A pilot double-blind, randomized, placebo-controlled trial of curcumin/bioperine for lung cancer chemoprevention in patients with chronic obstructive pulmonary disease
Amir Sharafkhaneh, J. Jack Lee, Diane Liu, Ruth Katz, Nancy Caraway, Cherise Acosta, Ignacio I. Wistuba, Bharat Aggarwal, Burton Dickey, Seyed J. Moghaddam, Nicola Hanania, Robert Newman, Hanan Abdel-Monem, Nga Bich Nguyen, Carol J. Farhangfar, Waun K. Hong, Jonathan M. Kurie
Department of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, USA.
Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, USA.
Department of Medicine, Baylor College of Medicine, Houston, USA.
Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, USA.
Department of Pulmonary Medicine, The University of Texas MD Anderson Cancer Center, Houston, USA.
Department of Thoracic/Head and Neck Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, USA.
Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, USA.
DOI: 10.4236/alc.2013.23008   PDF    HTML   XML   6,791 Downloads   12,911 Views   Citations

Abstract

Chronic obstructive pulmonary disease is an inflammatory condition with increased risk of lung cancer. We hypothesized that curcumin/ bioperine (CB), which has anti-inflammatory effects, may reduce cytological abnormalities in the sputum of patients with COPD. We conducted a 3-month, three-to-one randomized, doubleblind, pilot trial of escalating doses of CB in patients with moderate or worse COPD who were capable of producing sputum. The primary efficacy endpoint was changed in sputum cytology. We also explored changes in fluorescence in situ hybridization (FISH). We obtained sputum samples for cytology and chromosome abnormalities at baseline and each monthly follow-up visit. We enrolled 57 participants, with 35 completing the study. The participants’ mean age (standard deviation [SD]) was 66.6 (8.2) years, and they were mainly male (91.2%), with an average of 63.8 pack-years of smoking history. Also, 42.1% of participants were active smokers and the mean (SD) FEV1 was 37% (13%). At baseline, 13 subjects had moderate or worse dysplasia (22.8%). Subjects with moderate to severe sputum dysplasia had more chromosome abnormalities in epithelial cells and neutrophils, as measured by deletion and aneuploidy in 10q22.3. The changes in sputum cytology and chromosome abnormalities did not differ between the active and placebo arms. CB was well tolerated at the bid doses of 1, 1.5, and 2 gm of curcumin and 5 mg of bioperine, with minor side effects related to the gastrointestinal tract. In this short pilot trial, CB compared to placebo did not alter cytological and chromosomal abnormalities seen in sputum of patients with COPD.

Share and Cite:

Sharafkhaneh, A. , Lee, J. , Liu, D. , Katz, R. , Caraway, N. , Acosta, C. , Wistuba, I. , Aggarwal, B. , Dickey, B. , Moghaddam, S. , Hanania, N. , Newman, R. , Abdel-Monem, H. , Nguyen, N. , Farhangfar, C. , Hong, W. and Kurie, J. (2013) A pilot double-blind, randomized, placebo-controlled trial of curcumin/bioperine for lung cancer chemoprevention in patients with chronic obstructive pulmonary disease. Advances in Lung Cancer, 2, 62-69. doi: 10.4236/alc.2013.23008.

1. INTRODUCTION

Chronic obstructive pulmonary disease (COPD) is a debilitating disease that results in significant morbidity and mortality. Physiologically, COPD is characterized by expiratory airflow limitation that is partially reversible [1]. Pathologically, COPD is characterized by emphysema, small airway wall thickening, mucous metaplasia, occlusion of small airways with inflammatory mucus, and mucous gland hypertrophy and hyperplasia in large airways [2-4]. Various inflammatory cells including macrophages, neutrophils and CD8—T lymphocytes are increased in the airways of patients with COPD [2]. Associated with these inflammatory changes, COPD patients exhibit varying degrees of dysplasia upon cytologic examination of sputum or bronchial biopsy. Among smokers, there is a statistically significant increased risk of lung cancer in those patients with coexistent COPD [5]. Interestingly, cancer ensued up to 5 years after the initial abnormal sputum, with an accumulation of worsening cytopathologic findings until cancer was diagnosed. The association between inflammation and lung cancer in COPD patients has led to the hypothesis that targeting aspects of the inflammatory response will reverse premalignancy and reduce lung cancer risk in COPD patients.

