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At least 703 records · Page 39Linked to original sources
PubMed2000

Pharmacokinetics of gemcitabine and 2',2'-difluorodeoxyuridine in a patient with ascites.

Gemcitabine (dFdC) is a prodrug that undergoes metabolism by cytidine deaminase to form an inactive metabolite, 2',2'-difluorodeoxyuridine (dFdU). The pharmacokinetics of dFdC and dFdU have been studied; however, their disposition has never been evaluated in a patient with ascites. A patient with pancreatic cancer and malignant ascites was treated with dFdC 1,500 mg/m2 over 150 minutes weekly for 3 weeks, repeated every 4 weeks. Serial plasma and ascites samples were obtained on weeks 1 and 2 of cycle 2. High-pressure liquid chromatography was used to quantify dFdC and dFdU in plasma and ascites. The systemic dispositions of dFdC and dFdU were similar to those reported in patients without ascites. The concentration of dFdC in ascites approached 1 mg/ml. Ascitic fluid did not serve as a depot for dFdC, and the agent's concentration in ascites approached that at which its phosphorylation is saturated.

Abdominal Pain↗
PubMed1994

Nephrogenic ascites: a poorly understood syndrome.

Nephrogenic ascites is a condition characterized by the presence of massive ascites in a patient with ESRD. Neither the exact cause nor the pathogenesis of ascites formation is clearly understood. Patients frequently present with hypertension, moderate to massive ascites, minimal extremity edema, cachexia, and a history of dialysis-associated hypotension. The ascitic fluid is typically an exudate. Although treatment options are limited, continuous ambulatory peritoneal dialysis, peritoneovenous shunt placement, and renal transplantation appear to be effective in controlling ascites formation. Nephrogenic ascites is associated with a grave prognosis, especially if treatment is not instituted. One patient with nephrogenic ascites is described here.

Ascites↗
PubMed1995

The effects of chronic administration of indomethacin and misoprostol on renal function in cirrhotic patients with and without ascites.

BACKGROUND: Non-steroidal anti-inflammatory drugs (NSAIDs) often cause renal dysfunction in cirrhotic patients with ascites through inhibition of prostaglandin synthesis. However, their renal effects in cirrhotic patients without ascites are controversial. In addition, the role of prostaglandins in cirrhotic patients with ascites and in non-ascitic cirrhotic patients receiving NSAIDs also remains elusive. Thus we evaluated the chronic renal effects of indomethacin and misoprostol in 9 cirrhotic patients with ascites (protocol 1) and 21 cirrhotic patients without ascites (protocol 2). METHODS: The patients of protocol 1 received 200 micrograms of misoprostol every 6 h for 7 consecutive days. In protocol 2, 11 patients received 25 mg indomethacin three times a day for 7 consecutive days. The other 10 patients received 25 mg indomethacin three times a day plus 200 micrograms misoprostol every 6 h for 7 consecutive days. Renal function tests, plasma renin activity, and plasma aldosterone concentration were measured before and after treatment. RESULTS: In protocol 1, misoprostol tended to reduce the urinary sodium excretion (p = 0.08). In protocol 2, indomethacin alone greatly impaired renal plasma flow (p < 0.05), creatinine clearance (p < 0.05), blood urea nitrogen (p < 0.05), and serum creatinine (p = 0.06) in 11 patients. Similar magnitudes of renal dysfunction were observed in the other 10 patients despite the concomitant misoprostol treatment. CONCLUSION: Chronic administration of misoprostol may have caused a negative natriuretic effect in cirrhotic patients with ascites. In cirrhotic patients without ascites chronic administration of indomethacin may induce a renal dysfunction that cannot be reversed by misoprostol.

Aged↗
PubMed1999

Intravenous infusion ascitic fluid during hemodialysis: a study of 108 treatments in 13 uremic cases.

