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Update on ascites and hepatorenal syndrome.

Ascites is the most common complication occurring during liver cirrhosis. Even if a significant decrease in renal clearance may be observed in the first step of chronic active liver disease, renal impairment, at times complicated by the typical signs of hepatorenal syndrome, occurs only in patients with ascites, especially when tense and refractory. Experimental and clinical data seem to suggest a primary sodium and water retention in the pathogenesis of ascites, in the presence of an intrahepatic increase of hydrostatic pressure, which, by itself, physiologically occurs during digestion. Abnormal sodium and water handling leads to plasma volume expansion, followed by decreased peripheral vascular resistance and increased cardiac output. This second step is in agreement with the peripheral arterial vasodilation hypothesis, depicted by an increase in total blood volume, but with a decreased effective arterial blood volume. This discrepancy leads to the activation of the sympathetic nervous and renin-angiotensin-aldosterone systems associated with the progressive activation of the renal autacoid systems, especially, that of the arachidonic acid. During advanced cirrhosis, renal impairment becomes more sustained and renal autacoid vasodilating substances are less available, possibly due to a progressive exhaustion of these systems. At the same time ascites becomes refractory inasmuch as it is no longer responsive to diuretic treatment. Various pathogenetic mechanisms leading to refractory ascites are mentioned. Finally, several treatment approaches to overcome the reduced effectiveness of diuretic therapy are cited. Paracentesis, together with simultaneous administration of human albumin or other plasma expanders is the main common approach to treat refractory ascites and to avoid a further decrease in renal failure. Other effective tools are: administration of terlipressin together with albumin, implantation of the Le Veen shunt, surgical porto-systemic shunting or transjugular intrahepatic portosystemic stent-shunt, or orthotopic liver transplantation, according to the conditions of the individual patient.

Ascites↗

Pathogenesis of malignant ascites: Starling's law of capillary hemodynamics revisited.

Peritonitis carcinomatosa, indicating the presence of malignant cells in the peritoneal cavity, is a well-known complication of malignant disease. As a result, so-called malignant ascites develops. Malignant ascites is a debilitating condition for which no effective anti-tumor therapy is available. Frequent draining may be necessary to relieve pain and discomfort. Most studies regarding malignant ascites focus on diagnosis and treatment. In this paper. we will address the subject from a pathophysiologic perspective, using the characteristics of malignant ascites, Starling's equation of capillary forces, and recent knowledge regarding biologically active peptides produced by tumor cells. Following this approach. apart from decreased lymphatic ascites absorption, increased net capillary fluid-production can be identified as a contributing feature of ascites formation. The increased net filtration is due to an increase of overall capillary membrane-surface, increased capillary permeability and a subsequent increase of intraperitoneal protein concentration leading to increased intraperitoneal oncotic pressure. This sequence might be the result of biologically active peptides produced by tumor cells such as vascular endothelial growth factor and basic fibroblast growth factor. Interference with these mediators may serve as a target in future therapeutic strategies.

Ascites↗

Pancreatic ascites in an infant: lack of symptoms and normal amylase.

A 4-month-old boy presented with 9 days of abdominal distension. The abdomen was tense, distended, and nontender, with a fluid wave. Hypoalbuminemia, hyponatremia, high lipase, normal amylase, high ascitic fluid: lipase, amylase, and serum-ascites albumin gradient < 1.1 were present. Abdominal CT showed large ascites, edema, and pancreatic cyst. No improvement was noted with bowel rest, TPN, albumin, furosemide, octreotide, and paracentesis. Endoscopic retrograde cholangiopancreatography showed disrupted pancreatic duct and a cyst. Pancreatic duct stenting was complicated by early outward migration of the stent and was thus ineffective. An exploratory laporatomy revealed a cyst. Cystogastrostomy resolved the pancreatitis and ascites. The patient was discharged off TPN and tolerating enteral nutrition. Pancreatic ascites is rare, producing few or no symptoms in infants. In conclusion, our patient may have had viral pancreatitis, complicated by a disrupted duct and/or ruptured pseudocyst with ascites formation. Medical management was ineffective. Surgery appears to have been curative.

