SEARCH · Search PubMed

Results for “ASCITES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,531 records · Page 85Linked to original sources

PubMed1984

Ascites tumor fluid and bovine serum albumin as supplements in presomite mouse embryo cultures.

The growth of presomite mouse embryos in culture was studied using mouse Ehrlich ascites tumor fluid and bovine serum albumin as supplements to the tissue culture medium. The best development was observed with a mixture of 10-20% ascites fluid and 2% bovine serum albumin. During 48 h of culture under these conditions, embryos grew from egg cylinders to complex structures with neural folds and other organ rudiments. Most embryos had beating hearts, numerous pigmented red blood cells, and a fused chorioallantoic placenta. The results suggest that factors in ascites fluid support differentiation and growth of mouse embryos. Addition of bovine serum albumin was also beneficial for development. Differential sister chromatid staining of cultured embryos showed that ascites fluid increased the rate of cell proliferation as compared with medium containing bovine serum albumin alone, or bovine serum albumin and fetal calf serum. These results with abundant and readily available supplements may facilitate certain studies of mouse embryo development.

Animals↗

PubMed1994

Biotransformation of sodium nitroprusside into dinitrosyl iron complexes in tissue of ascites tumors of mice.

We have found that treatment of various types of murine ascites tumors with sodium nitroprusside (SNP) both in vitro (1.5 mM) and in vivo (25 mg/kg; i.p.) results in formation of EPR-detectable dinitrosyl nonheme iron complexes (DNIC) with RS- groups of proteins (g perpendicular = 2,037; g parallel = 2,012). The DNIC were mainly localized in the ascitic extracellular fluid. The appearance of DNIC was unaffected by an inhibitor of nitric oxide synthase, N omega-nitro-L-arginine (1 mM), but abolished with a SH-blockator, p-chloromercuribenzoate (0.1 mM). No DNIC formation was observed when ascitic fluid (after tumor cells separation) was incubated with SNP alone, but with SNP and L-cysteine (10 mM). Thus, ascites tumor cells contribute to the transformation of SNP into DNIC and thiols are essential in this process.

Animals↗

PubMed1996

Ovarian hemangioma associated with concomitant stromal luteinization and ascites.

A 62-year-old female presented with a pelvic mass and ascites. The Papanicolaou vaginal smear showed an unusual maturation, maturation index being 0/80/20. The serum level of estradiol was 48.7 pg/ml. The preoperative checkup suggested a pelvic malignancy with a differential diagnosis of hormone-secreting ovarian tumor. On surgical exploration, she had a hemangioma of the ovary without malignant cytology in the ascitic fluid. Histologically, this tumor was associated with stromal luteinization. This is the first case, reported in the literature, possessing ovarian hemangioma with stromal luteinization accompanying massive ascites. It should be noted that an ovarian hemangioma can be associated with stromal luteinization and ascites, and that MR imaging is sometimes of value for making a preoperative diagnosis of ovarian hemangioma.

Ascites↗

PubMed1985

Pharmacokinetics of teniposide (VM 26) after IV administration in serum and malignant ascites of patients with ovarian carcinoma.

Nine patients with ovarian carcinoma and malignant ascites treated with IV teniposide chemotherapy (30 mg/m2/30 min) entered this study. Plasma and peritoneal fluid levels were measured by an HPLC method with electrochemical detection. Plasma decay kinetics followed a triexponential function. A high variability of drug diffusion in ascites was noticed. Peak concentrations in ascites ranged from 1.6% to 20.5% of serum peak concentration. The concentration in peritoneal fluid reached a maximum level 6 h after the infusion ended. Teniposide was less slowly eliminated from ascites than from serum. The exposure of the inflammatory peritoneal fluid to the drug expressed by area under the concentration-time curve (AUC) was also subject to significant interindividual variation, ranging from 223 to 2332 micrograms/ml X min. However, the peritoneal AUC was correlated with serum AUC and with the systemic clearance of the drug. A significant relationship between gamma glutamyltranspeptidase and both systemic clearance and either the serum or the peritoneal AUC was found, suggesting that liver plays a role in drug disposition.

Aged↗

PubMed1987

Oral pharmacokinetics and ascitic fluid penetration of pefloxacin in cirrhosis.