Nephrogenic ascites is a clinical diagnosis defined as persistent ascites in an uremic patient without evidence for a causative underlying disease. It imperils the patient's life with intradialytic hypotension, however there is no effective therapy other than renal transplantation so far. In 13 cases, 108 treatments with i.v. ascites infusion were performed with hemofilter alone or combined with plasmafilter during hemodialysis over past 7-years. The ascitic fluid was filtrated and dialyzed before it was intravenously infused into the blood compartment of the hemofilter. There were a mean of 8.38 treatments per patient in a period of 56 days and 3,275.9 +/- 1,359.5 ml of ascitic fluid were removed per treatment. The patients' appetite and physical ability were considerably improved and the intradialytic hypotensions disappeared immediately following the initiation of ascitic fluid infusions. In this study, one patient was transplanted successfully. The longest interval without ascitic fluid infusion was 127 days. Main side effect was light pyrogenic reaction, which was presented in 12.96% of the total treatments. It is concluded that this method permits to continue hemodialysis, improves the nutritional condition and prolongs the lifespan by conserving and reusing the ascites protein.

Adult↗
PubMed2006

Myxedema ascites: case report and literature review.

Myxedema ascites caused by hypothyroidism is rare, so its diagnosis is often delayed and patients frequently receive unnecessary procedures such as liver biopsies and exploratory laparotomies. We report a 71-yr-old man with clinical ascites that was the first manifestation of hypothyroidism, and which resolved completely in response to thyroid hormone replacement therapy. To our knowledge, this is the first report of myxedema ascites in Korea. A review of the literature revealed 51 well-documented cases of myxedema ascites. Analyses of ascites from patients in this condition usually show high protein (>2.5 g/dL) and low white blood cell counts, with a high proportion of lymphocytes. A consistent feature is the good response to thyroid hormone replacement therapy, which has always led to resolution of the ascites. Myxedema ascites is thus rare but easy to treat; it should be borne in mind, especially if the ascites fluid has a high protein content.

Aged↗
PubMed1995

Bronchodilator, oxygen level, and temperature effects on ascites incidence in broiler chickens.

Oxygen level, ambient temperature, and bronchodilator (metaproterenol) effects on performance, ascites incidence, and hematology were investigated using commercial broilers. In Experiment 1, two atmospheric oxygen concentrations (17.6, 20.6%) and two ambient temperatures (26.7, 32.2 C) were examined in a factorial arrangement. The low-oxygen (17.6%), ambient temperature combination (26.7 C) reduced (P < .01) weight gain whereas the high-oxygen ambient temperature combination enhanced (P < .05) such performance. Ascites incidence for chicks housed at 32.2 C was higher (P < .01) for birds maintained at 17.6% oxygen but oxygen concentration did not impact ascites incidence at 26.7 C. White blood cell counts were elevated in the low-oxygen (17.6%) group at both 26.7 and 32.2 C, and hematocrit was positively (R = .84; P < .05) correlated with ascites incidence. In Experiment 2, two oxygen levels (17.6, 20.6%) at constant 26.7 C were examined with and without metaproterenol, a bronchodilator. Metaproterenol reduced (P < .01) ascites incidence at 17.6% oxygen and completely prevented ascites at 20.6% oxygen. The data suggest that therapeutic development may be enhanced by using hematocrit as an indices of ascites and further that studies directed at bronchodilation have potential to alleviate ascites.

Animals↗
PubMed1996

Artificial neural network prediction of ascites in broilers.

