Publications by authors named "Sachin R Shah"

12 Publications

  • Page 1 of 1

Race as a factor for intensification of diabetes medications.

Diabetes Educ 2013 May-Jun;39(3):335-43. Epub 2013 Mar 8.

Texas Tech University Health Sciences Center School of Pharmacy, Department of Pharmacy Practice; Veterans Affairs North Texas Health Care System (VANTHCS), Dallas, Texas (Dr Bullock, Dr Edwards, Dr Greene, Dr Shah, Dr Blaszczyk)

Purpose: The purpose of this study was to investigate if patients of nonwhite race are less likely to receive insulin therapy for treatment of poorly controlled diabetes than patients of white race.

Methods: A retrospective review was performed of patients with an A1C >10%. The primary objective was to determine any difference in the initiation of insulin between white and nonwhite patients. Secondary outcomes measured the impact of clinic type and provider specialty on the initiation of insulin therapy. Exclusion criteria included those patients with type 1 diabetes mellitus, those who were previously receiving insulin, and those without an outpatient clinic visit within 14 days of an A1C >10%.

Results: A total of 277 patients were included. Of these patients, 132 (47.7%) were white, followed by 95 (34.2%) black non-Hispanic patients and 30 (10.8%) Hispanic/Latino patients. No difference was found in receipt of insulin therapy for nonwhite patients as compared to white patients (12.5 vs 21.4, P = .117). Neither clinic type nor provider specialty impacted initiation of insulin therapy. No changes to medication regimen were made at 35% of clinic visits.

Conclusions: Failure to intensify diabetic medications was common in this outpatient setting. There were no disparities in the receipt of insulin therapy between white and nonwhite patients.
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http://dx.doi.org/10.1177/0145721713479145DOI Listing
January 2014

Vemurafenib: targeted inhibition of mutated BRAF for treatment of advanced melanoma and its potential in other malignancies.

Drugs 2012 Dec;72(17):2207-22

VA North Texas Health Care System, Dallas, TX 75216, USA.

Vemurafenib is the first molecularly targeted therapy to be licensed in the US and Europe for treatment of advanced melanoma. Its mechanism of action involves selective inhibition of the mutated BRAF V600E kinase that leads to reduced signalling through the aberrant mitogen-activated protein kinase (MAPK) pathway. Its efficacy is restricted to melanomas carrying the BRAF V600E mutation, which is seen in approximately 50% of all melanomas. In a randomized phase III trial, it was superior to dacarbazine in first-line treatment of advanced melanoma, with an overall response rate (ORR) of 48% (95% CI 42, 45), an estimated 6-month progression-free survival (PFS) of 5.3 versus 1.6 months (hazard ratio [HR] 0.26; 95% CI 0.20, 0.33; p < 0.001) and a statistically superior 12-month overall survival (OS) rate of 55% versus 43% (HR 0.62 [95% CI 0.49, 0.77]). Vemurafenib is generally well tolerated, but its use can be associated with development of cutaneous neoplasms such as squamous cell carcinoma (SCC) and keratoacanthoma (KA). These lesions can be excised safely without the need for withholding the drug or reducing its dose. Mechanisms of resistance to vemurafenib do not involve development of secondary mutations in the BRAF kinase domain, but may be related to BRAF V600E over-amplification, bypassing mechanisms via upregulation and overexpression of other components in the MAPK signalling cascade or activation of alternative pathways with potential to enhance cell growth, proliferation and survival. Clinical trials to test the efficacy of vemurafenib in combination with immunomodulatory agents, such as ipilimumab, and MAPK kinase (MEK) inhibitors, such as GDC-0973, in the treatment of advanced melanoma are currently underway. Also under investigation is the use of vemurafenib in other solid tumours with BRAF mutations, such as papillary thyroid cancer.
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http://dx.doi.org/10.2165/11640870-000000000-00000DOI Listing
December 2012

Evaluation of chemotherapy-induced severe myelosuppression incidence in obese patients with capped dosing.

J Oncol Pract 2011 Jan;7(1):13-7

Veterans Affairs North Texas Health Care System; School of Pharmacy, Texas Tech University Health Sciences Center, Dallas, TX.

