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Biomedical subjects

P Monroe

Publications and source records attributed to P Monroe.

17 recordsLinked to original sources

Phase I trial of a murine antibody to MUC1 in patients with metastatic cancer: evidence for the activation of humoral and cellular antitumor immunity.

BACKGROUND: BrevaRex mAb-AR20.5 is a murine anti-MUC1 monoclonal antibody generated to induce MUC1 antigen-specific immune responses through the formation of immune complexes with circulating MUC1 and/or MUC1-expressing tumor cells that may target these immune complexes (IC) to receptors on dendritic cells (DCs). PATIENTS AND METHODS: A phase I study focusing on safety and immunology evaluated 1, 2 and 4-mg doses. Seventeen patients with MUC1-positive cancers received intravenous infusions of the antibody over 30 min on weeks 1, 3, 5, 9, 13 and 17 of treatment. RESULTS: mAb-AR20.5 was well-tolerated, not associated with dose-limiting toxicity, and did not induce hypersensitivity reactions. Overall, five of 15 evaluable patients developed human anti-mouse antibodies (HAMA), five developed anti-idiotypic antibodies (Ab2) and seven developed anti-MUC1 antibodies. Immune responses were most prominent in the 2-mg dose cohort for all parameters tested, and treatment-emergent MUC1-specific T-cell responses were detected in five of 10 evaluable patients treated with mAb-AR20.5. CONCLUSIONS: The injection of a murine antibody to MUC1 induces MUC1-specific immune responses in advanced cancer patients. Anti-MUC1 antibody increases correlated with decrease or stabilization of CA15.3 levels (P=0.03). The 2-mg dose of mAb-AR20.5 showed strongest biological activity, and will be evaluated in future efficacy trials.

Adult↗

Pharmacokinetics and bioequivalence of a combined oral formulation of eniluracil, an inactivator of dihydropyrimidine dehydrogenase, and 5-fluorouracil in patients with advanced solid malignancies.

BACKGROUND: This study was performed to evaluate the pharmacokinetics, bioequivalence, and feasibility of a combined oral formulation of 5-flurouracil (5-FU) and eniluracil (Glaxo Wellcome Inc., Research Triangle Park, North Carolina), an inactivator of dihydropyrimidine dehydrogenase (DPD). The rationale for developing a combined eniluracil/5-FU formulation oral dosing form is to simplify treatment with these agents, which has been performed using separate dosing forms, and decrease the probability of severe toxicity and/or suboptimal therapeutic results caused by inadvertently high or conversely insufficient 5-FU dosing. PATIENTS AND METHODS: The trial was a randomized, three-way crossover bioequivalence study of three oral dosing forms of eniluracil/5-FU tablets in adults with solid malignancies. Each period consisted of two days of treatment and a five- to seven-day washout phase. Eniluracil at a dose of 20 mg, which results in maximal DPD inactivation, was administered twice daily on the first day and in the evening on the second day of each of the three treatments. On the morning of the second day, all patients received a total eniluracil dose of 20 mg orally and a total 5-FU dose of 2 mg orally as either separate tablets (treatment A) or combined eniluracil/5-FU tablets in two different strengths (2 tablets of eniluracil/5-FU at a strength (mg/mg) of 10/1 (treatment B) or 8 tablets at a strength of 2.5/0.25 (treatment C)). The pharmacokinetics of plasma 5-FU, eniluracil, and uracil, and the urinary excretion of eniluracil, 5-FU, uracil, and alpha-fluoro-beta-alanine (FBAL), were studied. To determine the bioequivalence of the combined eniluracil/5-FU dosing forms compared to the separate tablets, an analysis of variance on pharmacokinetic parameters reflecting eniluracil and 5-FU exposure was performed. RESULTS: Thirty-nine patients with advanced solid malignancies had complete pharmacokinetic studies performed during treatments A, B, and C. The pharmacokinetics of eniluracil and 5-FU were similar among the three types of treatment. Both strengths of the combined eniluracil/5-FU dosing form and the separate dosing forms were bioequivalent. Mean values for terminal half-life, systemic clearance, and apparent volume of distribution for oral 5-FU during treatments A/B/C were 5.5/5.6/5.6 hours, 6.6/6.6/6.5 liters/hour, and 50.7/51.5/50.0 liters, respectively. The intersubject coefficient of variation for pharmacokinetic variables reflecting 5-FU exposure and clearance in treatments ranged from 23% to 33%. The urinary excretion of unchanged 5-FU over 24 hours following treatments A, B, and C averaged 52.2%, 56.1%, and 50.8'%, of the administered dose of 5-FU, respectively. Parameters reflecting DPD inhibition, including plasma uracil and urinary FBAL excretion following treatments A, B, and C were similar. Toxicity was generally mild and similar following all three types of treatments. CONCLUSIONS: The pharmacokinetics of 5-FU and eniluracil were similar and met bioequivalence criteria following treatment with the separate oral formulations of 5-FU and eniluracil and two strengths of the combined formulation. The availability of a combined eniluracil/5-FU oral dosing form will likely simplify dosing and decrease the probability of severe toxicity or suboptimal therapeutic results caused by an inadvertent 5-FU overdose or insufficient 5-FU dosing in the case of separate oral formulations, thereby enhancing the overall feasibility and 0therapeutic index of oral 5-FU therapy.

