rifampin and Lung-Neoplasms

Actinomycosis was at one time a common diagnosis in this country. It still is fairly common in some parts of the world. As the numbers of antibiotics and indications for their use have increased, the disease has almost become a medical rarity in the United States. This fact might be thought a paradox in view of the universal presence of the actinomyces organisms in every human mouth. However, it is perhaps not well recognized that the actinomyces are true bacteria, and that they are particularly sensitive to most of the common antibacterials in current usage. These facts have combined to decrease the clinical frequency of the disease as well as effectively reduce the opportunity for securing a satisfactory specimen for laboratory culture in suspected cases. Actinomycosis can present in a variety of forms and may mimic other infections or even neoplasms. The clinical pattern of remission and exacerbation of symptoms occurring in parallel sequence with initiation and cessation of antibiotic administration is a phenomenon which should increase suspicion for actinomycosis in any of its manifestations.

Topics: Actinomyces; Actinomycosis; Actinomycosis, Cervicofacial; Adult; Age Factors; Aged; Anti-Bacterial Agents; Diagnosis, Differential; Female; Humans; Isoniazid; Lung Diseases; Lung Neoplasms; Male; Middle Aged; Rifampin; Sex Factors; Sputum; United States

SH-1028 is an irreversible third-generation EGFR tyrosine kinase inhibitor (EGFR-TKI) for the treatment of locally advanced or metastatic non-small cell lung cancer (NSCLC). Considering the possibility of combination therapy in patients with NSCLC, we investigated the drug-drug interaction (DDI) potential of SH-1028 both in vitro and in clinical trials. The in vitro studies were conducted to determine the potential of SH-1028 as a substrate, inducer, or inhibitor of cytochrome P450 (CYP) subtypes. A phase I drug-drug interaction study in healthy volunteers was performed to evaluate the impact of co-administering rifampicin (a strong CYP3A4 inducer) and itraconazole (a strong CYP3A4 inhibitor) on the pharmacokinetics of SH-1028. The in vitro experiments showed that SH-1028 was mainly metabolized by CYP3A4. The activities of CYP1A2, 2B6, 2C19, 2D6 and 3A4 enzymes were slightly inhibited in vitro with SH-1028. SH-1028 has no obvious induction effect on CYP1A2 and CYP2B6 activities, but has potential induction effect on CYP3A4 mRNA expression. However, SH-1028 may not induce or inhibit human CYPs significantly at the clinically expected dose (200 mg). The geometric mean ratios of pharmacokinetic parameters and their corresponding 90% confidence intervals for SH-1028 in combination and alone did not fall within the range of 80-125%. It is speculated that itraconazole and rifampicin affect the metabolism of SH-1028. In the clinical application of SH-1028, special attention should be paid to the interaction between SH-1028 and drugs or foods that affect the activity of CYP3A4. (Clinical trial registration number: CTR20210558).

Topics: Carcinoma, Non-Small-Cell Lung; Cytochrome P-450 CYP1A2; Cytochrome P-450 CYP3A; Cytochrome P-450 Enzyme System; Drug Interactions; ErbB Receptors; Humans; Itraconazole; Lung Neoplasms; Rifampin

Trilaciclib is a cyclin-dependent kinase 4/6 inhibitor indicated to decrease the incidence of chemotherapy-induced myelosuppression in patients with extensive-stage small-cell lung cancer. Trilaciclib is a substrate and time-dependent inhibitor of cytochrome P450 3A4 and an inhibitor of multidrug and toxin extrusion 1, multidrug and toxin extrusion 2-K, organic cation transporter 1, and organic cation transporter 2. Here, we investigate the pharmacokinetic drug-drug interaction potential of trilaciclib.. Coadministration with trilaciclib had minimal effects on the exposure (area under the plasma concentration-time curve from time 0 to infinity) of midazolam (geometric least-square mean ratio [GMR] vs midazolam alone 1.065; 90% confidence interval [CI] 0.984-1.154) but statistically significantly increased plasma exposure (GMR 1.654; 90% CI 1.472-1.858) and decreased renal clearance (GMR 0.633; 90% CI 0.572-0.701) of metformin. Coadministration of trilaciclib with rifampin or itraconazole decreased trilaciclib area under the plasma concentration-time curve from time 0 to infinity by 17.3% (GMR 0.827; 90% CI 0.785-0.871) and 14.0% (GMR 0.860; 0.820-0.902), respectively, vs trilaciclib alone. Population pharmacokinetic modeling showed no significant effect of trilaciclib on topotecan clearance.. Overall, the drug-drug interaction and safety profiles of trilaciclib in these studies support its continued use in patients with extensive-stage small-cell lung cancer.. Study 106: EudraCT number: 2019-002303-18; Study 114: not applicable; Study 03: Clinicaltrials.org: NCT02514447; August 2015.

