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Query: UMLS:C0341503 (
bacterial peritonitis
)
1,303
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
We report the case of a patient with peritonitis caused by Brucella melitensis who also had chronic liver disease. At first the patient was treated for
bacterial peritonitis
but when a lymphocytic ascites was aspirated antituberculosis chemotherapy was given. However, the serological tests for brucellosis were strongly positive and subsequently B. melitensis was isolated from ascitic fluid.
J Infect 1993
Sep
PMID:Brucella peritonitis. 822 98
Spontaneous or idiopathic perforation of the bile duct (IPBD) in neonates and infants is a rare disease. An 1-year-5-month-old female child admitted with progressive abdominal distension and generalized jaundice. She had previously been treated for
bacterial peritonitis
at another hospital by using strong antibiotics. Abdominal tapping revealed bilious ascites suggesting a possible biliary tree perforation and was later confirmed by the scintigraphy study. She was subsequently operated and recovered uneventfully. The mode of presentation, diagnosis and treatment are described and the literature reviewed.
Changgeng Yi Xue Za Zhi 1995
Sep
PMID:Idiopathic common bile duct perforation: a case report. 852 39
51 CAPD patients (age 55.5 +/- 14.5 yrs, 35 male, 16 female) on CAPD using 'O' set were studied retrospectively during the period January 1993 to April 1995. Etiology of ESRD was Diabetic nephropathy-25(49%) and the other causes-26(51%). The total duration of observation on 'O' set was 553 patient months, the mean duration was 10.8 +/- 6.1 months. 24 patients (47%) developed total of 30 episodes of peritonitis. The incidence of peritonitis was 18.4 patient months per episode of peritonitis. The organisms responsible for peritonitis were Gram positive-6(20%), Gram negative-3(10%), Fungal-1(3.3%), Mycobacterial-1(3.3%), Eosinophilic-1(3.3%), Sterile-12(40%) and unknown-6(20%) 2 patients of
bacterial peritonitis
and a patient with tuberculous peritonitis died while rest of the patients responded favourably to antibiotics. 13(52%) diabetic patients and 11(42%) non-diabetic patients had peritonitis (p-NS) and the peritonitis rates in diabetics and non diabetics were 18.3 and 18.6 patient months per episode respectively (p-NS). Exit site infection was seen in 5 patients (10%) (Staph aureus-4, Enterococci-1) and all responded to antibiotic therapy. 7 patients had total of 10 episodes of symptomatic accidental intraperitoneal sodium hypochlorite instillation, none had any long term adverse effects. The 'O' set procedure was done by self in 10(20%) and by others in 41(80%) cases. The peritonitis rates when performed by self and others were 18.5 and 18.4 patient months per episode respectively (p-NS). The cost of being on CAPD using 'O' set, Y-bag and twin bag were Rs. 1,50,000, 2,10,000 and 3,72,000 per annum respectively and cost of maintenance haemodialysis was 1,36,800 per annum. The cost of CAPD using 'O' set was comparable to that of maintenance haemodialysis. The 'O' set connector system in CAPD is found to be safe, cost effective and efficient.
J Assoc Physicians India 1996
Sep
PMID:'O' set connector system in CAPD. 925 69
Spontaneous bacterial peritonitis is a frequent and often serious complication of long-standing ascites in the presence of advanced liver disease. Coliform bacteria account for the infection in most cases and are thought to be related to translocation of bacteria from the bowel into the peritoneal cavity. The empiric use of cefotaxime is well established as most of the causative organisms are sensitive to this antibiotic. However, we report on a case of spontaneous
bacterial peritonitis
in a patient with hepatitis C related cirrhosis who was awaiting liver transplantation caused by infection with Listeria monocytogenes, in which the patient did not improve with empiric antibiotic therapy. This case adds to the 23 others reported in the literature since 1966. Our case raises some concerns about the universal empiric usage of cefotaxime for spontaneous
bacterial peritonitis
because it does not offer adequate coverage against organisms such as Listeria, enterococci, Pasturella, and anaerobes.