Purpose: Clinicians typically cap an obese patient's chemotherapy regimen as a result of concern for excessive toxicity, without adequate clinical evidence. The purpose of this study was to evaluate the incidence of grade 3 or 4 myelosuppression in obese patients versus nonobese patients with capped dosing on the basis of body surface area (BSA).

Methods: A retrospective chart review was conducted comparing obese patients (body mass index [BMI] ≥ 30 kg/m(2)) with capped dosing who received capped chemotherapy doses at a BSA of 2.2 m(2) with nonobese (BMI < 25 kg/m(2)) patients with lung, colorectal, or hormone-refractory prostate cancer.

Results: Forty-one obese patients with capped dosing and 244 nonobese patients were included. The obese patient group received on average significantly more cycles of chemotherapy (6 v 4 cycles) compared with the nonobese group. The overall incidence of any chemotherapy-related toxicity was 34% in the obese patient group, compared with 42% in the nonobese patient group (P = .356). The incidence of grade 3 or 4 myelosuppression was lower, but not statistically significant, in obese patients with capped dosing compared with the nonobese patient group (22% v 27%; P = .493).

Conclusions: Overall, obese patients with capped dosing experienced a lower incidence of severe myelosuppression and tolerated more cycles of chemotherapy compared with nonobese patients. The better tolerability of chemotherapy in obese patients with capped dosing suggests that there is room to increase the dose in obese patients above the nationally recognized BSA cap of 2.0 m(2), especially in early-stage lung or colon cancers in which the intention of treatment is curative.
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http://dx.doi.org/10.1200/JOP.2010.000045DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3014502PMC
January 2011

Pazopanib: the newest tyrosine kinase inhibitor for the treatment of advanced or metastatic renal cell carcinoma.

Drugs 2011 Mar;71(4):443-54

Texas Tech University Health Sciences Center School of Pharmacy, Dallas, Texas 75216, USA.

Treatment options for renal cell carcinoma (RCC) have multiplied in the past 5 years. Pazopanib is the third tyrosine kinase inhibitor (TKI) and the sixth targeted therapy that has received US FDA approval for the treatment of advanced or metastatic RCC. The primary mechanism of action of pazopanib in RCC is through its antiangiogenic properties via inhibition of the intracellular tyrosine kinase of vascular endothelial growth factor receptor and platelet-derived growth factor receptor. A placebo-controlled phase III study demonstrated that pazopanib significantly improved response rates and progression-free survival (PFS) in both treatment-naïve and cytokine-pretreated patients. Among treatment-naïve patients, the response rate was 32% and PFS was 11.1 months. In cytokine-pretreated patients, the response rate and PFS were 29% and 7.4 months, respectively. Common adverse effects of pazopanib include diarrhoea, hypertension and elevation of liver enzymes. Overall, the adverse effect profile of pazopanib is similar to that of other TKIs used for the treatment of RCC, but variation in the incidence and severity may exist. Pazopanib has an increased propensity to cause hepatotoxicity, which may be fatal in rare cases. Hepatic function must be monitored closely with dose interruption and/or reduction if elevation of hepatic function tests occurs. Pazopanib is administered on an empty stomach at a dose of 800 mg daily until disease progression, but dose reduction may be required in patients with baseline elevation of hepatic function tests, particularly total bilirubin. The minimum dose recommended for baseline hepatic dysfunction or toxicity is 200 mg daily. The potential for drug interactions exists for pazopanib. It is a substrate of cytochrome P450 (CYP) 3A4, P-glycoprotein and breast cancer resistance protein, and it weakly inhibits CYP3A4, CYP2C8 and CYP2D6, and potently inhibits UGT1A1 and OATP1B1. Currently, no study has directly compared pazopanib with other first- or second-line therapies in RCC. However, published clinical trials of pazopanib show similar efficacy outcomes to those of other targeted therapies. Therefore, pazopanib may be considered a first-line treatment option among other therapies including sunitinib, temsirolimus, and bevacizumab plus interferon-α. After failure of cytokine therapy, pazopanib is a treatment option as well as sorafenib or bevacizumab. No study has evaluated pazopanib treatment after failure of another targeted therapy. Future studies will further clarify the comparative efficacy of pazopanib with other agents as well as optimal sequencing with other agents. If similar efficacy is seen among the TKIs, it is likely that varying incidences of adverse effects may be analysed to tailor therapy according to the patient's individual co-morbidities and preferences.
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http://dx.doi.org/10.2165/11588960-000000000-00000DOI Listing
March 2011

Risk of renal failure in cancer patients with bone metastasis treated with renally adjusted zoledronic acid.