Amylases↗

Correlation of high levels of hyaluronan and cytokines (IL-1beta, IL-6, and TGF-beta) in ascitic fluid of cirrhotic patients.

Our objective was to investigate the relationship between endotoxin and hyaluronan synthesis and release in serum and ascitic fluid from cirrhotic patients. We studied hyaluronan, endotoxin, albumin, and creatinine levels in ascitic fluid and plasma and cytokine levels (IL-1beta, IL-6, TGF-beta) in ascitic fluid. TGF-beta, IL-6, and IL-1beta correlation analyses indicated a strong dependence of the production of these cytokines on endotoxin levels. Correlation analyses for TGF-beta and IL-6 indicated a strong dependence of the production of hyaluronan on cytokine levels and, to a lesser extent, on IL-1beta levels. Hyaluronan analysis indicated that a certain glycosaminoglycan level is required in ascites before its appearance in plasma. Our results disclosed elevated plasma hyaluronan concentrations. The simultaneous increased hyaluronan levels in ascitic fluid do not seem to be derived from the systemic circulation. In conclusion, the high hyaluronan-ascites/hyaluronan-plasma ratio suggests an intrinsic hyaluronan production from peritoneal cells induced by endotoxins.

Adult↗

Interleukin-1 receptor antagonist in ascites indicates acute graft rejection after pediatric liver transplantation.

Acute graft rejection is one of the most frequent complications after pediatric liver transplantation (LTx). In clinical practice, it is sometimes difficult to differentiate acute cellular graft rejection from other complications because clinical and chemical findings are often nonspecific. We therefore investigated the value of cytokine quantification in drained ascites, in addition to quantification of cytokine concentrations of serum, in 30 children in the first 2 weeks after orthotopic liver transplantation (OLT). Six of 30 patients showed acute graft rejection, with rising levels of alanine aminotransferase (ALT) and alpha-glutathione-S-transferase (alpha-GST) in serum up to 24 h prior to biopsy-proven rejection. There were no significant elevations of interleukin-2 receptor (IL-2r) and interleukin-6 (IL-6) in serum and ascites. In contrast to these findings, the concentration in ascites of the interleukin-1 receptor antagonist (IL-1ra) increased 48 h before rejection was proven by liver biopsy (p < 0.01, in comparison with the non-rejecting group, n = 24). The IL-1ra concentration in ascites was up to 11-fold higher than in serum during rejection (15.43 vs. 1.38 ng/mL). Two children with early infectious complication showed no significant increase in ascitic IL-1ra concentration. We conclude from these data that quantification of IL-1ra in ascites indicates the start of graft rejection after LTx. As long as abdominal drainage is performed, this non-invasive procedure may be of additional value in differential diagnoses and early diagnosis of rejection.

Acute Disease↗

Mononuclear-cell infiltration in ovarian cancer. I. Inflammatory-cell infiltrates from tumour and ascites material.

Malignant effusions and tumour tissue obtained at surgery provided material for a study of the prognostic value of the various inflammatory cells in the prognosis of human ovarian cancer. Ascitic fluids predominantly contained inflammatory cells; tumour cells, both singly and in clusters, were a minor component. Tumour cells were usually in excess in dispersed solid material. Some patients had significant proportions of lymphocytes and macrophages in their solid tumour, and these patients invariably responded to therapy. Sedimentation-velocity separation at unit gravity provided tow populations of inflammatory cells. One consisted of mononuclear cells similar in size to those in the patients blood: the other consisted of one or more large macrophage populations, distinct in morphology and enzymatic markers from both blood monocytes and each other. T lymphocytes were enriched in ascites fractions (78%) and in the tumour-derived mononuclear fraction (71%) compared to patient blood (60%). The T-cell subset characterized by ANAE reactivity was markedly depleted in the tumour-infiltrating fraction (17%) compared to patient blood (62%) or patient blood (51%). Esterase-positive monocyte-like cells were more frequent in the tumour-infiltrating fraction (17%) than ascites (7%) or blood (12%). B lymphocytes were infrequent in solid tumours and difficult to assess in ascites. Histiocyte-like macrophages were present in the higher-velocity tumour-cell containing fractions of both solid and ascitic material. The variation in infiltrating cells between patients and between tumour and ascites of the same individual was marked.