An artificial neural network was trained to predict the presence or absence of ascites in broiler chickens. The neural network was a three-layer back-propagation neural network with an input layer of 15 neurons (defining 15 physiological variables), a hidden layer of 16 neurons, and an output layer of 2 neurons (the presence or absence of ascites). Male by-products of a breeder pullet line were brooded at 32 and 30 C during Weeks 1 and 2, respectively. The training set for the neural network consisted of data from birds subjected to cool temperatures (18 C) to induce ascites. After training, the predictive ability of the neural network was verified with two new data sets. The second data set was from birds subjected to cool temperatures (18 C). The third data set was from birds subjected to clamping of the pulmonary artery to simulate the physiological processes involved in ascites (the temperature was 24 C). A comparison was made between laboratory diagnostic results and the neural network predicted ascites incidence. The neural network accurately identified the presence or absence of ascites in the first (training) set. Two false positives and one false positive were identified in the second and third verification sets, respectively. The birds identified as false positives were determined to be in the developmental stages of ascites before the occurrence of fluid accumulation. Artificial neural networks were found to effectively identify broilers with and without ascites.

Animals↗
PubMed1975

Lymphatic obstruction in carcinomatous ascites.

The i.p. inoculation of C3H mice with 5 times 10-6 cells of a transplantable ovarian carcinoma invariably evokes accumulation of large amounts of ascitic fluid. Histological and pharmacotherapeutic studies indicate that obstruction to peritoneal lymphatic drainage is a key factor in the formation of carcinomatous ascites in this model. In the early stages of ascites formation, an intense inflammatory reaction appears to occlude the condusts that connect the peritoneal cavity to the subdiaphragmatic lymphatic plexus. This inflammatory reaction, elicited by the presence of tumor cells within the peritoneal cavity, can be inhibited with high-dose systemic corticosteroid therapy. Ascitic fluid accumulation in animals so treated is markedly retarded. Tumor cells do not gain access to lymphatic capillaries draining the peritoneal cavity until ascitic fluid accumulation is massive. Systemic anticoagulation with heparin or sodium warfarin does not prevent lodgment of tumor cells within these lymphatic capillaries, nor does it alter the pattern of ascitic fluid accumulation. Various considerations suggest that excess production of ascitic fluid is not a likely pathogenetic factor in murine carcinomatous ascites.

Animals↗
PubMed2000

[Study on ascite of ovarian cancer].

OBJECTIVE: Analysis of correlative factors in ascite of ovarian cancer. METHODS: The clinical data of 72 patients with ovarian cancer admitted to our hospital from 1993 to 1998 were analyzed retrospectively. RESULTS: 73.5% of patients with ovarian cancer had cancer cells in ascite, the incidence of ascite was 81.9%, III and IV stage ovarian cancer with cancer cells in ascite were 91.2%, positive rate of tumor cells obviously increased in cases whose ascite were more than 1,000 ml, in cases with tumor surface infiltration as well as with metastasis to omentum, intestine and diaphragm. CA125 value in ascite without cancer cells was (324.94 +/- 527.64) kU/L, whereas in ascite with cancer cells it was (5,172.64 +/- 1,432.61) kU/L. Whether cancer cells were positive or negative. Chromosomal aneuploidy was detected in two third of the cases. CONCLUSION: Routine examination of cancer cells, chromosome and CA125 in ascite with ovarian cancer may improve the diagnostic accuracy.

Adolescent↗
PubMed2002

[The pathophysiology of ascites formation in cirrhosis of the liver].

Ascites is the most common complication in cirrhotic patients. The presence of ascites predisposes the cirrhotic patients to complications that significantly increase their morbidity and mortality. These include spontaneous bacterial peritonitis and the hepato-renal syndrome. The ascitic process has different stages, from the diuretic responsive ascites through the unresponsive ascites to the development of the hepato-renal syndrome. Until a few years ago there was a controversy regarding the pathophysiology of ascites in portal hypertension. Nowadays, the peripheral vasodilatation theory is accepted as the mechanism responsible for the development of the ascites. This theory proposes that elevated blood levels of vasodilators cause a systemic vasodilatation, that leads to the development of a hyperdynamic circulation. This vasodilatation causes activation of compensatory vasoconstrictive mechanisms. The vasoconstrictors cause functional kidney damage, which leads to the retention of sodium and water, and thus to the development of ascites.