Support Care Cancer 2012 Jan 1;20(1):87-93. Epub 2011 Jan 1.

Texas Tech University Health Sciences Center (TTUHSC) School of Pharmacy, 4500 S. Lancaster Rd., Dallas, TX 75216, USA.

Purpose: The purpose of this study was to evaluate the incidence of acute renal failure (ARF) in patients with mild to moderate renal dysfunction, receiving renally adjusted zoledronic acid (ZA) and compare it to patients with normal baseline renal function, receiving standard-dose ZA.

Methods: This was a retrospective study of patients receiving ZA for the treatment of bone metastasis due to cancer. Patients were divided into two groups: (1) normal group with baseline creatinine clearance (CrCl) of greater than 60 mL/min and standard ZA dose; (2) impaired group with baseline CrCl of 30-60 mL/min and renally adjusted ZA dose. Primary endpoint of ARF was defined as an increase in serum creatinine (SCr) of 0.5 mg/dL or 1.0 mg/dL from a baseline SCr of <1.4 mg/dL or ≥ 1.4 mg/dL, respectively.

Results: In total, 1,472 evaluable doses of ZA were given to 220 patients. Of these, 184 patients were in the normal group and 36 patients in the impaired group. There were 38 patients (20.7%) who developed ARF in the normal group versus 7 patients (19.4%) in the impaired group. There was no difference in the mean time to the incidence of ARF at 6.1 months in both groups. Incidence of ARF based on CrCl (≥ 25% decline in CrCl) was similar between groups (39.1% vs. 41.7%; p = 0.78).

Conclusion: The incidence of ARF is similar between patients in the normal group and impaired group when the ZA dose is renally adjusted.
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http://dx.doi.org/10.1007/s00520-010-1067-7DOI Listing
January 2012

Comparison of the 5-fluorouracil-warfarin and capecitabine-warfarin drug interactions.

Pharmacotherapy 2010 Dec;30(12):1259-65

School of Pharmacy, Texas Tech University Health Sciences Center, Dallas, Texas 75216, USA.

Study Objective: To compare the differences between the 5-fluorouracil-warfarin and capecitabine-warfarin drug interactions in patients receiving therapeutic doses of warfarin.

Design: Retrospective medical record review.

Setting: Large academic Veterans Affairs health care system.

Patients: Twenty-four patients who received concomitant therapeutic doses of warfarin and at least one dose of a fluoropyrimidine--5-fluorouracil or capecitabine--between January 2004 and May 2008.

Measurements And Main Results: The primary outcome was mean change in international normalized ratio (INR) from baseline to end of 90-day study period. Only patients who were taking warfarin before starting either fluoropyrimidine-based chemotherapy were included in the primary analysis. Of the 24 eligible patients, 15 (9 receiving 5-fluorouracil, 6 receiving capecitabine) were taking warfarin before receiving either fluoropyrimidine. No significant differences were noted in the average weekly warfarin dose or baseline INR between the 5-fluorouracil and capecitabine groups. The mean change in INR for patients taking warfarin before fluoropyrimidine use was 4.62 in the 5-fluorouracil group compared with 5.11 in the capecitabine group (p=0.87). The capecitabine group had a similar proportion of patients achieving an INR above 9 while taking warfarin compared with the 5-fluorouracil group (17% vs 22%). In those patients who required a warfarin dosage reduction, the dose was reduced by 38% and 41% in the 5-fluorouracil and capecitabine groups, respectively. No significant differences in bleeding events were reported within 90 days of concurrent use of either fluoropyrimidine with warfarin.

Conclusion: Our study suggests that in patients receiving concomitant warfarin and a fluoropyrimidine, no significant differences in INR elevation or bleeding events were noted with 5-fluorouracil compared with capecitabine.
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http://dx.doi.org/10.1592/phco.30.12.1259DOI Listing
December 2010

Retrospective analysis of the consequences of acid suppressive therapy on ketoconazole efficacy in advanced castration-resistant prostate cancer.