Curcumin (diferuloylmethane) is a potent anti-inflammatory agent that has shown substantial anticarcinogenic properties in cellular and animal models of cancer [6,7]. Its efficacy has been attributed to its capacity to inhibit the NFkB transcription factor, which regulates inflammation, angiogenesis, and tumor cell survival, invasion, and metastasis [8]. Several clinical trials have revealed activity of curcumin in cancer patients [9]. In a dose-escalation study of 15 patients with advanced colorectal cancer refractory to standard treatment, study subjects received doses of 440 to 2200 mg/day of curcuma extracts (containing 36 - 180 mg of curcumin) daily for 4 months. Five patients had radiologically stable disease during treatment for 2 to 4 months [10]. Cruz-Correa and colleagues demonstrated a dramatic reduction in polyps (60.4%) in patients with familial adenomatous polyposis (FAP) treated with curcumin and quercetin, further demonstrating the potential of the combination [11].

Because clinical and preclinical studies have shown that curcumin has poor bioavailability, Shoba and colleagues examined the effects of piperine on the bioavailability of curcumin in rats and healthy volunteers [12]. When curcumin was given to rats at a dose of 2 g/kg with concomitant piperine at a dose of 20 mg/kg, the serum concentration of curcumin increased and its bioavailability increased by 154% compared to that of curcumin given alone. Also, the time to maximum concentration significantly increased (P < 0.002), and the rate of clearance significantly decreased (P < 0.02). In healthy volunteers, serum levels of curcumin were very low or undetectable (approximately 0.006 pg/ml) 1 hr after a 2 g dose. When piperine was added at a dose of 20 mg, significantly higher concentrations of curcumin (as much as 0.18 pg/ml) were observed 1 hr after administration for up to 0.75 hours (P < 0.01). These concentrations decreased to 0 by 3 hr after administration. No toxicity with curcumin or piperine was reported at these doses.

Given the association between airway inflammation and lung cancer risk in COPD patients, in this study we evaluated the effects of the curcumin/bioperine (an extract of piperine) combination on epithelial and FISH detected abnormalities, lung function, and exercise capacity in a 3-month dose-escalation, double-blind, randomized, pilot clinical trial in patients with COPD.

2. MATERIALS AND METHODS

This was a pilot study with intent to evaluate cytology changes in sputum by treatment of curcumin plus bioperine (CB). The ultimate goal was to gain information for planning a large scale study using CB. A total of 40 patients were planned to be enrolled, 30 in CB and 10 in placebo groups. The protocol was approved by the Baylor College of Medicine Institutional Review Board and the Research and Development Committee of the Michael E. DeBakey Veterans Affairs Medical Center (MEDVAMC) in Houston, Texas, USA. The study was conducted between August 2006 and March 2008. The clinical investigation described herein was conducted in accordance with the guidelines in The Declaration of Helsinki. All subjects provided written informed consent.

2.1. Study Subjects

The potential subjects were recruited from our pulmonary clinics at the MEDVAMC. We enrolled subjects with COPD who were at least 40 years old and who had a smoking history of at least 10 pack-years and a history of chronic bronchitis to increase the likelihood of sputum production. Subjects with a history of COPD exacerbations within the previous 8 weeks; other chronic respiratory conditions, including asthma, symptomatic heart failure, liver failure, or renal failure; any cancer within the past 5 years; or any lung or upper airway cancer were excluded. After signing the consent form, the study subjects underwent spirometry to test for COPD, which we defined as an FEV1/FVC ratio < 70% (ref GOLD guideline). Subjects who did not meet the spirometry criteria for COPD were excluded from the study. Furthermore, subjects who were not able to produce sputum at the time of consent were excluded. We screened 75 subjects from who 59 subjects met the study criteria; 1 subsequently withdrew consent and 1 was already in another study and was excluded. Thus, 57 patients enrolled in the study and received at least one dose of the study agents/placebo. Thirty-five patients completed the study. Among the 22 patients who dropped out of the study, 12 dropped out after baseline evaluation, 5 after 1 month, and 5 after 2 months (Figure 1).

Figure 1. The consort diagram.

