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Diagnosing ascites: value of ascitic fluid total protein, albumin, cholesterol, their ratios, serum-ascites albumin and cholesterol gradient.

Ascitic fluid total protein, albumin, cholesterol, their ascites/serum ratios, serum-ascites albumin and cholesterol gradients were measured for their ability to differentiate cirrhotic, malignant and tuberculous ascites in 76 patients. The mean +/- s.d. ascitic fluid total protein, albumin, cholesterol, their respective ascitic fluid/serum ratios in cirrhotic ascites were lower than malignant and tuberculous groups (P < 0.001 for each). The difference between malignant and tuberculous groups was significant for ascitic fluid/serum total protein (P < 0.05) and ascitic fluid/serum albumin (P < 0.01) only. Mean serum-ascites albumin gradient in cirrhotics was higher than in the malignant and tuberculous groups (P < 0.001 for each). The difference between malignant and tuberculous groups was significant (P < 0.01). Mean +/- s.d. serum-ascites cholesterol gradient in cirrhotics was higher than that in malignant and tuberculous groups (P < 0.001 for each). The difference between malignant and tuberculous groups was also significant (P < 0.01). Both serum/ascitic fluid total protein less than 0.5 and ascitic fluid cholesterol less than 55 mg/dL had 94% diagnostic accuracy for differentiating cirrhotic from malignant and tuberculous differentiating cirrhotic from malignant and tuberculous ascites. Serum ascitic fluid albumin gradient greater than 1.1 g/dL, ascitic fluid/serum albumin less than 0.65 and ascitic fluid albumin less than 2 g/dL had diagnostic accuracy of 92, 92 and 91%, respectively. Ascitic fluid total protein had diagnostic accuracy of 88%. None of the tests was able to differentiate between malignant and tuberculous ascites. Measurement of ascitic fluid cholesterol concentration is a simple method of differentiating cirrhotic from non-cirrhotic ascites.

Albumins↗

Superiority of the serum-ascites albumin difference over the ascites total protein concentration in separation of "transudative" and "exudative" ascites.

The serum-ascites albumin difference, an index of the serum-ascites oncotic pressure difference, correlates directly with the pressure gradient between the portal capillaries and the peritoneal cavity. This test was compared with the ascites total protein concentration in the separation of "transudative" and "exudative" ascites. The serum-ascites albumin difference was large in patients with transudative ascites (1.6 +/- 0.5 g/dl) and small in patients with exudative ascites (0.6 +/- 0.4 g/dl, p less than 0.001) and provided significantly better discrimination of these categories than did the ascites total protein concentration. The serum-ascites albumin difference was especially useful in the separation of cardiac ascites, which usually has a high total protein concentration, from high protein exudative ascites. The serum-ascites albumin difference did not provide perfect discrimination of any category, however; in patients with mixed causes of ascites, this difference tended to be large, resembling ordinary transudative ascites, a potential source of diagnostic error. Nevertheless, the serum-ascites albumin difference has superior discriminatory power and should replace the ascites total protein concentration in the routine diagnostic examination of ascites.

Ascites↗

Diagnosis of malignant ascites. Comparison of ascitic fibronectin, cholesterol, and serum-ascites albumin difference.

The ascitic fluid concentrations of cholesterol and fibronectin and the serum-ascites albumin difference were compared with two conventional tests of ascitic fluid, total protein and LDH, in their diagnostic ability for detection of malignancy in ascitic samples from 69 patients with ascites: 54 with ascites due to liver disease and 15 whose ascites was caused by peritoneal metastases. Sixteen cirrhotic patients with superimposed hepatocellular carcinoma in whom ascites was of uncertain etiology were considered separately. The mean ascitic fluid total protein, LDH, cholesterol, and fibronectin values in the peritoneal metastases group were 3.70 +/- 1.20 g/dl, 247.26 +/- 148.14 units/liter, 109.06 +/- 29.85 mg/dl, and 91.57 +/- 41.52 micrograms/ml, respectively, and all were significantly higher than the corresponding values in the liver disease group (P less than 0.001), which were 1.37 +/- 0.59 g/dl, 75.40 +/- 110.70 units/liter, 23.75 +/- 11.22 mg/dl, and 31.86 +/- 10.51 micrograms/ml, respectively. Mean serum-ascites albumin difference in the peritoneal metastases group was 0.62 +/- 0.38 g/dl, which was significantly different from the corresponding value in the liver disease group (1.92 +/- 0.41 g/dl, P less than 0.001). Both ascitic cholesterol above 46 mg/dl and an ascitic fibronectin concentration greater than 50 micrograms/ml had high diagnostic accuracy (97%) for malignancy, being higher than that achieved using a serum-ascites albumin difference under 1.1 g/dl and an ascitic total protein above 2.5 g/dl, which had accuracies of 94% and 93%, respectively. Ascitic fluid LDH was the least reliable test. No differences in the ascitic fluid analysis were found between cirrhotic patients with and without hepatocellular carcinoma.(ABSTRACT TRUNCATED AT 250 WORDS)

