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J C Hoefs

Publications and source records attributed to J C Hoefs.

At least 19 recordsLinked to original sources
PubMed1995

The liver-spleen scan as a quantitative liver function test: correlation with liver severity at peritoneoscopy.

Sulfur colloid distribution on liver-spleen scan is determined by the perfused Kupffer cell mass. The perfused Kupffer cell mass is proportional to the perfused hepatocyte mass, but is less affected by acute changes in hepatocyte function. Thus, sulfur colloid distribution parameters (precisely measured by quantitative liver-spleen scan [QLSS]) may be an excellent test of the perfused hepatic mass. Although no gold standard exists for confirmation, a close correlation should exist between liver disease severity assessed at peritoneoscopy and sulfur colloid distribution. Peritoneoscopy severity (scored as total peritoneoscopy score [PS]; range, 0-5) was assessed in 76 patients who also had QLSS. Multivariate equation were generated to estimate liver disease severity from the QLSS. These were then applied prospectively in 20 consecutive patients to validate these equations. In 76 patients, 62 were evaluated because of chronic liver disease (CLD) and included those with micronodular (20) and macronodular (20) cirrhosis with various degrees of severity (Child's A, 16; B, 29; C, 17). Multivariate analysis yielded a number of combinations of QLSS parameters that correlated with peritoneoscopic severity. These equations were used to estimate liver disease severity. Estimates of liver disease severity (estimated PS [EPS]) correlated well with the PS in these 76 patients (r = .9064; r2 = .8216; P < .0001). Adding histological fibrosis to the QLSS parameters yields an equation for estimating PS that was even more effective (r = .9462; r2 = .8953; P < .001). However, validation of multivariate equations requires confirmation of their value in a second population.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Raising the dose of interferon does not improve the response in chronic hepatitis C.

We report results of dose escalation to 5 or 6 million units (MU) three times weekly (t.i.w.) of interferon-alpha in 17 consecutive patients with chronic active hepatitis C who were not responding to 3 MU t.i.w. after > or = 12 weeks of therapy. The mean pretreatment alanine aminotransferase (ALT) level was 206 +/- 62 U/L and, at the time of dose escalation, 113 +/- 71 U/L. Two patients could not tolerate the dose escalation. The remaining 15 patients were treated for an additional 10 +/- 3.5 weeks. Three patients had a complete response 3-8 weeks after dose escalation. At the end of high-dose therapy, the mean ALT level was 105 +/- 76 U/L (n = 15). During the 6-month posttreatment follow-up time, the mean ALT level was 147 +/- 85 U/L. All three responders had a relapse. Increasing the dose of interferon-alpha to 5-6 MU t.i.w. in chronic hepatitis C patients who are not responding to interferon-alpha, 3 MU t.i.w., at the 12th week of therapy is unlikely to result in sustained normalization of ALT levels.

Adult↗
PubMed1992

Globulin correction of the albumin gradient: correlation with measured serum to ascites colloid osmotic pressure gradients.

The albumin difference or gradient between serum ascites is presumed to be an effective estimate of the colloid osmotic pressure gradient, although this has never been directly demonstrated. The colloid osmotic pressure gradient is controlled by the degree of portal hypertension. Thus the albumin gradient is clinically useful in detecting patients with ascites caused by portal hypertension, although some overlap in such patients' albumin gradients exists compared with those of patients without portal hypertension. Part of this overlap is related to the inverse correlation of the albumin gradient with serum globulin; globulins also contribute to colloid osmotic pressure. The ability to calculate colloid osmotic pressure in serum and ascites with albumin and globulin concentration or to correct the albumin gradient for the impact of globulins might improve the clinical usefulness of the ascitic fluid analysis in determining the presence of portal hypertension in ascitic patients with borderline albumin gradients. Thus we developed equations to calculate colloid osmotic pressure from multivariate discriminate analyses of albumin and globulin concentrations in serial dilution samples of pooled serum and subsequently validated these equations, along with older methods of calculating colloid osmotic pressure. In an initial set of dilution experiments, globulin concentration was closely correlated with the colloid osmotic pressure to albumin concentration ratio (r = 0.956; p less than 0.001). Multivariate discriminate analysis yielded an equation for calculating colloid osmotic pressure from albumin (A) and globulin (G) concentration with a ratio of colloid osmotic pressure to albumin (calculated colloid osmotic pressure = A(1.058G + 0.163A + 3.11) and two other equations.(ABSTRACT TRUNCATED AT 250 WORDS)

Ascitic Fluid↗
PubMed1990

Diagnostic paracentesis. A potent clinical tool.

Diagnostic paracentesis is a potent diagnostic tool capable of rapidly detecting portal hypertension and peritonitis. Gram's stain and chemical analysis of ascitic fluid add additional information by determining the predisposition to SBP, the presence of organisms, and the severity of peritonitis. In patients with a narrow A-GRAD, the chemical analysis, cell count and differential, and cytology will add direction for the work-up if the etiology is not apparent and confirmation if it is. This information should be available within a few hours of admission if the paracentesis and blood are obtained immediately. The results should optimize patient care and minimize costs.