Ann Pharmacother 2010 Oct 14;44(10):1538-44. Epub 2010 Sep 14.

Texas Tech University Health Sciences Center, Dallas, USA.

Background: The area under the curve of a single ketoconazole dose has been shown to decrease significantly when administered with acid suppressive therapy. No published studies have examined the clinical impact of concurrent ketoconazole and acid suppressive therapy in patients with castration-resistant prostate cancer (CRPC).

Objective: To evaluate the effect of acid suppressive therapy on prostate-specific antigen (PSA) response rate in CRPC patients receiving ketoconazole.

Methods: This retrospective study evaluated CRPC patients treated with ketoconazole 3 times daily between January 1, 1999, and September 30, 2009. Patients included in the analysis had failed androgen deprivation therapy, and were subsequently initiated on ketoconazole. Response (PSA decline ≥50% maintained ≥4 weeks) was evaluated in patients receiving ketoconazole with (group 1 [G1]) or without (group 2 [G2]) concurrent acid suppressive therapy.

Results: Thirty patients (G1: 11 patients; G2: 19 patients) were included in the analysis. Mean age in G1 and G2 was 71.8 and 69.6 years, respectively. Most patients had received prior therapy with an antiandrogen (90.9% G1; 100% G2) and fewer patients received antiandrogen withdrawal therapy (27.3% G1; 21.1% G2). Median baseline PSA was 109.4 (G1) and 86.9 ng/mL (G2) (p = 0.55). Median duration of ketoconazole was 7.2 months in G1 and 5.8 months in G2 (p = 0.09). Ketoconazole adherence was 82% (G1) and 100% (G2). Median duration of concurrent acid suppressive therapy was 3.8 months (range 2.0-20.4) in G1. PSA response (72.7% and 47.4%; p = 0.26) and time to PSA response (1.2 vs 0.9 mo; p = 0.53) were statistically similar between G1 and G2, respectively. Median progression free survival was higher in G1 (11.5 vs 6.9 months in G2; p = 0.047).

Conclusions: Use of concurrent acid suppressive therapy and ketoconazole in CRPC patients did not decrease PSA response rate, and progression free survival was unexpectedly higher compared with the non-acid suppressive therapy group. Larger studies are needed to verify the clinical impact of acid suppressive therapy in combination with ketoconazole.
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http://dx.doi.org/10.1345/aph.1P225DOI Listing
October 2010

Intricacies of bevacizumab-induced toxicities and their management.

Ann Pharmacother 2009 Mar 3;43(3):490-501. Epub 2009 Mar 3.

Veterans Affairs North Texas Health Care System, Dallas, TX 75216, USA.

Objective: To review the serious and common toxicities of bevacizumab and describe their incidence, risk factors, presentation, pathophysiology, and management.

Data Sources: Literature for this review article was collected from PubMed, MEDLINE, and the proceedings of the American Society of Clinical Oncology (2000-November 2008). The key terms used in the search were: bevacizumab, vascular endothelial growth factor, angiogenesis inhibitors, toxicity, toxicity management, and adverse event.

Study Selection And Data Extraction: Review articles, preclinical studies, and all published Phase 1-3 clinical trials were reviewed. The references listed in identified articles were examined for additional publications.

Data Synthesis: The biomedical literature from 2000 to 2008 confirms that bevacizumab carries serious and potentially life-threatening toxicity risks and emphasizes the importance of early recognition, continuous monitoring, and prompt management of these toxicities. Such toxicities include hemorrhage/bleeding, wound healing complications, gastrointestinal perforation, arterial thromboembolism, congestive heart failure, hypertension, proteinuria/nephrotic syndrome, infusion-related hypersensitivity reactions, and reversible posterior leukoencephalopathy syndrome. Patients at the highest risk for these toxicities are individuals with a history of hypertension, thromboembolism, bleeding, cardiovascular disease, or preexisting proteinuria, as these conditions may be exacerbated by bevacizumab use. Additionally, particular tumor types correlate with risk for individual toxicities; for example, patients with squamous non-small-cell lung cancer or rectal cancer have a higher risk of bleeding, those with renal cell carcinoma have a higher proteinuria risk, and patients with colorectal cancer have a higher risk of gastrointestinal perforation. Further investigation is warranted to develop effective management strategies for these toxicities.