Ascites↗

[The tests for anti-TB and adenosine deaminase in ascites for distinguishing between tuberculous ascites and carcinous ascites].

OBJECTIVE: To evaluate the tests for anti-TB and adenosine deaminase (ADA) in ascites in an attempt to distinguish between tuberculous ascites and carcinous ascites. METHODS: DIGFA was used to test anti-TB and Martineck's method was used to determine the level of ADA in 35 cases of tuberculous ascites and 31 cases of carcinous ascites. RESULTS: The levels of anti-TB and ADA in ascites were significantly higher in tuberculous ascites than those in carcinous ascites (P < 0.01). When the level of ADA was higher than 45 U/L, the sensitivity, specificity and accuracy in the diagnosis of tuberculous ascites were 100%, 97.1% and 98.5%, respectively. When the result of anti-TB test was positive, the sensitivity, specificity and accuracy in the diagnosis of tuberculous ascites were 93.5%, 94.3% and 95.38%, respectively. CONCLUSION: The tests for anti-TB and ADA in ascites are of important clinical value to differential diagnosis in an attempt to distinguish between tuberculous ascites and carcinous ascites.

Adenocarcinoma↗

Ascitic pseudouridine discriminates between hepatocarcinoma-derived ascites and cirrhotic ascites.

Various biochemical indexes discriminate neoplastic from nonneoplastic ascites. However, within the latter group, the distinction between cirrhotic ascites and ascites caused by hepatocarcinoma (HC) is usually based on liver biopsy or cytology. HC-derived ascites is included in the group of nonneoplastic ascites because it is not associated with peritoneal spreading of neoplastic cells. In 54 cases of cirrhotic ascites and 17 cases of HC ascites, all histologically diagnosed, ascitic pseudouridine concentrations discriminated cirrhotic from HC ascites. For example, using the cutoff value of 4.25 mumol/L (obtained by ROC curve analysis) resulted in a diagnostic sensitivity of 88.2% and a diagnostic specificity of 90.8%. Moreover, in cirrhosis, the ascitic concentrations of pseudouridine were lower than serum concentrations, and the two sets of values were correlated; in HC, however, ascitic pseudouridine concentrations were higher than serum concentrations, and the two were unrelated. These findings strongly suggest that in cirrhotic patients ascitic pseudouridine derives from serum by diffusion, whereas in HC patients the mechanism appears to be more complex.

Aged↗

Serum-ascites albumin concentration gradient and ascites fibronectin in the diagnosis of malignant ascites.

BACKGROUND: The differential diagnosis between malignant and nonmalignant ascites by using laboratory parameters has not been completely achieved so far. METHODS: The authors studied serum-ascites albumin concentration gradients ([albumin]s - [albumin]a), ascites fibronectin and various parameters in 149 consecutive patients with ascites (including Group 1: 22 patients with intraabdominal malignant lesions; Group 2: 81 patients with chronic liver disease; and Group 3: 46 patients with hepatocellular carcinoma [HCC]). RESULTS: The concentrations of fibronectin, albumin, protein, lactate dehydrogenase, and carcinoembryonic antigen in ascites were significantly higher in Group 1 than in Group 2 (P < 0.001). By contrast, the [albumin]s - [albumin]a was significantly lower in Group 1 than in Group 2 (P < 0.001). None of these parameters was useful in differentiating the ascites of chronic liver disease from that of HCC. In this study, to differentiate malignant ascites from the ascites caused by liver diseases, [albumin]s - [albumin]a (< 1.5 g/dl) and the fibronectin level in the ascites (> 100 micrograms/ml) provided diagnostic accuracy (96.8% and 95.9%, respectively) as precise as those of the levels of albumin (> 1.6 g/dl), protein (> 2.5 g/dl), and lactate dehydrogenase (> 60 U/l; 97.9%, 96.7%, and 94.8%, respectively) in ascites. These results were better than that of carcinoembryonic antigen level (> 1.5 ng/ml, 80.9%). CONCLUSIONS: The authors concluded that [albumin]s - [albumin]a offered the best method to survey malignant ascites because of its sensitivity (100%).

