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Biomedical subjects

J B Gross

Publications and source records attributed to J B Gross.

At least 19 recordsLinked to original sources
PubMed2005

Non-responders to previous treatment for hepatitis C.

The main principle in treating chronic hepatitis C is the prevention of serious liver complications. Because curing hepatitis C virus infection has been demonstrated to prevent progression of liver disease and even promote regression of fibrosis, it remains the primary goal of treatment. However, nearly half of patients are not cured with our best treatment. Patients who failed older therapies should be treated with peginterferon and ribavirin, but those with advanced fibrosis or African heritage will have very low rates of response. Non-responders to peginterferon and ribavirin present a special challenge. If there were problems related to dosing, adherence, or access during treatment, then one can consider re-treating with the same regimen if the problems can be corrected. Otherwise, non-responders with early-stage fibrosis can observe without further treatment until newer drugs are available. Those with advanced fibrosis should consider low-dose peginterferon maintenance treatment or participation in an experimental trial. Experimental approaches include intensification of existing therapies, combination of new agents with existing drugs, long-term virus suppression, inhibition of liver fibrogenesis, and inhibition of hepatitis C RNA or hepatitis C viral enzymes.

Antiviral Agents↗
PubMed2001

Outcome of hospital care of liver disease associated with hepatitis C in the United States.

We describe mortality and resource utilization for inpatient care of hepatitis C (HCV) in comparison to alcohol-induced liver disease (ALD) in the United States and identify factors that affect outcomes. The Healthcare Cost and Utilization Project database, a national inpatient sample was used to identify hospitalization records with diagnoses related to liver disease from HCV and ALD. Outcome of hospitalizations was analyzed in terms of in-hospital deaths and health care resource utilization. For 1995, we estimate that there were 26,700 hospitalizations and 2,600 deaths in acute, nonfederal hospitals in the United States for liver diseases caused by HCV. Total charges for these hospitalizations were $514 million. In comparison, ALD was associated with 101,200 hospitalizations, 13,400 deaths, and $1.8 billion in charges. Simultaneous HCV and alcohol abuse was associated with younger ages at the time of hospitalization and death compared with HCV or ALD alone. In a logistic regression analysis, alcohol abuse (odds ratio [OR], 1.4; 95% confidence interval [CI], 1.2-1.5) and human immunodeficiency virus (HIV) infection (OR, 4.5; 95% CI, 4.0-4.9) were associated with an increased risk of death among those with HCV. Liver transplantation and patient death were associated with the largest increase in hospitalization charges. Major complications of cirrhosis, such as variceal bleeding, encephalopathy, and hepatorenal syndrome, and sociodemographic factors, such as race and health insurance, were also significantly associated with the risk of death and hospitalization charges, which were similar in HCV and ALD. This study provides new estimates regarding the public health impact of HCV, for use in health policy decisions and cost-effectiveness analyses of preventive and therapeutic interventions.

Adult↗
PubMed2000

Hepatitis A antibodies in liver transplant recipients: evidence for loss of immunity posttransplantation.

Liver transplant recipients frequently have chronic liver diseases and should be considered for vaccination against hepatitis A virus (HAV). However, persistence of protective antibodies after orthotopic liver transplantation (OLT) has not been shown in this population, which may have implications for future vaccine recommendations. We evaluated the prevalence and epidemiological significance of immunoglobulin G (IgG) antibody to HAV (anti-HAV) in a nonvaccinated population before OLT (immunity from previous exposure) and determined the persistence of IgG anti-HAV at 1 and 2 years after OLT. One hundred consecutive patients were identified who underwent OLT and had at least 2 years of follow-up post-OLT. They were not vaccinated against HAV infection at any time. Clinical data were summarized from medical records, and stored sera were tested for IgG anti-HAV before OLT and at 1 and 2 years after OLT by a commercially available enzyme immunoassay. Of 100 patients, 24 had IgG anti-HAV before OLT. No epidemiological differences were noted between those with or without detectable IgG anti-HAV before OLT. Among patients with detectable IgG anti-HAV before OLT, 4 of 22 patients (18%) and 7 of 24 patients (29%) became negative for IgG anti-HAV at 1 and 2 years post-OLT, respectively. None of the patients with undetectable IgG anti-HAV before OLT became positive at any time. Most of our patients with end-stage liver disease had no serological evidence for immunity against HAV. A significant proportion of patients with detectable protective antibodies before OLT lost their antibodies at 2 years after OLT.