Administration, Oral↗

Susceptibility of beta-hemolytic streptococci to nine antimicrobial agents among four medical centers in Salt Lake City, Utah, USA.

A multicenter study was performed to evaluate the susceptibility of beta-hemolytic streptococci to nine antimicrobial agents. MICs were performed in cation-supplemented Mueller-Hinton broth with 3.5% lysed sheep red blood cells according to NCCLS guidelines. A total of 646 isolates were tested: 300 (46%) group A; 170 (26%) group B; 38 (6%) group C, 35 (5%) group F; 83 (17%) group G; and 20 (3%) nongroupable. Six percent of the total isolates were resistant to one or more of the antibiotics tested. Approximately 7% of 387 strains from the University of Utah Hospital and Clinics were resistant to erythromycin. Four isolates were resistant to clindamycin. Six strains (3%) from Primary Children's Medical Center (207 tested) were resistant to one or more of the macrolides. Resistance was rare at the LDS Hospital and the Salt Lake Veteran's Affairs Hospital. Overall, resistance among beta-hemolytic streptococci in this geographic location does not seem to be a significant problem, except at the tertiary care university hospital.

Anti-Bacterial Agents↗

A novel high-dose chemotherapy protocol with autologous hematopoietic rescue in patients with metastatic breast cancer or recurrent non-Hodgkin's lymphoma.

In this phase II trial, we used a double dose-intensive chemotherapy and stem cell rescue protocol to treat breast cancer (BCA) patients or non-Hodgkin's lymphoma patients (NHL). The first cycle consisted of high-dose melphalan followed by ABMT. The second cycle used a novel chemotherapy combination; thiotepa, etoposide, carboplatin and cyclophosphamide (TECC) followed by ABMT. We treated 12 patients in total, nine with BCA, three with NHL. All nine BCA patients were treated with the two cycle protocol. The three NHL patients were treated with the second cycle only. Bone marrow (BM, 1 patient), peripheral blood stem cells (PBSC, 10 patients) or both (1 patient) were reinfused 60-72 h after completion of each cycle of chemotherapy. Recovery was rapid; the ANC rose to greater than 500/microl on day +11 (+8 to + 20) and the platelet count to greater than 20000/microl on day +12 (+6 to +20). The toxicities included the expected neutropenic fevers, severe mucositis, diarrhea, and a low incidence of mild renal insufficiency. No patients developed veno-occlusive disease, hemorrhagic cystitis or overt bleeding. With a mean follow-up of 37 months, 83.3% of the patients are alive. Six patients are in complete remission; one patient with BCA relapsed and expired; one patient with NHL is in CR now over 18 months after relapse and subsequent treatment with interferon; one patient is too early to evaluate. Progression-free survival overall is 75%, which is at least equivalent to many other recent studies using similar regimens. In addition, we have also found that delayed addition of G-CSF during the mobilization of PBSC was feasible and resulted in excellent CD34+ cell counts and engraftments, and reduced treatment costs. These results indicate that this chemotherapy is effective with good remission rates and high progression-free survival rates. It is also well tolerated with acceptable toxicities that are manageable. Long-term follow-up of a larger cohort of patients will be needed to ascertain the overall efficacy of this type of therapy.

Adult↗

The pulmonary hypertension of sclerosing agents is prevented by cyclooxygenase inhibitors.

