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J C Hoefs

Publications and source records attributed to J C Hoefs.

At least 37 records · Page 2Linked to original sources
PubMed1986

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↗
PubMed1986

Peritoneal lymphomatosis with ascites. A characterization.

Three patients had autopsy-proved peritoneal lymphomatosis with ascites. Ascitic fluid analysis was characteristic in that the total protein level was greater than 2.5 g/dL, the lactate dehydrogenase level was greater than 225 mU/mL (the upper limit of normal for serum), and the glucose level was less than 50 mg/dL in all patients. Atypical cells were noted on ascitic fluid cytologic studies, and peritoneoscopic biopsy specimens were diagnostic of lymphoma in all three cases. Gut ulceration was present in all patients; a gastric ulcer, a duodenal ulcer, and a colonic ulcer were found to have invasion by lymphoma at autopsy. No patient lived long enough to receive chemotherapy. Perhaps if the diagnosis of lymphoma could have been made earlier, their lives could have been prolonged.

Ascites↗
PubMed1985

Spontaneous bacterial peritonitis.

Spontaneous bacterial peritonitis is an infection of the ascitic fluid of patients who, in general, have severe chronic liver disease. Several variants of this disease exist including bacterascites, culture-negative neutrocytic ascites, and secondary bacterial peritonitis. Spontaneous bacterial peritonitis is frequently manifested by signs and symptoms of peritonitis although the findings may be subtle; however, occasionally it may be completely without clinical manifestation. The clinician must have a high index of suspicion in order to make this diagnosis at a relatively earlier stage of infection. An abdominal paracentesis is required to make the diagnosis of spontaneous bacterial peritonitis. This paracentesis should be performed on all patients who are admitted to the hospital for ascites and should be repeated if there is any manifestation of bacterial infection during the hospitalization. Patients with severe intrahepatic shunting--as manifested by marked redistribution of activity from the liver to the spleen and to the bone marrow on liver-spleen scan as well as patients with an ascitic fluid total protein concentration of less than 1 g/dl--appear to be particularly susceptible to bacterial infection of their ascites. In order to optimize the yield of ascitic fluid culture, it is probably appropriate to inject blood culture bottles with ascites at the bedside immediately after the abdominal paracentesis. The mortality of spontaneous bacterial peritonitis continues to be very high. Perhaps routine admission paracentesis and prompt empiric antibiotic therapy with a third-generation cephalosporin will decrease the mortality of this infection if the Gram stain of the ascitic fluid demonstrates bacteria or the ascitic fluid neutrophil count is greater than 250 cells/cu mm. Repeating the paracentesis after 48 hours of treatment to reculture the fluid and reassess the ascitic fluid neutrophil count appears to be the best way to assess efficacy of treatment. After 48 hours of treatment the ascitic fluid neutrophil count should be less than 50% of the original value if the antimicrobial therapy is appropriate. The optimal duration of antibiotic treatment is unknown; however, until controlled trials provide data regarding duration of treatment it is appropriate to treat with parenteral antibiotics for 10 to 14 days. Research is also needed to determine if there are measures which can be taken to prevent the development of spontaneous peritonitis.

Adolescent↗
PubMed1984

Mechanism for the abnormal liver scan in acute alcoholic liver injury.