Conclusions: As bevacizumab is becoming widely used in general oncology practice, it is important to understand the toxicities that can arise and to develop practice guidelines for their management.
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http://dx.doi.org/10.1345/aph.1L426DOI Listing
March 2009

Epidermal growth factor receptor monoclonal antibodies for the treatment of metastatic colorectal cancer.

Pharmacotherapy 2008 Jun;28(6):742-54

School of Pharmacy, Texas Tech University Health Sciences Center, Dallas, Texas 75216, USA.

Treatment of metastatic colorectal disease has evolved over the last decade. Two epidermal growth factor receptor (EGFR) monoclonal antibodies--cetuximab and panitumumab--have been developed in an effort to provide yet another therapeutic option. The EGFR is a transmembrane glycoprotein, expressed constitutively throughout the body and found on many epithelial tissues. The monoclonal antibodies bind to and inhibit the activation of the receptor in the body. This inhibition prevents tumor cell growth, angiogenesis, invasion, and metastasis, and induces apoptosis. Cetuximab and panitumumab exhibit nonlinear pharmacokinetics. Both monoclonal antibodies are approved for the treatment of refractory metastatic colorectal cancer. Cetuximab in combination with irinotecan has significantly better response rates and progression-free survival compared with those of cetuximab or irinotecan alone. Cetuximab and panitumumab as monotherapy have shown significantly better response rates and progression-free survival compared with best supportive care in patients refractory to irinotecan and oxaliplatin. In the Cetuximab Combined with Irinotecan in First Line Therapy for Metastatic Colorectal Cancer (CRYSTAL) trial, treatment-naïve patients received cetuximab in combination with the chemotherapy regimen infusional leucovorin, fluorouracil, and irinotecan (FOLFIRI) or FOLFIRI alone; the difference in progression-free survival was statistically significant but suggested only a modest benefit over FOLFIRI alone (8.9 vs 8 mo, p=0.036). Results of a preplanned analysis of the first 231 events in the Panitumumab Advanced Colorectal Cancer Evaluation (PACCE) trial favored the control group (chemotherapy regimen with folinic acid [leucovorin], fluorouracil, and oxaliplatin [FOLFOX] plus bevacizumab) instead of the control group plus panitumumab. For clinical consideration, many trials have shown that the intensity or absence of EGFR expression is not a clinically significant predictor of outcomes. Development and intensity of a rash are suggested to be a positive predictor of outcomes in patients. The most common adverse events of EGFR monoclonal antibody therapy are rash, diarrhea, and hypomagnesemia. Other serious but not common adverse events include hypersensitivity reactions and pulmonary toxicity. The availability of EGFR monoclonal antibodies has provided another weapon in the arsenal to treat refractory metastatic colorectal cancer. They have shown safety and efficacy in combination with other chemotherapy regimens and as monotherapy; however, their use as metastatic colorectal cancer therapy needs to be further explored.
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http://dx.doi.org/10.1592/phco.28.6.742DOI Listing
June 2008

A newer immunoglobulin intravenous (IGIV) - Gammagard liquid 10%: evaluation of efficacy, safety, tolerability and impact on patient care.

Authors:
Sachin R Shah

Expert Opin Biol Ther 2008 Jun;8(6):799-804

Associate Professor of Pharmacy Practice/Hematology-Oncology Clinical Pharmacist Texas Tech University Health Sciences Center, School of Pharmacy/Veterans Affairs North Texas Healthcare System, Dallas, TX 75216, USA.

Background: Even though all immunoglobulin intravenous (IGIV) end products have high IgG concentrations, variations in manufacturing processes lead to unique product characteristics.

Objective: Solvent/detergent-treated IGIV (IGIV-S/D) liquid 10% (Gammagard or Kiovig liquid) is one of the newer products, and this article will discuss and compare its efficacy, safety, tolerability and effect on patient care.

Methods: The search terms 'immunoglobulin,' 'IGIV,' 'IVIG,' and 'liquid' were entered into PubMed/Medline and Google for the literature search in preparation of this manuscript. Additional references were screened from researched literature.