2.2. Study Design

The curcumin, bioperine, and placebo were obtained pre-packaged from Sabinsa Corporation (East Windsor, New Jersey, USA). The study medication/placebo was stored in the MEDVAMC research pharmacy and was dispensed by the research pharmacist. Each capsule contained 500 mg of curcumin and each tablet contained 5 mg of bioperine. We initially enrolled 8 participants in an open-label study to evaluate the safety and tolerability of curcumin plus bioperine (CB). The dosing schedule was similar (see below) to the double-blinded part of the study. Subsequently, the participants were randomized (3 to 1) to receive CB versus placebo, a design intended to maximize the number of patients who receive the active drug. Each participant received CB at 1 g curcumin/5mg bioperine b.i.d. for a month, then CB at 1.5 g/5mg b.i.d. for a month, and finally, CB at 2 g/5 mg b.i.d. for an additional month. The escalating doses design was used for the concern of safety in the COPD population. The participants were seen at the research clinic at the MEDVAMC at baseline, one, two and three months after randomization. At each visit, the participants were asked to give a sputum sample. On the first visit, following inhalation of nebulized 3% saline, the participants were instructed to cough into a container filled with Sacommano’s fixative (90% alcohol, 5% acetic acid, and 5% polyethylene glycol). For subsequent visits, the participants were given containers with the fixative to take home. The participants were instructed to cough their morning sputum into the container on the day of their visit to the research center.

After the collection of sputum samples, spirometry tests were performed. For spirometry, we obtained at least three reproducible forced expiratory maneuvers. For the forced maneuvers, each subject was instructed to inspire to total lung capacity and then to expire with maximal effort to residual volume. Quality control measures as outlined by the American Thoracic Society were used to select appropriate maneuvers [13]. Each subject was instructed to expire forcefully for at least 6 seconds. Subsequently, the subjects underwent a 6-minute walk test according to the guidelines published by the American Thoracic Society [14].

2.3. Sputum Cytologic Analysis

The sputum samples were transferred to the cytology laboratory at The University of Texas MD Anderson Cancer Center for processing. Samples were transferred to 50-mL conical tubes and centrifuged at 1500 rpm for 10 minutes. Supernatant was removed, leaving behind 2 - 3 mL of the solution with the cell pellet. Four millimeters of 1X phosphate-buffered saline (PBS) was added to the cell pellet and centrifuged at 1500 rpm for 5 minutes. The supernatant was discarded and 4 mL of pre-warmed 3.25-mM Sputolysin (0.05 g DDT, 5 mL PBS, and 45 mL H2O) was added to the cell pellet and incubated for 5 minutes at 37˚C in the incubator. Next, the supernatant was discarded and the cell pellet was washed with 1X PBS and saved. Finally, 2 mL of 50% ethanol was added to the cell pellet, which was then divided and mounted on several super-frosted slides. One Diff Quick slide was made to check the cellularity and adequacy of the sample (at least 10 macrophages per slide were required for a slide to be deemed adequate). Once the cellularity and adequacy were determined, cytospins were made using a Shandon Cytocentrifuge (Thermo Fisher Scientific Inc., Waltham, MA). Two slides were fixed in 95% ethanol for Papanicolaou staining, and the rest of the slides were fixed in Carnoy’s fixative (3:1, methanol:acetic acid) for FISH analysis. Samples were given a score (negative, squamous metaplasia, or mild, moderate, or severe dysplasia) using standard criteria [15].

2.4. FISH Analysis

We used fluorescence in situ hybridization (FISH) to analyze abnormal gene amplifications and/or deletions in epithelial cells and neutrophils in sputum at baseline and at monthly follow-up. Two-color FISH was performed on sputum samples using in-house bacterial artificial chromosome probes for 3p22.1 and 10q22.3. For internal controls, we combined in-house 3p22.1 (green) probe with the centromeric 3 (orange) probe and the 10q22.3 (green) probe with the centromeric 10 (orange) probe (centromeric 3 and 10 probes obtained from Vysis, Inc.; Downers Grove, IL). One slide was used for centromeric 3 and 3p22.1 FISH assay and another slide was used for centromeric 10 and 10q22.3 FISH assay.

