Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031154 (peritonitis)
 15,372 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This previously healthy 43-year-old man was admitted to our hospital with a history of rash, dysphagia and severe myalgia for two months. Physical examination showed prominent edema and erythema over the face and the chest, scattered ulcerations on the trunk, and muscle atrophy most prominent proximally. Serum levels of muscle enzymes were remarkably increased. Two weeks of oral prednisolone therapy (40 mg/day) was not effective, and betamethasone intravenous pulse therapy (3 x 1000 mg) was followed by slight clinical improvement. However, 12 days after pulse therapy, he complained abdominal pain on the right lower quadrant. The surgical findings included peritonitis due to single perforation of the cecum. After operation, cyclosporine therapy was added and over the next 14 month a considerable clinical improvement was noted. Prednisolone was reduced from 80 mg to 10 mg daily. Biopsy specimens from ulcerated+ skin and perforated cecum showed prominent vascular abnormalities: arterial and venous intimal hyperplasia, occlusion of vessels by fibrin thrombi, and lymphocytic infiltration which affected veins of all sizes. The evidence strongly suggests that both skin ulcers and cecum perforation were caused by vasculitis and occlusion of vessels, which often seen in childhood dermatomyositis.
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PMID:[Adult dermatomyositis with angiopathy and cecum perforation]. 188 78

When the streptococcal preparation OK-432 was intraperitoneally injected for the treatment of carcinomatous peritonitis, antitumor polymorphonuclear leukocytes (PMNs) accumulated in the peritoneal cavity. We examined the mechanism of this PMN accumulation using an in vivo system in rats. FUT-175, EDTA and K76 inhibited C5a generation by OK-432 in vitro, but EGTA, prednisolone and inhibitors of arachidonic acid cascade did not. In in vivo experiments, EDTA, FUT-175, antirat C3 serum and K76 reduced the accumulation of PMNs onto filter membranes, when these reagents were reacted with OK-432 for 3 h through filter membranes placed on the turned rat peritoneum. EGTA failed to inhibit PMN accumulation. Prednisolone, indomethacin, OKY046 and AA861 inhibited PMN accumulation in a dose-dependent manner. These inhibitions of PMN accumulation were confirmed by histological examination. It was concluded that complement-derived chemotactic factor C5a generated by OK-432 induced PMN accumulation in association with chemotactic arachidonic acid metabolites.
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PMID:Mechanism of polymorphonuclear leukocytes accumulation examined using inhibitors of complement and arachidonic acid cascade in rats treated with OK-432. 251 82

A 78 year old man suffering from anaphylactoid purpura complained of abdominal pain and bloody stools. Combined therapy with Prednisolone and cyclophosphamide had been given against nephrotic syndrome caused by purpura nephritis. Severe abdominal pain with symptoms and signs of pan-peritonitis necessitated laparotomy. Rectosigmoid perforation due to necrotizing angiitis (phlebitis) was also demonstrated histologically. The patient died of septicemia 18 days after surgery. Perforation of the alimentary tract rarely occurs in anaphylactoid purpura. Twenty similar cases were briefly reviewed from the Japanese literature.
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PMID:Anaphylactoid purpura with intestinal perforation: report of a case and review of the Japanese literature. 804 97

We describe a case of systemic lupus erythematosus (SLE) with enteritis and peritonitis who later developed pneumatosis cystoides intestinalis (PCI). A 35-year-old woman with SLE relapsed with enteritis and peritonitis. Prednisolone (PSL) effectively improved her symptoms. However, 6 weeks later, she developed PCI. Tapering of PSL, administration of intravenous cyclophosphamide, prokinetic agents and antibiotics, bowel rest with intravenous hypernutrition therapy and hyperbaric oxygen therapy successfully improved PCI. Although PCI is a rare complication of SLE, the present case suggests that lupus enteritis could be a risk factor for PCI, and that high-dose PSL could cause additional insult to PCI.
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PMID:Pneumatosis cystoides intestinalis following lupus enteritis and peritonitis. 1859 54

Prednisolone and other glucocorticosteroids are used by some peritoneal dialysis patients because of underlying diseases such as peritonitis. Although corticosteroids are potent inhibitors of various processes during inflammation, their influence on the transport properties of peritoneum is little known. Our study investigated the influence of prednisolone (0.001 g/dL) on glucose (1.8 g/dL) and uric acid (0.02 g/dL) transfer across isolated parietal peritoneum taken from the anterior abdominal wall of white Hyplus 59 rabbits and placed inside a modified Ussing-type chamber. Values for transfer from the interstitial (I) to the mesothelial (M) side of membrane (I-->M) and in the opposite direction (M-->I) were calculated using the mathematical model of mass transport and are expressed as a coefficient of diffusive permeability [P (in centimeters per second)]. Four separate series of experiments were done. In the first and second series, we respectively examined glucose transport under control conditions (for 120 minutes) and then before (15-60 minutes) and after (75-120 minutes) introduction of prednisolone on the M side of the membrane. In the third and fourth series, similar studies of uric acid transfer were done. In the control (first and third) series, the stability of bidirectional transport for solute of interest was observed. The values of P +/- standard error of the mean (all x0.0001) for I-->M and M-->I transfer of glucose were, respectively, 2.489 +/- 0.329 cm/s and 2.259 +/- 0.493 cm/s. In the case of uric acid, the transport values were lower and amounted 1.936 +/- 0.324 cm/s and 1.895 +/- 0.596 cm/s for I-->M and M-->I respectively. Application of prednisolone on the M side of membrane lowered bidirectional transfer of glucose across peritoneal membrane by a mean of 73% (p < 0.02) and transport of uric acid by a mean of 19% (p < 0.003). These results show that, in vitro, prednisolone lowers glucose and uric acid transport across the peritoneal membrane, modifying the transfer dynamics of glucose to a greater extent. These observations may have clinical importance, especially in patients with disorders of peritoneal permeability, diabetes, and hyperuricemia.
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PMID:Influence of prednisolone on glucose and uric acid transport across peritoneal membrane in vitro. 2331 Dec 8

The clinical characteristic of gastrointestinal anisakiasis is severe abdominal pain after eating raw fish. Intestinal anisakiasis is more uncommon than gastric anisakiasis. Most patients with intestinal anisakiasis need hospitalization because anisakiasis can cause intestinal obstruction, ileus, peritonitis or intestinal perforation. We report a case of intestinal anisakiasis. A 43-year-old woman presented with symptoms of intermittent abdominal pain 2 days after eating raw fish. Her brother had eaten the same food and had been suffering from gastric anisakiasis. Abdominal ultrasonography in this patient showed localized jejunal wall thickening with dilated lumen of proximal jejunum and ascites. According to the clinical course and examinations, she was diagnosed with intestinal anisakiasis. Administration of prednisolone 5 mg/day and olopatadine hydrochloride 10 mg/day improved her symptoms quickly without hospitalization. Prednisolone was administered for 10 days, and olopatadine hydrochloride was administered for a total of 6 weeks according to ultrasonographic findings. Six months after the treatment, the abdominal ultrasonography demonstrated normal findings. This case demonstrates that ultrasonography was quite useful for the diagnosis and surveillance of intestinal anisakiasis. Furthermore, treatment with corticosteroid and an antiallergic agent could be an option for patients with intestinal anisakiasis.
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PMID:Intestinal Anisakiasis Treated Successfully with Prednisolone and Olopatadine Hydrochloride. 2740 99