Adolescent↗
PubMed2000

The pharmacodynamic effect of a remifentanil bolus on ventilatory control.

BACKGROUND: In doses typically administered during conscious sedation, remifentanil may be associated with ventilatory depression. However, the time course of ventilatory depression after an initial dose of remifentanil has not been determined previously. METHODS: In eight healthy volunteers, the authors determined the time course of the ventilatory response to carbon dioxide using the dual isohypercapnic technique. Subjects breathed via mask from a to-and-fro circuit with variable carbon dioxide absorption, allowing the authors to maintain end-tidal pressure of carbon dioxide (PET(CO2)) at approximately 46 or 56 mm Hg (alternate subjects). After 6 min of equilibration, subjects received 0.5 microg/kg remifentanil over 5 s, and minute ventilation (V(E)) was recorded during the next 20 min. Two hours later, the study was repeated using the other carbon dioxide tension (56 or 46 mm Hg). The V(E) data were used to construct two-point carbon dioxide response curves at 30-s intervals after remifentanil administration. Using published pharmacokinetic values for remifentanil and the method of collapsing hysteresis loops, the authors estimated the effect-site equilibration rate constant (k(eo)), the effect-site concentration producing 50% respiratory depression (EC50), and the shape parameter of the concentration-response curve (gamma). RESULTS: The slope of the carbon dioxide response decreased from 0.99 [95% confidence limits 0.72 to 1.26] to a nadir of 0.27 l x min(-1) x mm Hg(-1) [-0.12 to 0.66] 2 min after remifentanil (P<0.001); within 5 min, it recovered to approximately 0.6 l x min(-1) x mm Hg(-1), and within 15 min of injection, slope returned to baseline. The computed ventilation at PET = 50 mm Hg (VE50) decreased from 12.9 [9.8 to 15.9] to 6.1 l/min [4.8 to 7.4] 2.5 min after remifentanil injection (P<0.001). This was caused primarily by a decrease in tidal volume rather than in respiratory rate. Estimated pharmacodynamic parameters based on computed mean values of VE50 included k(eo) = 0.24 min(-1) (T1/2 = 2.9 min), EC50 = 1.12 ng/ml, and gamma = 1.74. CONCLUSIONS: After administration of 0.5 microg/kg remifentanil, there was a decrease in slope and downward shift of the carbon dioxide ventilatory response curve. This reached its nadir approximately 2.5 min after injection, consistent with the computed onset half-time of 2.9 min. The onset of respiratory depression appears to be somewhat slower than previously reported for the onset of remifentanil-induced electroencephalographic slowing. Recovery of ventilatory drive after a small dose essentially was complete within 15 min.

Adult↗
PubMed2000

Multiport epidural catheters: does the air test work?

BACKGROUND: Multiport epidural catheters are popular; however, the reliability of the air test has not been evaluated with this catheter design. The authors determined the effectiveness of aspirating for blood and the air test in detecting intravascular multiorifice epidural catheters. METHODS: Three hundred women in labor underwent placement of a blunt-tip, three-hole, 20-gauge, lumbar epidural catheter. If there were no signs of spinal anesthesia, 3 ml lidocaine or bupivacaine was injected and the patient was observed for signs of spinal anesthesia. If there were no signs of spinal anesthesia, the authors injected 1 ml air through the epidural catheter while listening to the maternal precordium using a Doppler fetal heart rate monitor. Catheters through which blood was aspirated were air-tested and replaced. Patients with air-test-positive, blood-aspiration-negative catheters received 100 mg lidocaine through the catheter and were questioned about toxicity symptoms. The authors injected bupivacaine-fentanyl through aspiration-negative,air-test-negative catheters and recorded the sensory analgesic level 20 min later. RESULTS: The authors aspirated cerebrospinal fluid through one catheter and documented intravascular placement in 11 catheters. Results of the air test and blood aspiration were positive for eight catheters. Blood could not be aspirated from one air-test-positive catheter; perioral numbness developed in the patient after lidocaine injection. Blood was freely aspirated from two air-test-negative catheters. In the remaining 288 catheters, bupivacaine-fentanyl injection produced epidural analgesia in 279 patients and no effect in 9 patients. CONCLUSIONS: The authors obtained false-negative results with both catheter aspiration and the air test. Fractionating the local anesthetic dose is important when using multiorifice epidural catheters.

