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1.
J Palliat Med ; 24(3): 347-353, 2021 03.
Artículo en Inglés | MEDLINE | ID: mdl-32721254

RESUMEN

Background: Nearly 3 million U.S. family caregivers support someone with cancer. However, oncology clinic-based service lines that proactively screen, assess, and support cancer caregivers are nearly nonexistent. Objective: To examine first-year experiences of a nurse-led clinic-based telehealth support service (FamilyStrong) for family caregivers of patients with recently diagnosed grade IV brain tumors. Methods: This is a retrospective evaluation of operational outcomes from initial implementation of the FamilyStrong Service, developed in partnership with Caregiver and Bereavement Support Services at the University of Alabama at Birmingham (UAB) and the UAB Center for Palliative and Supportive Care. From August 2018 to December 2019, 53 family caregivers were proactively identified and enrolled by a palliative care nurse, working approximately one day/week, who performed monthly caregiver distress thermometer screenings by phone and provided emotional, educational, problem-solving, and referral support. Results: Enrolled family caregivers were a mean age of 53.5 years and mostly female (62.3%), full- or part-time employed (67.9%), and the patient's spouse/partner (79.3%). Caregivers provided support 6.7 days/week for 11.2 hours/day. The palliative care nurse performed 235 distress screenings and provided support that included 68 documented instances of emotional, problem-solving, and educational support, 41 nurse-facilitated communications with the neuro-oncology team about patient issues, and 24 referrals to UAB and community services (e.g., counseling). The most common problems caregivers wanted assistance with included: managing their relative's health condition and symptoms (51%), coordinating care/services (21%), and planning for the future/advance care planning (17%). Discussion: The FamilyStrong Program is among the first "real world" oncology clinic-based formal support services for advance cancer family caregivers.


Asunto(s)
Neoplasias Encefálicas , Telemedicina , Cuidadores , Familia , Femenino , Humanos , Masculino , Persona de Mediana Edad , Cuidados Paliativos , Estudios Retrospectivos
2.
Anticancer Drugs ; 26(2): 224-6, 2015 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-25304989

RESUMEN

Patients with BRCA-1 and BRCA-2 germ line mutations are at an increased risk of developing pancreatic adenocarcinoma (PAC). In particular, the BRCA-2 mutation has been associated with a relative risk of developing PAC of 3.51. The BRCA-2 protein is involved in repair of double-stranded DNA breaks. Recent reports have suggested that in the setting of impaired DNA repair, chemotherapeutic agents that induce DNA damage, such as platinum-based antineoplastic drugs (platins) and poly(ADP-ribose) polymerase inhibitors (PARP inhibitors), have improved efficacy. However, because of the relative rarity of BRCA-related PAC, studies evaluating such agents in this setting are scarce. Patients with a known BRCA-2 mutation and PAC were retrospectively reviewed. Ten patients with PAC and BRCA-2 mutation were identified. Four patients (40%) were of Ashkenazi Jewish descent. Seven patients (70%) received platinum agents, two (20%) received mitomycin-C, one (10%) received a PARP inhibitor, and seven (70%) received a topoisomerase-I inhibitor. Overall, chemotherapy was well tolerated with expected side effects. Patients with a BRCA-2 mutation and PAC represent a group with a unique biology underlying their cancer. Chemotherapies such as platinum derivatives, mitomycin-C, topoisomerase-I inhibitors, and PARP inhibitors targeting DNA require further investigation in this population. Genetic testing may guide therapy in the future.


Asunto(s)
Adenocarcinoma/tratamiento farmacológico , Adenocarcinoma/genética , Antineoplásicos/uso terapéutico , Proteína BRCA2/genética , Neoplasias Pancreáticas/tratamiento farmacológico , Neoplasias Pancreáticas/genética , Inhibidores Enzimáticos/uso terapéutico , Femenino , Humanos , Judíos/genética , Masculino , Persona de Mediana Edad , Mitomicina/uso terapéutico , Compuestos Organoplatinos/uso terapéutico , Inhibidores de Poli(ADP-Ribosa) Polimerasas , Estudios Retrospectivos , Inhibidores de Topoisomerasa I/uso terapéutico , Resultado del Tratamiento
3.
Oncol Lett ; 8(3): 1302-1306, 2014 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-25120712