Ascitic Fluid↗

Mononuclear-cell infiltration in ovarian cancer. III. Suppressor-cell and ADCC activity of macrophages from ascitic and solid ovarian tumours.

Macrophages have been isolated from ascitic and collagenase-dispersed tumours from patients undergoing surgery for ovarian cancer. Macrophages were present in varying proportions in both sites, though the ration of macrophages to tumour cells was higher in ascites. Marked variation in size (as detected by sedimentation velocity) and cytochemical markers in the macrophages was noted. Highly enriched macrophage fractions were isolated from the ascites and collagenase-dispersed solid tumours by a combination of sedimentation velocity and selective EA RFC or adherence techniques. Suppressor activity in the PHA assay was detected in tumour macrophages (4/10 giving less than 50% inhibition), ascitic macrophages (1/15) and blood monocytes (2/7). Lymphocyte fractions from tumours were unresponsive to PHA and failed to suppress the blood response. Suppressor activity was also present in the purified tumour-cell fraction of 6/14 patients. ADCC activity was tested in a few patients. When the activity was determined against the SB target cells, tumour-derived macrophages were inactive, whereas the ascitic fraction showed low but significant activity which averaged much lower than patients blood values. The ADCC assays carried out with the CRC target cell indicated activity within the range of patient blood values in 4/4 ascites and 2/4 tumour macrophage fractions. Cytotoxicity was also assessed against co-purified autologous tumour cells. Although activity was detected in many of the tests, the results seemed to reflect target cell sensitivity. There appeared to be a correlation between cytotoxicity with test macrophages and normal blood mononuclear cells. The results indicate that the cytochemical heterogeneity and the variation in size between macrophage fractions is associated with a spectrum of activities.

Antibody-Dependent Cell Cytotoxicity↗

MDA435/LCC6 and MDA435/LCC6MDR1: ascites models of human breast cancer.

We have established a novel ascites tumour model (MDA435/LCC6) from the oestrogen receptor-negative, invasive and metastatic MDA-MB-435 human breast cancer cell line. MDA435/LCC6 cells grow as both malignant ascites and solid tumours in vivo in nude mice and nude rats, with a tumour incidence of approximately 100%. Untreated mice develop ascites following i.p. inoculation of 1 x 10(6) cells and have a reproducible life span of approximately 30 days, with all animals dying within a 48 h period. The in vivo response of MDA435/LCC6 ascites to several cytotoxic drugs, including doxorubicin, etoposide (VP-16), BCNU and mitomycin C, closely reflects the activity of these single agents in previously untreated breast cancer patients. MDA435/LCC6 cells also retain the anchorage-dependent and anchorage-independent in vitro growth properties of the parental MDA-MB-435 cells, and can be used in standard in vitro drug screening assays. The drug resistance pattern of the MDA435/LCC6 cells suggests that they may have few active endogenous drug resistance mechanisms. To generate a model for the screening of MDR1-reversing agents, MDA435/LCC6 were transduced with a retroviral vector directing the constitutive expression of the MDR1 cDNA, producing a cell line with a classical MDR1 resistance pattern (MDA435/LCC6MDR1). THese ascites models may be a viable alternative to the murine leukaemia ascites (L1210, P388) and, in conjunction with other breast cancer cell lines, facilitate the in vitro and in vivo screening of new cytotoxic drugs and drug combinations.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

Active immunization with EPF suppresses the formation of immune ascites in BALB/c mice.