The mechanism of liver scan abnormality was investigated in patients with acute alcoholic liver injury evaluated shortly after admission (18 patients) with repeat examination 1 month later (14 patients). Indocyanine green (ICG) and Tc99 sulfur colloid extraction ratios (ERICG and ERSC), elimination rate constants (KICG and KSC), total body clearance (TBCICG and TBCSC), and hepatic clearance of sulfur colloid (HCSC) were determined from sequential blood samples obtained at the time of hepatic vein catheterization after the intravenous injection of ICG and Tc99 sulfur colloid. Liver size and sulfur colloid redistribution expressed as a scan score (SS) and redistribution ratio (RR) were assessed from an external scan immediately after the procedure. Improvement in hepatic tests and function was noted between the first and second study. At both the first and second study, the SS (or RR) correlated with the hepatic removal of sulfur colloid (ERSC; r = -0.59; p less than 0.001; HCSC: r = -0.56; p = 0.003) and ICG (ERICG: r = -0.85; p less than 0.001; KICG: r = -0.83; p less than 0.001). ERSC correlated with ERICG (r = 0.76; p less than 0.007) and both correlated with SS and RR consistent with intrahepatic shunting as the mechanism of decreased hepatic clearance and of sulfur colloid redistribution. However, the systemic clearance of sulfur colloid (KSC) did not correlate with redistribution (SS: r = -0.25; NS) at either study period or to ICG clearance (r = 0.23; p = NS) in the first period. The KSC/KICG ratio in both study periods correlated with serum bilirubin (r = 0.83; p less than 0.001 and r = 0.73; p less than 0.001), but was significantly higher in the first period (3.37 +/- 2.37 versus 2.00 +/- 0.75; p less than 0.01). This lack of correlation between intrahepatic shunting and systemic clearance of sulfur colloid is consistent with an increase in the nonhepatic clearance of sulfur colloid in patients with alcoholic liver injury and deep jaundice. A decrease in liver size between the first and second study correlated inversely with change in portal pressure (r = -0.67; p = 0.004) and SS (r = -0.49; p = 0.038) and directly with change in KICG (r = 0.48; p = 0.04). By virtue of these relationships, redistribution of Tc99 sulfur colloid by liver scan may have prognostic significance in patients with alcoholic liver disease.

Acute Disease↗
PubMed1984

A new method for the measurement of intrahepatic shunts.

After transhepatic portal pressure determination, 96 patients were assessed for the presence of intrahepatic shunts by injection of microspheres (25 +/- 5 micron diameter) into the portal vein using RISA-131I as an indicator of dilution. Multiple portal vein injections in each patient allowed blood sampling from the hepatic vein (site 1) and from two inferior vena cava sampling sites (site 2, at the junction of the hepatic vein orifice with the inferior vena cava, and site 3, 2 to 3 cm closer to or within the right atrium). Intrahepatic shunting was calculated from each site: hepatic vein in 57 patients and inferior vena cava, site 2 in 43 patients and site 3 in 77 patients. At least one valid IHS calculation was available in 92 of the patients. Intrahepatic shunting calculated from sequential portal vein injections with sampling from the hepatic vein was highly correlated (r = 0.98, p less than 0.0001, slope = 1.0), with a mean difference of 1.9% +/- 1.9%. There was no significant difference by t test comparison of the mean IHS calculated from sites 1, 2, and 3. The IHShv was correlated with the IHSivc (site 2) (r = 0.79, p less than 0.0001, slope = 1.0) and IHSivc (site 3) (r = 0.82, p less than 0.0001, slope = 2.1). Occasional marked discrepancies were noted between IHS calculated from site 1 or site 2 compared with site 3, and the site 3 calculation was always greater. A shunt index in all patients included shunts calculated from the hepatic vein in 57 patients plus shunt calculation from the inferior vena cava in the remaining patients (site 2 in 26 patients and site 3 in nine). A control group with minimal chronic liver disease (10 patients) had a portal pressure (greater than IVC) of 4.1 +/- 1.4 mm Hg and shunt index of 0.5% +/- 0.6%. The 82 patients with portal hypertension or chronic liver disease had a higher portal pressure, 13.8 +/- 4.6 mm Hg, and a significantly greater shunt index, 13.7% +/- 24.5% (p less than 0.0001) compared with controls. The frequency distribution of IHS in patients with chronic liver disease demonstrated less than 2% IHS in 49% of patients and less than 5% IHS in 63%. The validity of our methods and the implications of the infrequent demonstration of a large IHS are discussed.

Hepatic Veins↗
PubMed1983

Serum-ascites albumin concentration gradient: a physiologic approach to the differential diagnosis of ascites.

Serum-ascites albumin concentration gradient, a parameter of oncotic pressure gradient reflecting presence or absence of portal hypertension, was compared with the usual parameters of ascitic fluid analysis in the differential diagnosis of ascites. Twenty-nine patients with liver disease and 15 patients with malignant neoplasm were prospectively studied. The group with malignant neoplasm showed higher ascitic fluid total protein level (3.70 +/- 1.28 vs. 1.66 +/- 1.20 g/dl), ascites to serum ratio of total protein level (0.58 +/- 0.14 vs. 0.26 +/- 0.14), ascitic fluid lactic dehydrogenase level (756 +/- 693 vs. 151 +/- 125 U/L), ascites to serum ratio of lactic dehydrogenase level (1.13 +/- 0.79 vs. 0.35 +/- 0.22), and lower serum-ascites albumin gradient (0.72 +/- 0.30 vs. 1.85 +/- 0.45) (p less than 0.001 for all parameters). Results of the serum-ascites albumin gradient overlapped the least between the two groups: all but 1 patient with malignant ascites while only 1 patient with liver disease had a gradient lower than 1.1. We conclude that the serum-ascites albumin gradient offers the best diagnostic discrimination between ascites caused by liver disease and ascites caused by a neoplasm.

