Severe and prolonged hypocalcemia after a single dose of denosumab for metastatic breast cancer with diffuse bone involvement without prior calcium/vitamin D supplementations.

INTRODUCTION: Denosumab is a human monoclonal antibody antiresorptive agent used for the treatment of bone metastasis in different cancer types, including breast cancer. Hypocalcemia is a known adverse effect of denosumab, and early supplementation plays an important role in the prevention and management of hypocalcemia. CASE REPORT: A 63-year-old female with stage IV estrogen receptor-positive breast cancer with diffuse bone metastasis experienced severe, prolonged hypocalcemia following a single dose of denosumab. The patient also had several risk factors for denosumab-associated hypocalcemia. Despite not receiving additional doses of denosumab, the patient required multiple hospitalizations and outpatient infusions of calcium to resolve her symptomatic hypocalcemia.Management and outcome: Severe hypocalcemia associated with denosumab can be prevented or mitigated by recognizing the risk factors for hypocalcemia and supplementing with vitamin D/calcium. Proposed risk factors include poor renal function, hypoparathyroidism, insufficient calcium intake, and diffuse metastatic bone disease. Studies suggest that early supplementation before starting denosumab can lower this risk. DISCUSSION: Several cases of severe hypocalcemia associated with denosumab have been reported. However, to the authors' knowledge, this is the first report that highlights the importance of early vitamin D/calcium supplementations for a patient with diffuse metastatic bone disease with pre-existing low levels of calcium.

Characterizing the impact of magnesium and potassium-supplemented hydration with cisplatin and the subsequent electrolyte replacement requirements.

BACKGROUND: Cisplatin-associated electrolyte dysregulation is a prevalent therapy-related adverse effect. There are numerous electrolyte-supplemented hydration regimens that have been evaluated, however these studies focused on the development of nephrotoxicity. The objective of this study was to characterize the impact of magnesium and potassium-supplemented hydration during cisplatin administration on subsequent magnesium and potassium imbalances. METHODS: A single-region retrospective study from central Texas at Baylor Scott & White Cancer Clinics who were treated with two or more cycles of cisplatin were included. Standard hydration for this study was defined as normal saline before and after cisplatin along with potassium chloride 10 mEq and magnesium sulfate 1 g added to the cisplatin bag. RESULTS: A total of 477 patients were included in the study with376 patients receiving the standard hydration. Overall, 17 percent of patients experienced a potassium level below 3.5 mEq/L, but no major depletion was observed. Thirty-three percent of the patients experienced a magnesium level below 1.8 mg/dL, and time to first rescue magnesium supplementation was 4 weeks. CONCLUSION: Our study demonstrated despite routine magnesium and potassium supplementation in hydration, magnesium imbalances were observed. Potassium levels post cisplatin administration were maintained with minimal routine supplementation in hydration.

Verapamil as a culprit of palbociclib toxicity.

A promising drug, palbociclib, received accelerated approval as a first line treatment when used with the aromatase inhibitor, letrozole, for postmenopausal women with hormone receptor positive advanced or metastatic breast cancer. We report a case of a patient who presented with febrile neutropenia, grade 3 stomatitis with lip swelling, periorbital edema, and transaminitis while on palbociclib and verapamil. Labs normalized upon discontinuation of verapamil and our patient was able to continue treatment with palbociclib and letrozole. Verapamil's inhibition of both permeability-glycoprotein (P-gp) and CYP3A4 is suspected to have led to the adverse side effects seen in our patient.

Altered methotrexate clearance in the treatment of CNS lymphoma with concurrent use of nitrofurantoin for a urinary tract infection.

Methotrexate is a widely used chemotherapy agent with a propensity for drug interactions placing the patient at risk for toxicities. There are several modes for altering methotrexate clearance including concomitant drugs leading to toxic effects on the kidneys, medications producing an acidic urine pH, and agents interfering with methotrexate transporters including the organic anion transporter and breast cancer resistance protein efflux pump. We report a case of a patient with central nervous system non-Hodgkin's lymphoma receiving high-dose methotrexate and being concomitantly treated for a urinary tract infection with nitrofurantoin. Subsequently, her initial methotrexate clearance was altered by the introduction of nitrofurantoin and returned to baseline when her nitrofurantoin was discontinued. This is the first case report describing the altered methotrexate clearance from concurrent administration of methotrexate and nitrofurantoin.