Sodium morrhuate and sodium tetradecylsulfate are injected during endoscopic sclerotherapy to control variceal bleeding. When administered to sheep they cause transient pulmonary hypertension and increase protein poor lung lymph flow. To determine the etiology of these alterations, we studied three groups of sheep after establishing acute lung lymph fistulas. In Group 1, indomethacin or ibuprofen was infused. In Group 2, 2.5 cc of sodium morrhuate was injected alone (2A) or after indomethacin or ibuprofen pretreatment (2B). In Group 3, 2.5 cc of sodium tetradecylsulfate was given intravenously either alone (3A) or after indomethacin or ibuprofen (3B). When sclerosing agents were given alone (Group 2A and 3A) pulmonary artery pressures increased three-fold at 30 seconds postinjection to 37 +/- 4.4 and 39 +/- 5.7 mmHg respectively with a slow return to baseline over two hours. Lymph flow increased significantly from 1.3 +/- 1.5 to 2.7 +/- 1.5 cc/30 minutes after sodium morrhuate and from 1.2 +/- .62 to 2.7 +/- 1.7 cc/30 mins at 30 minutes after sodium tetradecylsulfate and the lymph/plasma albumin ratio fell. Increased lymph flow persisted through 120 minutes. In those animals receiving a sclerosing agent after indomethacin or ibuprofen (2B and 3B) there was no change in pulmonary artery pressure, lymph flow, lymph plasma albumin ratio, or lung wet weight to dry weight ratios. We conclude that the pulmonary hypertension and increased protein poor lymph flow are mediated by prostaglandins.

Animals↗

Chromosomal breakage in normal and fragile X subjects using low folate culture conditions.

To investigate whether the fragile X syndrome is associated with a generalised chromosomal instability, we compared the frequency and distribution of chromosomal breakage in lymphocytes grown in low folate medium from normal subjects and from patients with the syndrome. Although low folate conditions increased the rate of chromosome breakage, no difference in frequency or distribution of chromosomal breakage was found between the two groups. This suggests that the fragile X syndrome is not associated with a generalised chromosome instability expressed in folate deficient medium and assessed in terms of chromosomal breakage.

Chromosome Aberrations↗

Acute respiratory failure after sodium morrhuate esophageal sclerotherapy.

Two of 30 patients with esophageal varices had respiratory distress develop within 8-24 h of esophageal sclerotherapy. Evidence of aspiration and sepsis were absent in these two patients with the clinical picture of adult respiratory distress syndrome. To investigate the possible etiologic role of sodium morrhuate in this syndrome, a sheep model was established and pulmonary hemodynamics, lung lymph flow, and albumin concentration were measured before and after the intravenous injection of 2.5-15.0 cm3 of sodium morrhuate. In all 8 animals studied, mean pulmonary artery pressures increased from 11.6 +/- 2.8 to 32.8 +/- 4.9 mmHg (p less than 0.01) 30 s after injection. These pressures returned to baseline values over 120 min. Lymph flow increased from 0.91 +/- 0.89 to 2.8 +/- 1.5 ml/30 min at 90 min postinjection (p less than 0.05) and returned to baseline values in animals monitored for 6-8 h. The lymph/plasma albumin ratio decreased from 0.856 +/- 0.08 to 0.74 +/- 0.01 (p less than 0.05) 120 min postinjection. Pulmonary edema was not evident histologically or gravimetrically (wet/dry weight ratio was 3.65 +/- 0.3 and not different from normal). It was concluded that sodium morrhuate injection in sheep causes marked but transient pulmonary hypertension associated with an increased lymph flow of relatively protein-poor lymph. Sodium morrhuate esophageal sclerotherapy may affect pulmonary hemodynamics and contribute to respiratory difficulties in patients.

Animals↗

In vivo evaluation of lipoprotein cholesterol ester metabolism in patients with liver disease.

Fifteen patients with liver disease were found to have marked reductions in both plasma lecithin-cholesterol acyltransferase activity (62%) and cholesterol ester concentration (46%) when compared with 11 normal subjects. The changes in cholesterol ester concentration were confined to high-density lipoprotein and very-low-density lipoprotein; the low-density lipoprotein fraction was not significantly altered. Examination of the plasma lecithin and lipoprotein cholesterol esters revealed that patients with liver disease had significantly greater amounts of saturated and monounsaturated fatty acids and less linoleic acid than normal subjects. Lipoprotein cholesterol ester kinetic studies were carried out in 2 normal subjects and 2 severely cirrhotic patients who simultaneously received [14C]mevalonic acid and high-density lipoprotein labeled with free [3H]cholesterol. A lipoprotein cholesterol ester model was developed that fit both the 3H and 14C data. The precursors of high-density lipoprotein cholesterol esters were free cholesterol and low-density lipoprotein cholesterol esters; the distribution pattern was in favor of low-density lipoprotein cholesterol esters in both groups of subjects (71% for normals and 88% for cirrhotics). The turnover of high-density lipoprotein cholesterol esters was similar in both groups of subjects, but the flux of free cholesterol into high-density lipoprotein cholesterol esters was greatly reduced in the cirrhotic patients. In cirrhotic patients, this represented only 9% and 12% of the total lipoprotein cholesterol ester synthesized; in the normal subjects, the values were 68% and 74%. The turnover of very-low-density lipoprotein cholesterol esters was greatly suppressed in the cirrhotic patients, and their precursor sources were high-density lipoprotein cholesterol esters and tissue free cholesterol. The low-density lipoprotein cholesterol ester precursors were very-low-density lipoprotein, low-density lipoprotein, and tissue free cholesterol. In the cirrhotic patients, much greater proportions (78% and 88%) of low-density lipoprotein cholesterol ester were derived from free cholesterol. Also, the turnover rates of these esters were reduced in the cirrhotic patients. The present report has provided evidence that cirrhotic patients derive most of their plasma lipoprotein cholesterol esters from an acyl-CoA-cholesterol acyltransferase free-cholesterol tissue source--most likely the intestine. By contrast, in normal subjects, the major contribution to plasma esters is via the introduction of newly formed cholesterol esters into the high-density lipoprotein fraction.