Plasma and ascitic fluid concentrations of pefloxacin in 10 cirrhotic patients and 8 healthy volunteers were determined following administration of a single oral dose of 400 mg. The mean elimination half-life was significantly increased in the patients (29.0 h) compared to in 8 healthy volunteers (12.3 h). In patients, the total plasma clearance (2.71 vs 6.85 l/h) and volume of distribution (1.12 vs 1.67 l/kg) were decreased. Estimated by the ratio of the AUC in peritoneal fluid and plasma, ascitic fluid penetration was 68% after one oral dose, and pronounced accumulation of pefloxacin in ascites was found after repeated doses. Oral pefloxacin would seem to be a convenient and useful treatment of spontaneous, gram-negative, bacterial peritonitis in cirrhosis. However, the decreased hepatic metabolism of the drug leads to a marked accumulation in plasma and ascites after repeated doses, and a reduced dose is required in these patients.

Adult↗

PubMed1994

Free, cytoskeletal-bound and membrane-bound polysomes isolated from MPC-11 and Krebs II ascites cells differ in their complement of poly(A) binding proteins.

A three-step detergent/salt extraction procedure (Vedeler et al., Mol Cell Biochem 100: 183-193, 1991) was used to isolate free polysomes (FP), cytoskeletal-bound polysomes (CBP) and membrane-bound polysomes (MBP) from MPC-11 and Krebs II ascites cells. Polysomes were pelleted, washed with high salt buffer and re-pelleted. Proteins in the dialysed high-salt extracts were subjected to poly(A) Sepharose chromatography and poly(A) binding and non-binding proteins were separated by SDS-PAGE. In MPC-11 cells the FP fraction contains thirteen poly(A) binding proteins and four non-poly(A) binding proteins while the corresponding fraction in Krebs II ascites cells has four poly(A) binding proteins and six proteins which do not bind poly(A). The CBP fraction isolated from MPC-11 cells has a complement of ten poly(A) binding proteins, four which are non-poly(A) binding, and a protein of 105 kDa which has both poly(A) binding and non-poly(A) binding properties. In the CBP fraction prepared from Krebs II ascites cells a protein band at 32 kDa exhibits both poly(A) binding and non-poly(A) binding properties. In this fraction there are six poly(A) binding proteins and an additional eight which do not bind poly(A). Of the total number of proteins eight of these have a molecular weight below 40 kDa. The MBP fraction in MPC-11 cells contains three poly(A) binding proteins and eleven with non-poly(A) binding properties. In contrast this fraction in Krebs II ascites cells has a complement of thirteen poly(A) binding and ten non-poly(A) binding proteins.(ABSTRACT TRUNCATED AT 250 WORDS)

3T3 Cells↗

PubMed1976

Myxedema ascites.

A 74-year-old man presented with mental obtundation and massive ascites without evidence of significant impairment of liver function. Thyroid function studies suggested hypothyroidism. Aspirated ascitic fluid had the characteristics of an exudate. Thyroid replacement therapy resulted in rapid clinical improvement with resolution of the ascites. Prompt recognition of myxedema ascites may prevent the inappropriate use of diuretic agents, therapeutic paracentesis, and sometimes unnecessary laparotomy.

Aged↗

PubMed1987

Intractable ascites in systemic mastocytosis treated by portal diversion.

A 50-year-old male presented with intractable ascites due to systemic mastocytosis. The diagnosis of systemic mastocytosis was established by histology of the bone marrow which showed mast cell infiltration and fibrosis. Ascites was related to portal hypertension which was documented by esophageal varices at endoscopy and by an increase of wedged-free hepatic venous pressure gradient. Liver biopsy disclosed dense fibrosis of hepatic arterial and portal venule walls, resulting in complete obstruction of some portal radicles. Peliosis hepatis and fibrous deposits in the walls of hepatic venules were also present. Because of intractable ascites and significant malnutrition, a portacaval shunt was performed which cleared ascites and dramatically improved the general condition of the patient.

Ascites↗

PubMed1985

Peritoneovenous shunts in malignant ascites.

A 51-year-old woman with malignant ascites secondary to hepatocellular carcinoma had a peritoneovenous (LeVeen) shunt inserted with effective control of ascites and amelioration of symptoms. The results of 12 recent series evaluating the efficacy of peritoneovenous shunts in the treatment of 198 patients with malignant ascites were reviewed. Peritoneovenous shunts effectively controlled malignant ascites in 77% of patients. Complications occurred in 25%, although the majority of these were related to shunt occlusion and transient congestive heart failure.

Ascites↗

PubMed1997

Neonatal chylous ascites--report of three cases and review of the literature.