Ascites↗
PubMed2003

Familial Mediterranean fever with massive recurrent ascites: a case report.

A 35-year-old woman had a history of recurrent massive ascites for 12 years. She had been examined to identify the etiology of ascites and was placed on antituberculous and subsequently steroid treatment at another center before admission to our hospital for fever, abdominal distention and abdominal pain. She had massive ascites with serum-ascites albumin gradient of 1.0 g/dl. We could not find any cause for ascites including tuberculosis. We thus performed exploratory laparotomy of the abdomen. There was no evidence of tuberculosis, peritoneal diseases or of any gynecological reason for ascites. Biopsies taken from the peritoneum revealed fibrinous peritonitis. Since she had a history of attacks of abdominal pain in her childhood, she was screened for mutations causing familial Mediterranean fever and was found to be homozygous for M694V. After definitive diagnosis of familial Mediterranean fever, she was put on colchicine treatment and relief of symptoms and reduction in ascites were seen on follow-up. To our knowledge this is the first documented case of massive ascites due to familial Mediterranean fever.

Adult↗
PubMedDate not supplied

Recurrent peritonitis with massive ascites as the initial manifestation of systemic lupus erythematosus: report of one case.

Systemic lupus erythematosus (SLE) rarely presents with massive ascites secondary to severe peritonitis before the occurrence of major diagnostic features. We described a 13-year-old girl who developed four episodes of severe abdominal pain with massive ascites. During the first episode, the patient experienced deterioration with massive ascites over a 3-day period, after a 3-month history of intermittent abdominal pain. This episode resolved under conservative treatment. During the second episode, her acute abdominal findings mimicked appendicitis or gynecologic emergency. An exploratory laparotomy was initially planned, but not performed. Thrombocytopenia postponed the surgical intervention and led to further investigation. Autoimmune studies confirmed SLE and prompted steroid therapy, which rapidly improved her painful ascites and spared an unnecessary operation. After improvement of peritonitis with ascites, and following discharge, other major clinical features of SLE ensued. The third episode of peritonitis with massive ascites responded well to steroid pulse therapy. The fourth episode of ascites was accompanied by intracranial hemorrhage that led to her death. To the best of our knowledge, this is the first case report of recurrent peritonitis with massive ascites as the initial and major manifestation of SLE in a pediatric patient.

Abdominal Pain↗
PubMed1992

Treatment of ascites in cirrhosis. Diuretics, peritoneovenous shunt, and large-volume paracentesis.

The medical treatment of ascites in cirrhosis is based on sodium restriction and the administration of diuretics. Because the natriuretic potency of spironolactone is greater than that of loop diuretics (i.e., furosemide) in patients with marked sodium retention, spironolactone is the basic drug for the treatment of ascites. The simultaneous administration of spironolactone and furosemide increases the natriuretic effect of each drug and diminishes their effects on potassium metabolism. Recent studies indicate that large-volume paracentesis associated with intravenous albumin infusion is more effective than diuretic therapy in eliminating the ascitic fluid; is associated with a lower incidence of complications (hepatic encephalopathy, renal impairment, and hyponatremia); and considerably reduces the duration of hospital stay. Therapeutic paracentesis associated with intravenous albumin infusion is therefore the treatment of choice for cirrhotic patients with tense ascites. The mobilization of the ascitic fluid by paracentesis without plasma volume expansion is constantly associated with a deterioration of effective circulating blood volume and may induce renal impairment and severe hyponatremia. Dextran 70 and polygeline appear as effective as albumin in preventing these abnormalities. Cirrhotic patients treated with paracentesis require the administration of diuretics to avoid reaccumulation of ascites. Peritoneovenous shunt, a prosthesis capable to correct most abnormalities involved in the accumulation of fluid in the abdominal cavity, is an effective treatment of ascites in cirrhosis. It is especially indicated in patients who do not respond to diuretics and develop repeated episodes of ascites despite adequate treatment. The use of peritoneovenous shunting is limited by the high incidence of complications induced by the procedure, however. In addition, approximately 40% of patients develop an obstruction of the prosthesis within the first postoperative year.