Adult↗

Fragile X.

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Chromosome Fragility↗

Effects of acute and chronic ethanol intake on bile acid metabolism.

Ethanol has been demonstrated to cause aberrations in lipoprotein metabolism, cholesterol synthesis, biliary secretion, and bile acid synthesis. Although there is interdependency of cholesterol and bile acid metabolism, a role of ethanol-induced lipid abnormalities in altering bile acid synthesis has not been found. The direct effects of ethanol administration on bile acid metabolism have been studied in animals and vary with the experimental design. Acutely, ethanol causes decreased bile acid secretion and synthesis, but other effects are less well defined. Chronic ethanol use in man may result in cirrhosis, a condition in which abnormalities of bile acid metabolism have been described in detail. Cholic acid synthesis and pool size are markedly depressed in advanced cirrhosis. Chenodeoxycholic acid synthesis is affected less than cholic acid synthesis, probably because 12 alpha-hydroxylase activity is markedly depressed in cirrhosis, although other steps may also be influenced such as 7 alpha-hydroxylation of cholesterol or availability of cholesterol precursor. The deoxycholic acid pool is depressed probably because of changes in fecal flora. Despite the decrease in total bile acid pool, lithogenicity of bile is not increased in cirrhotic patients because of a concomitant decline in cholesterol and phospholipid secretion. Changes in hepatic blood flow and hepatic extraction cause an increase in plasma bile acid levels which may have clinical relevance.

Animals↗

Aphasia outcome in stroke: a clinical neuroradiological correlation.

Fourteen aphasic patients with acute onset of thromboembolic cerebrovascular insults demonstrable by angiography or radioscintigrams who were available for long-term follow-up have been studied. Their aphasia evolution was compared with acute angiographical and radioisotopic findings, and the lesions shown by follow-up computerized axial tomography (CT). Angiographical site of occlusion, evidence of early reopening of occluded vessels, and radioisotopic flow asymmetries including the "hot-stroke" luxury perfusion failed to correlate with aphasia outcome. Radioisotopic static images were more helpful by depicting lesion location and number but lacked the definition seen on the CT scan. The long-term CT scan by showing the size, location and number of lesions had a good correlation with aphasia outcome. Those patients with large dominant hemisphere involvements, either one large or many smaller lesions, fared poorly while those with lesser lesions did better. Bilateral lesions, at times evasive clinically, helped to account for significant aphasia residuals.

Adult↗

Transient bacteremia due to suction abortion: implications for SBE antibiotic prophylaxis.

The incidence and character of the bacteremia associated with elective suction abortion was investigated in volunteer subjects aged 19 to 35 years who were to undergo first trimester abortion by suction curettage. One hundred and forty-four blood cultures were obtained from thirteen pregnant and four non-pregnant (control) subjects matched for age. Transient bacteremia occurred during or soon after suction abortion in 11 of 13 (84.7%) study subjects. Four of these patients were bacteremic after bimanual pelvic examination, just prior to initiation of the abortion procedure. Seven others developed bacteremia temporally related to cervical dilatation and suction abortion. The bacteremia was intermittent in some, persistent in others, existed as long as one hour after the procedure, and was transient in all patients. Microorganisms isolated from the blood were all normal genital tract flora and were predominantly anaerobes, although alpha hemolytic streptococci were also recovered. Mixed bacteremia occurred in six patients. In contrast, blood cultures from four non-pregnant women were sterile. This study indicates that the systemic circulation-uterine cavity barrier is significantly disrupted during abortion by suction curettage permitting endogenous genital tract microorganisms to gain access into the bloodstream. These observations also suggest that there may be some risk of developing endocarditis during suction abortion in patients with cardiac deformities, and lend some support to the current practice of giving antibiotic prophylaxis to abortion patients with cardiac lesions which predispose them to endocarditis.

Abortion, Induced↗