Analysis of carboplatin dosing in patients with a glomerular filtration rate greater than 125 mL/min: To cap or not to cap? A retrospective analysis and review.

The use of the Calvert formula to calculate carboplatin doses allows clinicians to achieve the appropriate carboplatin area under the concentration (AUC) curve. Thrombocytopenia is the dose limiting toxicity of carboplatin and optimizing AUC minimizes the risk of thrombocytopenia. Carboplatin clearance directly correlates with glomerular filtration rate (GFR) and, therefore, an accurate estimation of the renal function is needed. The Calvert formula was designed using the GFR measured by 51Cr-EDTA; however, many clinicians substitute estimated creatinine clearance (CrCl) as calculated by the Cockcroft-Gault (C-G) equation. The potential for overestimating AUC occurs when clinicians substitute actual weight in obese patients or use a low serum creatinine when calculating C-G estimated CrCl. In 2010, the National Cancer Institute recommended the GFR value within the Calvert formula should not exceed 125 mL/min, thereby capping the carboplatin dose. However, there are studies demonstrating that certain patients' actual GFR values do exceed 125 mL/min. Therefore, capping the carboplatin dose in these patients may lead to underestimating the carboplatin AUC. A single-center, retrospective study was performed to evaluate the change in platelet count pre- and post-carboplatin exposure in patients with C-G estimated CrCl greater than 125 mL/min receiving capped versus uncapped carboplatin doses. A review of carboplatin dosing strategies is also presented. This study indicated there was a larger mean difference in pre- and post-platelet count in patients receiving uncapped carboplatin compared to patients receiving capped carboplatin with no differences in toxicities. Dose capping this patient population will likely lead to a lower AUC rather than the intended AUC target, which could ultimately lead to substandard outcomes.

Cetirizine versus diphenhydramine in the prevention of chemotherapy-related hypersensitivity reactions.

OBJECTIVE: This study evaluated the role of cetirizine compared to diphenhydramine as premedications for patients receiving paclitaxel, cetuximab, and rituximab infusions. Historically, diphenhydramine has been linked with more sedation in comparison to cetirizine; however, it is unknown if cetirizine can replace diphenhydramine in the prevention of hypersensitivity reactions in patients receiving chemotherapy. METHODS: This is a retrospective study designed to assess infusion reactions occurring in patients receiving diphenhydramine or cetirizine premedication for rituximab, paclitaxel, or cetuximab therapies. Infusion reactions were defined as various symptoms such as flushing, itching, alterations in heart rate and blood pressure, and dyspnea plus the clinical setting of a concurrent or very recent infusion. RESULTS: A total of 207 patients were evaluated in this study with 83 patients receiving cetirizine and 124 diphenhydramine patients. Overall, the percentage of patients with at least one chemotherapy-related infusion event in the cetirizine group was 19.3% (95% CI 11.4-29.4) compared to diphenhydramine group 24.2% (95% CI 17.0-32.7), P = 0.40. Of the patients who received cetirizine and then experienced an event in the first cycle, 41.7% (95% CI 13.7-74.3) of the events were due to paclitaxel, 50.0% (95% CI 19.4-80.6) were due to rituximab, and 8.3% (95% CI 0.1-43.6) were due to cetuximab. Of the patients who received diphenhydramine and then experienced an event in the first cycle, 26.1% (95% CI 5.7-51.4) were due to paclitaxel, 73.9% (95% CI 48.6-94.3) were due to rituximab and none due to cetuximab. CONCLUSION: Cetirizine appears to be a viable substitute for diphenhydramine for the prevention of infusions reactions with cetuximab, paclitaxel, and rituximab infusions in adults. Prospective studies are needed to determine the efficacy and safety of cetirizine compared with diphenhydramine in the prevention of chemotherapy-related infusion reactions.