Three cases of neonatal chylous ascites (CCA) were managed in the neonatal unit, University Hospital, Kuala Lumpur, over the past 9 years. Fetal ascites and polyhydramnios were the sole abnormalities detected in all three babies by antenatal ultrasonography. They were born at 36 weeks' gestation and their birth weights ranged from 3.0 kg to 3.8 kg. All three infants had abdominal distension at birth. Milky ascitic fluid was obtained after starting enteral feedings. Analysis of the ascitic fluid revealed a raised white blood cell count (predominantly lymphocytic) and triglycerides (1.4 - 3.8 mmol/l), cholesterol (1.6 - 2.8 mmol/l), and protein levels (25 - 41 g/l). Conservative management with skimmed milk and medium-chain triglycerides in one infant and Pregestimil in another was instituted. these two infants with CCA were clinically normal when reviewed at 19 months and 3.5 years of age. The third infant had a gut malrotation and associated pyloric septum; he died from complications of a laparotomy. The literature on this rare condition is reviewed.

Chylous Ascites↗

PubMed1995

Continuous ascitic recirculation in severe ovarian hyperstimulation syndrome.

Massive ascites, hydrothorax, acute renal failure and thromboembolism are clinical manifestations of severe ovarian hyperstimulation syndrome (OHSS) which may complicate the induction of ovulation with exogenous gonadotrophins. We report a case of severe OHSS with ascites formation in excess of five litres per day. Massive ascites and bilateral pleural effusions resulted in respiratory failure. Continuous ascitic recirculation (AR) was commenced after repeated paracentesis and i.v. fluid therapy failed to improve the patient's condition. The procedure was undertaken for a total of 15 days and rapidly resulted in marked improvement of impaired respiratory function. Febrile episodes occurred on 3 occasions, but we did not observe coagulation disturbances or adverse haemodynamic effects. Continuous AR is a safe and effective treatment of complicated severe OHSS.

Adult↗

PubMed1984

[Ascites as a complication of hepatic storage of hydroxyethyl starch in long-term dialysis].

Three adult dialysis patients developed ascites after having received repeatedly the plasma substitute hydroxyethyl starch (HES 40/0.5). In two cases (total dose 180, and 330 g HES, respectively) the ascites was reversible after discontinuation of the HES administration. In the third case (total dose 915 g HES) the ascites could be controlled only by implantation of a Denver shunt. In this latter case it was shown by histological, electron microscopical, and biochemical findings that the ascites was caused by hepatic sinusoidal obstruction due to an extreme storage of HES in the sinusoidal lining cells. Additional storage was detected in hepatocytes, bile duct epithelia, endothelial cells, and fibroblasts in the portal tracts. Biochemically HES was found in liver tissue at a concentration of 4% (w/w). Although in renal impairment plasma clearance of HES is not significantly different from normal individuals, long-term administration of HES must be regarded inadvisable because of tissue storage which apparently is especially significant in this condition.

Ascites↗

PubMed1994

Peritoneal Kaposi's sarcoma: a cause of ascites in acquired immunodeficiency syndrome.

The investigation of ascites in a homosexual man with acquired immunodeficiency syndrome and mucocutaneous Kaposi's sarcoma (KS) revealed only numerous purplish nodules of KS in the parietal and serosal peritoneum, observed at laparoscopy. KS lesions of the peritoneum, a finding not reported in the literature previously, was the only and likely cause of ascites in our patient. Increased red cells and high serum-ascites albumin gradient in a patient with acquired immunodeficiency syndrome should suggest the possibility of peritoneal KS as a cause of ascites.

Acquired Immunodeficiency Syndrome↗

PubMed1989

Induction of endogenous tumor necrosis factor by OK-432 in ovarian cancer patients with ascites.

To four ovarian cancer patients with malignant ascites, 10 KE of OK-432 was intraperitoneally administered four times at 2 day intervals for priming, and 40 KE of OK-432 was given on the 13th day after the first injection for triggering. The changes in blood monocyte and peritoneal macrophage levels and the production of tumor necrosis factor (TNF) by blood mononuclear cells (BMCs) and ascitic lymphoid cells (ALCs) were examined. In the two patients in whom TNF was induced in the ascites, TNF production by BMCs and ALCs was noted during priming. After triggering, increases in both the number of peritoneal macrophages and TNF production by ALCs were noted. In the other two patients, in whom TNF was not detected in the ascites, the ratio of peritoneal macrophages to ALCs did not change throughout the study period, and TNF production by the ALCs was not augmented. These findings suggest that OK-432 can exert a primary effect on both peritoneal macrophages and blood monocytes, and that OK-432 triggering can promote an increase in primed peritoneal macrophages and the release of TNF from these cells.

Ascites↗

PubMed1991

Renal function in experimentally induced acute pancreatitis in dogs: how it is affected by the nephrotoxic substance in pancreatic exudate from ascitic fluid.