Am J Gastroenterol 1998
Sep
PMID:Spontaneous bacterial peritonitis caused by infection with Listeria monocytogenes: a case report and review of the literature. 1048 37
The present study assessed whether peritoneal macrophages isolated from cirrhotic patients produce nitric oxide (NO) and express NO synthase type II (NOS II) mRNA and protein. Patients with cirrhosis and ascites without peritonitis or with unresolved or resolved spontaneous
bacterial peritonitis
(SBP) were studied. Following paracentesis, ascites NO(2)(-) + NO(3)(-) content (NOx) was measured. Peritoneal macrophages from ascites were seeded on well plates, and NO(2)(-) in the medium was determined. NOx was higher in patients with unresolved or resolved SBP than in cirrhotic patients without peritonitis. Macrophages of patients with SBP or resolved SBP produced NO(2)(-) after 30 hours in culture, but those obtained from patients without peritonitis did not. Reverse-transcription polymerase chain reaction (RT-PCR) and immunocytochemical analysis revealed the presence of a clear signal for NOS II mRNA and protein in macrophages of SBP patients, regardless of whether or not the infection subsided. Therefore, peritoneal macrophages isolated from cirrhotic patients with unresolved or resolved SBP produce NO and express the NOS II mRNA and protein, suggesting that NOS II may contribute to the control of SBP, or to its associated pathology, in human cirrhosis.
Hepatology 1999
Sep
PMID:Nitric oxide production and inducible nitric oxide synthase expression in peritoneal macrophages of cirrhotic patients. 1046 73
Bacterial infection coincides with migration of leucocytes from the circulation into the bacterium-infected tissue. Recently, we have shown that endothelial cells, upon binding and ingestion of Staphylococcus aureus, exhibit proinflammatory properties including procoagulant activity and increased intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression on the cell surface, resulting in hyperadhesiveness, mainly for monocytes. The enhanced extravasation of monocytes to bacterium-infected sites is facilitated by the local production of chemotactic factors. From another study we concluded that the locally produced chemokine MCP-1 is important in the recruitment of monocytes to the peritoneal cavity in a model of
bacterial peritonitis
. In the present study we investigated whether cultured human endothelial cells after infection with bacteria produce and release MCP-1, which in turn stimulates monocyte chemotaxis. We observed that endothelial cells released significant amounts of MCP-1 within 48 h after ingestion of S. aureus. This was dependent on the number and the virulence of the bacteria used to infect the endothelial cells. The kinetics as well as the amount of MCP-1 released by S. aureus-infected endothelial cells differed markedly from that released by endothelial cells upon stimulation with IL-1beta. Supernatant from S. aureus-infected or IL-1beta-stimulated cells promoted monocyte chemotaxis which was almost entirely abrogated in the presence of neutralizing anti-MCP-1 antibody, indicating that most of the chemotactic activity was due to the release of MCP-1 into the supernatant. Our findings support the notion that endothelial cells can actively initiate and sustain an inflammatory response after an encounter with pathogenic microorganisms, without the intervention of macrophage-derived proinflammatory cytokines.
Clin Exp Immunol 1999
Sep
PMID:Infection of human endothelial cells with Staphylococcus aureus induces the production of monocyte chemotactic protein-1 (MCP-1) and monocyte chemotaxis. 1046 52
A case of undiagnosed renal abscess complicated by intraperitoneal rupture with generalised
bacterial peritonitis
is presented. Prompt surgical intervention was essential for saving the patient's life. Early imaging of the kidney in unresolved renal infection is essential if renal abscess, its delayed presentation and complications are to be avoided. Most patients will be cured without operation by antibiotics and if necessary, by additional percutaneous drainage where an abscess has formed.