Phase II open label pilot trial of aprepitant and palonosetron for the prevention of chemotherapy-induced nausea and vomiting (CINV) in patients receiving moderately emetogenic FOLFOX chemotherapy for the treatment of colorectal cancer.

PURPOSE: Chemotherapy-induced nausea and vomiting (CINV) causes significant morbidity among colorectal cancer patients, receiving fluorouracil, oxaliplatin, and leucovorin (FOLFOX) chemotherapy even with standard antiemetic prophylaxis. The purpose of this study is to determine if the addition of aprepitant to standard antiemetic therapy improves CINV in these patients. METHODS: Patients receiving FOLFOX for colorectal cancer were given antiemetic prophylaxis with aprepitant 125 mg orally on day 1 and 80 mg on days 2 and 3. Palonosetron 0.25 mg was given IV push on day 1 only. Dexamethasone 12 mg was administered orally on day 1 and 8 mg each morning on days 2 through 4. Assessments including emetic events, rescue doses, nutritional intake, and appetite were recorded in a patient diary which was returned to study personnel in the following cycle. RESULTS: Of the 53 patients screened, 50 were evaluable and had a complete dataset for cycle 1. For the first cycle, 74% of patients achieved a complete response (CR), 22% achieved a major response and 4% experienced treatment failure. The percentage of patients achieving a CR remained high throughout each cycle at 83, 83, and 86% for cycles 2, 3, and 4, respectively. Appetite and nutritional status remained largely unchanged throughout treatment. Adverse events occurring in more than 10% of patients included diarrhea (13.6%), fatigue (12.6%), and neutropenia (11%). CONCLUSIONS: Aprepitant added to standard antiemetic therapy appears to be an effective and safe regimen for prevention of CINV in patients receiving FOLFOX.

Retrospective comparison of low molecular weight heparin vs. warfarin vs. oral Xa inhibitors for the prevention of recurrent venous thromboembolism in oncology patients: The Re-CLOT study.

Background There is increasing evidence indicating oral factor Xa inhibitors can be used for secondary prevention of venous thromboembolism. Studies are needed to compare oral factor Xa inhibitors, low molecular weight heparins, and warfarin in the oncology population. The purpose of this study is to evaluate the recurrent venous thromboembolism incidence in oncology patients utilizing oral Xa inhibitors, low molecular weight heparins, or warfarin. Methods Using retrospectively collected data, we compared the recurrent venous thromboembolism incidence in oncology patients taking rivaroxaban/apixaban, enoxaparin, or warfarin with at least three months of follow-up. Patients were included if they had an active cancer, venous thromboembolism, and taking warfarin, enoxaparin, or rivaroxaban/apixaban. The primary endpoint was the first episode of recurrent venous thromboembolism at three months. Secondary endpoints included recurrent venous thromboembolism after six months, major bleeding, and mortality. Results Of 127 venous thromboembolism patients, 48 received rivaroxaban or apixaban, 23 received enoxaparin, and 56 received warfarin. The three most common cancer diagnoses were lung (21%), colorectal (14%), and breast (14%). There was no difference in venous thromboembolism recurrence at three months between the rivaroxaban/apixaban (0%), warfarin (3.6%), and the enoxaparin cohorts (4.4%) (p = 0.8319). Major bleeding at three months was only seen in one patient in the enoxaparin arm (4.2%). Mortality at three months was 0%, 3.6%, and 17.4% in the rivaroxaban/apixaban, warfarin, and enoxaparin cohorts, respectively. Conclusion The results of this retrospective study suggest that oral factor Xa inhibitors are potential options for cancer patients with venous thromboembolism. However, randomized, controlled trials are needed to confirm these results.

Concurrent gastrointestinal perforation and pulmonary embolism due to bevacizumab in an adult undergoing treatment for stage IV colon cancer.

Bevacizumab is an important component in the treatment of metastatic colorectal cancer when used with 5-fluorouracil, leucovorin and oxaliplatin or irinotecan. As a molecular target agent, it is considered to be less toxic than traditional chemotherapy; however, bevacizumab has been shown to cause serious, life-threatening adverse effects. The following report describes a case of bevacizumab-associated pulmonary embolism with simultaneous gastrointestinal perforation in a patient with stage IV adenocarcinoma of the descending colon. This case report and literature review describes the risk factors, etiology, and typical presentation of bevacizumab-induced gastrointestinal perforation and pulmonary embolism.