Albumins↗
PubMed1992

Ascites: a portent of cardiopulmonary complications in the preeclamptic patient with the syndrome of hemolysis, elevated liver enzymes, and low platelets.

OBJECTIVE: Maternal ascites is frequently found at cesarean delivery in patients with severe preeclampsia or eclampsia expressed as hemolysis, elevated liver enzymes, and low platelets (HELLP syndrome). We attempted to determine whether large-volume maternal ascites present at cesarean delivery in HELLP syndrome patients is correlated with disease severity or with any specific form of increased maternal morbidity. METHODS: For this retrospective case series, we reviewed the medical records of 190 patients and noted the presence or absence of large-volume maternal ascites, peripartum complications, laboratory data, and specific operative techniques. RESULTS: The incidence of large-volume ascites in patients with HELLP syndrome who underwent abdominal delivery was approximately 10% in classes 1, 2, and 3. Compared with HELLP syndrome patients without ascites, those with HELLP-associated ascites at surgery had a significant sixfold increase in the incidence of congestive heart failure and a ninefold increase in the incidence of adult respiratory distress syndrome, both of which usually became clinically apparent within 24 hours postpartum. Those HELLP syndrome patients without ascites at surgery developed congestive heart failure or adult respiratory distress syndrome infrequently, and more than 24 hours postoperatively. CONCLUSION: Cautious fluid administration and observation for cardiopulmonary deterioration are crucial in management of the critically ill, high-risk group of HELLP syndrome patients with large-volume ascites.

Adult↗
PubMed2006

[A case of paclitaxel-resistant cancerous ascites secondary to gastric carcinoma responding well to TS-1 therapy].

Paclitaxel was used as the first-line drug for treatment of a case with peritoneal recurrence of gastric cancer, accompanied by cancerous ascites. Because paclitaxel was ineffective, TS-1 was used as the second-line drug, resulting in disappearance of cancerous ascites on diagnostic imaging. This case was an 81-year-old male patient. In February 2004, he underwent resection of the pyloric side of the stomach (D 2) based on a diagnosis of advanced gastric cancer. CT scans, conducted in February 2005, revealed ascites, and a diagnosis of cancerous peritonitis was made on the basis of subsequent cyto-diagnostic findings. He was later hospitalized because of anorexia and difficulty with oral ingestion, and received paclitaxel therapy (60 mg/m(2)). Abdominal CT scans in May of the same year showed the disappearance of ascites. Thereafter, he was managed as an outpatient. In June of the same year, relapse of ascites was detected by CT scans, and exacerbation of ascites was seen in August. In October, paclitaxel was switched to TS-1 (80 mg/m(2)). CT scans, obtained at the end of two cycles of TS-1 therapy, revealed complete disappearance of ascites. This therapy was administered for 4 cycles in total. CT scans, performed at the end of each cycle of TS-1 therapy, confirmed the absence of ascites. At present (July 2006), the patient is managed on an outpatient basis. Our experience with this case suggests that if paclitaxel therapy fails to exert satisfactory efficacy, switching to second-line TS-1 therapy is a promising means of treating gastric cancer complicated by cancerous peritonitis.

Aged, 80 and over↗
PubMed1991

Ascitic fluid protein and cellular changes during diuretic therapy in cirrhosis of liver.

