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Eosinophilic gastrointestinal diseases with overall gastrointestinal tract causing liver abscess in an older patient: a case report and literature review

BMC Geriatrics volume 24, Article number: 945 (2024) Cite this article

Abstract

Background

Eosinophilic gastrointestinal diseases are the rare gastrointestinal disorders. To our knowledge, there have been no reports of eosinophilic gastrointestinal diseases with overall gastrointestinal tract involvement causing liver abscess in an older patient.

Case presentation

We report a 68-year-old man with eosinophilic gastrointestinal disease with overall gastrointestinal tract involvement. He was admitted with suspected acute gastroenteritis, and histological examination showed eosinophilic infiltration accompanied by liver abscess. The collected pus was tested for Metagenomics Next-Generation Sequencing and confirmed the presence of Klebsiella pneumoniae.

Conclusions

We conducted a literature review on the complications of eosinophilic gastrointestinal diseases and discussed how eosinophilic gastrointestinal diseases lead to liver abscess caused by Klebsiella pneumoniae.

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Background

Eosinophilic gastrointestinal diseases (EGIDs) are disorders of the gastrointestinal (GI) tract characterized by pathologic infiltration of the specific region by eosinophils [1]. Involvement of individual GI tract locations are named specifically: eosinophilc gastritis (EoG), eosinophilic enteritis (EoN), eosinophilic colitis (EoC) and eosinophilic esophagitis (EoE) [2]. These disorders are considered to be chronic, Th2 antigen-mediated [3, 4].

Pyogenic liver abscess (PLA) is a potentially life-threatening suppurating infection of hepatic parenchyma disease, which have a global distribution [5]. PLA may be caused by a variety of organism and Klebsiella pneumoniae (KP) is the main causative pathogenic bacterium of PLA in China [6, 7]. At present, KP-induced pyogenic liver abscess (KP-PLA) has become a globally emerging disease.

Here, we present an older patient who had EGIDs with overall GI tract involvement causing KP-PLA and review the literature on the clinical characteristics and the reasons of this condition.

Case presentation

A 68-year-old man presented to our clinic for further work-up in the context of abdominal distension, nausea and no vomiting for a week. He was previously treated with conventional antibiotics therapies in a local hospital for suspected acute gastroenteritis, but the symptoms did not improve. He denied any recent travel, sick contacts or antibiotics used prior to onset of symptoms, and did not use tobacco, alcohol or illicit drugs. There was no family history of similar symptoms. Abdominal examination showed a distended abdomen with shifting dullness. Blood analysis demonstrated a leucocyte count of 13.3 × 109 / L (lymphocyte: 2.0 × 109 / L, eosinophil: 5.56 × 109 / L, neutrophils: 5.1 × 109 / L) and total IgE of 455.3 IU / mL, C-reactive protein (CRP) 27.5 mg/L (Table 1). A computed tomography (CT) scan was performed on the patient, which revealed significant wall edema thickening in the lower-middle section of esophagus, gastric antrum and small bowel; ascites; liver abscess (Figs. 1 and 2). Subsequently, an abdominal diagnostic paracentesis was performed on the patient. The ascitic fluid study revealed that eosinophils account for 34% of the total cells, and the total number of nucleated cells count was 6756 × 106 / L by microscope. We also performed an ultrasound-guided percutaneous liver abscess puncture and drainage on the patient. Metagenomics Next-Generation Sequencing (mNGS) analysis of the pus detected KP, with no evidence of fungi, viruses, or parasites.