High- versus low-dose leucovorin in the modified FOLFOX6 regimen for first-line treatment of metastatic colorectal cancer.

Background In response to the national leucovorin shortage in 2008, our institution adjusted the modified FOLFOX6 (leucovorin, fluorouracil, and oxaliplatin) protocol to utilize a lower dose of leucovorin (20 mg/m2). This adjustment was based on prospective studies suggesting that lower doses of leucovorin may be equally effective in other fluorouracil containing regimens. This retrospective study evaluates outcomes in metastatic colorectal cancer (mCRC) patients treated with low- (20 mg/m2) vs. high-dose (400 mg/m2) leucovorin in the FOLFOX6 regimen for mCRC. Methods This retrospective analysis included consecutive mCRC patients from 2004 to 2011 if they received at least one cycle of modified FOLFOX6 as first line therapy. Patients who received an initial leucovorin dose other than 20 mg/m2 or 400 mg/m2 on their first cycle were excluded. Patient characteristics included demographics, metastatic site at initial diagnosis, and treatment history including chemotherapy and surgery. Primary outcome was date of death or last contact. Cox proportional hazards regression analysis and Kaplan-Meier survival curves were utilized to evaluate the effect of leucovorin dose on overall survival. Log-rank tests were used to compare median survival times by dose group. Results Of the 93 mCRC patients who received first line modified FOLFOX6, leucovorin 400 mg/m2 was administered to 47 (51%) patients and 20 mg/m2 to 46 (49%) patients. There were no differences of baseline characteristics between the groups with exception of primary site of cancer ( p = 0.038). The overall survival time was 22.5 months (95% CI 16.6-29.6). The median survival time in the leucovorin 400 mg/m2 group was 23.1 months (95% CI 16.2-35.7) compared to leucovorin 20 mg/m2 which was 20.5 months (95% CI 14.2-34.2); p = 0.573. The median survival times in patients with one versus two or more sites with metastasis were statistically different (26.9 vs. 16.2 months, p = 0.009). Metastatic site removal or ablation showed differences in the median survival, 34.2 months (95% CI 20.8-50.9) vs. 16.6 months (95% CI 14.1-23.6) without metastatic disease removal ( p = 0.004). The odds of dying for patients with two metastatic sites was higher compared with the odds of those patients with one site, HR 1.8 (95% CI 1.08-3.0). Patients without metastatic site removal or ablation had higher odds of dying compared to those patients without this procedure, HR 0.47 (95% CI 0.27-0.81). Conclusion In this single center retrospective study, there was no difference in overall survival for mCRC patients treated with first line FOLFOX6 with low- vs. high-dose leucovorin.

Severe palmar-plantar erythrodysesthesia and aplasia in an adult undergoing re-induction treatment with high-dose cytarabine for acute myelogenous leukemia: a possible drug interaction between posaconazole and cytarabine.

High-dose cytarabine is recommended for re-induction chemotherapy in patients less than 60 years of age with acute myelogenous leukemia. This case describes a patient receiving high-dose cytarabine for re-induction and subsequently developed tingling and numbness in her hands and feet followed by severe pain, swelling, and erythema consistent with a diagnosis of palmar-plantar erythrodysesthesia. Furthermore, the patient's hemoglobin, platelets, and neutrophils did not recover after over 30 days post high-dose cytarabine. The patient was concurrently receiving posaconazole for fungal prophylaxis which was initiated after the induction therapy. We speculate that posaconazole may inhibit the cytarabine efflux through P-glycoprotein inhibition leading to the patient's palmar-plantar erythrodysesthesia and subsequent aplasia. Future pharmacokinetic studies need to be conducted to ascertain if posaconazole does influence the pharmacokinetics of cytarabine.

Effect of ceftriaxone and cefepime on high-dose methotrexate clearance.

