Acute septic cholelithiasic cholecystitis and adenocarcinoma of the gallbladder; an interesting association.

BACKGROUND AND STUDY AIMS: Primary carcinoma of the gallbladder may present as acute lithiasic cholecystitis that leads to severe septic complications. The correlation between severe sepsis of the gallbladder and primary carcinoma is unclear. The goal of the present study is to examine the relation between severe septic complications of lithiasic cholecystitis and primary carcinoma of the gallbladder. PATIENTS AND METHODS: A group of 72 patients (22 males, 50 females, age range: 45-99, mean age: 68.6 years), with severe septic cholelithiasic cholecystitis was treated with emergency surgery after failure of conservative treatment, and patients found with primary carcinoma of the gallbladder were registered. The resectability and operability of the tumor were studied, as well as tumor staging and overall patient survival. RESULTS: During urgent surgery for severe septic lithiasic cholecystitis, 12 patients (12/72, 16.6%) were found with gallbladder carcinoma. Patients with septic acute lithiasic cholecystitis and carcinoma had a higher mean age compared to those without carcinoma (74.8 vs. 67.4 yrs). Eleven of 12 (91.6%) carcinomas were inoperable, despite resectability of 8 out of 12 (66.6%), and overall patient survival was limited to a few months after surgery. CONCLUSIONS: Severe septic complications in elderly patients with a long-standing history of gallbladder stones may co-exist with primary carcinoma of the gallbladder. The percentage of a gallbladder carcinoma detected in septic patients reaches up to 16.6%. Even if these patients have a poor general health, surgical intervention is a solution when they appear with severe septic clinical symptoms caused by gallstones or carcinoma, in order to avoid lethal sepsis. The possibility of a carcinoma hidden in the gallbladder must be in mind during surgery. Imaging studies before surgery may detect the carcinoma; in most cases carcinomas are inoperable, although colecystectomy may be performed during surgery.

Biliary bacterial factors determine the path of gallstone formation.

BACKGROUND: Bacteria cause pigment gallstones and can act as a nidus for cholesterol gallstone formation. Bacterial factors that facilitate gallstone formation include beta-glucuronidase (bG), phospholipase (PhL), and slime. The current study sought to determine whether bacterial factors influence the path of gallstone formation. METHODS: A total of 382 gallstones were cultured and/or examined using scanning electron microscopy (SEM). Bacteria were tested for bG and slime production. Gallstone composition was determined using infrared spectrography. Ca-palmitate presence documented bacterial PhL production. Groups were identified based upon bacterial factors present: slime and bGPhL (slime/bGPhL), bGPhL only, and slime only. Influence of bacterial stone-forming factors on gallstone composition and morphology was analyzed. RESULTS: Bacteria were present in 75% of pigment, 76% of mixed, and 20% of cholesterol stones. Gallstones with bGPhL producing bacteria contained more pigment (71% vs. 26%, P < .0001). The slime/bGPhL group was associated (79%) with pigment stones, bGPhL was associated (56%) with mixed stones, while slime (or none) only was associated (67%) with cholesterol stones (P < .031, all comparisons). CONCLUSIONS: Bacterial properties determined the path of gallstone formation. Bacteria that produced all stone-forming factors promoted pigment stone formation, while those that produced only bGPhL promoted mixed stone formation. Bacteria that only produced slime lacked the ability to generate pigment solids, and consequently were more common in the centers of cholesterol stones. This shows how bacterial characteristics may govern the process of gallstone formation.

DNA sequences and proteic antigens of H. pylori in cholecystic bile and tissue of patients with gallstones.

BACKGROUND: Although Helicobacter pylori DNA sequences have been detected in cholecystic bile and tissue of patients with gallstones, controversial results are reported from different geographic areas. AIM: To detect H. pylori in cholecystic bile and tissue of patients with gallstones from a previously uninvestigated geographic area, southern Italy. Detection included both the bacterial DNA and the specific antigen (H. pylori stool antigen) identified in the stools of infected patients for diagnostic purposes. PATIENTS AND METHODS: The study enclosed 33 consecutive patients undergoing laparoscopic cholecystectomy for gallstones. DNA sequences of H. pylori were detected by polymerase chain reaction in both cholecystic bile and tissue homogenate. Moreover, we assayed H.pylori stool antigen on gall-bladder cytosolic and biliary proteins after their extraction. Bacterial presence in the stomach was assessed by urea breath test in all patients and Deltadelta13CPDB value assumed as marker of intragastric load. Fisher's exact probability and Student's t-tests were used for statistical analysis. RESULTS: DNA sequences of H. pylori in bile were found in 51.5% and significantly correlated with its presence in cholecystic tissue homogenate (P<0.005), H. pylori stool antigen in gall-bladder (P=0.0013) and bile (P=0.04) proteins, gastric infection (P<0.01) and intragastric bacterial load (P<0.001). No correlation was found, however, with sex and age of the patients. CONCLUSIONS: Our prevalence value of bacterial DNA in bile and gall-bladder of patients with gallstones agreed with that of the only other Italian study. The simultaneous presence of both bacterial DNA and proteic antigen suggests that the same prototype of bacterium could be located at both intestinal and cholecystic level and, therefore, the intestine represents the source of biliary contagion.

Campylobacter jejuni: unusual cause of cholecystitis with lithiasis. Case report and literature review.

A 51-year-old man presented with acute cholecystitis and the routine intraoperative culture of the bile grew Campylobacter jejuni. The patient was cured by laparoscopic cholecystectomy without specific antimicrobial treatment. Cholecystitis owing to Campylobacter spp. could be missed because a culture for Campylobacter is not routinely requested nor is it cost effective to look for it in bile or gallbladder specimens. Moreover, the fastidious nature of these bacteria dictates against their recovery in routine culture. Because this is a rare infection at this site, a review of the literature on this infection is included.

[Nanobacteria in serum, bile and gallbladder mucosa of cholecystolithiasis patients].

OBJECTIVE: To find the distribution of nanobacteria in the serum, bile and gallbladder mucosa of cholecystolithiasis patients. METHODS: The infection rate of nanobacteria was identified by ELISA in the serum samples from 338 healthy people and 76 patients with cholecystolithiasis (chi(2) = 0.89, P > 0.05). Nanobacteria were cultured from the bile samples in 57 patients with cholecystolithiasis and 18 non-cholelithiasis patients and identified by immunohistochemical staining and TEM (chi(2) = 29.80, P < 0.05). Forty samples of gallbladder mucosa randomly selected from the 57 cholecystolithiasis patients were identified by immunohistochemical staining and compared with the corresponding bile samples. RESULTS: The infection rate of nanobacteria was 8.0% and 31.6% for the serum samples of the healthy people and cholecystolithiasis patients, respectively. The positive rate of nanobacteria in the bile samples was 61.3% and there was no significant difference in the bile of the cholecystolithiasis patients and the control group (61.4% vs. 61.1%). Fourteen positive patients had infection of nanobacteria in the gallbladder mucosa, submucosa, and calcific field. CONCLUSIONS: The infection rate of nanobacteria was 8% in the serum samples from the healthy people. There are nanobacteria in the serum, bile, and gallbladder mucosa. The infection of the nanobacteria may result in calcification and fibrosis of the gallbladder.