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There are several pathologies associated with the peritoneum, such as mesothelioma and peritonitis. Moreover, the peritoneum is widely used in ultrafiltration procedures, i.e., peritoneal dialysis, presenting advantages over hemodialysis. On the other hand, ultrafiltration failure may lead to dialysis-induced fibrosis and hypervolemia. Therefore, the pathophysiological study of this tissue is of extreme biomedical importance. Studies investigating the biology of the cells dwelling in the peritoneum wall provide evidence of their plasticity and progenitor features. For instance, both mesothelial and submesothelial cells present characteristics similar to mesenchymal stem cells, including osteogenic and adipogenic differentiation potential, support of extramedullary hematopoiesis, modulation of inflammatory responses, and regulation of tumor progression. Indeed, the participation of each cell type in peritoneal pathological and physiological phenomena is still under debate, especially regarding a possible differentiation pathway connecting these peritoneal cells. The primary aim of this review is to raise this discussion. In order to do so, we will firstly provide an overview of the peritoneum anatomy, histology, and ontology, and finally we will address how a better understanding of peritoneal cell biology may contribute to future cell therapy and tissue engineering approaches., (© 2017 S. Karger AG, Basel.)

Background/aims: Peritoneal fibrosis is one of the long-term complications in peritoneal dialysis (PD) patients. Recent evidences have suggested that hydrogen sulfide (H2S) is beneficial in treating various fibrotic diseases, including pulmonary fibrosis, cirrhosis, kidney fibrosis and cardiac hypertrophy. However, no information is known about the effect of H2S on peritoneal fibrosis. In the present study, we investigated the effect of H2S on peritoneal fibrosis and explored its potential mechanisms., Methods: We developed a model of peritoneal fibrosis by intraperitoneally injecting 4.25%-glucose PD fluids and lipopolysaccharide to Sprague-Dawley rats. The rats received daily intraperitoneal injections of NaHS (56 μg/kg), an H2S donor. After 28 days, the peritoneal equilibration test (PET) was used to assess peritoneal function. At the end of dialysis, the rats were killed and parietal peritoneum was harvested for microscopic examination and immunohistochemistry., Results: On the 28th day, the parietal peritoneum of the PD rats markedly thickened as a result of increased depositions of type III collagen and fibronectin. Moreover, the number of ED-1-positive cells and the expressions of monocyte chemoattractant protein-1, transforming growth factor-β1 (TGF-β1), α-smooth muscle actin and CD31 were significantly increased in the fibrotic peritoneum. Administration of NaHS markedly decreased the biomarkers of inflammation, fibrosis and angiogenesis in the peritoneum. NaHS also improved peritoneal function assessed by PET., Conclusion: Exogenous H2S ameliorates the pathologic process of peritonitis via attenuating inflammatory events and TGF-β1 synthesis. These results suggest that H2S may be a potential therapy against peritoneal fibrosis during chronic PD. In the future, compounds releasing H2S at controlled rate will be assessed as potential candidates to treat peritoneal fibrosis., (© 2015 S. Karger AG, Basel.)

Aim: To evaluate peritoneal resorption capacity for lipopolysaccharide (LPS) and interleukin-6 (IL-6) in a model of chemical peritonitis., Methods: Zymosan peritonitis was induced in anesthetized rats. LPS was injected intraperitoneally to different groups at 4 h (n = 10), 8 h (n = 9), 12 h (n = 9), and 24 h (n = 9) after peritonitis and to a control group (n = 8). Similarly, IL-6 was injected intraperitoneally to different groups at 4 h (n = 9), 8 h (n = 10), 12 h (n = 10), and 24 h (n = 10) after peritonitis, and to a control group (n = 10). Plasma levels of LPS or IL-6 were measured immediately after intraperitoneal injections of LPS or IL-6, respectively, and at 5, 15, 30, 45, and 60 min later., Results: There was no change over time in plasma LPS levels in the groups receiving LPS intraperitoneally (p = 0.4). There was highly significant change over time in the IL-6 level in the studied time periods in the groups receiving IL-6 intraperitoneally (p < 0.0001). There was an increase in the plasma IL-6 level when sampled at 4 h after peritonitis., Conclusion: There was a reduction of resorption capacity of inflamed peritoneum for inflammatory mediators in acute chemical peritonitis., (Copyright © 2011 S. Karger AG, Basel.)