Numerous drug interactions with methotrexate have been identified, which can lead to serious life-threatening effects. Up to 90% of methotrexate is excreted unchanged in the urine with primary excretion dependent on organic anion transport in the renal proximal tubule. The two pathways responsible for methotrexate secretion are organic anion transport 1 and primarily organic anion transport 3. Penicillins undergo tubular secretion via organic anion transport, and cephalosporins are believed to also possess a similar risk when administered with methotrexate; however, there are no human studies observing this interaction with cephalosporins and methotrexate. Ceftriaxone undergoes biliary clearance and has low affinity for the same organic anion transports as methotrexate; therefore, ceftriaxone has a low potential to interact with methotrexate. Cefepime is primarily secreted by organic cation transport N2, and also has a low potential to interact with methotrexate. This case report describes the pharmacokinetic effect of concomitant beta-lactam therapy in a patient receiving high-dose methotrexate.

Cytarabine syndrome despite corticosteroid premedication in an adult undergoing induction treatment for acute myelogenous leukemia.

Cytarabine syndrome is a rare clinical condition characterized by fever, malaise, myalgia, arthralgia, and/or rash that occurs after receipt of cytarabine. Our patient developed fever, malaise, and diffuse body pain shortly following cytarabine initiation despite receiving prophylactic dexamethasone. The patient's discomfort was treated with intravenous morphine and her other symptoms were controlled with a higher dose of dexamethasone. Although the exact cause is not fully understood, cytarabine syndrome is hypothesized to be an immune-mediated response following cytarabine-induced apoptosis that results in a rapid increase in proinflammatory cytokines. While there is no standard therapy for cytarabine syndrome, corticosteroids appear to play a role in the treatment and prevention of the condition by suppressing the proinflammatory response. Since our case describes the development of cytarabine syndrome despite dexamethasone, clinicians should monitor for this adverse event if patients begin exhibiting characteristics of this syndrome.

Outcomes of hospitalized neutropenic oncology patients with Pseudomonas aeruginosa bloodstream infections: focus on oral fluoroquinolone conversion.

BACKGROUND: Pseudomonas aeruginosa bacteremia is a major cause of morbidity and mortality, especially in neutropenic oncology patients. Few studies have been published in the last decade on treatment outcomes of neutropenic oncology patients with Pseudomonas aeruginosa bacteremia. In addition, there is a lack of data addressing the role of oral fluoroquinolones in this patient setting. METHODS: A retrospective chart review from 1999 to 2013 was conducted at a large academic medical center in neutropenic oncology patients with documented Pseudomonas aeruginosa bacteremia, who were initially treated with intravenous anti-pseudomonal antibiotics and then converted to an oral anti-pseudomonal fluoroquinolone. Patients were evaluated for the rate of cure and for the time from onset of intravenous antibiotic therapy to conversion to oral fluoroquinolones. RESULTS: Twenty-nine patients with Pseudomonas aeruginosa bacteremia were evaluated. The median absolute neutrophil count at the time of the first positive blood culture was 50 cells/mm(3), and the median duration of time below an absolute neutrophil count of 1000 cells/mm(3) was five days. The change to oral fluoroquinolones occurred at a median (range) of six (2-18) days after initiation of intravenous antibiotics and at a median absolute neutrophil count of 2610 (110-24790) cells/mm(3). The initial cure was 93.1%, while ultimate cure was 91.7%. CONCLUSION: Converting to oral fluoroquinolones after initial intravenous antibiotic therapy for Pseudomonas aeruginosa bacteremia in clinically stable neutropenic oncology patients appears to achieve successful outcomes. However, prospective trials are needed to validate these results in neutropenic oncology patients with Pseudomonas aeruginosa bacteremia who are converted to oral fluoroquinolones.

Fixed, low-dose rasburicase for the treatment or prevention of hyperuricemia in adult oncology patients.

