Microscopic evaluation of giant peritoneal loose body: A case report

Abstract

BACKGROUND

Giant peritoneal loose body (PLB) occurs in the abdominal or pelvic cavity. It is rare and the causes of its occurrence are unclear. Here, we report a case of giant PLB and further reveal the related metabolic products and microorganisms within it.

CASE SUMMARY

A 74-year-old man presented with lower back discomfort for two weeks. Abdominal computed tomography revealed a large, well-circumscribed solid mass at the left pelvic margin. The symptoms improved after surgical removal. A giant PLB with central calcification and necrotic adipose tissue was identified by pathological investigation. While metabolomic profiling showed an enrichment of arachidonic acid (AA) and palmitoylethanolamide (PEA), additional metagenomic analysis confirmed the presence of Aspergillus, Acinetobacter and Aeromonas.

CONCLUSION

Fat necrosis and microbial stimulation in patients with intestinal inflammation, surgery or trauma, and AA/PEA imbalance may result in giant PLB formation.

Key Words: Peritoneal loose body; Microbiota; Arachidonic acid; Palmitoylethanolamide; Inflammatory microenvironment; Case report

Core Tip: An instance of a giant peritoneal loose body (PLB) is described. We, for the first time, examined the interior microbial composition and metabolite profile using metagenomic sequencing and liquid chromatography–mass spectrometry. Arachidonic acid and palmitoylethanolamide, the two lipid bioactive mediators, were found along with microorganisms such as Aspergillus, Acinetobacter and Aeromonas. We speculate that continuous stimulation by fat necrosis and microorganisms on abdominal macrophages may be the fundamental cause of giant PLB formation.

INTRODUCTION

Peritoneal loose body (PLB) are typically small, white or light-gray, pea-shaped nodules with smooth and shiny surfaces, and they are more commonly observed in males. Most PLBs range from 5 mm to 20 mm in diameter, while those exceeding 50 mm are extremely rare[1]. PLBs can present with a variety of clinical symptoms, such as intestinal obstruction, urgency of urination, and abdominal pain. They are frequently misinterpreted as benign or malignant abdominal tumors or as tuberculous granulomas[2]. The factors contributing to the formation of giant PLBs remain unclear. Currently, it is believed that PLB may originate from appendages epiploicae, omentum majus, as well as autoerotic ovaries or uterus[3,4]. Fat necrosis induced by ischemia facilitates saponification and calcification[5]. Its gradual expansion developed subsequently with aberrant collagen deposition[4]. Here, we report a case of a 74-year-old male patient diagnosed with a giant PLB measuring approximately 5.0 cm × 4.2 cm, and explore the potential pathogenic mechanisms using metagenomic and metabolomic analyses.

CASE PRESENTATION

Chief complaints

A 74-year-old male patient attended our department for the treatment of low back discomfort.

History of present illness

The patient’s back pain had lasted 2 months.

History of past illness

The patient had a medical history of coronary artery stenosis and cerebral infarction. He took ginkgo biloba extract, atorvastatin, loratadine, and ezetimibe orally. The patient previously underwent an appendectomy. He had no history of pancreatic disease, spinal disorders, or trauma.

Personal and family history

His personal history included tobacco use (10 cigarettes/day for 40 years). The patient denied any family history of genetic diseases.

Physical examination

Upon physical examination, the patient’s general condition was satisfactory; blood pressure was 117/72 mmHg, pulse rate was 72 beats per minute, and pain score was 3, with no alleviation of pain on positional changes. An old surgical scar was visible on the abdomen; no masses or ascites were detected.

Laboratory examinations

Laboratory tests revealed no significant abnormalities. The patient had a normal white blood cell count; normal carcinoembryonic antigen, prostate-specific antigen, albumin, and alanine aminotransferase levels; and a normal absolute T-lymphocyte count. The triglyceride level was 1.94 mmol/L (reference range: 0.3-1.7 mmol/L).

Imaging examinations

Abdominal computed tomography revealed a 5.0 cm × 4.2 cm cystic-solid mass within the left pelvic margin with well-defined borders (Figure 1).

Figure 1 Abdominal computed tomography. A: Plain abdominal computed tomography (CT) shows a 5.0 cm × 4.2 cm cystic-solid mass within the left pelvic margin with well-defined borders; B: Contrast-enhanced abdominal CT shows no obvious enhancement or significant blood supply within the mass.

FINAL DIAGNOSIS

Based on the above findings, the patient was diagnosed with a giant PLB, warranting consideration of surgical intervention.

TREATMENT

Laparoscopic resection was chosen after preoperative departmental discussion and anesthetic evaluation. A whitish, oval-shaped mass on the left side of the pelvic cavity was discovered during surgery. The mass measured approximately 4.5 cm × 5.0 cm, with a smooth surface, firm consistency, and well-defined borders. A tiny portion of the growth was stuck to the peritoneum (Figure 2A and B). The patient’s back pain disappeared after the tumor was removed, and on the fourth day following the procedure, he was discharged from the hospital without incident.

Figure 2 Lesion morphology. A: Morphology of the lesion under laparoscopy; B: The lesion was approximately 4.5 centimeters × 5.0 centimeters in size, with a smooth surface, a consistent, solid texture, and a distinct border; C: The lesion could be separated into three layers, with visible gravel-like material in the center; D: Hematoxylin and eosin staining of the lesion.