During peritoneal dialysis, peritoneal cells are repeatedly exposed to a non-physiological hypertonic environment with high glucose content and low pH. Current sterile dialysis solutions cause inflammation in the submesothelial compact zone that leads to fibrosis, neoangiogenesis, progressive increases in solute transfer and even ultrafiltration failure. The peritoneal dysfunction will further be amplified with the development of an epithelial-to-mesenchymal transition of mesothelial cells and the dissipation of the osmotic driving force through increased area and solute transport that accompanied neoangiogenesis of the submesothelial microvasculature. The alteration in the peritoneal membrane will further be aggravated by peritonitis, advanced glycation end-products and glucose degradation products. Finally, there are emerging new data supporting a pro-inflammatory role of peritoneal adipocytes.

Background and Aims: The aim of this study was to analyze intestinal integrity after temporary abdominal wall repair with absorbable mesh., Methods: Rats underwent abdominal wall repair with absorbable mesh or sham operation. Myeloperoxidase-positive cells in the intestinal muscularis were histochemically quantified. Intestinal transit was visualized 48 h after surgery. Local and systemic inflammatory response was measured with TNF-alpha and IL-6 ELISA as well as malondialdehyde (MDA) expression in serum and peritoneal fluid., Results: Neutrophil count of the intestinal muscularis revealed that infiltration in the mesh-implanted and in the mesh-free animals 48 h postoperatively was similar. Gastrointestinal transit was similarly unaffected 48 h after surgery, with or without mesh implantation. TNF-alpha, IL-6 and MDA concentration in serum and peritoneal fluid showed no significant differences between the two groups., Conclusion: Intestinal contractility and local and systemic inflammatory response remained unaffected. Therefore, absorbable mesh augmentation is a safe and reliable method for temporary repair of the abdominal wall without affecting the intestinal integrity., ((c) 2008 S. Karger AG, Basel.)

Background/aim: Ascites tumor cells from patients with peritonitis carcinomatosa were tested for cis-diamminedichloroplatinum (CDDP) sensitivity. The patients were divided into CDDP-sensitive and resistant groups. Survival and time to progression (TTP) rates were compared., Materials and Methods: 18 peritonitis carcinomatosa patients with class V ascites based on cytologic diagnosis were enrolled in this study. Chemosensitivity testing of the ascites tumor cells was done to determine their sensitivity to CDDP using a three-dimensional culture matrix of thermoreversible gelation polymer (TGP). CDDP at a dose calculated to achieve ascitic fluid drug levels equivalent to the IC(50) was given intraperitoneally to 12 CDDP-sensitive patients and 6 CDDP-resistant patients., Results: Both the median survival time and the median TTP were significantly longer in CDDP-sensitive patients than in CDDP-resistant patients (survival time 105 vs. 13 days, p = 0.019; TTP 90 vs. 5 days, p = 0.029)., Conclusion: The results indicate the potential feasibility of controlling ascites in cancer patients in whom a maximal dose effect can be achieved with a minimal dose of chemotherapy.