Topics: Area Under Curve; Drug Interactions; Healthy Volunteers; Humans; Itraconazole; Lung Neoplasms; Metformin; Midazolam; Prospective Studies; Pyrimidines; Pyrroles; Rifampin; Topotecan

Lorlatinib is a third-generation tyrosine kinase inhibitor approved for the treatment of anaplastic lymphoma kinase (ALK)-positive metastatic non-small cell lung cancer; cytochrome P450 (CYP) 3A plays an important role in the metabolism of lorlatinib.. This phase 1, open-label, two-period, crossover study estimated the effect of oral rifampin (a strong CYP3A inducer) on the pharmacokinetics and safety of oral lorlatinib (NCT02804399). Healthy participants received single-dose lorlatinib 100 mg in period 1 followed by rifampin 600 mg/day (days 1-12) and single-dose lorlatinib 100 mg (day 8) in period 2. Blood samples were collected for 120 h after each dose of lorlatinib.. When a single dose of lorlatinib was administered during daily dosing with rifampin (period 2), the area under the plasma concentration-time profile extrapolated to infinity (AUC. The addition of a single dose of lorlatinib to daily dosing with rifampin significantly reduced lorlatinib plasma exposure relative to a single dose of lorlatinib administered alone and was associated with severe but self-limiting transaminase elevations in all healthy participants. These observations support the contraindication in the product label against concomitant use of lorlatinib with all strong CYP3A inducers.. ClinicalTrials.gov identifier, NCT02804399.

Topics: Adult; Aminopyridines; Antineoplastic Agents; Area Under Curve; Carcinoma, Non-Small-Cell Lung; Cross-Over Studies; Drug Interactions; Female; Healthy Volunteers; Humans; Lactams; Lactams, Macrocyclic; Lung Neoplasms; Male; Middle Aged; Pyrazoles; Rifampin; Young Adult

In vitro data support involvement of cytochrome P450 (CYP)2C8 and CYP3A4 in the metabolism of the anaplastic lymphoma kinase inhibitor brigatinib. A 3-arm, open-label, randomized, single-dose, fixed-sequence crossover study was conducted to characterize the effects of the strong inhibitors gemfibrozil (of CYP2C8) and itraconazole (of CYP3A) and the strong inducer rifampin (of CYP3A) on the single-dose pharmacokinetics of brigatinib. Healthy subjects (n = 20 per arm) were administered a single dose of brigatinib (90 mg, arms 1 and 2; 180 mg, arm 3) alone in treatment period 1 and coadministered with multiple doses of gemfibrozil 600 mg twice daily (BID; arm 1), itraconazole 200 mg BID (arm 2), or rifampin 600 mg daily (QD; arm 3) in period 2. Compared with brigatinib alone, coadministration of gemfibrozil with brigatinib did not meaningfully affect brigatinib area under the plasma concentration-time curve (AUC

Topics: Administration, Oral; Adult; Aged; Anaplastic Lymphoma Kinase; Area Under Curve; Carcinoma, Non-Small-Cell Lung; Cross-Over Studies; Cytochrome P-450 CYP2B6 Inducers; Cytochrome P-450 CYP2C8; Cytochrome P-450 CYP2C8 Inhibitors; Cytochrome P-450 CYP3A Inducers; Cytochrome P-450 CYP3A Inhibitors; Drug Interactions; Drug Therapy, Combination; Female; Gemfibrozil; Healthy Volunteers; Humans; Itraconazole; Lung Neoplasms; Male; Middle Aged; Organophosphorus Compounds; Protein Kinase Inhibitors; Pyrimidines; Rifampin