Albumins↗

Total discrimination of peritoneal malignant ascites from cirrhosis- and hepatocarcinoma-associated ascites by assays of ascitic cholesterol and lactate dehydrogenase.

No laboratory test completely distinguishes malignant ascites (MA) from ascites associated with cirrhosis and (or) hepatocellular carcinoma (A/C-HC). Ascitic cytology is highly specific but has a diagnostic sensitivity of only 40-60%. We determined 11 ascitic analytes and cytology in 58 patients with cirrhosis, 15 with hepatocellular carcinoma, and 21 with MA (10 ovarian cancers, 4 mesotheliomas, 6 gastrointestinal neoplasias, 1 leukemia). Ascitic total protein, cholesterol, pseudouridine, and lactate dehydrogenase (LD), and the ascitic:serum ratios of total protein and of LD showed the most significant differences between the two groups of patients. Stepwise multiple linear discriminant analysis (applying the Wilks' lambda criterion) of several variables, corroborated by the "jack-knife" reallocation procedure, showed that the ascitic cholesterol and ascitic LD association correctly identified 100% of MA and A/C-HC; cytology had a diagnostic specificity of 100%, but identified only 48% of MA. This association may represent a primary tool for the discrimination of ascites of unknown origin, particularly in the presence of negative cytology findings.

Ascites↗

Pathophysiology of elevated ascites fluid cholesterol in malignant ascites. Increased ascites to serum relation of proteins and lipoproteins in patients with peritoneal carcinomatosis as compared to patients with cirrhosis of the liver.

The existence of marked elevations of ascitic fluid cholesterol has been observed in patients with peritoneal carcinomatosis compared to patients with cirrhosis and has been found useful in differential diagnosis. This finding could be caused by an enhanced movement of plasma lipoproteins into the peritoneal cavity. To test this hypothesis we determined the fasting concentrations of total, high density lipoprotein (HDL)- and low density lipoprotein (LDL)-cholesterol, apolipoprotein-A1 (apo-A1) and apolipoprotein-B (apo-B) in serum and ascites of 17 patients with cirrhosis and 16 patients with peritoneal carcinomatosis. The movement of proteins from plasma to ascites was calculated from the ascites/serum concentration ratios of six different sized proteins with a molecular mass ranging from 54 kDa to 971 kDa. Mean values (mg/dl) for total cholesterol (92.6 vs. 21.0), HDL-cholesterol (15.6 vs. 1.8), LDL-cholesterol (63.4 vs. 16.1), apo-A1 (50.2 vs. 13.6) and apo-B (41.2 vs. 12.9) in ascites were significantly higher in peritoneal carcinomatosis than in cirrhosis. These differences could only partially be explained by the higher serum concentrations of these parameters in peritoneal carcinomatosis, but were mainly due to a lower selectivity for the movement of plasma proteins and lipoproteins into ascites (mean ascites/serum (A/S) ratio: 0.30-0.77) in peritoneal carcinomatosis as compared to cirrhosis (mean ascites/serum ratio: 0.11-0.21). In both groups about 85% of the total cholesterol in serum and ascites consisted of HDL- and LDL-cholesterol. These findings support the hypothesis that elevations in ascitic cholesterol in peritoneal carcinomatosis compared to cirrhosis are mainly caused by the increased movement of plasma HDL and LDL into the peritoneal cavity.

Apolipoprotein A-I↗

Renal effects of transjugular intrahepatic portosystemic shunt in cirrhosis: comparison of patients with ascites, with refractory ascites, or without ascites.