The mass comprised three layers. Gravel-like material comprised the innermost layer, with distinct brown and white gravel particles. The inner layer was surrounded by a ring-shaped plate of white, stiff, fibrous material (middle layer). The outermost layer, which formed a brown ring enclosing the middle layer, had a similar texture to the middle layer but a noticeably different color (Figure 2C).

Histologically, the region surrounding the core zone comprised annular fibrous tissue, whereas the center zone comprised calcified and necrotic adipose tissue (Figure 2D).

Liquid chromatography–mass spectrometry revealed 52 metabolites in the lesion: 25 in the inner layer, 28 in the middle layer, and 40 in the outer layer. Arachidonic acid (AA) and palmitoylethanolamide (PEA) were the most abundant metabolites in the inner layer (Figure 3A).

Figure 3 Metabolite distribution. A: Metabolite distribution inside the lesion area; B: Kyoto Encyclopedia of Genes and Genomes pathway enrichment study of inner-layer metabolites.

Further metagenomic sequencing of the inner layer revealed bacteria and fungi, with Aspergillus, Acinetobacter, and Aeromonas being the most abundant (Table 1).

Table 1 Abundance of microorganisms identified by metagenomic sequencing.

Type	Genus	Relative abundance (%)	Sequence count (genus)	Species	Identification confidence (%)	Sequence count (species)
/	Aspergillus	24.4	1233	Aspergillus oryzae	99	8
				Aspergillus flavus	99	4
				Aspergillus fumigatus	99	4
G-	Aeromonas	16.1	11340	Aeromonas caviae	99	5197
G-	Acinetobacter	19.5	10040	Acinetobacter junii	99	5013
G+	Microbacterium	2.6	1379	Microbacterium arborescens	99	955
G-	Moraxella	2.2	782	Moraxella catarrhalis	99	4
G-	Pseudomonas	2.1	1759	Pseudomonas aeruginosa	99	335
G-	Serratia	0.3	264	Serratia marcescens	99	211
G-	Enterobacter	0.2	128	Enterobacter cloacae	99	27
G+	Enterococcus	0.2	68	Enterococcus faecium	99	4
G-	Escherichia	0.1	64	Escherichia coli	99	64

OUTCOME AND FOLLOW-UP

At the six-month follow-up after the operation, the patient remained free of complications such as lower abdominal discomfort, fever or intestinal obstruction.

DISCUSSION

PLB is a very rare abdominal lesion typically found by accident during autopsy or abdominal surgery. It is generally believed to originate from the fatty appendices epiploicae. Torsion of the appendices epiploicae blocks the blood supply, which causes fat necrosis and calcification[6].

We discovered polyunsaturated fatty acid synthesis in the core area of the lesion, in which AA was the most abundant metabolite (Figure 3B). Strong biological activity was exhibited by AA and its metabolites, which can activate multiple signaling pathways contributing to inflammatory reactions[7]. Abnormal fatty acid metabolism can exacerbate the inflammatory response to infection by influencing the p38 MAPK signaling pathway[8]. Interestingly, another metabolite present in significant quantities, PEA, prevents scar formation by alleviating inflammation and fibrosis through the activation of peroxisome proliferator-activated receptor alpha[9]. This antagonistic effect, and the disparity in local metabolite proportions, may explain why cellulose fibers continuously accumulate around the core of the PLB without adhering to surrounding tissues.

We confirmed the presence of bacteria and fungi within the inner layer of the PLB through metagenomic sequencing. These microorganisms most likely originated from appendicitis. Generally, neither bacteria nor fungi create metabolites like AA and PEA. AA and PEA are typically derived from the hydrolysis of membrane phospholipids by phospholipase, and by the hydrolysis of the membrane by the phospholipid precursor N-acyl-phosphatidylethanolamine (NAPE) by NAPE-PLD[10,11]. Therefore, peritoneal macrophages that possess these two catalytic enzymes are the most likely candidates for catalyzing the production of AA and PEA[12,13].

What role do bacteria and fungi play in this process? Pathogen specificity and highly conserved molecular architectures influence phospholipase and NAPE-PLD expression in macrophages[11,14]. Macrophages can also respond to exotoxin stimulation by producing proinflammatory cytokines and activating the AA pathway[15]. Therefore, necrotic adipose tissue primarily provides the raw materials for generating bioactive mediators such as AA and PEA, while microorganisms enhance hydrolytic enzyme activity. Their collaborative action stimulates sustained release of pro- and anti-inflammatory factors by macrophages, thereby forming PLB within the peritoneal cavity.

In summary, we reported a case of giant PLB and provided the first exploratory multi-omics characterization of a giant PLB and offers preliminary insights into possible microbiota-metabolite interactions in the PLB microenvironment. However, as a single-case exploratory study, its findings from metagenomic and metabolomic analyses are observational in nature and cannot establish direct causal relationships between the identified microorganisms, AA/PEA metabolic alterations, and PLB formation. Therefore, future studies integrating larger clinical cohorts, prospective specimen collection, additional histological and molecular validation, functional experiments, and animal models are required to validate and further elucidate these potential mechanisms.

CONCLUSION

We report a case of a giant PLB in the abdominal cavity and, for the first time, analyzed the etiology in terms of metabolites and nucleic acids. The findings suggest that continuous stimulation of peritoneal macrophages by fat necrosis and microorganisms may be the cause of PLB formation. Therefore, any factors for development of fat necrosis and the retention of microorganisms in the abdominal cavity can potentially trigger PLB, such as intestinal inflammation, intestinal surgery, and abdominal trauma. And inflammatory factors such as AA and PEA, as well as their ratios, may also play a significant role in the occurrence and progression of PLB.