The efficacy and safety of alectinib, a central nervous system-active and selective anaplastic lymphoma kinase (ALK) inhibitor, has been demonstrated in patients with ALK-positive (ALK+) non-small cell lung cancer (NSCLC) progressing on crizotinib. Alectinib is mainly metabolized by cytochrome P450 3A (CYP3A) to a major similarly active metabolite, M4. Alectinib and M4 show evidence of weak time-dependent inhibition and small induction of CYP3A in vitro. We present results from 3 fixed-sequence studies evaluating drug-drug interactions for alectinib through CYP3A. Studies NP28990 and NP29042 enrolled 17 and 24 healthy subjects, respectively, and investigated potent CYP3A inhibition with posaconazole and potent CYP3A induction through rifampin, respectively, on the single oral dose pharmacokinetics (PK) of alectinib. A substudy of the global phase 2 NP28673 study enrolled 15 patients with ALK+ NSCLC to determine the effect of multiple doses of alectinib on the single oral dose PK of midazolam, a sensitive substrate of CYP3A. Potent CYP3A inhibition or induction resulted in only minor effects on the combined exposure of alectinib and M4. Multiple doses of alectinib did not influence midazolam exposure. These results suggest that dose adjustments may not be needed when alectinib is coadministered with CYP3A inhibitors or inducers or for coadministered CYP3A substrates.

Topics: Adult; Anaplastic Lymphoma Kinase; Carbazoles; Carcinoma, Non-Small-Cell Lung; Cytochrome P-450 CYP3A; Dose-Response Relationship, Drug; Female; Humans; Lung Neoplasms; Male; Midazolam; Middle Aged; Piperidines; Receptor Protein-Tyrosine Kinases; Rifampin; Treatment Outcome; Triazoles; Young Adult

A total of forty-three compounds were synthesized, including thirty-two new ones. Among those compounds, seventeen were selected and tested on human tumor cell lines: PC-3 (prostate adenocarcinoma), HCT-116 (colorectal tumor), NCIH-460 (lung carcinoma), SKMEL-103 (melanoma) and AGP-01 (gastric tumor). Alkynylated 1,2,4-oxadiazoles 2m, 3g and 3k exhibited antiproliferative activities against NCIH-460 in culture. Alkynylated N-cyclohexyl-1,2,4-oxadiazoles 3a-m and bis-heterocycle glucoglycero-1,2,3-triazole-N-cyclohexyl-1,2,4-oxadiazole derivatives 5a-k and 6-11 were evaluated for their in vitro efficacy towards Mycobacterium tuberculosis (Mtb) H

Topics: Alkynes; Animals; Antineoplastic Agents; Antitubercular Agents; Carcinoma, Squamous Cell; Cell Line; Cell Proliferation; Cell Survival; Chlorocebus aethiops; Dose-Response Relationship, Drug; Drug Discovery; Glycoconjugates; Humans; Lung Neoplasms; Mice; Microbial Sensitivity Tests; Molecular Structure; Mycobacterium tuberculosis; Oxadiazoles; Structure-Activity Relationship; Triazoles

Topics: Aged; Crizotinib; Humans; Lung Neoplasms; Male; Rifampin; Tomography, X-Ray Computed; Treatment Outcome

Small-cell lung cancer (SCLC) rarely coexists with pulmonary Mycobacterium avium intracellular complex (MAC) infection. The key drug for SCLC treatment is etoposide, which is metabolized by cytochrome P-450 (CYP) 3A4. Meanwhile, the key drugs for pulmonary MAC infection are clarithromycin (CAM) and rifampicin (RFP), and their metabolism influences CYP3A4. Therefore, treatment of concurrent SCLC and pulmonary MAC infection is difficult, and to the best of our knowledge, no report of treatments for concurrent SCLC and pulmonary MAC infection has been published. Patient Concerns and Diagnoses: A 65-year-old man presented to our hospital with abnormal findings of chest computed tomography: (1) a hilar region nodule in the left lung and mediastinal lymphadenopathy and (2) a thick-walled cavity lesion in the right upper lobe of the lung. After further examinations, the former lesions were diagnosed as SCLC, cT4N3M0, stage IIIC and the latter as pulmonary MAC infection, fibrocavitary disease.. Concurrent treatment was conducted with discontinuation of CAM and RFP before and after etoposide administration. Specifically, intravenous cisplatin and etoposide were administered on day 1 and days 1-3, respectively, and CAM, RFP, and ethambutol (EB) were administered orally on days 6-22 every 4 weeks. Concurrent radiotherapy was added to the drug administration on days 1-27 of the first cycle. The chemotherapy was continued for 4 cycles, followed by continuation of CAM and RFP administration. EB was discontinued because of optic nerve disorder. The treatments were conducted completely and safely, and both of the SCLC lesions and the MAC lesion were improved.. Treatments for concurrent SCLC and pulmonary MAC infection may be successfully conducted with discontinuation of CAM and RFP before and after etoposide administration.