Renal effects of the transjugular intrahepatic portosystemic shunt (TIPS) were compared in 6 patients without ascites (group 1), 11 patients with ascites responding to diuretic treatment (group 2), and 6 patients with refractory ascites (group 3). Seven days after insertion of TIPS, 24-hour urinary sodium excretion had increased in patients with ascites: 113 +/- 16 mmol to 170 +/- 30 mmol (P = .012) in group 2, and 22 +/- 8 mmol to 77 +/- 27 mmol (P = .050) in group 3. In group 3, fractional sodium excretion tended to increase from 0.26% +/- 0.14% to 0.62% +/- 18% (P = .081). The relative increase of urinary sodium excretion (to 444% +/- 122%) and fractional sodium excretion (to 413% +/- 127%) in group 3 was significantly (P < .05) higher than in group 1 and group 2, respectively. Creatinine clearance and 24-hour urinary volume were not significantly changed in either group. Patients with Child-Pugh class C had a more pronounced effect of TIPS on urinary sodium excretion (increase to 396% +/- 115% vs. 139% +/- 15%; P = .066) and on fractional sodium excretion (increase to 415% +/- 103% vs. 94% +/- 15%; P = .020) than patients with less-severe liver disease. Fractional sodium excretion of less than 0.35% before TIPS was found to be an indicator of renal response to TIPS. The effect of TIPS on urinary sodium excretion and on fractional sodium excretion was related to the patients' Child-Pugh score (r = .55; P = .007 and r = .68; P = .001, respectively) and inversely to their fractional sodium excretion (r = -.44; P = .047 and r = -.54; P = .012, respectively) before TIPS. These data demonstrate that TIPS affects renal sodium handling in patients with ascites, particularly in patients with refractory ascites. Severity of liver disease and fractional sodium excretion before TIPS are parameters to predict the extent of the renal response.

Adult↗

[Studies on fibrinolysis and ascites accumulation associated with peritonitis carcinomatosa--effects of protease inhibitors (PI) on MM2 ascites tumor growth, ascites accumulation and fibrinolysis].

The effects of protease inhibitors(PI), t-AMCHA, gabexate, aprotinin and heparin on the growth of mouse MM2 ascites tumor (MAT) and on several components of fibrinolysis were studied. The drugs were administered intraperitoneally one time daily for 12 days, one day after the tumor transplant. The volumes of ascites, total packed cell volume (TPCV) and fibrinolytic parameters (FDP, whole plasmin, plasminogen activator (PA)) were measured on the 8, 10 and 12th days of therapy. Fibrinolytic activity was assayed by the lysin sepharose affinity chromatography-radio caseinolytic method. Fibrinolytic activity in the ascites increased during the tumor growth. The ascites accumulation as well as levels of FDP, whole plasmin and PA in the drug treated group were significantly decreased when compared to the control group. In these drug-treated groups, MAT cells agglutinated in the abdominal cavity, but in contrast to this, no agglutination was observed in the control group. It was uncertain whether PI directly inhibited tumor growth. The fact that PI inhibited the ascites accumulation and also decreased fibrinolytic activity suggest the involvement of protease in the neoplastic process and indicates another therapeutic approach to malignant ascites tumors.

Animals↗

[Value of ascitic lipids and sero-ascitic gradient of albumin in the differential diagnosis of ascites].

In order to compare its diagnostic value in the differentiation between malignant and hepatic ascites, we analysed the ascitic fluid concentrations of cholesterol (Ct) and triglycerides (Tg) and the serum-ascites albumin gradient (S-A alb grad) in 58 patients--forty one with chronic liver disease (CLD) and 17 with malignancy. In CLD group the mean values +/- SD for Ct (27.1 +/- 20.1 mg/dl), Tg (34.2 +/- 33.8 mg/dl) and S-A alb grad (1.9 +/- 0.6 g/dl) were significantly different from those obtained in malignant ascites (Ct 103.1 +/- 45.1 mg/dl; Tg 62.1 +/- 43.0 mg/dl; S-A alb grad 0.5 +/- 0.4 g/dl) (p less than 0.001 for all parameters). Application of the cutoff concentrations given in the literature revealed the following results: Ct-Sensitivity (Se) 82.4%, Specificity (Sp) 85.4%, Efficiency (E) 84.5%; Tg-Se 29.4%, Sp 95.1%, E 75.9%; S-A alb grad- Se 88.2%, Sp 97.6%, E 94.8%. The exclusion of the 4 patients with massive hepatic metastasis from malignant group by ultrasound or computer tomography gave an efficiency of 87.0% for Ct, 88.9% for Tg and 98.1% for S-A alb grad. We conclude that: 1) S-A alb grad is the best analysed parameter in the discrimination between malignant and hepatic ascites, 2) the combination with non-invasive imaging methods increases its diagnostic value.