The production of early pregnancy factor (EPF) is not confined to pregnancy--EPF has been detected as a product of tumour and transformed cells in vivo and in vitro. In this study, EPF (or an EPF-like substance) was detected also in the serum of BALB/c mice, 7 days after intraperitoneal (i.p.) administration of the mineral oil pristane. Furthermore, EPF was present in serum from mineral oil-induced plasmacytoma-susceptible mice throughout the latent period potentially leading to tumour development, peaking around the time neoplastic cells were identified in ascites. Since mineral oil-induced granuloma is essential to development of immune ascites, involvement of EPF in this process was investigated. Active immunization of BALB/c mice with EPF was shown to suppress the production of immune ascites, induced by multiple i.p. injections of antigen in complete Freund's adjuvant. Of the mice immunized with EPF (n = 19), only 47% produced ascites, compared with 94% of mice receiving saline or human chorionic gonadotrophin and 100% of mice receiving keyhole limpet haemocyanin. Further investigations revealed that ascites was only produced in mice that maintained free-circulating EPF. These mice displayed the classic mineral oil-induced granuloma covering the tissues of the peritoneum. In contrast, the serum of mice that did not produce ascites tested negative for EPF and the peritonea of these mice were devoid of the oil granuloma. These studies suggest that EPF is involved in the initiation and maintenance of the inflammatory response of the peritoneum to mineral oil.

Animals↗

Hyperdynamic circulation of cirrhotic rats with ascites: role of endotoxin, tumour necrosis factor-alpha and nitric oxide.

1. Hyperdynamic circulation observed in portal hypertensive states is characterized by generalized vasodilation, increased cardiac index and increased systemic and regional blood flows. Endotoxin, tumour necrosis factor-alpha (TNF-alpha) and nitric oxide (NO) have been reported to be involved in the pathogenesis of hyperdynamic circulation, but the interactions between endotoxin, TNF-alpha and NO in cirrhotic rats with ascites have never been specifically addressed. 2. This study was designed to determine systemic and portal haemodynamics and plasma levels of endotoxin, TNF-alpha and nitrate/nitrite in cirrhotic rats with ascites and investigate the relationships between these substances. 3. Plasma concentrations of endotoxin, TNF-alpha and nitrate/nitrite (an index of NO production) were determined in 25 cirrhotic rats with ascites and 17 control rats using the Limulus assay, ELISA and a colorimetric assay respectively. In addition, haemodynamic studies were performed in another ten cirrhotic rats with ascites and ten control rats. 4. Cirrhotic rats with ascites had hyperdynamic circulation accompanied by increased plasma levels of endotoxin, TNF-alpha and nitrate/nitrite, as compared with control rats. Significant correlation existed between plasma levels of endotoxin and nitrate/ nitrite (r = 0.59, P < 0.0001) and between plasma levels of endotoxin and TNF-alpha (r = 0.63, P < 0.0001). No correlation was detected between plasma levels of TNF-alpha and nitrate/nitrite (r = 0.24, P > 0.05). 5. This study suggests that endotoxaemia developed in cirrhotic rats with ascites may stimulate NO formation directly or indirectly via cytokine cascade, and consequently participate in the development and/or maintenance of hyperdynamic circulation.

Animals↗

Phenotype and antitumor activity of ascitic fluid monocytes in patients with ovarian carcinoma.

Monocytes/macrophages (MO/MA) represent a major leukocyte population in the peritoneal cavity of patients with epithelial ovarian cancer (EOC). We examined the phenotypic characteristics and antitumor cell activity of ascitic MO in patients with EOC. MO/MA phenotype was compared with MO in peripheral blood by two- and three-color flow cytometry. Cytotoxic/cytostatic effects of different cytokines on cultured EOC cells were measured by initial labeling or uptake inhibition of [methyl-3H] thymidine. Malignant ascites had higher proportion of MO/MA with the CD14brightCD16+ phenotype than peripheral blood. Cell surface antigen expression of activation and differentiation in peripheral blood and ascites, including CD38, CD40, CD64, and CD86, was higher on CD14brightCD16- and CD14brightCD16+ than on CD14dimCD16- cells. HLA-DR expression was higher on ascitic MO/MA than peripheral blood MO. Significant cytotoxic/cytostatic activity was elicited by treating ascitic MO/MA with interferon-gamma (IFN-gamma) and interleukin-2 (IL-2), but not with interleukin-12, paclitaxel, granulocyte-monocyte colony-stimulating factor (GM-CSF), or tumor necrosis factor-alpha (TNF-alpha). Soluble CD40Lt did not enhance MO/MA cytotoxic activity, and inhibited IFN-gamma or IL-2 induced cytoxicity. We conclude that MO/MA from ascites have elevated proportions of CD14brightCD16+ cells, showing phenotypic features of activation. IFN-gamma induces the cytotoxic and cytostatic activity of MO/MA that is inhibited by CD40Lt.