PURPOSE: Rasburicase is a recombinant urate oxidase enzyme administered to high risk patients or to those with preexisting hyperuricemia from tumor lysis syndrome (TLS). The objective of this retrospective review is to evaluate and characterize the use of fixed, low-dose rasburicase for the treatment of hyperuricemia in adult patients. PATIENTS/METHODS: A retrospective chart review from 1 October 2005 to 31 December 2011 was conducted in adult oncology patients who received fixed, low-dose rasburicase. Patients who met the inclusion criteria were evaluated for the uric acid level change from baseline and the achievement of uric acid level less than 8 mg/dL. RESULTS: Forty-five patients were included in the analysis in which 26 (58%) patients received 3 mg rasburicase. For the 39 patients with baseline uric acid levels 8 mg/dL or higher, 80% achieved a uric acid level lower than 8 mg/dL with a single rasburicase dose. Six patients (13%) required renal replacement therapy despite rasburicase. The median uric acid level reduction 24 h post rasburicase dose 1.5 mg, 3 mg, 4.5 mg, and 6 mg were 5.5, 5.8, 3.8, and 10.05 mg/dL, respectively. There was no clinical difference between obese and non-obese patients in terms of their median uric acid reduction, 5.5 vs. 7 mg/dL, respectively. CONCLUSION: Fixed, low dose rasburicase produced a consistent lowering of uric acid levels and may be utilized in the management of hyperuricemia in TLS. Further study is necessary to determine if a larger fixed dose would be required in those patients with a higher baseline uric acid level.

Single premedication dose of dexamethasone 20 mg IV before docetaxel administration.

BACKGROUND: The administration of docetaxel requires the use of dexamethasone for the prevention of hypersensitivity reactions (HSRs) and fluid retention reactions (FRRs). The manufacturer recommends dexamethasone for 3 days starting the day before docetaxel. This regimen has the potential for nonadherence so the utility of a single dexamethasone dose would be welcomed. OBJECTIVE: To ascertain the incidence of HSRs and FRRs after receiving a single dose of intravenous dexamethasone before docetaxel administration. DESIGN: Retrospective chart review. SETTING: Data set from an oncology clinic affiliated with a large, tertiary, academic, teaching hospital. PATIENTS: Ninety patients (median age 59 years, range 40-92 years) with cancer (primarily breast cancer, nonsmall cell lung cancer and head/neck cancer) who received docetaxel. MEASUREMENTS AND RESULTS: Patients with heart failure, renal failure, chronic edema, current steroid use and/or prostate cancer were excluded from the study. Seven patients (7.8%) experienced a HSR requiring a treatment intervention (fluid bolus, oxygen, steroid, and/or diphenhydramine). Eleven patients (12.2%) had documented fluid retention. The mean docetaxel dose at the onset of fluid retention was 247.2 ± 134.5 mg/m(2). LIMITATIONS: This single center evaluation with a small sample size had the potential for incomplete collection of the adverse events from the medical records due its retrospective nature. CONCLUSION: Hypersensitivity reactions and FRRs occurred in 7.8% and 12.2% of patients, respectively. This is lower than the rates reported by the manufacturer with the oral premedication regimen.

Pegfilgrastim-induced hyperleukocytosis leading to hospitalization of a patient with breast cancer.

In patients receiving dose-dense chemotherapy, adverse effects such as neutropenia can be reduced by colony-stimulating factors. Pegfilgrastim, a colony-stimulating factor, has associated adverse effects, including bone pain, fever, and, rarely, hyperleukocytosis. We describe a 45-year-old woman with breast cancer receiving dose-dense Adriamycin and cyclophosphamide chemotherapy. She presented with hyperleukocytosis after receiving pegfilgrastim, which resulted in hospitalization. This case report reviews the strategy to minimize the risk of hyperleukocytosis from pegfilgrastim administered in dose-dense chemotherapy.

Lipid-lowering efficacy and safety after switching to atazanavir-ritonavir-based highly active antiretroviral therapy in patients with human immunodeficiency virus.

