Clinical management of porcelain gallbladder: A case report

Abstract

BACKGROUND

This case report highlights the clinical significance and management of porcelain gallbladder, a rare condition with malignant potential, aiming to enhance clinicians’ awareness of its association with gallbladder cancer and emphasize the importance of imaging and timely surgical intervention.

CASE SUMMARY

An elderly female with asymptomatic gallstone history presented with upper abdominal pain. Imaging supported porcelain gallbladder diagnosis, and laparoscopic cholecystectomy was performed successfully. Postoperative pathology confirmed chronic calculous cholecystitis with wall calcification, and the patient recovered well. Literature review underscores the link between porcelain gallbladder and gallbladder carcinoma, supporting surgical resection as key for diagnosis and prevention.

CONCLUSION

Porcelain gallbladder requires early surgical management due to its malignant potential and reliance on imaging for diagnosis.

Key Words: Gallbladder carcinoma; Gallbladder calcification; Porcelain gallbladder; Computed tomography; Case report

Core Tip: Porcelain gallbladder, a rare condition marked by gallbladder wall calcification, carries a significant risk of malignancy. Contrast-enhanced computed tomography is the definitive imaging modality for diagnosis. Prophylactic cholecystectomy is the standard treatment, with laparoscopic approach feasible in selected cases. Intraoperative frozen section is mandatory to rule out carcinoma, which dictates the extent of surgery.

INTRODUCTION

The gallbladder is a vital digestive organ primarily responsible for the storage, concentration, and excretion of bile[1-3]. Gallbladder dysfunction is a common cause of various biliary tract diseases, such as cholecystitis and gallstones[4,5]. Among the numerous gallbladder disorders, porcelain gallbladder is a rare condition characterized by extensive gallbladder wall calcification. This condition derives its name from the bluish-white, porcelain-like appearance and brittle texture of the calcified wall found on macroscopic inspection[6,7].

Although the incidence of porcelain gallbladder is extremely low in the general population, it poses a notable clinical concern due to its well-established association with gallbladder carcinoma[8,9]. Despite advances in imaging techniques that have improved preoperative diagnosis, the precise pathogenesis, malignant transformation risk, and optimal management strategies remain debated.

In light of these factors, we present a case of a patient admitted with upper abdominal pain who was ultimately diagnosed with porcelain gallbladder, which was further confirmed by surgery and pathology. In this case report, we systematically explore the etiology, clinical features, diagnostic approaches, treatment options, and prognosis of this rare condition by reporting this case and reviewing the relevant literature, aiming to provide valuable insights to enhance clinical understanding and management.

CASE PRESENTATION

Chief complaints

A 60-year-old female patient presented to our hospital with persistent pain in the upper abdomen. The pain was described as a dull, deep discomfort that had developed gradually over several days and localized predominantly in the epigastric region. No specific aggravating or relieving factors were reported by the patient at the time of admission. This symptom represented the primary reason for seeking medical attention.

History of present illness

A 60-year-old female patient was admitted to our hospital with a primary complaint of upper abdominal pain. The pain was the symptom that prompted the current medical visit.

History of past illness

The patient had a documented history of gallstones for over 20 years. Notably, she had remained entirely asymptomatic throughout this prolonged period prior to the current presentation.

Personal and family history

No significant personal or family medical history relevant to the current condition was reported.

Physical examination

Upon admission, physical examination revealed deep tenderness localized to the upper abdomen. No other positive signs, such as jaundice, fever, or palpable masses, were detected.

Laboratory examinations

Laboratory tests indicated cholestatic liver injury. The key findings included markedly elevated alanine aminotransferase (482.7 U/L), aspartate aminotransferase (256.6 U/L), and γ-glutamyl transferase (923.8 U/L). Total bilirubin was mildly increased to 22.7 μmol/L.

Imaging examinations

Imaging studies played a decisive role in the diagnostic process. Abdominal ultrasonography revealed a gallbladder extensively filled with stones (Figure 1A). Subsequently, contrast-enhanced computed tomography (CT) of the upper abdomen was performed. The CT scan clearly demonstrated diffuse calcification of the gallbladder wall, exhibiting the characteristic features of a porcelain gallbladder (Figure 1B and C).

Figure 1 Imaging, intraoperative, and pathological findings of porcelain gallbladder. A: Abdominal ultrasonography; B and C: Sagittal and coronal views of contrast-enhanced abdominal computed tomography; D and E: Laparoscopic intraoperative views; F and G: Resected gallbladder specimen (yellow arrows: Gallbladder body; orange arrows: Gallbladder infundibulum); H and I: Histological examination with hematoxylin-eosin staining (yellow arrows: Calcification foci; orange arrows: Hyaline degeneration).