Adult↗

[A rare cause of malignant ascites--peritoneal mesothelioma].

HISTORY AND CLINICAL FINDINGS: A 56-year-old patient (case 1) with recurrent haemorrhagic ascites for one year was admitted to our hospital for further investigation. Besides massive ascites he did not show abnormal physical signs. In addition, two 45-year-old patients were admitted (case 2 and 3) with clinical signs of acute abdomen--one having muscular guarding in the epigastric angle, the other in the right lower quadrant. All 3 patients did not have serious illnesses in the past; the first 2 patients had occupational asbestos exposure. INVESTIGATIONS: In patient 1 the ultrasound did not reveal abnormal findings besides ascites. Patients 2 and 3 underwent explorative laparotomy. DIAGNOSIS, TREATMENT AND COURSE: In the first case a diagnostic laparoscopy revealed diffuse tumor proliferations with nodular formations over the entire peritoneum--histologically a malignant peritoneal mesothelioma of the epithelial subtype. Patient 2 showed intraoperatively metastatic spread of tumour formations with infiltration of the peritoneum and transverse mesocolon. The histologic finding was similar to that in the first case. Patient 3 had a perforated sigma diverticulitis which was treated by resection of the sigmoid. Incidentally a well differentiated papillary peritoneal mesothelioma was found in the resected specimen. The first two patients were treated with alpha-interferon subcutaneously resulting in a decrease of ascites production. Because patient 3 showed neither ascites nor evidence for malignancy no interferon was administered. CONCLUSION: In case of haemorrhagic ascites of unknown cause a histological clarification by either laparoscopy or laparotomy is mandatory. Immunomodulation with interferon may be a promising approach.

Antineoplastic Agents↗

Metabolic rate and its relationship with ascites in chicken genotypes.

1. Male chickens of 7 genetic lines, consisting of two pure sire and two pure dam populations, a commercial broiler cross and two slow-growing chicken lines (Label Rouge, LR and Mechelse Koekoek, MK) were reared from 1 to 37 d of age. The chickens received a two-phase dietary regime and were subjected to low ambient temperature. 2. The experimental aim was to investigate relationships between susceptibility to ascites and heat production. 3. Body weight gain (BWG), food intake and food conversion ratio (FCR) were determined. Ascites mortality, arterial pressure index (API=right ventricular/total ventricular weight ratio), haematocrit values, proportional lung weight (lung weight/body weight x 100), plasma thyroid hormones (thyroxine, T4 and triiodothyronine, T3) and arterial blood gas pressures (pCO2 and pO2) were determined. The heat production per kg metabolic body weight (H/W0.75) and total heat production (H) were calculated for the period 16 to 33 d using an energy balance study according to the comparative slaughter method. 4. The two breeder sire lines had high BWG and low FCR and high but different incidences of ascites compared with the slow-growing ascites resistant LR and MK lines with notable high FCR. The broiler cross and slower-growing breeder dam lines had a similar and relatively lower incidence of ascites mortality. 5. The fast-growing chickens had low H/W0.75 values compared with slow-growing lines. 6. These fast-growing breeder sires had lower plasma thyroid hormone, reduced proportional lung weights, low arterial pO2 and high arterial pCO2 pressures compared with the slower-growing lines. 7. In conclusion, ascites incidence was associated with lower heat production per metabolic body weight and therefore a lower oxygen requirement per metabolic weight.

Animals↗

Progressive bradycardia, a possible factor in the pathogenesis of ascites in fast growing broiler chickens raised at low altitude.