Albumins↗

Ascites kinetics in cirrhosis: relationship to plasma-ascites hydrostatic-oncotic balance and intensity of renal sodium retention.

The factors controlling ascites formation and reabsorption, as well as the relationship of ascites dynamics to renal sodium retention complicating cirrhosis, are not defined. We measured, using labeled albumin, the ascites albumin clearance rate, the plasma-ascites and ascites-plasma albumin filtration rates, the ascites albumin exit rate, and the plasma-ascites and ascites-plasma albumin transfer rates in seven patients with cirrhosis and ascites. Wedged hepatic vein pressure (WHVP), right atrial pressure (RAP), ascites pressure (AP), and serum and ascites oncotic pressure (SOP, AOP) were used to calculate the net hydrostatic (WHVP - AP), oncotic (SOP - AOP) and hydrostatic-oncotic pressure, or "transfer" pressure, favoring ascites formation [(WHVP - AP) - (SOP - AOP)], and the net hydrostatic pressure favoring ascites reabsorption (AP - RAP). Over 4 hours: the ascites albumin exit rate greater than the plasma-ascites albumin transfer rate greater than the ascites-plasma albumin transfer rate (P less than 0.05), and the ascites albumin clearance rate greater than the plasma-ascites and ascites-plasma albumin filtration rates (P less than 0.05). The ascites-plasma albumin filtration rate was inversely related to ascites volume (r = 0.91, P less than 0.01). Calculating the ascites-plasma albumin transfer rate from the extrapolated ascites-plasma albumin filtration rate at an ascites volume of 0 (0.031 L/hr/m2) produced values similar to the mean plasma-ascites albumin transfer rate (0.20 + 0.11 gm/hr/m2 vs. 0.24 + 0.13 gm/hr/m2, not significant).(ABSTRACT TRUNCATED AT 250 WORDS)

Albumins↗

Ascitic fluid analysis in malignancy-related ascites.

A prospective study identified 45 patients with malignancy-related ascites among 448 ascites patients (10% of the total). Patients were categorized into five subgroups based on the pathophysiology of ascites formation. Each subgroup had a distinctive ascitic fluid analysis. Patients with peritoneal carcinomatosis but without massive liver metastases (53.3% of the patients with malignancy-related ascites) had a uniformly positive ascitic fluid cytology, high ascitic fluid protein concentration and low serum-ascites albumin gradient. Patients with massive liver metastases and no other cause for ascites formation (13.3% of the series) had a negative cytology, low ascitic fluid protein concentration, high serum-ascites albumin gradient and markedly elevated serum alkaline phosphatase. Those with peritoneal carcinomatosis and massive liver metastases (13.3% of the series) had a nearly uniformly positive ascitic fluid cytology, variable protein concentration, high serum-ascites albumin gradient and markedly elevated serum alkaline phosphatase. Chylous ascites (6.7%) was characterized by a milky appearance, negative cytology and an elevated ascitic fluid triglyceride concentration. Patients with hepatocellular carcinoma superimposed on cirrhosis (13.3%) had negative ascitic fluid cytology, low ascitic fluid protein concentration, high serum-ascites albumin gradient and elevated serum and ascitic fluid alpha-fetoprotein concentration. Two-thirds of patients with malignancy-related ascites had peritoneal carcinomatosis; 96.7% of patients with peritoneal carcinomatosis had positive ascitic fluid cytology. Ascitic fluid analysis is helpful in identifying and distinguishing the subgroups of malignancy-related ascites.

Alkaline Phosphatase↗

Usefulness of serum-ascites albumin difference in separating transudative from exudative ascites. Another look.

