Perforation with extravasation of barium is a rare complication of contrast enema examination of the large bowel with a high associated mortality rate. The experience of performing a re-laparotomy in a patient previously exposed to barium peritonitis is even less common. We describe an elderly male patient with a Hartmann's procedure performed a year previously, presenting with peritonitis following barium enema evaluation of the proximal colon via an end descending colon stoma. Emergency laparotomy, segmental bowel resection and liberal peritoneal toilet resulted in a satisfactory outcome. The patient had a subsequent successful reversal of his Hartmann's procedure nine months later despite the presence of dense barium induced adhesions. This potentially preventable iatrogenic complication is discussed in this report, which is supplemented by a brief review of the English literature.
Barium Sulfate/administration & dosage ; Barium Sulfate/*adverse effects ; Colon ; Colostomy ; Enema/*adverse effects ; *Iatrogenic Disease ; Peritonitis/*chemically induced

The possibility of inducing peritoneal inflammation in three murine species (gerbils, rats and mice) via the oral administration of indomethacin was investigated with the overall aim of developing an experimental animal model for human peritonitis. Gerbils given high doses of indomethacin at a rate of 30 mg and 40 mg/kg body weight showed swelling of the abdomen, depression and dyspnea within 4 days after the treatment. The severity of the clinical symptoms increased with time. The animals were confirmed as having developed peritonitis based on the pathological features including inflammation of the peritoneum, and fibrinous adhesion of the abdominal organs in the abdominal cavity. The severity of peritonitis increased with increasing dose of indomethacin, and was not related to the gender of the animal. On the other hand, peritoneal inflammation did not develop in the rats and mice even at high doses. Therefore, the administration of 30 mg/kg body weight of indomethacin is an effective and simple method of inducing peritonitis in 5-week-old Mongolian gerbils. The animal peritonitis model used in this study can be used as an effective tool for examining potential therapeutic compounds for preventing peritoneal damage during peritonitis, and provide insight into the pathophysiology of peritonitis.
Administration, Oral ; Animals ; Dose-Response Relationship, Drug ; Female ; *Gerbillinae ; Indomethacin/*administration&dosage/*toxicity ; Inflammation/chemically induced/pathology ; Male ; Mice ; Mice, Inbred ICR ; Peritonitis/*chemically induced/pathology ; Rats ; Rats, Sprague-Dawley ; Specific Pathogen-Free Organisms

BACKGROUNDThe nervous system, through the vagus nerve and its neurotransmitter acetylcholine, can down-regulate the systemic inflammation in vivo, and recently, a role of brain cholinergic mechanisms in activating this cholinergic anti-inflammatory pathway has been indicated. Galanthamine is a cholinesterase inhibitor and one of the centrally acting cholinergic agents available in clinic. This study aimed to evaluate the effect of galanthamine on circulating tumor necrosis factor alpha (TNF-alpha) in rats with lipopolysaccharide-induced peritonitis and the possible role of the vagus nerve in the action of galanthamine.

METHODSRat models of lipopolysaccharide-induced peritonitis and bilateral cervical vagotomy were produced. In the experiment 1, the rats were randomly divided into control group, peritonitis group, and peritonitis groups treated with three dosages of galanthamine. In the experiment 2, the rats were randomly divided into sham group, sham plus peritonitis group, sham plus peritonitis group treated with galanthamine, vagotomy plus peritonitis group, and vagotomy plus peritonitis group treated with galanthamine. The levels of plasma TNF-alpha were determined in every group.

RESULTSThe level of circulating TNF-alpha was significantly increased in rats after intraperitoneal injection of endotoxin. Galanthamine treatment decreased the level of circulating TNF-alpha in rats with lipopolysaccharide-induced peritonitis, and there was significant difference compared with rats with lipopolysaccharide-induced peritonitis without treatment. The 3 mg/kg dosage of galanthamine had the most significant inhibition on circulating TNF-alpha level at all the three tested doses. Galanthamine obviously decreased the TNF-alpha level in rats with lipopolysaccharide-induced peritonitis with sham operation, but could not decrease the TNF-alpha level in rats with lipopolysaccharide-induced peritonitis with vagotomy.

CONCLUSIONCholinesterase inhibitor galanthamine has an inhibitory effect on TNF-alpha release in rats with lipopolysaccharide-induced peritonitis, and the vagus nerve plays a role in the process of the action of galanthamine.

Animals ; Cholinesterase Inhibitors ; therapeutic use ; Galantamine ; therapeutic use ; Lipopolysaccharides ; toxicity ; Male ; Peritonitis ; blood ; chemically induced ; drug therapy ; Rats ; Rats, Sprague-Dawley ; Tumor Necrosis Factor-alpha ; blood

OBJECTIVETo observe the effect of the antibody TSP-2 against a single epitope of mouse Toll-like receptor 2 extracellular domain (mTLR2ECD) on the inflammation in mice with zymosan A-induced peritonitis.