STUDY OBJECTIVE: To evaluate the efficacy, safety, and lipid-lowering effects after switching from a non-atazanavir-containing, protease inhibitor-based highly active antiretroviral therapy (HAART) to atazanavir-ritonavir-based HAART in patients infected with human immunodeficiency virus (HIV). DESIGN: Multicenter, noncontrolled, retrospective study. SETTING: Three tertiary teaching hospitals. PATIENTS: Thirty-six patients with HIV infection, aged 18 years or older, who were receiving non-atazanavir-containing, protease inhibitor-based HAART that was switched to atazanavir 300 mg-ritonavir 100 mg-based HAART without changes in nucleoside reverse transcriptase inhibitors and confounders known to alter serum lipid levels. MEASUREMENTS AND MAIN RESULTS: Lipid profiles measured 4 weeks-6 months before the switch, as well as follow-up lipid profiles measured 4 weeks-6 months after receiving the new HAART regimen, were evaluated. The switch resulted in the following changes in lipid levels: total cholesterol -9% (p=0.002), low-density lipoprotein cholesterol -13% (p<0.001), high-density lipoprotein cholesterol (HDL) -2% (p=0.431), triglycerides -23% (p=0.007), non-HDL -11% (p=0.002), total cholesterol:HDL ratio -10% (p=0.004), and triglyceride:HDL ratio -24% (p=0.019). A subgroup analysis was conducted on the lipid profiles of nine patients who still met the strict inclusion and exclusion criteria up to 9 months after the switch; it showed that the reductions in their lipid profiles were sustained. In addition, 33% more patients achieved their National Cholesterol Education Panel (NCEP) Adult Treatment Panel (ATP) III cholesterol goals. No significant changes were noted in median (interquartile range) CD4+ counts (372 [236-551] and 361 [217-464] cells/mm(3), p=0.118) or in number of patients with undetectable HIV viral loads ([defined as < 50 copies/ml] 32/36 and 31/36 patients, p>0.05) between baseline and after the switch, respectively. CONCLUSION: Switching to an atazanavir-ritonavir-based HAART regimen was associated with significant improvement in lipid profiles, similar to those seen in clinical trials, without compromising safety or viral and immunologic control. In addition, more patients were able to achieve their NCEP ATP III goals.

Dipping into the Clostridium difficile pool: Are alcohol-based dispensers fomites for C difficile?

The purpose of this study was to evaluate alcohol-based dispensers as potential fomites for Clostridium difficile. A convenience sample of 120 alcohol-based dispensers was evaluated for the presence of C difficile either by culture or polymerase chain reaction for C difficile toxin. The results demonstrated that C difficile was not cultured, and C difficile toxin was not detected using polymerase chain reaction; however, gram-positive rods, Clostridium perfringens, Pantoea agglomerans, coagulase-negative Staphylococcus, Peptostreptococcus, Bacillus spp, and microaerophilic Streptococcus were present within the overflow basins of the alcohol-based dispensers.

Prospective evaluation of carboplatin AUC dosing in patients with a BMI>or=27 or cachexia.

When determining the carboplatin dosage from the Calvert formula, there are a lack of data when evaluating patients with cachexia or body mass index (BMI)>or=27. If the Cockcroft and Gault (C-G) creatinine clearance (CrCl) equation is utilized and substituted for glomerular filtration rate in the Calvert formula, the chance for inaccurate dosing occurs especially in these populations. Therefore, the purpose of this study is to evaluate and compare the target carboplatin area under the concentration (AUC) with the actual AUC achieved in cachectic or BMI>or=27 patients. In a prospective manner, we evaluated 19 patients with a BMI>or=27 and nine cachectic patients. In the C-G equation to determine creatinine clearance, the adjusted body weight was used for BMI>or=27 patients and serum creatinine value of 70.7 microM (0.8 mg/dl) for the cachectic patients. The carboplatin dose was calculated, administered to the patients, and subsequent carboplatin blood samples were obtained for pharmacokinetic determination. Once the AUC was determined, the results were compared with the expected outcomes from the modified C-G CrCl equation for the Calvert formula, Chatelut and Bénézet equations. The results demonstrated that the modified C-G CrCl equation for the Calvert formula had less bias and more precision than using actual weight in the C-G CrCl equation or using the Chatelut and Bénézet equations. Using the actual weight in overweight and especially obese patients and using a serum creatinine<70.7 microM in cachectic patients will lead to overestimation of the carboplatin clearance and thus AUC.