Table 1 Laboratory tests of the patient
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Fig. 1
figure 1

Plain scan and enhanced CT images. A, E Esophagus; B, F Gastric antrum; C, G Small intestine; D, H Pelvic cavity CT plain scan shows diffuse thickening of the lower esophagus, gastric antrum, duodenum, and jejunum walls, local narrowing of the lumen, and a large amount of fluid accumulation in the abdomen and pelvis. Enhance CT scan shows diffuse and uniform enhancement of the thickened lumen, with no obvious abnormal enhancement lesions

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Fig. 2
figure 2

Enhanced CT images from the arterial and venous phases of the liver. A circular low-density shadow with a diameter of about 20 mm can be seen in the right lobe of the liver, with unclear boundaries. There are a few flocculent high-density shadows around the lesion, with unclear boundaries. On enhanced scanning, circular enhancement can be seen at the edge of the lesion in the arterial phase, and circular low-density shadows can be seen at the edge. In the portal and delayed phases, the enhancement fills inward. There are a few flocculent arterial phase enhancement shadows around the lesion, and the enhancement exits in the portal and delayed phases, presenting a relatively equal density shadow

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The patient underwent gastrointestinal endoscopy. Gastroscopy revealed edema in the esophagus, gastric antrum, and the descending part of the duodenum near the bulb, while colonoscopy showed scattered erythema throughout the colon (Fig. 3). Biopsies were taken from the esophagus, gastric antrum, descending duodenum, ascending colon, transverse colon, and descending colon (Fig. 4). Pathological examination revealed significant eosinophil infiltration in the gastric antrum, ascending colon, transverse colon, and descending colon. Eosinophil abscesses, eosinophil degranulation, and eosinophilic infiltration in the muscularis mucosae were also observed. The eosinophil count in the gastric antrum exceeded 30 per HPF and in the ascending colon exceeded 100 per HPF, both exceeded the diagnostic thresholds for EGIDs [8, 9]. Simultaneously, we conducted stool microscopy, tumor marker screening (including CEA, AFP, CA125, and CA199), allergen profile testing, antinuclear antibody panel, anti-neutrophil antibody testing, and ascitic fluid culture. Except for an elevated CA125 level (420.3 kU/L). All results were either within the reference range or showed no abnormalities. The elevated CA125 level in the patient can be attributed to the presence of ascites.

Based on the medical history and the aforementioned tests, we ruled out tumors, connective tissue diseases, allergies, parasitic infections, and other related conditions. The patient was diagnosed with EGIDs complicated by a KP liver abscess.

Fig. 3
figure 3

Endoscopic images. A Esophagus: esophageal edema; B Gastric antrum: edema of the gastric antrum with congestion; C Duodenum: entrance of the descending duodenum; D-F Ascending colon, Transverse colon, and Sigmoid colon: scattered congestion and erosions of the colonic mucosa(arrows)

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Fig. 4
figure 4

Histopathology results. A Esophagus: Lymphocytic infiltration was observed in the lamina propria(arrows), scale bar: 100 μm; B Gastric antrum: Numerous eosinophils infiltration can be seen in the lamina propria and submucosal layer., scale bar: 100 μm; C Duodenum: Focal accumulation of eosinophils in the lamina propria(arrows), scale bar: 100 μm; D Ascending colon: infiltration of eosinophils in the lamina propria, scale bar: 100 μm; E- F Transverse colon and Descending colon: There is a large amount of eosinophil infiltration in the lamina propria and submucosal layer, scale bar: 100 μm; G Transverse colon: eosinophilic infiltration in the muscularis mucosae(arrows), scale bar: 50 μm; (H) Descending colon: eosinophil degranulation(arrows), scale bar: 50 μm; (I) Descending colon: eosinophil abscesses(arrows), scale bar: 50 μm. Hematoxylin and eosin stain