Peritoneal sclerosis is very common in peritoneal dialysis (PD) patients. It can vary from the mild, clinically silent sclerosis always present after years of PD, to rare but dramatic and often fatal cases. In our opinion, peritoneal sclerosis is a single disorder, so its variable manifestations are different stages of one nosological entity: this opinion relies mainly on strong connections in pathophysiology. In our view, the frequency, pathology, animal models, etiology and pathogenesis often show a bimodal configuration with suggests that peritoneal sclerosis is actually two distinct nosological entities: simple sclerosis and sclerosing peritonitis. The former is very frequent, with minor anatomical alterations and low clinical impact; it is reproducible in animals by means of PD, and is clearly due to the poor biocompatibility of PD. The latter is rare, with radical anatomical alterations and high mortality; it can only be reproduced in animal models by means other than PD and seems to be due to factors both related and unrelated to PD.

Background: We aimed at investigating the effects of unfractionated heparin (UFH) and low-molecular-weight heparin (LMWH) on the healing process of colonic anastomoses in the presence of peritonitis which is known to adversely affect the healing process., Study Design: Three groups of Wistar albino rats (n = 15 in each group) with experimental fecal peritonitis were studied. A 1-cm colonic segment was resected, and an end-to-end anastomosis was performed. The control group (group 1) was given no treatment; group 2 animals received 50 IU/kg s.c. UFH twice a day, and group 3 rats received LMWH at a dose of 1.5 mg/kg daily for 7 days postoperatively. Relaparotomy was done on day 7 in the surviving rats. The rats were sacrificed by resection of the colonic segment. The anastomosis bursting pressures were measured and the tissue samples from anastomosis lines were histopathologically examined., Results: The bursting pressures were significantly higher in UFH and LMWH groups as compared with the controls (p = 0.021 and p < 0.001, respectively), while there was no statistically significant difference between UFH and LMWH groups. Positive bacterial culture results were more common in controls (90%) than in the other two groups (p = 0.029 and p = 0.002, respectively). Also the polymorphonuclear leukocyte counts were higher (p = 0.005) and the fibrin formation more common (p = 0.007) in the controls. On the other hand, the number of fibroblasts was higher (p = 0.002) and collagen formation and revascularization more frequent (p = 0.001 and p = 0.001, respectively) in the UFH and LMWH groups., Conclusion: UFH and LMWH may have positive effects on the healing process of colonic anastomoses in the presence of peritonitis.

Sclerosing encapsulating peritonitis (SEP) is characterized by the diffuse appearance of marked sclerotic thickening of the peritoneal membrane. We experienced a case with SEP accompanied by regional changes of peritoneum. A 37-year-old woman with end-stage renal failure was started on continuous ambulatory peritoneal dialysis in 1985 and was transferred to hemodialysis in 1997. She was admitted because of ileus in 1998 with SEP and died of septicemia. The diagnosis of SEP was confirmed via the autopsy. The root of the mesentery was retracted and shortened. Since the peritoneal change was marked in the regions with free margin of mesentery and was less apparent in the regions not adhered to mesentery, it is indicated that mechanical stress also contributes to the occurrence of SEP. Since calcification and ossification were only seen in a free margin of small bowel from mesentery, it is suggested that there is a close relationship between calcification and ossification. Since fibrosis invaded into the muscle layer, dysfunction of bowel movement as well as bowel obstruction contributed to the appearance of ileus. It is suggested that mechanical stress by the root of mesentery which is retracted and shortened also contributes to the appearance of SEP., (Copyright 2002 S. Karger AG, Basel)

