Search PubMed⌕ Search

PubMed · 8303315

Refractory ascites.

Abstract

The first step in the approach to the ascites patient, after the history and physical examination, is to perform a diagnostic abdominal paracentesis for SAAG to determine whether portal hypertension is present (SAAG 1.1 g/dl or higher) or not (SAAG less than 1.1 gm/dl) (Table 1). Patients without portal hypertension probably do not have liver disease as the cause of their ascites formation and probably should not be treated with dietary sodium restriction and diuretics. Patients with portal hypertension-related ascites usually have chronic parenchymal liver disease and usually require hospitalization for diet education, diuretic treatment, and evaluation of the underlying liver disease. Approximately 90% of patients with ascites due to chronic parenchymal liver disease respond to dietary sodium restriction and diuretics. Because of the poor prognosis associated with ascites, patients who are good candidates for transplantation should be considered for listing when they develop this complication of their underlying liver disease. The 10% of patients with cirrhosis whose ascites is refractory to routine medical treatment must be offered alternative therapy. Transplant candidates should be listed, in my opinion, once they are documented to have diuretic-resistant ascites. Fortunately, alcoholics (who are usually not good candidates for transplantation) who abstain from alcohol may revert from diuretic-resistant to diuretic-sensitive ascites over a period of months. Chronic outpatient therapeutic paracentesis is the most popular short-term treatment for patients with diuretic-resistant ascites. Paracentesis can be used as a "bridge" to alternative therapies or can be continued indefinitely.(ABSTRACT TRUNCATED AT 250 WORDS)

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

B A Runyon. 1993. Refractory ascites.. https://doi.org/10.1055/s-2007-1007362

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Growth-suppressive effect of non-steroidal anti-inflammatory drugs on 11 colon-cancer cell lines and fluorescence differential display of genes whose expression is influenced by sulindac.

In addition to an anti-inflammatory effect, sulindac, one of the non-steroidal anti-inflammatory drugs (NSAIDs), has been shown to have a protective effect against the incidence and mortality of colorectal cancer. However, the molecular basis of its anti-proliferative function remains unclear. To investigate its molecular mechanism, we exposed 11 colon-cancer cell lines to NSAIDs such as aspirin, sulindac and the sulfide and sulfone metabolites of sulindac. Sensitivity to these drugs was dose- and time-dependent but varied from one cell line to another. Among the cell lines examined, sulindac showed a moderate anti-proliferative effect on HT-29 colon cancer cells and caused morphological changes, including an increase of cells with abnormal DNA content. We used the mRNA fluorescence differential display method with these cells to identify molecules that might contribute, through altered expression, to cellular changes in response to NSAIDs. Sixty-eight cDNA fragments were confirmed by RT-PCR to have significantly different expression levels following sulindac treatment. Thirty of these fragments proved to be novel cDNA sequences or identical to expressed sequence tags; the other 38 fragments were identical, or showed significant homology, to genes whose function was already known. Among the known genes differentially expressed in HT-29 cells after sulindac treatment were those encoding acetylglucosaminyltransferase, ferritin heavy chain, zinc finger protein 165, aldose reductase, carcinoembryonic antigen, aldoketoreductase, NF-kappaB-activating kinase, lysosome-associated protein, RhoE = 26 kDa GTPase homologue, NADH oxidoreductase, G/T mismatch bindingprotein, TM7SF3, ADP/ATP carrier-like protein and chromosome segregation protein. This variety among classes of proteins affected by sulindac in our experiments underscores the complexity of anti-proliferative mechanisms that may operate in colon-cancer cells treated with NSAIDs. Furthermore, identification of genes regulated by NSAIDs in colon-cancer cells should provide useful information to identify novel therapeutic targets for treatment and/or prevention of colon cancer.

Anti-Inflammatory Agents, Non-Steroidal↗