METHODSIn mice with peritonitis induced by intraperitoneal injection of zymosan A, pretreatments with PBS, normal rabbit IgG and TSP-2 antibody at two different doses (2.5 and 5.0 mg/kg) were administered via the tail vein. Six hours after intraperitoneal injection of zymosan A, Evans blue was injected through the tail vein, and the frequency of writhing of the mice within 20 min were recorded. The mice were then sacrificed for peritoneal lavage, and the lavage fluid was collected to assess the exudation of Evans blue in the supernatant. The peritoneal leukocyte count, mast cell degranulation and release of such inflammatory mediators as platelet activating factor (PAF) and tumor necrosis factor-alpha (TNFalpha) in the lavage fluid were observed by cell counting, specific cell staining, immunohistochemistry and enzyme-linked immunosorbent assay (ELISA).

RESULTSCompared with PBS or rabbit IgG groups, TSP-2 treatment resulted in significantly reduced writhing response of the mice and lowered Evans blue exudation and leukocyte count in the peritoneal lavage, with also decreased degranulation of the mast cells induced by C48/80.

CONCLUSIONTSP-2 antibody against a single epitope of mTLR2ECD inhibits the inflammatory response in mice with zymosan A-induced peritonitis.

Animals ; Antibodies ; immunology ; Behavior, Animal ; Epitopes ; immunology ; Extracellular Space ; Female ; Leukocyte Count ; Mast Cells ; immunology ; Mice ; Peritoneal Lavage ; Peritonitis ; chemically induced ; immunology ; Protein Structure, Tertiary ; Toll-Like Receptor 2 ; chemistry ; immunology ; Zymosan ; pharmacology

Tuberculous liver abscesses are rare. Paradoxical response in tuberculosis is common and occurred between 2 weeks and 12 weeks after anti-tuberculous medication. We report here a case of tuberculous liver abscess that developed in a paradoxical response during chemotherapy for tuberculous peritonitis in a 23-year-old male. He was hospitalized, complaining of ascites, epigastric pain. He was diagnosed tuberculous peritonitis by expiratory laparoscopic biopsy and took medication for tuberculosis. After 2 months, a hepatic lesion was detected with CT scan incidentally. Chronic granulomatous inflammation was seen in ultrasound-guided liver biopsy, and tuberculous liver abscess was diasnosed. It was considered as paradoxical response, rather than treatment failure or other else because clinical symptoms of peritoneal tuberculosis and CT scan improved. After continuing initial anti-tuberculous medication, he was successfully treated. Herein, we report a case of tuberculous liver abscess as paradoxical response while treating peritoneal tuberculosis without changing anti-tuberculous treatment regimen.
Antitubercular Agents/*adverse effects/*therapeutic use ; DNA, Bacterial/analysis ; Humans ; Laparoscopy ; Liver/pathology/ultrasonography ; Liver Abscess/*chemically induced/*diagnosis/microbiology ; Male ; Mycobacterium tuberculosis/genetics/isolation & purification ; Necrosis/pathology ; Peritoneum/pathology ; Peritonitis, Tuberculous/*drug therapy ; Tomography, X-Ray Computed ; Tuberculosis/*diagnosis/microbiology ; Young Adult

Pannexin-1 (Panx1) forms nonselective large channel in cell plasma membrane and has been shown to be associated with NLRP3 inflammasome activation, ATP release and phagocytes recruitment. In the current study, by manipulation of Panx1 expression in human myeloid cells and application of Panx1 deficient mice, we failed to find a correlation between Panx1 and NLRP3 inflammasome activation, although an interaction between these two proteins was evident. However, in thioglycollate induced peritonitis, Panx1 deficient mice showed much more phagocytes infiltration. Further analyses showed that mice deficient for Panx1 exhibited enlarged F4/80(low)Gr1(-)Ly6C(-)cell population in the peritonea. Our study thus reveals an important role for Panx1 in regulation of peritoneal cell population and peritonitis development.
Animals ; Carrier Proteins ; metabolism ; Cell Line ; Connexins ; antagonists & inhibitors ; deficiency ; genetics ; metabolism ; HEK293 Cells ; Humans ; Inflammasomes ; metabolism ; Macrophages ; cytology ; metabolism ; Mice ; Mice, Inbred C57BL ; NLR Family, Pyrin Domain-Containing 3 Protein ; Nerve Tissue Proteins ; antagonists & inhibitors ; deficiency ; genetics ; metabolism ; Peritoneal Cavity ; cytology ; Peritonitis ; chemically induced ; metabolism ; pathology ; RNA Interference ; RNA, Small Interfering ; metabolism ; Thioglycolates ; toxicity