Adult↗
PubMed2000

Human leukocyte antigen DR markers as predictors of progression to liver transplantation in patients with chronic hepatitis C.

OBJECTIVE: Because many patients with chronic viral hepatitis do not progress to end-stage liver disease, it is possible that host factors such as human leukocyte antigen (HLA) differences are important. Our aims were to determine HLA marker-specific rates of progression to liver transplantation among patients with chronic hepatitis C; and to determine if polymerase chain reaction (PCR)-based HLA DRB1 typing can be performed on stored serum samples. METHODS: Forty-two hepatitis C virus RNA-positive liver transplant patients and 87 untransplanted patients were included in a Cox proportional hazards model to test whether the occurrence of certain HLA DRB1 markers were associated with progression to liver transplantation. HLA DRB1 typing was performed on stored serum samples using a PCR method. RESULTS: There were no differences among the HLA DRB1 markers with regard to the HLA marker-specific rate of progression to transplantation among patients with chronic hepatitis C. CONCLUSIONS: HLA DRB1 markers do not appear to be associated with progression of disease in chronic viral hepatitis C. It is possible to perform PCR-based HLA DRB1 typing on stored frozen serum samples.

Adult↗
PubMed1999

Unrecognized bulimia nervosa: a potential cause of perioperative cardiac dysrhythmias.

PURPOSE: To report serious cardiac dysrhythmias in two patients whose bulimia nervosa was not revealed during preoperative screening. CLINICAL REPORT: Case #1: A 25-yr-old woman with preoperative hypokalemia (K+ = 3.1 mEq x l(-1)) required anesthesia for removal of a wrist ganglion. She claimed the hypokalemia was of unknown etiology, and denied other medical problems. Shortly after induction of anesthesia with thiopental and isoflurane, the ECG revealed two runs of torsades de pointes. This was successfully treated by decreasing pulmonary ventilation, allowing P(ET)CO2 to increase from 32 to 45 mm Hg. Case #2: A 39-yr-old woman who denied any medical problems received propofol, rocuronium sevoflurane and N2O during general anesthesia for breast augmentation. In the PACU, the patient complained of light-headedness, and the ECG revealed a heart rate of 44 bpm with P-R interval of 0.42 sec. Following 0.5 mg atropine, the heart rate increased but the P-R interval remained prolonged (0.36 sec) and the corrected Q-T interval was 0.51 sec. Treatment with 2.5 g MgSO4, 20 mEq KCl, and 9.4 mEq calcium gluconate i.v. normalized the Q-T interval, and decreased the P-R interval to 0.22 sec. Upon specific questioning, she admitted to a remote history of bulimia, but denied any bulimic behavior for the last 16 yr. CONCLUSION: Two patients with histories of eating disorders failed to disclose this information during preoperative evaluation. Perioperative cardiac dysrhythmias developed in these patients, even though they claimed that eating behavior had returned to normal.

Adult↗
PubMed1999

A comparison of midazolam and diazepam for conscious sedation during colonoscopy in a prospective double-blind study.

BACKGROUND: Midazolam and diazepam are commonly used for conscious sedation, but their comparative respiratory depressive effects have not been accurately studied. We used a novel real-time, on-line, computerized data acquisition system to compare the two agents in a randomized double-blind study. METHODS: One hundred patients undergoing colonoscopy were studied. The maximum end-tidal carbon dioxide tension (PetCO2) and the minimum oxygen saturation by pulse oximetry (SpO 2) were recorded by computer every minute. Patients received meperidine (25 to 50 mg) and incremental doses of either midazolam or diazepam to an identical end point of slurred speech and/or ptosis. Sedation was scored from 1 (unarousable) to 5 (wide awake). RESULTS: Sedation scores were 3.6 +/- 0.1 (mean +/- standard error) after each agent. The doses of midazolam and diazepam were 0. 031 +/- 0.002 and 0.106 +/- 0.009 mg/kg, respectively. In the first 45 minutes (PetCO2) was significantly higher with midazolam than with diazepam (p < 0.05). SpO2 was significantly depressed for 80 minutes after each agent, and the number of minutes when the minimum Sp O2 was less than 90% did not differ between the two agents. CONCLUSIONS: Midazolam was 3.4 times more potent than diazepam. The duration of oxygen desaturation emphasizes the importance of monitoring SpO2 until ventilation and oxygenation have recovered. Although the degree of hypoxemia was comparable, midazolam led to higher end-tidal carbon dioxide tensions.