Ascites↗
PubMed1983

Serum protein concentration and portal pressure determine the ascitic fluid protein concentration in patients with chronic liver disease.

UNLABELLED: The ascitic fluid and serum concentrations of albumin and globulin were measured simultaneously with transhepatic portal pressure determination in 56 patients with chronic liver disease to determine whether (1) portal pressure correlated with (S-Asc)A and (2) the majority of variation in ascitic fluid protein concentration between patients was related to fluid balance from serum to ascites. The mean ascitic fluid albumin concentration was 1.04 +/- 0.73 gm/dl; globulin concentration 1.31 +/- 0.80 gm/dl; and ascitic fluid total protein concentration 2.35 +/- 1.49 gm/dl. The mean serum albumin concentration was 2.58 +/- .57 gm/dl; globulin concentration 3.91 +/- .86 gm/dl; and total protein concentration 6.49 +/- 1.30 gm/dl. The (S-Asc)A was 1.54 +/- .45 gm/dl. The mean PPIVC was 14.5 +/- 4.3 mm Hg. The (S-Asc)A correlated directly with PPIVC (r = 0.73; p less than 0.0001). The ascitic fluid protein correlated with three variables that did not correlate with each other: serum albumin (r = 0.67; p less than 0.0001), serum globulin (r = 0.44; p less than 0.001), and PPIVC (r = -0.48; p less than 0.0005). The sum of the squared correlation coefficients with these latter uncorrelated variables equaled 0.87 and partial correlation coefficient analyses demonstrated an increase in the correlation of the ascitic fluid protein with the serum albumin concentration when corrected for serum globulin and (S-Asc)A (r = 0.97; p less than 0.0001) or PPIVC (r = 0.90; p less than 0.0001). Thus most of the variation in ascitic fluid protein between patients in this study could be related to serum protein concentrations and PPIVC or (S-Asc)A. Furthermore, multivariate discriminant analysis of patients with an ascitic fluid protein less than or equal to 2.5 vs. greater than 2.5 gm/dl indicated that the majority of differences between the two groups could be attributed to differences in serum albumin and serum globulin in combination with the (S-Asc)A (canonical correlation = 0.808) or PPIVC (canonical correlation = 0.806). These factors could correctly identify the low or high ascitic fluid protein groups in 96% and 93% of patients, respectively. IN CONCLUSION: (1) the (S-Asc)A is associated with the degree of portal pressure elevation and (2) the majority of variation in ascitic fluid protein concentration between patients with chronic liver disease is associated with differences in portal pressure and serum protein concentrations.

Analysis of Variance↗
PubMed1981

Immune complexes and cryoproteins in ascitic fluid of patients with alcoholic liver disease.

27 paired specimens of ascitic fluid and serum obtained from patients with alcoholic liver disease were tested for cryoproteins and immune complexes by the C1q binding assay. 20 sera (74%) and ten ascitic fluid (37%) had significant amounts of cryoproteins. The cryoproteins were of the 'mixed' type of cryoglobulins consisting of IgG, IgM, IgA, C3 and C1q. The C1q binding test was positive in 17 sera (63%) and in 16 ascitic fluid (59%). Intracytoplasmic inclusions of immunoglobulin and complement were found within the ascitic fluid leukocytes by direct immunofluorescence. The presence of immune complexes in the ascitic fluid may be important in the reduction of the complement level of cirrhotic ascitic fluid.

Antibodies↗
PubMed1981

Renal kallikrein excretion in alcoholic cirrhosis. Relationship to other vasoactive systems.