Ascitic Fluid↗
PubMed1990

Diagnosis and hemodynamic assessment of portal hypertension.

Rational treatment of portal hypertensive complications requires a knowledge of the cause of portal hypertension and an assessment of the severity of liver disease. In the United States, chronic liver disease, usually due to alcohol, is the most common underlying cause. The history, physical examination, and laboratory analysis are usually sufficient to confirm the presence of underlying liver disease. If there is any question as to the etiology of portal hypertension, however, a more complete evaluation is required, whether the presenting complication is ascites, variceal bleeding, or hypersplenism. Usually, such an evaluation will require a liver biopsy, portal pressure measurement, and angiography. Occasionally, a noninvasive evaluation will be sufficient, but the value of these noninvasive parameters is still under investigation. Surgical mortality generally depends on the severity of the liver disease. Therefore, surgical intervention must be carefully considered in comparison to other therapeutic modalities depending on the patient's hepatic functional reserve. Secondary bacterial peritonitis due to perforation requires surgery regardless of the severity of the underlying liver disease.

Esophageal and Gastric Varices↗
PubMed1989

Measurement of portal shunting in dogs.

A new method for measuring the quantity of portal blood bypassing the liver (shunted) has been developed and tested in the dog. Shunts were mimicked by the simultaneous infusion of glycocholic acid into a small peripheral portal venule and a peripheral vein. The total infused amount was kept constant, but the ratio at the two infusion sites varied. Determination of the extraction efficiency of the liver by simultaneously measuring the hepatic vein and arterial blood for systemically infused [14C]glycocholic acid permitted the calculation of shunted blood from information provided by the concentration of glycocholic acid in the hepatic vein, artery, and portal vein blood. This method was tested for various proportion of shunting from none to complete. The total hepatic flow was determined with single injection of indocyanine green and the individual arterial and portal vein flows determined with flowmeters. The input ratios of shunting related quite closely to that calculated from the flowmeters or the hepatic extraction ratio.

Animals↗
PubMed1986

Polymicrobial bacterascites. A unique entity in the spectrum of infected ascitic fluid.

A retrospective analysis of 1578 abdominal paracenteses revealed ten cases of polymicrobial bacterascites, ie, growth of multiple organisms in ascitic fluid with a neutrophil count less than 250 cells/cu mm. Six of the ten paracenteses that documented this condition were traumatic (bloody or producing feculent material). Clinical peritonitis developed in only one patient. No one died as a result of the infection. Polymicrobial bacterascites is rare (0.6% of paracenteses). It is frequently due to a traumatic paracentesis (bowel entry by the paracentesis needle), and is associated with low morbidity.

Ascitic Fluid↗
PubMed1986

Spontaneous vs secondary bacterial peritonitis. Differentiation by response of ascitic fluid neutrophil count to antimicrobial therapy.

A retrospective chart review revealed 24 patients who had at least one subsequent ascitic fluid neutrophil count within 14 days of the ascitic fluid analysis that was diagnostic of spontaneous bacterial peritonitis. The neutrophil count decreased (after antibiotic therapy was started) at an exponential rate, with a half-life of 34 +/- 35 hours. In none of four episodes of secondary bacterial peritonitis was there an exponential decline in neutrophil count after antimicrobial therapy was initiated. In fact, the first follow-up neutrophil count was greater than the baseline value in all four episodes. The response pattern of the ascitic fluid neutrophil count to antimicrobial therapy is helpful in differentiating spontaneous from secondary bacterial peritonitis.

Anti-Bacterial Agents↗
PubMed1986

Noninvasive evaluation of hepatic fibrosis using frequency demodulation of ultrasound signals.

A new ultrasound image can be produced by frequency demodulation (FM) of the conventional ultrasound signal. This new FM image appeared to produce a more accurate representation of the fine structure of the liver. The individual features of the FM image were correlated with hepatic portal fibrosis and cirrhosis on liver biopsy in 34 patients with minimal hepatic fat and sinusoidal collagen. An overall ultrasound score correlated with portal fibrosis (r = 0.788; P less than 0.001). We conclude that the FM image may be helpful in measuring and following the progression of hepatic fibrosis in patients with chronic liver disease.

Biopsy↗
PubMed1986

Estimation of acoustic attenuation in liver using one megabyte of data and the zero-crossings technique.

Statistical fluctuations due to scatter-induced frequency variations in reflected acoustic pulses are a major problem when estimating acoustic attenuation. Disagreement exists in the ultrasound community as to how much data is sufficient to overcome these statistical fluctuations. The range of attenuation values for normal livers and a tissue equivalent phantom, using 1 megabyte of data per liver and the zero-crossings technique, was investigated. The significance of statistical fluctuations and their effects on attenuation are discussed.

Acoustics↗
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↗