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The patient received 2 g of cefoxitin twice daily via intravenous injection. Glucocorticoid therapy was not considered, as the patient has a liver abscess caused by KP, which could exacerbate the infection. After 10 days of antibiotic treatment, a liver ultrasound was performed, showing a reduction in the size of the liver abscess. Consequently, the patient was discharged with follow-up instructions and continued on cefixime 100 mg twice daily. Ten days after discharge, the patient came to our hospital for follow-up. A repeat complete blood count showed the eosinophil count was 4.34 × 109 /L, the white blood cell count was 10.4 × 109 /L, the neutrophils count was 2.9 × 109 /L, CRP 2.1 mg/L (Table 1). These results indicated that the patient’s bacterial infection was under control. However, the patient’s eosinophil count remained elevated, we initiated hormone therapy. The eosinophil counts significantly decreased within 2 weeks (the eosinophil count was 0.65 × 109 /L) (Table 1). One month after initiating hormone therapy, a follow-up abdominal CT showed no abnormal density in the liver parenchyma. There was significant relief of edema in the small intestine, esophagus, and gastric antrum. Additionally, a marked reduction in ascites was observed (Fig. 5). The patient reported no abdominal pain during follow-up over the phone.

Fig. 5
figure 5

Plain scan CT images. A-B CT plain scan showed significant improvement in wall thickening of the lower esophagus and gastric antrum; C The walls of the duodenum and jejunum are still thickened but have improved compared to before treatment; D A large amount of fluid in the abdomen and pelvic cavity has been completely absorbed

Full size image

Discussion

EGIDs encompass a spectrum of diseases characterized by prominent eosinophilic inflammation affecting different regions of the GI tract that occur in the absence of secondary causes (e.g., infections, drug reactions) [10] (Table 2). The patient initially presented with abdominal distension accompanied by nausea. CT imaging revealed segmental thickening of the esophagus, gastric antrum, and small intestine, along with ascites. Gastrointestinal biopsies showed significant eosinophil infiltration in both the stomach and colon. After ruling out other conditions that could cause elevated eosinophil levels, a diagnosis of EGIDs was established. Although the eosinophil count in the esophageal biopsy was less than 15 per HPF, below the diagnostic threshold [11]. But CT and gastroscopy revealed esophageal edema, and the patient responded well to hormone therapy. Therefore, we concluded esophageal involvement. The absence of eosinophils in the biopsy potentially attributed to factors such as the biopsy site and depth. For the same reasons, we also believe that the small intestinal was involved. In summary, this was diagnosed as EGIDs with overall GI tract involvement.

Table 2 Summary of the complications from EGIDs cases
Full size table

PLA is an intrahepatic infection caused by purulent bacteria that invade the liver. In China over 80% of PLA cases are caused by KP [17]. KP is a Gram-negative bacterium widely in nature [18,19,20]. In humans, KP is a member of the human microbiota that is found in the nasopharynx, skin, and GI tract [21]. Although KP typically does not cause disease in healthy individuals, it is an opportunistic pathogen that primarily affects individuals with weakened immune systems [22]. Reports indicate that the prevalence of KP-PLA is significantly elevated in patients with diabetes, malignancies, and renal disease [23,24,25]. However, in this case, the patient did not have diabetes, malignancies, renal disease, or cholelithiasis.

The GI tract is the dominant site of colonization and serves as a silent reservoir for the infection and transmission of KP [26, 27]. To successfully colonize these sites, KP must overcome the defenses established by both the microbiome and the immune system [28, 29]. For example, the commensal colonization factors (CCF) promote the association of Bacteroidetes with the mucosa and create an immune barrier within the intestine preventing colonization by KP [30]. Gut dysbiosis leads to the intestinal barrier damaged and intestinal permeability increased because of the decreased beneficial bacteria and enhanced harmful bacteria. Eventually, KP translocates across a leaky gut barrier and accesses the liver via the portal circulation, where it triggers inflammation and liver abscess.

In the GI tract under steady-state conditions, eosinophils are scattered in the lamina propria of the stomach, small intestine, and colon, except for the esophagus. Eosinophils promote generation and maintenance of IgA-expressing plasma cells and contribute to gut immune homeostasis [31]. They also maintain the integrity of the epithelial barrier by participating in the dynamic regulation of the gut bacterial community and responding to microbial stimuli [32].