East Afr Med J 2001
Sep
PMID:Undiagnosed renal abscess presenting as acute bacterial peritonitis: case report. 1192 88
Hepatic IVC disease (HVD), a disease caused by complete obstruction or stenosis of inferior vena cava (IVC) near cava-atrial junction is endemic in Nepal. It is a chronic disease characterized by upper abdominal pain, hepatomegaly, splenomegaly and dilated superficial veins in the body trunk. Ascites commonly, with high protein content is a feature of acute and subacute stages and during acute exacerbation of the chronic disease. We assessed the occurrence of
bacterial peritonitis
among patients of HVD with ascites. One hundred and sixty seven consecutive patients with ascites, which included 91 patients with HVD were examined for the presence of
bacterial peritonitis
. The ascitic fluids were examined for total and differential WBC count. The fluid and the blood were cultured for aerobic microorganisms by bedside inoculation in blood culture bottles. HVD is a common cause of non-cirrhotic high protein content ascites in Nepal. It was uniquely associated with high incidence of bacteremia (61%) and high incidence of mono-
bacterial peritonitis
(67%) from Gram-negative enteric bacteria (58.5%) and Staphylococcus aureus (42.5%). Ascites and
bacterial peritonitis
generally occurred almost simultaneously in these patients. It is postulated that when bacteremia occurred the defective portion of IVC near the cava-atrial junction become infected resulting in hepatic venous outflow obstruction and formation of ascites with high protein content. And spread of infection from the infected IVC to the peritoneum resulted in
bacterial peritonitis
.
Hepatol Res 2002
Sep
PMID:Bacterial peritonitis in hepatic inferior vena cava disease: a hypothesis to explain the cause of infection in high protein ascites. 1224 91
A decreased effective arterial blood volume is the principal haemodynamic disturbance in cirrhosis, leading to activation of the renin angiotensin aldosterone and the sympathetic nervous systems, sodium and water retention and renal impairment. Albumin is a plasma expander that could be used in clinical settings in cirrhosis in which plasma expansion would reverse some of the decreased effective arterial blood volume, or prevent its iatrogenic (i.e., paracenteses) or spontaneous worsening (spontaneous
bacterial peritonitis
). However, apart from the issue of transmission of prion agents, which may become an important issue in clinical risk management of the use of albumin in the future, the problem with albumin is its expense. Every effort must thus be made to definitely prove albumin is always the best colloid for all clinical settings in cirrhosis. Further randomized trials are justified.
Dig Liver Dis 2003
Sep
PMID:Is the use of albumin of value in cirrhosis? The case not so in favour, or is there an alternative? 1456 92
Hepatorenal syndrome (HRS) is a complex syndrome. In addition to severe reduction of renal function due to renal vasoconstriction, there is impairment in systemic haemodynamics, activation of the renin-angiotensin and sympathetic nervous systems and antidiuretic hormone, vasoconstriction of the brain, muscle and skin, and dilutional hyponatraemia. Treatment in patients with type 2 HRS, the most frequent form of HRS, is directed towards managing refractory ascites. Paracentesis is the treatment of choice. TIPS is also effective but is more expensive, is associated with higher incidence of hepatic encephalopathy, and does not increase survival. Although a rapidly progressive renal failure is the most characteristic manifestation of type 1 HRS, there is failure in other organs such as the liver and the brain. A decrease in cardiac output develops in these patients, associated with a decrease in cardiopulmonary pressures. Since type 1 HRS mainly occurs in patients with spontaneous
bacterial peritonitis
and massive release of cytokines within the peritoneal cavity, it may be considered as a special form of multiorgan failure of circulatory origin. Not surprisingly, the treatment of choice in type 1 HRS is the combination of vasoconstrictors to reduce arterial vasodilation and plasma volume expansion with albumin to increase cardiac preload. TIPS is also effective in these patients and the combination of pharmacological treatment followed by TIPS may be the most effective approach.
Aliment Pharmacol Ther 2004
Sep
PMID:Review article: hepatorenal syndrome--how to assess response to treatment and nonpharmacological therapy. 1533 2
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