Slides were pretreated in 2X sodium saline citrate (SSC) for 2 minutes at 73˚C, digested in Protease (Vysis, Inc.) solution (50 mL of 1X PBS [pH < 2.0] at 37˚C and 25 mg of protease), washed with 1X PBS, fixed with 1% formaldehyde, and rinsed again with 1X PBS. Slides were then dehydrated in a series of 70%, 85%, and 100% ethanol. Seven microliters of probe preparation was applied to each slide, slides were covered with a small coverslip, and rubber cement was applied. Slides were kept in a Hybrid machine (Vysis, Inc.; Downers Grove, IL) using a melting temperature of 77˚C for 5 minutes and then incubated at 37˚C for 18 - 20 hrs.

The next day after hybridization, the slides were washed using 0.4X SSC/0.3% NP-40 for 2 minutes at 74˚C and then 2X SSC/0.1% NP-40 at room temperature for 1 minute. Slides were counterstained with 10 µL of DAPI (4,6-diamidino-2-phenylindole) and visualized under a fluorescent microscope equipped with triple, red and green dual band, single green, and red filters.

2.5. Manual and Automated Scoring of FISH Signals

For each sample, at least 100 epithelial cells were scored manually for deletions of centromeric 3, 3p22.1, centromeric 10, and 10q22.3 and for other chromosomal abnormalities, including aneusomy or gain of any chromosomal material compared to an internal centromeric probe. Single non-overlapping cells with good FISH signals were scored. Cells with chromosomal abnormalities were selected. At the same time and in the same fields, neutrophils were also scored for similar abnormalities.

For centromeric 3 and 3p probes, 2 orange (centromeric 3) and two green (locus specific 3p21) signals were classified as normal, cells with 2 orange signals and 1 green signal were put in the 3p deletion class, cells with 2 orange signals and 3 green signals were classified as having polysomy, and cells with more than 2 signals for green and orange were classified as aneuploid. At least 100 consecutive non-overlapping epithelial cells and 100 neutrophils were analyzed for each sample. A similar scheme of classification existed for scoring abnormalities of chromosome 10 and locus specific 10q22.3 where chromosome 10 was orange and 10q22.3 was green.

Slides for 3p22.1/centromeric 3 and 10q22.3/centromeric10 probes were scanned separately using the Bioview Duet automated scanner (Bioview Ltd., Nes Ziona, Israel). The automated system scans and classifies each FISH probe into normal class (2 green [G]:2 orange [O]), 3p deletions (1 G:2 O), 10q deletions (1 G:2 O), polysomy of 3p (3 G:2 O), polysomy of 10q (3 G:2 O), and abnormal class (>2 G:>2 O). After automated scanning, the operator checks the accuracy of the machine classification and reclassifies the cells visually as defined above, based on the number of orange and green signals present, if there is disagreement with the machine classification.

2.6. Statistical Analysis

The original sample size calculation of this study was based on modulation of a continuous marker in the sputum over time. With 40 patients, 30 and 10 in the active treatment and placebo groups (3:1), respectively, we would have 86% power to detect an effect size of 1.14 using two-sided t-test with a two-sided significance level of 0.05. With a 10% drop-out rate, the study will still have more than 80% power. Subsequently, the primary endpoint was revised to be the change of cytology score by one or more level in the sputum. The percentage of changes in each group from baseline to 3 months after treatment would be estimated. Fisher’s exact test will be applied to compare the percentage of changes between the CB and the placebo group.

Summary statistics, including frequency tabulation, means, and standard deviations, were given to describe subject characteristics, cytology readings, and FISH results. Fisher’s exact test was applied to compare the proportions of improved cytology from baseline to posttreatment between the two treatment groups. The Wilcoxon rank sum test was used to compare baseline FISH results between two cytology groups and the difference in FISH results between two treatment groups.

3. RESULTS

Table 1 shows the demographic data for the 57 subjects who were randomized in this study. The mean age was 66.6 years, and subjects had smoked substantially, with average pack-years of 63.8. Pulmonary function tests showed that the patient population suffered from severe COPD, defined as forced expiratory volume in 1 second (FEV1) ≤ 50% of predicted.

Conflicts of Interest

The authors declare no conflicts of interest.