Severe liver disease is often associated with renal hemodynamic changes, and these changes may involve vasoactive hormones. The vasodilatory renal kallikrein-kinin system has received little previous study in these patients. We measured urinary kallikrein in nine patients with alcoholic cirrhosis under rigid metabolic conditions and simultaneously evaluated renin, aldosterone and urinary prostaglandins. Plasma renin and aldosterone were generally increased as expected but urinary kallikrein was surprisingly diminished (13.3 +/- 3.7 vs. 38.8 +/- 11.1 SE, E.U./day, P less than 0.05), despite adequate creatinine clearance (81 +/- 9 ml./min.). Administration of prostaglandin inhibitors reduced urinary prostaglandin E by 72% and creatinine clearance by 56% but did not alter urinary kallikrein. Mineralocorticoid inhibition by spironolactone induced a natriuresis in four patients with ascites (from 1.4-140 mEq.Na+/day) but also failed to alter kallikrein. Thus, kallikrein excretion is paradoxically reduced and seemingly unresponsive to alterations in the prostaglandin and renin-aldosterone systems. If urinary kallikrein quantitatively reflects intrarenal kallikrein-kinin activity, the impairment in this vasodilatory system may mediate the altered renal hemodynamics of severe liver disease.

Adult↗
PubMed1981

Ascites.

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Ascites↗
PubMed1981

The mechanism of ascitic fluid protein concentration increase during diuresis in patients with chronic liver disease.

The mechanism of increase in the protein concentration of ascitic fluid during diuresis was investigated in 27 patients with chronic liver disease. The albumin concentration increased in ascites from .58 +/- .49 gm.% in the initial paracentesis to 1.48 +/- .69 gm.% in the final paracentesis (P less than .001) as the serum albumin concentration increased from 2.40 +/- .44 gm.% 2.94 +/- .56 gm.% (P less than .001). The serum to ascites albumin concentration gradient decreased significantly from 1.82 +/- .39 gm.%-1.46 +/- .45 gm.% (P less than .001). Despite this decrease, the serum to ascites albumin concentration gradient was relatively constant (decrease of .36 gm.% or 20% of initial value) compared to either the absolute or percentage change in ascites total protein concentration (increase of 1.48 gm.% or 107% of initial value). In four patients studied prospectively, the plasma volume did not change (3.53 +/- .80 1.-3.73 +/- .59 1.) during diuresis, despite increase in total intravascular albumin (85.7 +/- 25.6 gm.-99.9 +/- 22.3 gm.; P less than .05) and decrease in total albumin in combined intravascular and peritoneal compartments (156.0 +/- 30.1 gm.-143.4 +/- 35.3 gm.; P less than .05). Since neither concentration without decrease in plasma volume or synthesis of protein without increase in total compartmental protein appear to be the major mechanism of serum protein concentration increase, the increase in serum protein concentration was attributed to redistribution of protein from ascites to the intravascular compartment. The increase in ascitic fluid protein concentration during diuresis can be attributed to an increase in serum protein concentration in the presence of the relatively stable serum to ascites albumin concentration gradient.

Ascitic Fluid↗
PubMed1980

Hepatitis B surface antigen in pancreatic and biliary secretions.

Pure pancreatic juice (PPJ) and pure bile (PBJ) were obtained by endoscopic retrograde cannulation of the pancreatic duct and common bile duct in 26 patients with acute (15) and chronic (11) hepatitis B infections and the specimens were tested for HBsAg. HBsAg was detected in PPJ in 8 of 15 patients with acute infections and 3 of 10 with chronic infections. HBsAg was detected in PBJ in 7 of 10 with acute infections and only 2 of 5 with chronic type B infection. Since normal PPJ was shown to be inhibitory to the detection of HBsAg, it is suggested that the HBsAg-positive PPJ represents heavy viral excretion.

Adult↗
PubMed1979

Prostaglandins: modulators of renal function and pressor resistance in chronic liver disease.

Prostaglandins may modulate renal function and play a role in the hyperreninism and angiotensin pressor resistance of chronic liver disease. To study this possibility, we evaluated 12 patients with alcoholic cirrhosis and ascites. Urine immunoassayable prostaglandin E in 5 female patients was 3.3 +/- 0.5 micrograms/day [normal, 0.3 +/- 0.1 (SE)], renin was 14.6 +/- 3.7 ng/ml.h, and aldosterone was 76 +/- 19 ng/dl. After either indomethacin (200 mg) or ibuprofen (2000 mg) for 1 day, urine immunoassayable prostaglandin E fell to 0.8 +/- 0.4 micrograms/day, renin to 8.0 +/- 2.4 ng/mol.h, and aldosterone to 54 +/- 14 ng/dl (all P less than 0.01). Pressor sensitivity increased dramatically, and creatinine clearance transiently fell from 73 +/- 10 to 32 +/- 7 cc/min (P less than 0.01). Because a primary effect on renin might explain the renal impairment, an additional study used propranolol to lower renin activity. Renal function was unaltered by propranolol. We conclude that prostaglandins play a supportive role in maintaining renal function and are involved in the hyperreninism and pressor resistance of patients with liver disease.