In patients with EGIDs, intestinal eosinophils directly release substances such as eosinophil-derived neurotoxin (EDN), eosinophil cationic protein (ECP), major basic proteins (MBP-1 and MBP-2), and eosinophil peroxidase (EPO) through degranulation, causing damage to intestinal tissue and increasing intestinal permeability [33]. Additionally, the gut microbiota in EGIDs patients becomes significantly dysregulated, which increases the invasiveness of KP [34, 35]. Although there are currently no reports on the incidence of pyogenic liver abscess in EGIDs, cases of liver microabscesses have been reported in premature neonates with EoC [36]. Hepatic abscesses in premature infants are rare with less than 100 case reports documented in literature. Furthermore, in inflammatory bowel disease, which is primarily characterized by intestinal inflammation, the incidence of liver abscesses is notably elevated [37]. Therefore, we believe that EGIDs may increase the risk of PLA.

Meanwhile, antibiotic treatments can weaken the protective effect of the gut microbiota, which is a protective factor against KP [38, 39]. The patient had been treated at a local hospital with conventional antibiotics, which may have caused dysbiosis of the gut microbiota. Overall, the basic hypothesis is that gut microbes translocate across a leaky gut barrier (due to inflammation) and access the liver via the portal circulation, where they trigger liver abscess.

Conclusions

We present a case of EGIDs with overall GI tract involvement, complicated by PLA in an older patient, and discuss potential mechanisms through which EGIDs may lead to PLA formation. This case suggests that bacterial infection could be a complication of EGIDs. Therefore, clinicians should perform thorough evaluations to rule out possible bacterial infections in patients with EGIDs, particularly before starting hormone therapy.

Data availability

All the data supporting this study are available from the corresponding author upon reasonable request.

Abbreviations

EGIDs:

Eosinophilic gastrointestinal diseases

GI:

Gastrointestinal

EoG:

Eosinophilc gastritis

EoN:

Eosinophilic enteritis

EoC:

Eosinophilic colitis

EoE:

Eosinophilic esophagitis

PLA:

Pyogenic liver abscess

KP:

Klebsiella pneumoniae

KP-PLA:

KP-induced pyogenic liver abscess

mNGC:

Metagenomics Next-Generation Sequencing

CT:

Computed tomography

CRP:

C-reactive protein

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Authors and Affiliations

  1. Gastroenterology Department, Wenzhou Central Hospital, Wenzhou, Zhejiang, 325000, China

    Yifan Ke, Yi Jiang, Yuping Yuan, Yihan Chen, Jianbin Huang & Chunwei Huang

  2. The Second Affiliated Hospital of Shanghai University, Wenzhou, Zhejiang, 325000, China

    Yifan Ke, Yi Jiang, Yuping Yuan, Yihan Chen, Jianbin Huang & Chunwei Huang

  3. The Dingli Clinical College of Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China

    Yifan Ke, Yi Jiang, Yuping Yuan, Yihan Chen, Jianbin Huang & Chunwei Huang

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Contributions

HCW contributed to the study conception and design; KYF wrote the first draft of the manuscript and prepared the table and figures; KYF and YYP acquired, analyzed, and interpreted the clinical data; JY provided an analysis of the pathology aspects; HJB provided the endoscopic images; HCW and CYH revised the manuscript. All authors have read and agreed to the published version of the manuscript.

Corresponding author

Correspondence to Chunwei Huang.

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The protocol of this study was approved by the Ethics Committee of the Wenzhou Central Hospital (NO. L2024-01-025).

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Written informed consents for publication were obtained from the patient and his family prior to the study.

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The authors declare no competing interests.

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Ke, Y., Jiang, Y., Yuan, Y. et al. Eosinophilic gastrointestinal diseases with overall gastrointestinal tract causing liver abscess in an older patient: a case report and literature review. BMC Geriatr 24, 945 (2024). https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s12877-024-05541-w

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Keywords

BMC Geriatrics

ISSN: 1471-2318

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