1. The first objective was to evaluate baseline heart rate (HR) responses in fast growing broilers fed ad libitum from 1 to 45d or subjected to a food restriction (85%, 70% and 55% of ad libitum from 7 to 21d) and a refeeding (22 to 45d) regimen in a normal thermal environment. The second was to evaluate HR and haematocrit responses in fast growing broilers reared at a low environmental temperature and fed ad libitum (A-L) from 1 to 42d, subjected to food restriction (70% ad libitum) between 7 to 21d and refed thereafter (R-R), or subjected to food restriction between 7 to 42d (R), and to follow the changes in normal birds and those prone to ascites. 2. The baseline HR in the normal thermal environment at 21 and 45d in birds fed ad libitum was lower (P < 0.001) than at 7d. The food-restricted groups had higher HRs at 21d than at 7d, with the differences significant (P < 0.01) for the 70% and 55% treatments. At 21d the HRs in restricted groups were significantly higher (P < 0.01) than in ad libitum-fed birds. After returning to ad libitum feeding the HRs in these birds tended to decline, with the differences significant (P < 0.05) for the 70% and 55% treatments. 3. In the birds exposed to cold, each feeding regimen produced distinct patterns of change in HR and haematocrit. Both feeding regimen and age had significant (P < 0.001) effects on the changes of both variables. Relative to 7d, on 14d and 21d the HRs decreased and haematocrits increased in all groups, but the rates of change were highest in the A-L and R-R birds. The first fulminant cases of ascites were observed during the third week in the A-L group and during the fourth week in the R-R group. None of the chickens from the R group developed ascites. Altogether, the incidence of ascites was 48% in the A-L group and 28% in the R-R group. 4. Among the birds exposed to cold, the ascitic birds had significantly (P < 0.001) lower HRs and higher haematocrits than normal birds from the same feeding regimen group. The time trends in the rates of change in HR and haematocrit were distinctly different (P < 0.001) for ascitic and normal birds. The change in feeding regimen from restricted to ad libitum in the R-R group resulted in a significant (P < 0.001) decrease in HR and increase in haematocrit. 5. In view of the evidence presented, it appears that hypoxaemia and tissue hypoxia in broiler chickens may be a result of circulatory insufficiency associated with progressive bradycardia rather than, as commonly believed, pulmonary insufficiency. In this situation the pulmonary hypertension may be a secondary symptom.

Analysis of Variance↗

Ascites fluid and plasma calprotectin concentrations in liver disease.

BACKGROUND: Calprotectin, a marker of neutrophil activation, has been associated with a poor prognosis in alcohol-induced cirrhosis. The aims were to study concentrations of calprotectin in patients with various liver diseases, and to further investigate the prognostic value of calprotectin in cirrhosis. METHODS: Plasma calprotectin concentrations were determined in 84 patients with alcohol-induced liver disease, 32 hepatitis B or C infected patients, 33 patients with liver disease of other aetiologies, 7 patients with combined aetiologies and in 24 patients with malignant disease. Thirty healthy individuals were included as controls. Ascites calprotectin concentrations were determined in patients with ascites (n = 75). Follow-up for survival was performed after a median observation period of 10 months. RESULTS: Increased plasma and ascites calprotectin concentrations were observed in malignant disease compared to non-malignant disease (P < 0.0001). Plasma calprotectin concentrations were low in viral liver disease compared to patients with non-viral liver disease (P = 0.02) and to controls (P = 0.0002). Plasma calprotectin (>median) was a highly significant marker of poor survival in alcohol-induced cirrhosis (P = 0.001), but was of no prognostic value in non-alcohol-induced cirrhosis (P = 0.88). In decompensated cirrhosis high (>upper quartile) ascites calprotectin concentrations were associated with an increased mortality (P = 0.002), as were high (>median) plasma calprotectin levels (P = 0.009). CONCLUSION: The prognostic importance of calprotectin in alcohol-induced cirrhosis is confirmed and demonstrated as specific for alcohol-induced liver disease. Low calprotectin levels are indicated in viral liver disease, and an association between high ascites calprotectin levels and malignant ascites was observed.