Topics: Aged; Animals; Anti-Bacterial Agents; Antineoplastic Agents, Phytogenic; Bronchoscopy; Clarithromycin; Drug Therapy, Combination; Etoposide; Humans; Lung; Lung Neoplasms; Male; Mycobacterium avium; Peptide Fragments; Recombinant Proteins; Rifampin; Small Cell Lung Carcinoma; Tomography, X-Ray Computed; Tuberculosis, Avian

Topics: Adenocarcinoma; Adenocarcinoma of Lung; Adult; Antibiotics, Antitubercular; Drug Therapy, Combination; Dysphonia; ErbB Receptors; Ethambutol; Female; Gene Expression Regulation, Neoplastic; Humans; Isoniazid; Lung Neoplasms; Pyrazinamide; Rifampin; Treatment Outcome; Tuberculosis, Laryngeal

BACKGROUND Oxycodone is a semisynthetic opioid receptor agonist, and is frequently used for pain control in patients with cancer. Most oxycodone is metabolized by N-demethylation to noroxycodone by CYP3A. Rifampin is a strong inducer of several drug-metabolizing enzymes, including CYP3A. Hence, rifampin-induced CYP3A activity may decrease the effect of oxycodone. CASE REPORT Osteosarcoma is a highly aggressive primary bone tumor of childhood and adolescence. Here, we report a 30-year-old male with osteosarcoma of the femur with lung metastases in the upper lobe. The lung also contained small, scattered nodular lesions that were identified as tuberculosis. Multi-drug therapy, including rifampin, was administered. The upper-lobe metastatic lesion extended to the brachial plexus and caused severe pain. Over 1000 mg per day of oxycodone was ineffective for pain control. However, morphine was able to control his pain at about one-third the equivalent dose. CONCLUSIONS Our patient demonstrated oxycodone resistance due to rifampin. Chemotherapy may have compromised the patient's immune system, thus theoretically increasing the risk of tuberculosis. Recognition of the interactions between rifampin and oxycodone is important in this and other cancers. Notably, for patients using high doses of oxycodone to manage severe pain, stopping rifampin may lead to oxycodone overdose.

Topics: Adult; Analgesics, Opioid; Antibiotics, Antitubercular; Bone Neoplasms; Cancer Pain; Drug Resistance; Humans; Lung Neoplasms; Male; Osteosarcoma; Oxycodone; Rifampin; Tuberculosis, Pulmonary

Recent studies have demonstrated that efflux pumps of Mycobacterium tuberculosis (M. tb) provide a crucial mechanism in the development of drug resistant to antimycobacterial drugs. Drugs that inhibit these efflux pumps, such as verapamil, have shown the potential in enhancing the treatment success. We therefore hypothesized that the combined inhaled administration of verapamil and a first-line rifamycin antibiotic will further improve the treatment efficacy. An inhalable dry powder consisting of amorphous verapamil and crystalline rifapentine with l-leucine as an excipient was produced by spray drying. The in vitro aerosol characteristic of the powder, its microbiological activity and stability were assessed. When the powder was dispersed by an Osmohaler, the total fine particle fraction (FPFtotal, wt % of particles in aerosol <5 μm) of verapamil and rifapentine was 77.4 ± 1.1% and 71.5 ± 2.0%, respectively. The combination drug formulation showed a minimum inhibitory concentration (MIC90) similar to that of rifapentine alone when tested against both M. tb H37Ra and M. tb H37Rv strains. Importantly, the combination resulted in increased killing of M. tb H37Ra within the infected macrophage cells compared to either verapamil or rifapentine alone. In assessing cellular toxicity, the combination exhibited an acceptable half maximal inhibitory concentration (IC50) values (62.5 μg/mL) on both human monocytic (THP-1) and lung alveolar basal epithelial (A549) cell lines. Finally, the powder was stable after 3 months storage in 0% relative humidity at 20 ± 3 °C.