Adult↗
PubMed1999

The clinical significance of simultaneous infection with hepatitis G virus in patients with chronic hepatitis C.

OBJECTIVES: Hepatitis G virus (HGV) is a recently discovered member of the flavivirus family that has been associated with acute and chronic hepatitis. HGV infection has been reported to coexist in 10-20% of patients with chronic hepatitis C. The significance of simultaneous infection with HGV and hepatitis C virus (HCV) remains to be clarified, as do the effects on HGV of therapeutic interventions such as interferon treatment or liver transplantation. THE AIMS OF OUR STUDY WERE: 1) to examine the frequency of HGV infection in the settings of liver transplantation and interferon therapy for hepatitis C; and 2) to compare HGV RNA levels before and after liver transplantation or interferon treatment. METHODS: Pre-treatment sera were available in 65 patients with chronic hepatitis C treated with interferon; pretransplant sera were available in 49 patients transplanted for end stage liver disease associated with chronic hepatitis C. Information collected included age, sex, risk factors for hepatitis, concurrent liver disease, patient and allograft survival, biochemical response to interferon, histological activity index, and degree of fibrosis/cirrhosis. HCV genotyping was performed by sequencing the NS-5 region. HGV quantitation was performed using a research-based branched DNA (bDNA) assay with a set of probes directed at the 5' untranslated region. RESULTS: HGV was detected in 10 of 49 patients (20%) before transplant and in 13 of 65 patients (20%) treated with interferon. There was a female predominance among HGV-positive compared with HGV-negative transplant patients (80% vs 20%; p < 0.01), but such a difference was not observed in the interferon-treated group. Hepatic iron concentration was lower in hepatic explants from patients who were HGV-positive than in those who were HGV-negative (318 +/- 145 microg/g dry weight vs 1497 +/- 2202 microg/g dry weight; p = 0.02). HCV exposure after 1980 was more common in the HGV-positive patients than in those who were HGV-negative for the entire study population (10 of 20 [50%] vs 16 of 66 [24%]; p = 0.03), as well as for the nontransplant subgroup (8 of 12 [67%] vs 12 of 39 [31%]; p = 0.03). HGV RNA levels declined at 1 yr after transplant in seven of eight patients. Among nine patients tested during or after interferon treatment, HGV RNA levels declined from pretreatment levels in all and disappeared in three. CONCLUSIONS: Among patients with chronic hepatitis C treated with either interferon or liver transplantation, the frequency of coinfection with HGV is about 20%. HGV may be a more recent virus in the US than HCV. Coinfection with HGV does not appear to affect the likelihood of response to interferon in patients with hepatitis C. Finally, HGV RNA levels appear to decline after both liver transplantation and interferon therapy, suggesting possible suppression by increased HCV replication in the former case, and a possible drug treatment effect in the latter.

Adult↗
PubMed1999

Clinical significance of TT virus infection in patients with chronic hepatitis C.