Background: Sclerosing encapsulating peritonitis (SEP) is a serious complication seen in patients on long-term continuous ambulatory peritoneal dialysis (CAPD). We have previously reported that mesothelial cells in effluent dialysate significantly increased in size as the duration of CAPD progressed. In this study, we investigated the relationship between mesothelial cytology, histopathology of the peritoneum, and clinical outcomes of 34 CAPD patients., Methods: When peritoneal dialysis catheters were inserted (n = 7) or removed (n = 27), a peritoneal biopsy was performed and results compared with mesothelial cytology in effluent dialysate., Results: A significant positive correlation was noted between the duration of CAPD and the surface area of peritoneal mesothelial cells (r = 0.721, p < 0.0001). The surface area of mesothelial cells in peritoneal sclerosis (n = 9; 584 +/- 97 microm(2)) was significantly greater than in peritoneal fibrosis (n = 14; 389 +/- 26 microm(2), p < 0.05), pathologic acute peritonitis (n = 3; 223 +/- 10 microm(2), p < 0.005), and normal peritoneum (n = 7; 247 +/- 12 microm(2), p < 0.001). The surface area in sclerosing peritonitis (n = 1; 1,200 microm(2)) was greater than that of all the others. Giant cells were found in the 1 case with sclerosing peritonitis and in 3 of 9 cases with peritoneal sclerosis, although they were found in only 1 of 14 patients with peritoneal fibrosis and in none of those with pathologic acute peritonitis or normal peritoneum. As the surface area of mesothelial cells increased to more than 400 microm(2) and giant cells appeared in the effluent, the frequency of peritoneal sclerosis and/or clinical SEP increased., Conclusion: An increase in the mesothelial cell surface area and the emergence of giant cells in the effluent indicate advanced peritoneal histopathology, and may be useful indicators to determine appropriate timing of discontinuation of CAPD to prevent the development of SEP., (Copyright 2001 S. Karger AG, Basel)

Leukocyte accumulation during peritonitis leads to an injurious microenvironment which is involved in the host defense reaction but is also thought to cause peritoneal damage. We tested the hypothesis that mesothelial cells (MC) respond to the injurious microenvironment during peritonitis by an increased expression of heat shock proteins (HSP 72/73), a basic way by which cells are protected against injury. Comparison of resting MC and activated MC during peritonitis in vivo by means of immunohistochemistry revealed an increased expression of HSP 72/73. As assessed by Western immunoblotting, incubation of MC in vitro with tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) caused a time-dependent induction of HSP 72/73 expression, which was maximal 6 h after stimulation. We suggest that the increased HSP 72/73 expression of MC during peritonitis is in part induced by TNF-alpha and IL-1beta and may exert a cell-protective function, lessening MC damage during peritonitis., (Copyright 2000 S. Karger AG, Basel.)

This study aimed to evaluate the possibility to detect early changes in gut-associated lymphoid tissue related to an inflammatory response. Anaesthetised pigs were subjected to faecal peritonitis (n = 9) or to a sham procedure (n = 8). Blood from the vena cava and the superior mesenteric vein was repeatedly sampled, and the levels of interleukin-6 (IL-6) were analysed. Biopsies of the small intestine and mesenteric lymph nodes (MLNs), harvested at 300 min, were incubated with monoclonal antibodies specific for CD2 (T lymphocytes), IgM (B lymphocytes) and CD11a/CD18 (leucocyte adhesion molecule). The number of positive (+) cells was scored. During peritonitis, IL-6 increased significantly. Compared to controls, the number of CD2+ cells decreased, IgM+ cells tended to increase and CD11a/CD18+ cells increased in the mucosa during peritonitis. In MLNs, the number of cells positive for all studied markers increased during peritonitis. We conclude that peritonitis causes an inflammatory response in the gut reflected by changes in the distribution of immune cells in gut-associated lymphoid tissue and release of IL-6 to venous blood.

Using a rat peritonitis model, we examined the pattern of expression of adhesion molecules and H2O2 productivity of neutrophils by indirect immunofluorescence and flow cytometry. H2O2 production in blood neutrophils was significantly increased after peritonitis induction. The expression of CD11b and CD18 antigens on blood neutrophils was also significantly increased after peritonitis induction. In contrast, H2O2 production in peritoneal neutrophils was significantly lower than that in blood neutrophils. The expression of CD11b and CD45 antigens on peritoneal neutrophils was significantly higher than on blood neutrophils. Although no function has been assigned to LFA-1 on neutrophils, the expression of LFA-1 (CD11a/CD18) on peritoneal neutrophils was significantly decreased.

