprazole 30 mg q.d and sucralfate.

She had a history of intermittent asthma, like her younger sister, and used salbutamol inhaler only if necessary. The physical examination results and obtained vital signs were unremarkable. An abdominal examination also revealed tenderness in the epigastric and upper left quadrant. Ultrasound of the upper abdomen, in the left quadrant, did not show any gastric wall thickening or mass and no evidence of splenomegaly. In the right quadrant, there was no evidence of gallstones, gall bladder wall thickening, or hepatomegaly. Laboratory findings were as follows: leukocyte count of 7600/mm3 (reference range, 3600–11 000/mm3; neutrophil, 53.2%; lymphocytes, 35.4%; eosinophil, 1%), total eosinophil count of 49/mm3, and total IgE of 845 IU/mL (reference range, 0–120 IU/mL), 2 times higher than that of her younger sister.

The patient then underwent a gastroscopic procedure; the EGD results showed the esophageal mucosa showed multiple erythematous mucosae, mild mucosal break, and incompetence in the lower esophageal sphincter in accordance with the appearance of esophagitis (Los Angeles grade A). The EGD results also showed fundus and antral gastritis in the gastric mucosa. Then, biopsy was carried out on 3 gastric sites, with the results showing muscularis mucosa with the sign of chronic inflammatory and eosinophils infiltration > 40 per HPF on 3 HPFs. The biopsy was negative for helicobacter pylori (Figure 2).

The results of the prick test and IgE atopy indicated multiple foods and environmental allergies, as shown in Table 1. A further examination of the ANA profile was negative. The patient was treated with desloratadine 5mg q.d, lansoprazole 30 mg q.d, and an elimination diet for 4 weeks. We decided not to use steroid therapy in this patient because the symptoms were mild and the patient refused to use any steroid therapy due to the possible adverse effects. The intervention showed significant improvement in clinical symptoms, and therapy was then not continued. However, 1 month after oral therapy was discontinued, the patient experienced multiple episodes of vomiting, which required hospitalization. After further history taking, it was found that the patient re-consumed the food that caused the allergy. Desloratadine and lansoprazole therapy were then recommenced.

Discussion

Our 2 cases demonstrate that there is a strong genetic component in the pathogenesis of EGID. These cases also shown that having a sibling with EGID can be a positive predictive risk factor, especially in families with a history of atopy.

EGIDs are a group of rare diseases in the gastrointestinal tract caused by allergic inflammation and induced gastrointestinal dysfunction manifestation. However, epidemiological research on the incidence of EGID in the family population has not been widely studied, especially in populations who are still in closely related family or sibling relationships [11,12,16–18]. EGID is diagnosed by the presentation of gastrointestinal symptoms, histological demonstration of eosinophilic infiltration into the GI tract or presence of high eosinophil count in ascetic liquid (serosal disease), and exclusion of other causes of tissue eosinophilia (differential diagnosis) [12].

EGID can affect all parts of the gastrointestinal tract, and the term includes eosinophilic esophagitis (EoE), eosinophilic gastritis (EoG), EG, and eosinophilic colitis [12]. However, the only established guideline for diagnosis and treatment is for EoE. Furthermore, compared with EoE, the knowledge about other non-esophageal EGID is barely understood [19].

In contrast to the esophagus, which is normally free from eosinophil infiltration, eosinophilic infiltration is ordinarily present in gastric, small, and large bowel mucosa. However, eosinophilic infiltration is found less in the gastric mucosa than in the small intestine and colon [12,17]. Therefore, the previous consensus recommended that the diagnosis of EGID is only available for EoE because histologically, the concentration of infiltrating eosinophils in the esophageal mucosa is minimal and does not even contain resident eosinophils at all. Thus, increasing concentrations can lead to clinical manifestations of specific dysphagia [12,14].