The serum-ascites albumin difference is reported to be superior to ascitic total protein, ascitic-to-serum total protein ratio, lactic dehydrogenase, and ascitic-to-serum lactic dehydrogenase ratio in differentiating between ascites from liver disease and malignant ascites, S-A greater than 1.1 reflecting portal hypertension. We analyzed ascitic fluid from 46 consecutive patients with chronic liver disease, 28 patients with ascites associated with malignancy, 10 patients with right-sided heart failure, 4 patients with hypothyroidism, and 6 patients with miscellaneous causes of ascites to determine if this albumin difference is indeed a more valuable parameter. Analysis of our data confirms with a larger number of patients that the serum-ascites albumin difference is a more reliable indicator of transudative ascites, better termed portal hypertensive ascites. Malignant ascites without liver metastases had features of nonportal hypertensive ascites, and the serum-ascites albumin difference confirms this. The characteristics of malignant ascites associated with liver metastases, however, resemble those of the portal hypertensive ascites complicating liver disease. This new parameter is also helpful in distinguishing congestive heart failure with high protein ascites and portal hypertensive ascitic features from malignant ascites without liver metastases. Of particular note, myxedematous ascitic fluid, classically categorized as exudative, had an S-A greater than 1.1, indicating the possible role of portal hypertension in the development of ascites in these patients.

Ascitic Fluid↗

[Usefulness of cholinesterase determination in ascitic fluid in the differential diagnosis of ascites].

BACKGROUND: Cholinesterase is an enzyme mainly synthesized in the liver that might play a role in the differential diagnosis of ascites. We prospectively compared the sensitivity, specificity and diagnostic usefulness of the ascites cholinesterase and the classical parameters, ascites total protein concentration and serum-ascites albumin gradient in the differential diagnosis of ascites. In addition, we evaluated the relationship between those parameters and the degree of liver failure. METHODS: A total of 91 patients with ascites were analyzed. According the final diagnosis, patients were classified in two groups, patients with signs of portal hypertension [n = 78] (60 with chronic liver disease, 5 chronic liver disease and hepatocellular carcinoma, 3 chronic liver disease and spontaneous bacterial peritonitis, 3 chronic liver disease and secondary peritonitis, 7 malignancy with liver involvement) and patients with no signs of portal hypertension [n = 13] (12 patients with peritoneal neoplasia without liver involvement and 1 tuberculous peritonitis). RESULTS: The sensitivity of the test for detecting portal hypertensive ascites was lowest for ascites cholinesterase less than 600 U/L (71.7%); intermediate with ascites total protein concentration less than 25 g/l (87.2%) and highest with serum-ascites albumin gradient at least 11 g/l (93.6%). The specificity for ruling out portal hypertensive ascites was 100 percent for ascites total protein > or = 25 g/l and ascites cholinesterase > or = 600 U/L and, 76.9 percent for serum-ascites albumin gradient < 11 g/l). Diagnostic efficiency (percentage of patients accurately classified) was greater for serum-ascitis albumin gradient (91.2%; IC95: 83-95.8), and lower for ascites total protein content (89%, IC95: 80.3-94.3) and, ascites cholinesterase (75.8%; IC95: 65.5-83.9). Ascites cholinesterase showed a significant relationship (p = 0.007) with the degree of liver failure measured by Pugh's classification. CONCLUSION: Serum-ascites albumin gradient was the test with best performance characteristics to identify patients with ascites related with portal hypertension. Our results suggest that ascites cholinesterase is more associated with the degree of liver failure than with the presence of portal hypertension.

Ascites↗

Ascitic fluid polymorphonuclear cell count and serum to ascites albumin gradient in the diagnosis of bacterial peritonitis.

The analysis of ascitic fluid has been complicated by several recently reported new tests. To simplify this assessment, we evaluated nine parameters prospectively and simultaneously in blood and ascitic fluid from 285 patients with ascites to determine which were the most reliable for immediate diagnosis of the etiology of the ascites and of its complications. Subjects were first divided into four groups: sterile cirrhotic ascites (n = 201), spontaneous bacterial peritonitis (n = 41), malignant ascites (n = 34), and miscellaneous ascites (n = 9). An ascitic fluid polymorphonuclear count greater than 500/microliters was the test with the greatest accuracy (96%) for the diagnosis of spontaneous bacterial peritonitis. Neither the most precise cutoff values for ascitic fluid pH (less than 7.32) and ascitic fluid lactate (greater than 32 mg/dl), nor their respective blood-ascitic fluid gradients (greater than 0.11 and less than -20 mg/dl) were more reliable indexes of spontaneous bacterial peritonitis, mainly due to the decreased ascitic fluid pH and increased ascitic fluid lactate observed in malignant ascites, tuberculous peritonitis, and pancreatic ascites. A blood-ascitic fluid albumin gradient less than 1.1 g/dl was the most accurate parameter for the diagnosis of malignant ascites (diagnostic efficacy, 93%). Therefore, the etiologic analysis of ascitic fluid might be simplified and the single practice of two tests, ascitic fluid polymorphonuclear cell count and blood-ascitic fluid albumin gradient, provides immediately useful information.