Results/conclusion: Gammagard liquid 10% has shown significant activity in primary immunodeficiency and immune thrombocytopenic purpura. It is a sugar- and sodium-free product with improved safety, tolerability and convenience. Overall, Gammagard liquid is a valuable addition to available therapies that has utility in life-threatening and complicated diseases, and its use will continue to grow.
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http://dx.doi.org/10.1517/14712598.8.6.799DOI Listing
June 2008

Lenalidomide in myelodysplastic syndrome and multiple myeloma.

Drugs 2007 ;67(13):1869-81

Texas Tech University Health Sciences Center-School of Pharmacy/VA North Texas Health Care System, Dallas, Texas, USA.

The use of thalidomide is limited by adverse effects of sedation, constipation, neuropathy and thromboembolism. In order to discover more potent and less toxic immunomodulators than thalidomide, its chemical structure was modified and lenalidomide was formed. Lenalidomide is approved by the US FDA for the treatment of patients with low-risk myelodysplastic syndrome (MDS) with deletion 5q cytogenetic abnormality. Two studies and a case report have evaluated lenalidomide in these MDS patients and showed significantly higher cytogenetic responses and durable red blood cell transfusion independence. Lenalidomide should be the drug of choice for patients with low and intermediate-1 risk MDS (based on the International Prognostic Scoring System) with chromosome 5q31 deletion with or without other karyotype abnormalities. Lenalidomide, in combination with dexamethasone, has been compared with dexamethasone alone in patients with relapsed or refractory multiple myeloma (MM) in two studies (MM-009 in North America and MM-010 in Europe, Israel and Australia). In these two phase III trials, lenalidomide demonstrated impressive (58-59%) response rates with dexamethasone. Lenalidomide has also been shown to overcome thalidomide resistance in MM patients. Therefore, the lenalidomide plus dexamethasone regimen provides another treatment option, in addition to first line MM treatment regimens of bortezomib, thalidomide or high-dose dexamethasone, for the treatment of relapsed or refractory MM. Lenalidomide does not produce significant sedation, constipation or neuropathy, but does lead to significant myelosuppression, unlike thalidomide. The prescribing information has a black box warning for risk of myelosuppression, deep vein thrombosis/pulmonary embolism and teratogenicity. Administration of lenalidomide is recommended at a starting dose of 10 mg/day orally for deletion 5q in MDS patients. Significant risk of myelosuppression may lead to dose reduction in the majority of these patients. Clinical trials of relapsed and refractory MM have shown that lenalidomide is clinically efficacious at a dosage of 25 mg/day when administered in combination with dexamethasone. Lenalidomide should be continued until disease progression in both MDS and MM patients.
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http://dx.doi.org/10.2165/00003495-200767130-00005DOI Listing
December 2007

Pemetrexed, a novel antifolate therapeutic alternative for cancer chemotherapy.

Pharmacotherapy 2006 May;26(5):641-54

School of Pharmacy, Texas Tech University Health Sciences Center, Dallas, 75216, USA.

Pemetrexed is a newly approved antifolate agent for the treatment of malignant pleural mesothelioma (MPM) and metastatic non-small cell lung cancer (NSCLC). We performed a PubMed/MEDLINE database search to identify relevant literature from January 1966-April 2005. Bibliographies from identified references were searched as well, as were abstracts from the 2004 and 2005 proceedings of the American Society of Clinical Oncology. We discuss the pharmacology of pemetrexed, describing its mechanism of action and comparing it with methotrexate. The pharmacokinetics and pharmacodynamics of pemetrexed are described to provide a better understanding of the properties of this drug. Therapeutic uses are assessed, beginning with the approved indications of MPM and NSCLC. However, pemetrexed has been studied in numerous phase II trials for other types of solid malignancies, and completed trials are reviewed. Data on adverse effects and drug interactions are also provided. Finally, dosing and administration are reviewed, including appropriate premedication. Premedication, including administration of steroids and vitamin supplements, has been shown to decrease the frequency and severity of pemetrexed toxicities. Pemetrexed should be used as a standard of care for unresectable MPM and recurrent metastatic NSCLC.
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http://dx.doi.org/10.1592/phco.26.5.641DOI Listing
May 2006