Topics: Adenocarcinoma; Administration, Inhalation; Aerosols; Anti-Arrhythmia Agents; Antibiotics, Antitubercular; Cell Survival; Chemistry, Pharmaceutical; Humans; In Vitro Techniques; Lung Neoplasms; Microbial Sensitivity Tests; Monocytes; Mycobacterium tuberculosis; Particle Size; Rifampin; Tuberculosis; Verapamil

Topics: Antitubercular Agents; Cough; Dyspnea; Humans; Lung Neoplasms; Male; Middle Aged; Mycobacterium tuberculosis; Rifampin; Thorax; Tomography, X-Ray Computed; Trachea; Tuberculosis, Pulmonary

Topics: Actinomycetales Infections; Aged; Anti-Bacterial Agents; Bacteremia; Ciprofloxacin; Diagnosis, Differential; Drug Therapy, Combination; Fertilizers; Humans; Imipenem; Immunocompromised Host; Leukemia, Myelomonocytic, Chronic; Lung Abscess; Lung Neoplasms; Male; Manure; Opportunistic Infections; Rhodococcus equi; Rifampin; Shock, Septic; Tomography, X-Ray Computed

Tuberculosis (TB) remains the "great pretender." We report the case of a 10-year-old female, who presented with a mass in the left chest that was suspected initially to be a tumor. This was later confirmed to be tuberculous in nature, with dissemination to the liver. A large granuloma eventually replaced the left lung, leaving her with "tuberculous destroyed lung" (TDL), an extremely rare, life-threatening sequela of the disease. We review the pathophysiology, radiologic findings, and management options, which includes pneumonectomy, for this seldom seen but preventable condition.

Topics: Antitubercular Agents; Child; Drug Therapy, Combination; Ethambutol; Female; Granuloma; Humans; Isoniazid; Lung; Lung Neoplasms; Mycobacterium tuberculosis; Pyrazinamide; Radiography; Rifampin; Treatment Outcome; Tuberculosis, Hepatic; Tuberculosis, Pulmonary

Topics: Aged, 80 and over; Anti-Bacterial Agents; Cardiology; Daptomycin; Diabetes Mellitus, Type 2; Diabetic Nephropathies; Endocarditis, Bacterial; Female; Humans; Incidental Findings; Interdisciplinary Communication; Lung Neoplasms; Medical Oncology; Pacemaker, Artificial; Patient Care Team; Pulmonary Disease, Chronic Obstructive; Pulmonary Medicine; Radiography; Referral and Consultation; Rifampin; Streptococcal Infections; Streptococcus sanguis; Thoracic Surgery

Topics: Adenocarcinoma; Administration, Cutaneous; Aged; Analgesics, Opioid; Antibiotics, Antitubercular; Drug Interactions; Fentanyl; Humans; Lung Neoplasms; Male; Pain; Parotid Neoplasms; Rifampin; Tuberculosis, Pulmonary

This report describes a patient with small-cell lung cancer who was infected with both Mycobacterium tuberculosis and non-tuberculous mycobacterium. He received irinotecan plus cisplatin, with and without rifampin. Rifampin slightly reduced the conversion of irinotecan to 7-ethyl-10-hydroxycamptothecin (SN-38), as determined by pharmacokinetic analysis. Rifampin may influence the metabolism and toxicity of irinotecan to some extent. However, there are possibilities to control M. tuberculosis and Mycobacterium avium complex infections in patients with small-cell lung cancer by using rifampin in combination with irinotecan plus cisplatin.