The EoE recommendations were first published in 2007 regarding the diagnosis and treatment of EoE. According to the latest guidelines, the threshold for the eosinophil count in the esophageal mucosa is >15 eosinophils in at least 1 HPF from at least 1 site in the esophagus as the pathological criteria for diagnosis [12,13,17]. The current definition of EoE refers to a chronic, immune-antigen-mediated esophageal disease that is clinically characterized by symptoms of esophageal dysfunction and histologically characterized by inflammation with a predominance of eosinophils [20,21]. The diagnosis of EoE itself has been agreed to be a clinicopathologic diagnosis whose diagnosis is based on clinical and pathological considerations from the clinician [12,15,17,20].

Recently, the EoE histological scoring system was also available to assess the density of eosinophils to pathological features of the esophageal mucosa [12,20]. In contrast, for non-esophageal EGIDs, such as EoG, EG, and eosinophilic colitis, making a diagnosis is more difficult, and there are no established guidelines for diagnosis and treatment. Experts are still in debate, especially regarding histological eosinophil concentration in the gastric, enteral, and colonic mucosa [12,14,22].

However, in our daily clinical practice, there are several cases of chronic abdominal disorders, especially in young patients with a strong history of atopy. Some cases present diverse abdominal manifestations, such as abdominal pain, dyspepsia, bloating, and chronic diarrhea, that did not improve with conventional pharmacological therapy for dyspepsia after advanced examination using biopsy revealed eosinophil infiltration with varying degrees of densities [12]. In the end, therapy with anti-inflammatory and anti-allergic agents gave more satisfactory results [9], especially with a combination of elimination diets according to allergy test results [9,12]. Some patients could also develop hypereosinophilia [9], but others can have a normal range of eosinophil serum [7]. Hypereosinophilia can be associated with the severity of the disease and the presence of atopic disease [9,23]. Although there are no specific guidelines for EoG, EG, and eosinophilic colitis yet, a review of the literature showed that the presence of eosinophil sheets in expanded lamina propria, excessive intraepithelial eosinophils, eosinophil cryptitis/abscess, and eosinophils in the muscularis mucosa and submucosa are all required histological diagnostic criteria for EoG. These criteria are 30 per HPF in 5 HPFs or 70 per HPF in 3 HPFs [10,12].

The following are the biopsy criteria listed in other literature for EoG, EG, and eosinophilic colitis. Endoscopic findings may seem normal at first glance; however, erythema, white specks, focal erosions, ulcerations, fold thickening, polyps, nodules, and friability have all been documented [1,12].

More than 30 eosinophils per HPF was recommended as a reasonable threshold to diagnose EoG due to the variable histo-logical appearance of EGID, whereas more than 50 eosinophils per HPF in the right colon, more than 35 eosinophils per HPF in the transverse colon, or more than 25 eosinophils per HPF in the left colon was recommended to diagnose eosino-phil infiltration [1,12,15].

The patient in case 1 also had clinical manifestations of gastric inflammation without other causes, with a picture of gastric mucosal inflammation with eosinophil infiltration in the lamina propria to the muscularis mucosa eosinophil count >30 per HPF at 5 HPFs. Improved clinical changes were seen in both patients after 4 weeks of therapy with anti-allergic administration (desloratadine 5 mg q.d) and even without proton-pump inhibitor therapy in the second to fourth week of therapy in combination with an elimination diet. In case 1, the patient 1 had a strong family history of atopy accompanied by evidence of specific allergy markers from the skin prick test and IgE atopy results. Although the data showed a low ANA immunofluorescence of 1: 100 with a speckled pattern, blood serology test of the ANA-profile, DSF70 antibodies were found, which is a strong marker of allergy and can exclude the possibility of autoimmune involvement [16]. Additionally, the patient’s screening findings for systemic lupus erythematosus using the SLICC grading system did not match.