Renal failure occurring in dogs during experimental acute pancreatitis and the effect on renal function of intravenous injections of ascitic fluid which accumulated during the acute pancreatitis were studied. Five hours after the induction of acute pancreatitis, the accumulation of 200 to 400 ml of ascitic fluid, and an elevation in hematocrit as well as a decreased mean arterial pressure were observed, which suggested hypovolemia due to plasma loss. At the same time, the renal blood flow, glomerular filtration rate, and urinary output decreased significantly. Hypovolemia was observed to be the main cause of renal failure in accordance with previous reports. When the sterile ascitic fluid was injected into healthy dogs, temporary hypotension was observed without changes in the hematocrit. However, the renal blood flow, glomerular filtration rate and urinary output decreased, together with an elevation in renal vascular resistance, even after the hypotension had returned to normal. This study shows that renal failure associated with acute pancreatitis occurred mainly as a direct result of hypovolemia but also that the sterile ascitic fluid contained nephrotoxic substances which were suspected to be unrelated to vasoactive substances or protease. Their removal is therefore necessary for the treatment and prevention of renal failure complicating acute pancreatitis.

Acute Disease↗

PubMed1988

Peritoneovenous shunting for intractable cirrhotic and cancerous ascites using different types of shunting tubes.

A total of twenty six peritoneovenous shuntings were performed in our department between 1978 and 1984, on twelve cirrhotic and ten cancerous patients with intractable ascites, using Pudenz, LeVeen or Denver type shunting tubes. Reduced ascites was noted postoperatively with statistical significance in both the cirrhotic group (p less than 0.05) and the cancerous group (p less than 0.01), of whom eight cirrhotic and seven cancerous patients exhibited an abdominal girth reduced by 9.7 cm (a 10.9 per cent reduction) in two weeks. A larger urinary output was noted in 13 patients, with a mean increase of 587 ml/day compared with the pre-shunting output. These patients lost a mean weight of 6.13 kg in two weeks, while the nonreduced ascites group gained weight. The post-shunting serum albumin level was higher in the reduced ascites group. The mean functioning periods of the shunts were 5.1 and 2 months, respectively for the cirrhotic and cancerous patients whose shunts were patent. The patients' outcome was shown to depend on the disease itself, with the exception of one patient who died of disseminated intravascular coagulopathy following shunting. In comparing several types of shunting systems, the Denver-type was proven as being the most unlikely to plug or malfunction because of its simpler structure.

Adult↗

PubMed2003

Ascites in ventriculoperitoneal shunt.

OBJECTIVE: To fetch out the factors responsible for ascites, following shunt CSF diversion in cases of intracarnial lesions. Four children developing ascites/abdominal psuedocyst following ventriculoperitoneal shunt were analyzed to see the factors responsible for such complication. METHODS: Records of 4 cases developing ascites were studied retrospectively. These children developed ascites at 8 months, 6 months, 1 year and 1 year 2 months interval following their shunt installation. RESULTS: The primary etiology of hydrocephalus was demonstrated as thalamic glioblastoma, choroid plexus papillomas of third ventricle, post tubercular meningitis hydrocephalus and suprasellar craniopharyngioma. CONCLUSION: The proposed etiology of ascites in these cases was peritoneal metastasis from thalamic glioblastoma through ventriculoperitoneal shunt in first case, excessive production of CSF by choroid plexus papilloma in second, infection in the third case and craniopharyngioma causing excessive production of CSF in the fourth child. All the children were treated by reasonable laparotomy and fenestration of cyst along with the repositioning of shunt tip at another site.

Ascites↗

PubMed1998

Neonatal total parenteral nutrition ascites from liver erosion by umbilical vein catheters.

BACKGROUND: A preterm infant was found to have total parenteral nutrition (TPN) ascites after infusion through a low umbilical vein catheter (UVC). Objective. To evaluate the clinical and imaging findings of neonates with TPN ascites after infusion through UVCs. MATERIALS AND METHODS: Eight patients with TPN ascites were identified over three years. Charts were abstracted for clinical data. Plain-film, ultrasound (US), and contrast studies through the UVCs were examined to determine UVC placement, presence of liver injury, and confirmation of intraperitoneal extravasation from the UVC. RESULTS: All eight patients with TPN ascites presented with hypotension and abdominal distension. All had UVCs overlying the liver on plain film. Catheters were in place a mean of 8.9 days prior to TPN extravasation. US in four patients showed hepatic parenchymal damage around the UVC tip. Contrast studies in six patients showed intraperitoneal spill. CONCLUSION: While low UVC placement may sometimes be clinically unavoidable, TPN administered through abnormally positioned UVCs is not without risk.

Ascites↗