Topics: Antibiotics, Antitubercular; Antineoplastic Agents, Phytogenic; Camptothecin; Carcinoma, Small Cell; Drug Interactions; Glucuronates; Humans; Irinotecan; Lung Neoplasms; Male; Middle Aged; Mycobacterium avium-intracellulare Infection; Rifampin; Tuberculosis, Pulmonary

The bioassay- and spectroscopic-guided fractionation of the antimalarial extract from a Jamaican sponge, Plakortis sp., resulted in the isolation of three metabolites. The previously reported bromoaromatic filiformin (1) was obtained from our sample of Plakortis sp., and the potential origins of this compound are discussed. The peroxide-containing metabolite, plakortide F (2), is a more typical Plakortis metabolite and was shown to exhibit significant activity against Plasmodium falciparum in vitro. The isolation, structure, and bioactivity of a new lactone, plakortone G (3), are also reported.

Topics: Animals; Antimalarials; Bromobenzenes; Chromatography, High Pressure Liquid; Colonic Neoplasms; Dioxanes; Gas Chromatography-Mass Spectrometry; Hepatitis B; HIV; Humans; Jamaica; Lactones; Leukemia P388; Lung Neoplasms; Mice; Molecular Structure; Mycobacterium tuberculosis; Neoplasms, Unknown Primary; Nuclear Magnetic Resonance, Biomolecular; Plasmodium berghei; Plasmodium falciparum; Porifera; Spectrometry, Mass, Electrospray Ionization; Tumor Cells, Cultured

Several cytochrome P450 (CYP) enzymes are expressed in the human lung, where they participate in metabolic inactivation and activation of numerous exogenous and endogenous compounds. In this study, the expression pattern of all known xenobiotic-metabolizing CYP genes was characterized in the human alveolar type II cell-derived A549 adenocarcinoma cell line using qualitative reverse transcriptase/polymerase chain reaction (RT-PCR). In addition, the mechanisms of induction by chemicals of members in the CYP1 and CYP3A subfamilies were assessed by quantitative RT-PCR. The expression of messenger RNAs (mRNAs) of CYPs 1A1, 1B1, 2B6, 2C, 2E1, 3A5, and 3A7 was detected in the A549 cells. The amounts of mRNAs of CYPs 1A2, 2A6, 2A7, 2A13, 2F1, 3A4, and 4B1 were below the limit of detection. 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induced CYP1A1 and CYP1B1 mRNAs 56-fold and 2.5-fold, respectively. CYP3A5 was induced 8-fold by dexamethasone and 11-fold by phenobarbital. CYP3A4 was not induced by any of the typical CYP3A4 inducers used. The tyrosine kinase inhibitor genistein and the protein kinase C inhibitor staurosporine blocked TCDD-elicited induction of CYP1A1, but they did not affect CYP1B1 induction. Protein phosphatase inhibitors okadaic acid and calyculin A enhanced TCDD-induction of CYP1B1 slightly, but had negligible effects on CYP1A1 induction. These results suggest that CYP1A1 and CYP1B1 are differentially regulated in human pulmonary epithelial cells and give the first indication of the induction of CYP3A5 by glucocorticoids in human lung cells. These results establish that having retained several characteristics of human lung epithelial cell CYP expression, the A549 lung cell line is a valuable model for mechanistic studies on induction of the pulmonary CYP system.

Topics: Adenocarcinoma; Anti-Inflammatory Agents; Aryl Hydrocarbon Hydroxylases; Cytochrome P-450 CYP1A1; Cytochrome P-450 CYP1B1; Cytochrome P-450 CYP3A; Cytochrome P-450 Enzyme System; Dexamethasone; Enzyme Inhibitors; Epithelial Cells; Excitatory Amino Acid Antagonists; Gene Expression Regulation, Enzymologic; Gene Expression Regulation, Neoplastic; Humans; Lung Neoplasms; Phenobarbital; Pulmonary Alveoli; Rifampin; RNA, Messenger; Tumor Cells, Cultured; Xenobiotics