Adult↗
PubMedDate not supplied

Increase in ascites white blood cell and protein concentrations during diuresis in patients with chronic liver disease.

Serum and ascites protein concentration and ascites cell concentration alterations with determined serially during diuresis in 27 patients with uncomplicated liver disease. The total protein concentration in ascites increased from 1.38 +/- 0.96 gm% to 2.86 +/- 1.28 gm% (p less than 0.001); the serum protein concentration from 6.26 +/- 0.81 gm% to 7.24 +/- 0.93 gm% (p less than 0.001), and the ascites to serum ratio of the total protein concentration from 0.21 +/- 0.13 to 0.38 +/- 0.14 (p less than 0.001). The white blood cell (WBC) concentration in ascites increased from 289 +/- 179 cells per mm3 to 1,108 +/- 924 cells per mm3 (p less than 0.001). Despite the increase in WBC concentration, the polymorphonuclear cell concentration remained constant (42 +/- 52 cells per mm3 to 68 +/- 96 cells per mm3). Protein concentration of the ascitic fluid greater than 3.0 gm% was demonstrated in 12 patients before completion of diuresis and ascitic fluid WBC concentration was greater than 750 cells per mm3 in 17 patients. Ten of 27 patients eventually developed ascites which had a combination of more than 3.0 gm% total protein concentration and greater than 750 cells per mm3. Ascitic fluid protein and WBC concentrations are not "fixed" at a low level in chronic liver disease since each rose during diuresis. Thus, the interpretation of these parameters must be made with caution in patients following significant diuresis.

Ascitic Fluid↗
PubMedDate not supplied

Spontaneous bacterial peritonitis.

Forty-three patients with spontaneous bacterial peritonitis (SBP) between 1973 and 1978 were identified. Criteria for SBP included a positive ascites culture and polymorphonuclear cell concentration greater than 250 cells per mm3. Chronic liver disease was documented by varices in 91%, severe histologic fibrosis or cirrhosis in 94%, splenomegaly in 91%, and past hospitalization for liver disease in 57% of the patients. SBP was detected within 7 days of admission in 17 patients (40%) and within 35 days in 38 patients. Single organisms were isolated from 38 patients and multiple organisms from 5 patients. Twenty-six of 43 patients survived the episode of SBP, but only 13 survived the hospitalization. Analysis of the survival curve from the onset of SBP revealed a rapid death rate and a slow death rate set of patients. Rapid death (less than or equal to 7 days from SBP onset) correlated with a lack of prior hospitalization for liver disease (p less than 0.001), hepatomegaly (p less than 0.001), increased serum bilirubin (p less than 0.005), serum creatinine (p less than 0.05), and peripheral white blood cell concentrations (p less than 0.05). Survival during hospitalization was associated with prior hospitalization with liver disease (p less than 0.001) and chills during the episode of SBP (p less than 0.001). The 43 patients were divided into Group 1 patients on the basis of a serum bilirubin greater than 8 mg% and/or serum creatinine greater than 2.1 mg%; Group 2 patients had lower values. Survival was greater in Group 2 patients with advanced, relatively quiescent liver disease compared to Group 1 patients for both the episode of SBP (91 vs. 29%; p less than 0.001) and for hospitalization (50 vs. 9%; p less than 0.05). Death in Group 2 patients was related to inadequate antibiotic therapy (p less than 0.05), nonhepatic factors, and new onset of renal failure. Although SBP in the setting of severe acute liver injury has a dismal prognosis, SBP with minimal acute liver injury has a relatively good prognosis for hospital survival even with advanced chronic liver disease. Long-term survival is also possible since 4 of 9 patients with prolonged follow-up have survived 3 years.

Anti-Bacterial Agents↗