Adult↗

Low protein concentration in cirrhotic ascites is related to low ascitic concentrations of immunoglobulins G and A.

OBJECTIVE: To analyse the differences in ascitic and serum levels of immunoglobulins and albumin between two groups of cirrhotic patients (with ascitic total protein levels higher and lower than 10 g/l). DESIGN: A prospective study. PATIENTS AND METHODS: We studied 39 cirrhotic patients with sterile ascites. The patients were classified into two groups: group A (18 patients) comprised those with an ascitic total protein level less than 10 g/l and group B (21 patients) those with an ascitic total protein level higher than 10 g/l. Ascitic and serum levels of albumin and immunoglobins G, A and M were analysed. RESULTS: Ascitic immunoglobulin G and A levels in group B were higher than ascitic immunoglobulin G and A levels in group A. Ascitic levels of these immunoglobulins correlated linearly with ascitic total protein levels. The serum levels of immunoglobulins G and A in groups A and B were not significantly different. Ascitic and serum immunoglobulin M concentrations in the two groups were similar. Transfer of immunoglobulins G and A and albumin from plasma to ascites seemed to be similar in group B. Transfer of immunoglobulins G and A seemed to be impaired in group A. Differences in ascitic immunoglobulin levels between groups A and B were also observed in the presence of diuretic treatment. Differences in ascitic immunoglobulin levels were related to the Child-Pugh score. CONCLUSION: Patients with a low ascitic total protein level show low ascitic immunoglobulin G and A concentrations. The low ascitic immunoglobulin G and A levels could be related to an impairment in the transfer of these immunoglobulins from plasma in those patients who have poor liver function. Ascitic immunoglobulin M is not related to ascitic total protein, and its origin is not clear. The putative transfer of immunoglobulin M to the peritoneal cavity is not related to the mechanism of transfer of albumin or of immunoglobulins G and A from serum. The physiological significance of ascitic immunoglobulin M is unclear.

Adult↗

Relationships between haemodynamic alterations and the development of ascites or refractory ascites in patients with cirrhosis.

OBJECTIVE: In patients with cirrhosis, the relationships between haemodynamic alterations and the development of ascites or the occurrence of refractory ascites are unknown. The aim of the present study was to compare haemodynamic measurements obtained in patients with non-refractory ascites to haemodynamic measurements obtained in patients without ascites and in patients with refractory ascites. METHODS: A cohort of 121 patients was prospectively studied, of whom 29 patients did not have ascites, 45 had non-refractory ascites and 47 had refractory ascites. Splanchnic, renal and systemic haemodynamics were measured in all patients. RESULTS: The hepatic venous pressure gradient was significantly higher in patients with non-refractory ascites than in patients without ascites (18.5 +/- 0.8 mmHg versus 15.8 +/- 0.7 mmHg). Renal and systemic haemodynamics did not significantly differ between patients with non-refractory ascites and patients without ascites. The glomerular filtration rate and renal blood flow were significantly lower in patients with refractory ascites than in patients with non-refractory ascites (77 +/- 4 versus 107 +/- 5 ml/min and 867 +/- 62 versus 1,008 +/- 68 ml/min, respectively). Splanchnic and systemic haemodynamics did not significantly differ between patients with refractory ascites and patients with non-refractory ascites. CONCLUSIONS: In patients with cirrhosis, an increase in portal hypertension was the sole haemodynamic alteration related to the development of ascites. Renal vasoconstriction (and subsequent renal hypoperfusion and hypofiltration) was the only haemodynamic alteration related to the occurrence of refractory ascites. The development of ascites or refractory ascites was not associated with any alteration in systemic haemodynamics.

Aldosterone↗