Thirty four patients with peritoneoscopy and/or biopsy proven uncomplicated cirrhosis of liver with ascites were studied for the effect of diuretic therapy on ascitic fluid protein and cell count. Renal function tests, liver function tests, ascitic fluid protein concentration and cell count were estimated prior to diuretic therapy and once every week till the end of therapy. There was no change in mean total serum protein (5.71 +/- 0.58 g/dl to 5.72 +/- 0.63 g/dl). The rise in mean ascitic fluid protein from 1.55 +/- 0.77 g/dl to 1.76 +/- 0.79 g/dl was not significant (P greater than 0.05). Twenty one patients (Group I) showed a rise in ascitic fluid protein concentration while 13 patients (Group II) did not show a rise or showed a fall in protein concentration during diuretic therapy. The rise in ascitic fluid protein concentration in Group I from 1.62 +/- 0.69 g/dl to 2.05 +/- 0.67 g/dl was statistically significant (P less than 0.05). Group I patients had a mean weight loss of 6.21 +/- 3.66 kg as compared to 3.15 +/- 2.00 kg in Group II patients (p less than 0.05). There was no other difference between Group I and Group II patients. Only 5 patients showed a rise in ascitic fluid cell count (more than 50 cell/mm3). It is concluded that diuretic therapy alters ascitic fluid protein concentration in a majority of patients but has no significant effect on cell count.

Adolescent↗
PubMed1991

Measurements of total body and extracellular water in cirrhotic patients with and without ascites.

Using H2[18O] tracer isotope dilution and corrected bromide space as standard reference techniques, we determined total body water and extracellular water in cirrhotic patients with (four men and four women) and without (seven men and six women) ascites and compared them with a normal control group (eight men and six women). These results were then compared with calculations of total body and extracellular water determined by the bioelectrical impedance analysis technique. According to H2[18(O)] dilution, total body water was similar in cirrhotic patients without ascites and in controls (60.8% +/- 2.1% vs. 60.3% +/- 1.4% body wt), but was increased in patients with ascites (69.7% +/- 1.2% body wt; p less than 0.002). Correlation was excellent between the H2[18(O)] dilution and bioelectrical impedance measurements of total body water in controls and cirrhotic patients without ascites (r = 0.98; p less than 0.0001). However, this correlation was poor in cirrhotic patients with ascites (r = 0.17; not significant). According to the bromide space, extracellular water (expressed as a percentage of total body water) was increased in cirrhotic patients with (57.8% +/- 1.8%; p less than 0.001) and without (44.0% +/- 1.2%; p less than 0.001) ascites compared with controls (36.6% +/- 1.0%). A poor correlation (r = 0.41; p less than 0.13) was seen for extracellular water measurements between the bromide space method and the bioelectrical impedance method, which failed to detect the differences among the three groups observed with the bromide space technique. Furthermore, bioelectrical impedance failed to detect any change in total body or extracellular water after paracentesis, with a degree of inaccuracy that increased linearly as the amount of ascitic fluid removed increased (r = 0.97; p less than 0.001). All these intergroup comparisons remained the same, whether the analysis was of both men and women combined or for each gender individually. However, we saw differences between men and women in the control group and cirrhotic group without ascites. These results demonstrate that abnormalities in water homeostasis and compartmentalization between intracellular (the difference between total body and extracellular water fluid) and extracellular water may exist in cirrhosis whether or not fluid accumulation is clinically evident. These data further indicate that alterations in the metabolically active body cell mass (as represented by intracellular water) in cirrhosis may occur independently of total body water and calculated fat-free body mass. In addition, gender is an important variable to control for in studies of this type.(ABSTRACT TRUNCATED AT 400 WORDS)

Abdomen↗
PubMed1990

[Validity of biochemical examinations in ascites in clinical practice].

The authors examined, using biochemical, cultivation and cytological methods, ascites in 94 patients. They divided the patients into four groups: group 1 (36 patients)--malignant ascites, group 2 (35 patients)--cirrhotic ascites, group 3 (11 patients)--cardial ascites, group 4 (12 patients)--nephrogenic ascites. The authors tried to differentiate malignant ascites from non-malignant, based on biochemical parameters. As the composition of ascites is influenced by some factors (diuretics, dialysis) the authors recommend the use of biochemical analyses of ascites in clinical practice.

Ascites↗