The efficiency of continuous ambulatory peritoneal dialysis depends on the permeability of the peritoneal membrane. Peritoneal fibrosis (PF) causes loss of the dialytic function. Several studies have indicated that PF is closely related to the proliferation of peritoneal fibroblasts and the deposition of extracellular matrix. Transforming growth factor-beta 1 (TGF-beta1) plays a major role in stimulating extracellular matrix deposition. Frequent peritonitis occurrence may cause persistent TGF-beta1 mRNA expression. In an attempt to search for a factor related to PF, we designed a longitudinal study to measure TGF-beta1 levels in dialysate and TGF-beta1 mRNA expression in peritoneal mononuclear cells from peritoneal dialysate before onset, once a week during peritonitis, and after peritonitis in high and low peritonitis occurrence (HPO and LPO) patients. Fifteen patients with a LPO rate and 5 patients with a HPO rate were followed up longitudinally. Meanwhile, TGF-beta1 levels and TGF-beta1 mRNA expression were augmented in peritoneal dialysate effluents before, during, and after the episodes of peritonitis. The peritoneal permeability was evaluated by the peritoneal equilibration test. The results revealed that in the LPO group, TGF-beta1 and TGF-beta1 mRNA were detectable at early stages of peritonitis, but the levels decreased rapidly and were undetectable 2 weeks after peritonitis. On the other hand, in the HPO group, TGF-beta1 and TGF-beta1 mRNA persisted for a long time. We could detect TGF-beta1 and TGF-beta1 mRNA in dialysate effluents and peritoneal mononuclear cells even 2, 3, and 4 weeks after episodes of peritonitis. When compared with that of first or second episode of peritonitis, the peritoneal function evaluated with the peritoneal equilibration test was found to obviously deteriorate during the third episode of peritonitis. These findings were confirmed by an in situ hybridization technique to evaluate the relationship between TGF-beta1 mRNA expression and PF from biopsied peritoneal specimens. These findings suggest that the high TGF-beta1 levels in the dialysate are related to an increased expression of TGF-beta1 in the peritoneum. Thus, the persistent TGF-beta1 expression in the peritoneum may serve as a useful parameter in predicting PF in continuous ambulatory peritoneal dialysis patients with frequent peritonitis occurrence.

Human peritoneal mesothelial cells lie on a basement membrane-like material consisting of fibronectin (FN), type I collagen (CI), type III collagen (CIII) and laminin (LA). To understand how these extracellular matrix (ECM) proteins affect mesothelial cell behavior, we investigated their effect on the adhesion and proliferation of mesothelial cells. A modified methyltetrazolium dye method was used to assess cell number. The results showed that FN, CI, CIII and LA, all increased adhesion of mesothelial cells. The adhesive effect was blocked dose-dependently by a synthetic Arg-Gly-Asp-containing (RGD) peptide. When coated as a substratum (immobilized form), FN, CI, CIII and LA, all enhanced serum-stimulated and epidermal-growth-factor-stimulated cellular proliferation as compared with bovine-serum-albumin-blocked plastic surfaces. When added in a soluble form, all matrix proteins except FN inhibited serum-stimulated and epidermal-growth-factor-stimulated cellular proliferation at high concentrations (CI and CIII: 1-10 micrograms/ml, LA: 3-10 micrograms/ml). We conclude that peritoneal mesothelial cells possess an RGD-sensitive receptor and that the ECM can modulate adhesion and proliferation of peritoneal mesothelial cells. The growth-modulating effect depends on the form and concentration of the ECM proteins.