References

[1] Rabe, K.F., Hurd, S., Anzueto, A., et al. (2007) Global strategy for the diagnosis, management, and prevention of COPD—2006 update. American Journal of Respiratory and Critical Care Medicine, 176, 532-555.
[2] Hogg, J.C., Chu, F., Utokaparch, S., et al. (2004) The nature of small-airway obstruction in chronic obstructive pulmonary disease. The New England Journal of Medicine, 350, 2645-2653. doi:10.1056/NEJMoa032158
[3] Hogg, J.C., Macklem, P.T. and Thurlbeck, W.M. (1968) Site and nature of airway obstruction in chronic obstructive lung disease. The New England Journal of Medicine, 278, 1355-1360. doi:10.1056/NEJM196806202782501
[4] Hogg, J.C., Chu, F.S., Tan, W.C., et al. (2007) Survival after lung volume reduction in chronic obstructive pulmonary disease: Insights from small airway pathology. American Journal of Respiratory and Critical Care Medicine, 176, 454-459. doi:10.1164/rccm.200612-1772OC
[5] Omenn, G.S., Goodman, G.E., Thornquist, M.D., et al. (1996) Effects of a combination of beta carotene and vitamin A on lung cancer and cardiovascular disease. The New England Journal of Medicine, 334, 1150-1155. doi:10.1056/NEJM199605023341802
[6] Moghaddam, S.J., Barta, P., Mirabolfathinejad, S.G., et al. (2009) Curcumin inhibits COPD-like airway inflammation and lung cancer progression in mice. Carcinogenesis, 30, 1949-1956. doi:10.1093/carcin/bgp229
[7] Gupta, S.C., Kim, J.H., Prasad, S., et al. (2010) Regulation of survival, proliferation, invasion, angiogenesis, and metastasis of tumor cells through modulation of inflammatory pathways by nutraceuticals. Cancer Metastasis Reviews, 29, 405-435. doi:10.1007/s10555-010-9235-2
[8] Gupta, S.C., Kim, J.H., Kannappan, R., et al. (2011) Role of nuclear factor kappaB-mediated inflammatory pathways in cancer-related symptoms and their regulation by nutritional agents. Experimental Biology and Medicine (Maywood), 236, 658-671. doi:10.1258/ebm.2011.011028
[9] Goel, A. and Aggarwal, B.B. (2010) Curcumin, the golden spice from Indian saffron, is a chemosensitizer and radiosensitizer for tumors and chemoprotector and radioprotector for normal organs. Nutrition and Cancer, 62, 919-930. doi:10.1080/01635581.2010.509835
[10] Sharma, R.A., McLelland, H.R., Hill, K.A., et al. (2001) Pharmacodynamic and pharmacokinetic study of oral Curcuma extract in patients with colorectal cancer. Clinical Cancer Research, 7, 1894-1900.
[11] Cruz-Correa, M., Shoskes, D.A., Sanchez, P., et al. (2006) Combination treatment with curcumin and quercetin of adenomas in familial adenomatous polyposis. Clinical Gastroenterology and Hepatology, 4, 1035-1038. doi:10.1016/j.cgh.2006.03.020
[12] Shoba, G., Joy, D., Joseph, T., et al. (1998) Influence of piperine on the pharmacokinetics of curcumin in animals and human volunteers. Planta Medica, 64, 353-356. doi:10.1055/s-2006-957450
[13] (2005) ATS/ERS recommendations for standardized procedures for the online and offline measurement of exhaled lower respiratory nitric oxide and nasal nitric oxide, 2005. American Journal of Respiratory and Critical Care Medicine, 171, 912-930. doi:10.1164/rccm.200406-710ST
[14] (2002) ATS statement: Guidelines for the six-minute walk test. American Journal of Respiratory and Critical Care Medicine, 166, 111-117. doi:10.1164/ajrccm.166.1.at1102
[15] Katz, R.L., Zaidi, T.M., Fernandez, R.L., et al. (2008)Automated detection of genetic abnormalities combined with cytology in sputum is a sensitive predictor of lung cancer. Modern Pathology, 21, 950-960. doi:10.1038/modpathol.2008.71

Copyright © 2024 by authors and Scientific Research Publishing Inc.

Creative Commons License

This work and the related PDF file are licensed under a Creative Commons Attribution 4.0 International License.