In case 2, the first clinical manifestation that appeared and stood out was profuse nausea and vomiting. In addition, the patient experienced abdominal pain in several locations, specifically in the left upper quadrant to the lower left quadrant. Hence, the gastroenterologist decided to do an EGD and colonoscopy examination. The endoscopy results showed inflammation in the esophagus to the colon, but biopsies were performed only on the gastric and colonic mucosa. Since the patient did not have dysphagia symptoms, the decision was made because the inflammation in the esophagus was mild (Los Angeles classification grade A), which may have been caused by the patient’s recurrent reflux. The patient in case 2 had an increase in serum IgE, which was higher than that in case 1; however, the ANA immunofluorescence was negative. Desloratadine and lanzoprazole were administered for 4 weeks, and the patient’s symptoms improved after that time; they had previously not improved with oral proton-pump inhibitor, sucralfate, and prokinetic agents, such as domperidone. Re-exposure to the allergic food brought on the symptoms again; thus, dietary elimination and anti-allergy administration proved effective to improve the symptoms.

The prevalence of EGID, in general, is still not known with certainty, but the number of cases is increasing in both adults and children. This can be related to the increasing awareness of clinicians about this disease, especially EoE [10,11,24]. The current research and literature mainly discuss EoE because the diagnostic guidelines for EoE have been established. However, strategies for risk prevention and mitigation for both EoE and EGID, in general, are still limited [11,17]. As with EoE, one of the mechanisms for the high risk of EGID is genetic variation [10,11,18]. In a genome-wide association study, clinicopatho-logically confirmed EoE patients underwent identification of common variants associated with disease risk, and a significant association of genetic variants with higher risk for EoE events was found [14,25]. The study succeeded in identifying the first genetic association with the predisposition to EoE event. Specifically, gene 5q22 implicates TSLP and/or WDR36, as these genes are potentially involved in the pathogenesis of EoE [25]. Other genetic variants, such as CAPN14, TSLP, TSLPR, CCL26, and FLG, have also been associated with the mechanism and pathogenesis of EoE [18], [26].

The association of consanguinity with the incidence of EGID has not been widely studied, but in the last decade, much scientific evidence shows that EoE, in particular, has a strong familial relationship. In a case report, Patel and Falchuk reported that 3 siblings with clinical symptoms of dysphagia, history of family atopy, and biopsy results supported the diagnosis of EoE, indicating a possible familial form of the EoE entity [27]. In another study, in pediatric patients, Blanchard et al found that from 300 probands, 26 of them had at least 1 sibling or parent with EoE. Furthermore, Blanchard et al estimated up to an 80-fold increase in the risk of developing EoE in siblings compared with population prevalence; this indicates a decisive genetic factor [17,28]. This is also in accordance with the theory proposed by Rothenberg et al that there is familial EoE with autosomal dominance, which may explain the occurrence of this disease in one family line. Interestingly, Rothenberg’s hypothesis suggests a relationship between respiratory inflammation (asthma) and eosinophilic inflammation of the esophagus [14].

This phenomenon may suggest that some individuals sensitized to either aeroallergens via respiration or those ingested via the esophagus can develop an eosinophilic inflammation of the esophagus in response to exposure to these allergens [14,29]. This may explain the association of a strong history of asthma atopy in our 2 patients, both of whom had a history of asthma and strong atopy similar to that of the mother, who had a history of asthma but no history of EGID. However, the role of allergens in the induction of eosinophilia, especially in the esophagus, is still being debated and needs further research [14,30].

Conclusions

This report has highlighted that atopic disease, such as asthma, is often familial, and can be associated with generalized eosinophilia, including EG. In these 2 sisters, the clinical history and histological findings on colonic biopsy were important to confirm the diagnosis. We further suggest screening for the possible involvement of gastrointestinal eosinophilic infiltrates in patients with recurrent and unexplained functional gastrointestinal complaints of other causes and who have substantial familial risk factors for atopy. This is due to the different therapeutic approaches in patients with eosinophilic gastrointestinal disease who may respond better to the combined use of anti-allergic and anti-inflammatory treatment and allergen elimination. In future research, it would be interesting to investigate whether there is gene involvement in patients with EGID.

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American Journal of Case Reports eISSN: 1941-5923
American Journal of Case Reports eISSN: 1941-5923