FINAL DIAGNOSIS

The final diagnosis was porcelain gallbladder, confirmed by comprehensive postoperative histopathological examination. The pathological findings were consistent with chronic calculous cholecystitis with acute exacerbation, featuring extensive gallbladder wall calcification, fibrous tissue hyperplasia, hyaline degeneration, and purulent inflammatory changes.

TREATMENT

The patient subsequently underwent laparoscopic cholecystectomy. Intraoperative findings closely corresponded to the imaging results, with the gallbladder wall exhibiting typical porcelain-like hardening and dense adhesions to surrounding tissues, accompanied by an obscured anatomy of the Calot’s triangle (Figure 1D and E). Dissection of the specimen further revealed a stone-filled gallbladder lumen and a hardened wall texture (Figure 1F and G). Intraoperative frozen section pathology indicated acute exacerbation of chronic calculous cholecystitis with gallbladder wall calcification, while postoperative pathological examination confirmed the diagnosis of porcelain gallbladder, presenting as acute exacerbation of chronic calculous cholecystitis with purulent changes, along with fibrous tissue hyperplasia, hyaline degeneration, and gallbladder wall calcification (Figure 1H and I).

OUTCOME AND FOLLOW-UP

The patient tolerated the procedure well with no immediate postoperative complications such as bleeding, bile leakage, or infection. Pain was adequately controlled, and the patient was discharged on the third postoperative day with stable vital signs and satisfactory wound healing. Final paraffin-embedded histopathology confirmed the diagnosis of porcelain gallbladder with no evidence of malignancy, consistent with the intraoperative frozen section findings. Given the benign nature of the pathology, long-term oncological surveillance was deemed unnecessary. The patient was advised to attend a routine postoperative follow-up appointment at one month for clinical assessment and wound review. As the risk of malignancy in this completely resected benign porcelain gallbladder was considered negligible, no further imaging or tumor marker monitoring was scheduled. At the one-month follow-up, the patient remained asymptomatic, with complete resolution of preoperative abdominal pain and no new complaints.

DISCUSSION

The formation of porcelain gallbladder represents a pathological process driven primarily by chronic inflammation, progressive tissue damage, and aberrant repair. Its mechanism can be summarized as a classic pathway of “chronic stimulation - inflammatory cascade - fibrosis and calcification”. Persistent gallstones and recurrent chronic cholecystitis establish a foundation of sustained injury[10]. On one hand, chronic inflammatory responses activate both the innate and adaptive immune systems, leading to the infiltration of inflammatory cells such as macrophages and lymphocytes, which release a large number of inflammatory cytokines and profibrotic mediators. This directly drives the progression of gallbladder wall fibrosis and eventual calcification. On the other hand, certain pathogens may also trigger autoimmune responses targeting the biliary epithelium through molecular mimicry, further exacerbating local inflammation and tissue damage[11-13]. Under the sustained influence of chronic inflammation and a hypoxic microenvironment, gallbladder wall fibroblasts become abnormally activated, resulting in excessive deposition of extracellular matrix, progressive fibrosis, thickening, and even hyaline degeneration of the gallbladder wall. Ultimately, driven by imbalances in local calcium and phosphorus metabolism, the formation of an alkaline microenvironment, and inflammation-mediated heterotopic calcification, the gallbladder wall undergoes diffuse or patchy deposition of calcium salts, forming the characteristic “porcelain” change[11,14]. Therefore, the immune-inflammatory response is a key component throughout the development of porcelain gallbladder, directly participating in and promoting its final formation by regulating the processes of fibrosis and pathological calcification[15].

Porcelain gallbladder presents with non-specific clinical manifestations, and the condition is often detected incidentally during imaging studies or when complications arise. This condition most commonly affects middle-aged and older populations, with the highest incidence observed between those aged 50 years and 70 years. Women are slightly more affected than men, a demographic distribution that aligns with the prevalence pattern of cholelithiasis[16]. Most patients remain asymptomatic for extended periods or present only with underlying chronic cholecystitis-related or gallstone-related non-specific symptoms, such as right upper quadrant discomfort, abdominal bloating, and dyspepsia. Characteristic biliary colic is relatively uncommon because of the loss of contractile function that results from extensive gallbladder wall calcification. The onset of symptoms such as severe right upper quadrant pain, fever, or jaundice typically indicates complications including acute cholecystitis, choledocholithiasis, or, most critically, gallbladder carcinoma[17,18]. Therefore, the paradoxical combination of frequent asymptomatic presentation and prominent malignant potential is the primary rationale for recommending surgical intervention upon diagnosis.