The multidrug resistance-associated protein (MRP) is a drug efflux membrane pump conferring multidrug resistance on tumor cells. In order to look for compounds that can lead to reversal of such a resistance, the antituberculosis compound rifampicin, belonging to the chemical class of rifamycins, was examined for its effect on MRP activity in human multidrug resistant lung cancer GLC4/ADR cells. Rifampicin was shown to increase accumulation of the MRP substrate calcein in GLC4/ADR cells in a dose-dependent manner by inhibiting its MRP-mediated efflux from the cells; it also enhanced intracellular retention of another substrate of MRP such as the anticancer drug vincristine in the resistant cells. By contrast, the antituberculosis drug did not alter cellular levels of accumulation of either calcein or vincristine in parental drug-sensitive GLC4 cells. Other rifamycins such as rifamycin B and rifamycin SV were also demonstrated to increase intracellular accumulation of calcein in GLC4/ADR cells. These results therefore indicate that rifamycins, including rifampicin, probably constitute a new chemical class of modulators down-regulating MRP-mediated drug transport.

Topics: Antibiotics, Antitubercular; ATP-Binding Cassette Transporters; Dose-Response Relationship, Drug; Drug Resistance, Multiple; Fluoresceins; Humans; Lung Neoplasms; Models, Chemical; Multidrug Resistance-Associated Proteins; Rifampin; Rifamycins; Tumor Cells, Cultured

We reported a human immunodeficiency virus type 1-infected patient with a small solitary pulmonary nodule mimicking adenocarcinoma, who was treated successfully with antituberculosis therapy. We believe that high-resolution CT scans of thorax are important examinations to detect pulmonary inflammatory findings, such as ectasis of the bronchi leading to the nodules and calcifications in the nodules, and also as follow-up tests for evaluating effectiveness of treatment on pulmonary inflammatory nodules in human immunodeficiency virus type 1-infected patients.

Topics: Acquired Immunodeficiency Syndrome; Adenocarcinoma; Adult; Antitubercular Agents; Diagnosis, Differential; Drug Therapy, Combination; Ethambutol; HIV-1; Humans; Isoniazid; Lung Neoplasms; Male; Pyrazinamide; Rifampin; Solitary Pulmonary Nodule; Tomography, X-Ray Computed

The effect of rifampicin on transplantable tumor growth and antitumor immunity was studied. The growth of transplantable lung sarcoma was significantly enhanced in mice when rifampicin was given for 7 days or longer. Also, the antitumor effects of preimmunization of the animals with killed tumor cells were abrogated by this antibiotic. In vitro studies showed that spleen cells from tumor-bearing animals expressed significantly lower specific cytotoxicity toward syngeneic tumor cells, when the animals had been previously treated with rifampicin. Also, natural killer activity in healthy animals was diminished in mice receiving the antibiotic.

Topics: Animals; Antigens, Neoplasm; Cytotoxicity, Immunologic; Immunization; Immunosuppressive Agents; In Vitro Techniques; Killer Cells, Natural; Lung Neoplasms; Male; Mice; Mice, Inbred BALB C; Rifampin; Sarcoma, Experimental; Spleen

Topics: Humans; Lung Neoplasms; Male; Middle Aged; Neoplasms, Multiple Primary; Rifampin; Tuberculosis, Pulmonary

Topics: Adult; Carcinoma; Carcinoma, Small Cell; Humans; Lung Neoplasms; Male; Middle Aged; Rifampin; Tuberculosis, Pulmonary

Topics: Adult; Carcinoma, Small Cell; Diagnostic Errors; Humans; Lung Neoplasms; Male; Rifampin; Tuberculosis, Pulmonary

Topics: Adult; Aged; Female; Hodgkin Disease; Humans; Lung Neoplasms; Middle Aged; Remission, Spontaneous; Rifampin; Time Factors

Topics: alpha 1-Antitrypsin; Anniversaries and Special Events; Antibody Formation; Congresses as Topic; Finland; Humans; Legislation, Medical; Lung Neoplasms; Public Relations; Rifampin; Scandinavian and Nordic Countries; Smoking; Societies, Medical; Tuberculosis; World Health Organization

Topics: Carcinoma, Small Cell; Humans; Immunity; Lung Neoplasms; Male; Middle Aged; Rifampin; Tuberculosis, Pulmonary

Topics: Antitubercular Agents; Bronchitis; Cycloserine; Humans; Italy; Lung Diseases; Lung Neoplasms; Pyrazines; Rifampin; Tuberculosis; Tuberculosis, Pulmonary