OBJECTIVE: The TT virus (TTV) is a novel DNA virus that has recently been identified. The clinical significance of TTV infection in patients with chronic hepatitis C has not been determined. The aim of this study was to determine the prevalence and possible role of TTV in a well characterized population with chronic hepatitis C infection. METHODS: Ninety patients with chronic HCV and known time of HCV acquisition were selected from approximately 250 patients followed at our institution. Characteristics including age, sex, histology, and length of disease were recorded. Direct sequencing of the NS5 region was used for HCV genotyping. TTV DNA detection was based on PCR. RESULTS: TTV infection was present in 24 of 90 (27%) HCV patients. Patients were divided into four groups based on stage of disease; chronic hepatitis (CH, 29 patients), compensated cirrhosis (CC, 17 patients), decompensated cirrhosis (DC, 28 patients), and hepatocellular carcinoma (HCC, 16 patients). TTV was present in 2/29 (7%), 2/17 (12%), 11/28 (39%), and 9/16 (56%) in those with CAH, CC, DC, and HCC respectively. TTV was significantly more prevalent among those with advanced disease (DC and HCC) compared to those with stable disease (CH and CC; p = 0.001). Mean age, sex, and the time from exposure to HCV to development of complications were similar in TTV-positive and -negative patients. TTV infection was more common in patients infected with HCV genotype 1b. Univariate analysis showed that length of HCV infection, HCV genotype 1b, and TTV infection were important in predicting the stage of liver disease in HCV patients. However, after adjusting for length of HCV infection, TTV but not HCV genotype was important in predicting the stage of liver disease. CONCLUSIONS: We conclude that 1) TTV infection is common in patients with chronic HCV; 2) TTV infection is more prevalent among patients with advanced HCV-associated liver disease (DC and HCC) than in those with stable disease (CH and CC); and 3) TTV infection is more common in patients with HCV genotype 1b but is independent from genotype in predicting the stage of HCV-associated liver disease.

Base Sequence↗
PubMed1998

Hepatitis G virus infection in patients transplanted for cryptogenic cirrhosis: red flag or red herring?

BACKGROUND: The significance of hepatitis G (HGV) infection in liver transplant recipients is not known. We set out to determine the pre-orthotopic liver transplantation (OLT) prevalence, the pre- and postoperative viral titers of HGV, and the allograft histology in patients infected with HGV who underwent OLT for cryptogenic cirrhosis. METHODS: HGV RNA was measured using a research-based branched DNA assay. The assay used a target-specific probe set that was based on the 5'-untranslated region of the HGV genome. Allograft histology was assessed with protocol liver biopsies in all patients who survived longer than 6 months. RESULTS: The preoperative prevalence of HGV infection in recipients transplanted for cryptogenic cirrhosis was 26%. Thirty-seven percent (12 of 33) of recipients who had serum available in the first postoperative month had HGV infection. Mean HGV RNA levels were 9.8 (+/-4.2) (viral molecular equivalents/ml x 10[6]) before OLT and 37.5 (+/-10.7) at 1 year after OLT. In 4 of the 11 cryptogenic recipients in whom HGV RNA was detectable in the first postoperative month, HGV RNA fell to undetectable levels at the most recent follow-up (mean 70 months). Of the five cryptogenic recipients who continue to have measurable HGV RNA, three have unexplained hepatitis histologically. CONCLUSIONS: These findings suggest the following: 1) The prevalence of HGV infection in patients undergoing OLT for cryptogenic cirrhosis is about 25%. 2) In recipients persistently infected with HGV, mean HGV RNA titers increase after OLT. 3) HGV RNA becomes undetectable in about one third of recipients who had detectable HGV RNA in the first month after OLT. 4) Hepatitis of uncertain etiology occurs in 60% (3 of 5) of persistently HGV-infected cryptogenic recipients.

Adult↗
PubMed1998

Clinician's guide to hepatitis C.

Hepatitis C virus infection is common, often silent, and almost always chronic and can lead to cirrhosis and hepatocellular cancer. Deaths related to chronic hepatitis C are expected to increase dramatically in the future. Many cases of infection are asymptomatic and are undiagnosed because of a lack of recognition by patients and physicians. All patients currently or previously at risk of infection should undergo screening, including those who received blood transfusions before 1992. Interferon is the only effective therapy, but disappearance of virus is sustained in only 10 to 15% of patients. The combination of interferon and oral ribavirin therapy may increase the sustained response rate to about 40%. New agents such as hepatitis C virus-specific protease inhibitors may be available in the next 5 to 10 years, and treatment is evolving toward multiple-drug regimens analogous to those used for human immunodeficiency virus (HIV) infection. In contrast to public funding for drug development in HIV, such funding for hepatitis C has been limited.

Biopsy↗