Porcelain gallbladder diagnosis relies predominantly on imaging modalities. CT is considered the gold standard for diagnosis and classification, as it effectively reveals diffuse or focal calcification of the gallbladder wall and allows the precise characterization of the calcification pattern and extent[8,19]. Furthermore, CT offers unparalleled advantages for detecting potential coexistence with gallbladder cancer. Moreover, the differential diagnosis should include gallstones, gallbladder adenomyomatosis, and most importantly, gallbladder carcinoma[20,21].

Surgical intervention remains the primary treatment for porcelain gallbladder. Given its well-established association with gallbladder carcinoma, prophylactic cholecystectomy is recommended once radiological diagnosis is established, regardless of the clinical symptoms or their absence[22,23]. The surgical approach should be carefully considered based on preoperative assessment and intraoperative findings. Laparoscopic cholecystectomy is the preferred initial option considering its minimally invasive advantages; however, its feasibility may be limited by local pathological changes characteristic of porcelain gallbladder. Calot’s triangle frequently has a “frozen” appearance due to chronic inflammation and fibrosis, resulting in obscured anatomical planes and dense adhesions between the gallbladder and surrounding tissues, which increase intraoperative bleeding and biliary injury risks. Consequently, prompt conversion to open surgery is warranted when severe adhesions, unclear anatomical relationships, or suspected malignancy are encountered. Intraoperative frozen section examination is mandatory, and if gallbladder carcinoma is confirmed, the surgical scope should be expanded according to tumor staging to perform a standard radical cholecystectomy, including wedge liver resection and regional lymph node dissection, which is critical for determining patient prognosis.

The prognosis and postoperative management of porcelain gallbladder are fundamentally guided by risk stratification based on pathological findings. For simple (benign) porcelain gallbladder, prognosis after cholecystectomy is excellent, and specialized oncological follow-up is generally unnecessary. If pathological examination reveals malignant transformation, prognosis depends directly on tumor staging: Patients with early-stage gallbladder cancer (e.g., T1a) can achieve a postoperative 5-year survival rate exceeding 85%, whereas survival rates decline significantly in advanced cases. Postoperative management should be tailored according to the pathological diagnosis: Benign cases require only routine postoperative review; malignant or high-risk cases should establish a structured follow-up protocol based on imaging (contrast-enhanced CT/magnetic resonance imaging) and tumor marker surveillance, with some advanced cases requiring multidisciplinary evaluation to determine the need for additional radical surgery or adjuvant therapy. In summary, postoperative paraffin pathological diagnosis serves as the cornerstone for prognostic assessment and clinical decision-making.

The clinical significance of this case is demonstrated through critical decision-making optimizations in three key aspects: First, preoperative evaluation should not rely solely on abdominal ultrasonography but must incorporate enhanced CT or other precise imaging modalities to anticipate surgical complexity. Second, given the frequent intraoperative finding of a “frozen” fibrotic adhesion in the gallbladder triangle that obscures anatomical planes, comprehensive preoperative planning for managing difficult adhesions is essential to minimize the risk of biliary injury. Most importantly, due to the well-established malignant potential of porcelain gallbladder, standardized intraoperative frozen section biopsy must be rigorously implemented as a critical procedure. This integrated diagnostic-therapeutic pathway - spanning precise preoperative assessment, strategic intraoperative management, and pathological confirmation - systematically illustrates a standardized management protocol for complex biliary diseases, providing a valuable reference model for managing similar cases in clinical practice.

CONCLUSION

Porcelain gallbladder is a rare biliary condition with noteworthy clinical implications because of its established association with gallbladder carcinoma. This case report underscores CT as the definitive imaging modality for preoperative diagnosis and classification. Furthermore, prophylactic cholecystectomy remains the standard treatment choice. However, the surgical approach should be carefully individualized, and the selection between laparoscopic and open techniques should be based on intraoperative findings, supplemented by routine frozen section examination to exclude malignancy. This comprehensive approach allows clinicians to optimally determine the surgical extent and improve patient prognosis.

ACKNOWLEDGEMENTS

The authors would like to sincerely thank the colleagues from the Department of Hepatobiliary Surgery, Department of Radiology, and Department of Pathology for their professional support throughout the diagnosis and treatment process, particularly in clinical evaluation, imaging interpretation, and pathological analysis.