Ascitic Fluid↗

Intestinal permeability in cirrhotic patients with and without ascites.

OBJECTIVE: It has been suggested that increased intestinal permeability plays a pathogenic role in bacterial infections, such as spontaneous bacterial peritonitis, in patients with liver cirrhosis. The aim of this study was to assess whether intestinal permeability is altered in cirrhotic patients with and without ascites. MATERIAL AND METHODS: Intestinal permeability was assessed by a (51)Cr-EDTA permeability test in 20 cirrhotic patients (10 with and 10 without ascites) along with 20 age- and gender-matched healthy controls. In six patients with ascites, the test was performed before and after therapeutic paracentesis. RESULTS: The median (IQR) 24-h urinary excretion of (51)Cr-EDTA was higher in patients with cirrhosis (1.94% (1.21-2.70%)) compared with that in controls (1.40% (1.09-1.99%); p<0.05). Patients with (2.05% (1.50-3.46%); p<0.05) but not those without ascites (1.94% (1.13-2.53%); p>0.1) had significantly higher excretion values compared with those of controls. Only one patient without ascites and a total of four patients with ascites had increased intestinal permeability ((51)Cr-EDTA excretion > 95% confidence than that of controls; p>0.1). Paracentesis did not affect urinary (51)Cr-EDTA excretion significantly (1.69% (1.16-2.86%) versus 1.30% (1.08-1.79%) before and after, respectively; p>0.1). No significant correlation was found between clinical severity scores for liver disease and intestinal permeability. CONCLUSIONS: Only a small proportion of patients with liver cirrhosis have increased intestinal permeability and it is unlikely that this plays any major role in predisposing these patients to infections.

Adult↗

An ascites tumor appearing during the passage of Eperythrozoon coccoides in mice.

A strain of Eperythrozoon coccoides was maintained in a pure state for 16 months in unsplenectomized Princeton mice by the intraperitoneal injection of parasitized blood, at intervals of 1 to 3 weeks. In the 39th passage three out of five mice developed marked ascites with innumerable neoplastic cells in the peritoneal fluid. By passage of this fluid the tumor cells and the eperythrozoon were transferred together, with the rapid development of ascites and early death of the animals. On continued passage of ascitic fluid and blood from the mice of the 39th successive group both the tumor and the eperythrozoon were ultimately obtained in a pure state. Development of the passaged tumor was uninfluenced by the eperythrozoon but growth of the latter appeared enhanced in the presence of the neoplastic cells. Throughout 50 passages in mice the ascites tumor has not altered in character. The intraperitoneal injection of ascitic fluid was irregularly followed by the appearance of tumor cells in the blood, the rate of the carriage being 26 per cent in sixty-five animals. The subcutaneous and intramuscular injection of the fluid resulted in solid, highly invasive, local growths which did not metastasize. The solid growths proved transferable in series yet after 20 passages still produced the ascites tumor on intraperitoneal injection of their cells.

Animals↗

The opacity of portal hypertension-related ascites correlates with the fluid's triglyceride concentration.

To determine if an elevated triglyceride concentration can explain the opacity of some cirrhotic ascites specimens, the authors measured triglyceride concentration by Coulter DACOS (Hialeah, FL) on 133 paired serum and ascitic fluid specimens. The specimens were categorized as clear or cloudy by coded visual inspection. In addition, the ascitic fluid specimens were inspected for a lipid supernatant after 48 hours of refrigeration at 4 degrees C. The ascitic fluid triglyceride concentration of the 87 clear specimens was 1.9 +/- 1.0 mmol/L compared with 7.0 +/- 4.6 mmol/L for the opalescent specimens (P less than 0.001). Only 17% of the clear specimens demonstrated any lipid layer after refrigeration, compared with 94% of opalescent specimens (P less than 0.001). The triglyceride concentrations were not significantly different between the serum samples obtained from patients with clear compared with opalescent ascites. The opacity of portal hypertension-related ascites appears to be related to the triglyceride concentration of the fluid.

Ascites↗