Spontaneous bacterial peritonitis (SBP) is defined as infection of preexisting ascites without evidence for any intraabdominal source for secondary infection. SBP is now recognized with rising frequency and has mainly been reported in patients with alcohol-induced cirrhosis of the liver. We report SBP in a female dialysis patient whose ascites was not due to liver disease, but was possibly due to lupus erythematosus or represented 'nephrogenic ascites'. The patient had severe abdominal pain and a positive rebound phenomenon, fever and an elevated peripheral white cell count of 21,000 cells/microliters. Ascitic fluid analysis revealed an exudate with a protein concentration of 5.2 g/dl, 13,000 white cells/microliters with 94% neutrophils and positive cultures for Streptococcus morbillorum. Because of the dramatic clinical features the patient underwent laparotomy which did not reveal a source for secondary infection and in retrospect was unnecessary. The patient responded well to antibiotic therapy. This case report draws attention to SBP as a cause of acute abdomen in patients on chronic hemodialysis.

A continuous ambulatory peritoneal dialysis patient developed eosinophilic peritonitis and was followed for 7 months. After 1 month, the peritonitis resolved, with a concomitant drop in percentage of hypodense eosinophils (Eos) recovered from peritoneal dialysate (PD) as well as a drop in fluid major basic protein levels. Blood eosinophil differential percentages were low, but the percentage of hypodense Eos in the blood tended to be relatively increased. Stool samples showed no evidence of parasitic infection, and epicutaneous skin tests were negative. Leukotriene C4 levels remained relatively constant as did white blood cell counts. Flow cytometric analysis of lymphocytes and granulocytes from PD and blood revealed high levels of CD23-positive lymphocytes.

From January 1987 to July 1988, 30 patients suffering from end-stage renal disease were treated with continuous ambulatory peritonitis dialysis (CAPD) therapy. Serial cell number, size and cycle of the peritoneal macrophage (PM) in these patients were measured before and during episodes of peritonitis from the time they started CAPD therapy. Patients with peritonitis were divided into high peritonitis occurrence (HPOG) and low peritonitis occurrence (LPOG) groups. Both before and during occurrence of peritonitis, there were no significant differences in the number of PM cells in the dialysate taken from patients in the HPOG and LPOG. When peritonitis occurred, the size and cell cycle S/Go-G1 ratio decreased about 3 days after the onset of peritonitis. It progressed to the lowest level 7-10 days later, then progressively recovered. However, the dialysate PM cells from the HPOG took a much longer time to recover to the preperitonitis size. When dialysate PM cells from patients without peritonitis were put into the dialysate of HPOG patients on day 10 of peritonitis and incubated for 24 h, an obvious decrease in cell size could be identified. On the other hand, when the PM cells from HPOG patients with peritonitis on day 10 were incubated 24 h with the dialysate from patients without peritonitis, there were obvious increases in cell size. These results suggest there may be a substance (or substances) in the peritonitis dialysate, which contribute(s) to the shrinkage of PM cell size.

Clinical experience gives evidence of the increasing importance of chronic-abscess-forming peritonitis with a general physical impairment in spite of a well-controlled abdominal situation. The number of unsolved problems led us to develop a standardized and reproducible experimental animal model, using Wistar rats. We induced peritonitis by intraperitoneal injection of a mixture containing a capsulated strain of Bacteroides fragilis and DEV agar. The histologic changes in the parietal and visceral peritoneum, lymphnodes and liver were recorded in the course of the disease. The data largely correlate with those recorded in human peritonitis. Bacteriologic examinations gave evidence of bacteria passing through the intestinal wall into the abdomen. This is the first model for peritonitis which is defined by its histological and bacteriological course. It enables one to examine pathophysiological problems and the consequences of harm and stress for the course of the disease.

Thirty-eight peritoneal biopsies from 37 patients with normal renal function or with end-stage renal failure without replacement therapy or utilizing continuous ambulatory peritoneal dialysis (CAPD), haemodialysis (HD) or a functioning transplant were examined histologically. No abnormality in peritoneal membrane morphology was observed in uraemia in the absence of dialysis. Significant abnormalities of peritoneal membrane morphology were observed in association with CAPD, the predominant finding being the development of peritoneal fibrosis which had a deleterious effect on membrane function. Abnormal peritoneal morphology was less commonly observed in patients on maintenance HD and with functioning transplants but may have implications regarding the future use of CAPD in these patients.

Peritoneal fluids from 41 patients on continuous ambulatory peritoneal dialysis (CAPD) were examined. The patients were divided into a short-term group (18 patients with CAPD up to one year) and a long-term group (23 patients with CAPD for one to seven years). Peritoneal fluids from a control group, consisting of ten nondialysis patients with ascites, were also examined. The cellular background of the peritoneal fluids and, in particular, the morphology of the mesothelial cells were studied. The following were found to be significantly increased in the CAPD groups: background lymphocytes, mesothelial exfoliation in three-dimensional clusters, mesothelial nuclear size and the number of mesothelial nucleoli. All of these features increased slightly with an increased duration of the dialysis. These findings emphasize that peritoneal dialysis of any duration can induce significantly atypical changes in mesothelial cells.

A cirrhotic patient with ascites was apparently well managed with diuretics and salt and water restriction for 9 months. A spontaneous bacterial peritonitis (SBP) developed and the patient finally died following septic shock. There were enough findings indicating that SBP in this case had been existing silently for some time. During this period the only apparent manifestation of this complication was a cutaneous pigmentation on the abdomen. It is suggested that pigmentation may be incuded among other presentations of this frequently silent process.

Continuous ambulatory peritoneal dialysis (CAPD) lavage can be interpreted as an artificial short-term ascites. The cellular content of 362 CAPD specimens from 32 patients was investigated. Irregular inflammatory reactions were seen in 85.3% of the specimens and eosinophilia in 27.6%. Mesothelial aggregates of great variability were registered in 59.4% of the specimens and mainly atypical mitoses in 7.5%. The cytologic changes seen in those patients from whom lavage fluids were examined over 10 to 12 months did not correlate with the changes in blood chemistry (BUN and creatinine) in those cases.

We have developed a rabbit model for intraabdominal candidiasis by the intraperitoneal injection of Candida albicans. The most reliable early predictor of induction of disease was positive paracentesis cultures for C. albicans during the 1st week post-inoculation (p.i.). Cultures of mesenteric and renal abscess were mean log 6.20 and 3.18 colony-forming units (CFU) per gram tissue, respectively, 1 week p.i., and remained positive for the 21-day i.p. period. Incidence of hematogenous dissemination, judged by chorioretinal cultures, was 69%. Histopathology of involved organs demonstrated suppurative abscesses at 1 week p.i.; lesions became more granulomatous at 2 and 3 weeks p.i.

The question of whether the presence of peritonitis has any influence upon the process of healing and the load capacity of a standard enterotomy was studied in guinea pigs. Laparotomy was performed 4 h after induction of peritonitis by a standardized method. Fecal peritonitis could be confirmed clinically, histologically and bacteriogically in all cases. A standardized enterotomy was carried out. The animals were killed 3 or 5 days later, anastomoses inspected, and the intraluminal pressures for anastomotic rupture measured. Comparison with a control group showed: (1) there can be normal healing of an enterotomy even with coexisting peritonitis; (2) anastomotic breakdown takes place at the same pressure as in the control group (p less than 0.01), and (3) primary lethality is significantly higher in cases operated in the presence of peritonitis (33 vs. 20%).

The cytologic findings in a case of endosalpingiosis presenting in peritoneal washings taken at the time of staging laparotomy for endocervical adenocarcinoma are described. Dense papillary epithelial clusters with distinct ciliated cell borders were found in the cytologic specimens. Cell nuclei were oval, with finely dispersed chromatin and uniform nuclear membranes. These findings, in conjunction with the discovery of tubal-type epithelial inclusions in pelvic and periaortic lymph nodes, established a diagnosis of endosalpingiosis or benign glandular inclusions involving the pelvic peritoneum and lymph nodes.