RESUMEN

Therapeutic options for locally advanced pancreatic cancer (LAPC) include concurrent chemoradiation, induction chemotherapy followed by chemoradiation or systemic therapy alone. The original Gastro-Intestinal Study Group and Eastern Cooperative Oncology Group studies defined fluorouracil (5-FU) with concurrent radiation therapy followed by maintenance 5-FU until progression, as the standard therapy for this subset of patients. Although this combined therapy has been demonstrated to increase local control and median survival from 8 to 12 months, almost all patients succumb to the disease secondary to either local or distant recurrence. Our earlier studies provided a strong rationale for the use of capecitabine in combination with concurrent radiation followed by maintenance capecitabine therapy. To report our clinical experience, we retrospectively evaluated our patients who were treated with maintenance capecitabine. We reviewed the medical records of patients with LAPC who received treatment with capecitabine and radiation, followed by a 4-week rest, then capecitabine alone 1,000 mg twice daily (ECOG performance status 2 or age >70 years) or 1,500 mg twice daily for 14 days every 3 weeks until progressive disease. We treated 43 patients between September 2004 and September 2012. The population consisted of 16 females and 25 males, with a median age of 64 years (range, 38-80 years). Patients received maintenance capecitabine for median duration of 9 months (range, 3-18 months). The median overall survival (OS) for these patients was 17 months, with two patients still living and receiving therapy. The 6-month survival rate was 91% (39/43), 1-year survival rate was 72% (31/43) and 2-year OS rate was 26% (11/43). Grade 3 or 4 toxicity was observed rarely: Hand-foot syndrome (HFS) in two patients, diarrhea in one patient and peripheral neuropathy in one patient, and there was no mortality directly related to treatment. Capecitabine maintenance therapy following chemoradiation in LAPC offers an effective, tolerable and convenient alternative to 5-FU. To the best of our knowledge, this is the largest study of its kind which has determined the safety and efficacy of capecitabine maintenance therapy for patients with LAPC.

6.
JOP ; 8(6): 799-805, 2007 Nov 09.
Artículo en Inglés | MEDLINE | ID: mdl-17993734

RESUMEN

CONTEXT: Capecitabine has shown efficacy in treatment of metastatic pancreatic cancer. Several researchers have identified thymidine phosphorylase, dihydropyrimidine dehydrogenase, or their ratio as indicators of response to capecitabine in various cancers. CASE REPORT: We report two patients with metastatic pancreatic carcinoma who had long-term survivals on capecitabine after gemcitabine failure. These two cases prompted us to measure thymidine phosphorylase and dihydropyrimidine dehydrogenase levels to facilitate discourses regarding their relationship with efficacy of capecitabine. We also describe a novel method of measuring thymidine phosphorylase level from serum without an invasive tissue biopsy. One patient is alive as of today, with improved performance status, 50 months after capecitabine was started. CA 19-9 and CT scans remained stable during 57 cycles. Her thymidine phosphorylase level was 1.77 compared to a control level of 1.00. Dihydropyrimidine dehydrogenase level was 4.14 compared to a control level of 1.00. Their ratio was 0.43. The other patient was alive on capecitabine for 24 months. His performance status, bilirubin, AST, and ALT improved on capecitabine. CT scans and CA 19-9 remained stable during this period. He had thymidine phosphorylase level of 5.56, dihydropyrimidine dehydrogenase level of 2.74, and their ratio of 2.03. CONCLUSION: Capecitabine resulted in long term survivals in two patients with metastatic pancreatic cancer after gemcitabine failure. The use of capecitabine as second-line treatment in metastatic pancreatic cancer should be further explored along with the role of thymidine phosphorylase and dihydropyrimidine dehydrogenase levels in its activity. A non-invasive method of thymidine phosphorylase measurement we described should be validated in larger trials.


Asunto(s)
Adenocarcinoma/tratamiento farmacológico , Antimetabolitos Antineoplásicos/uso terapéutico , Desoxicitidina/análogos & derivados , Fluorouracilo/análogos & derivados , Neoplasias Pancreáticas/tratamiento farmacológico , Adenocarcinoma/metabolismo , Biomarcadores/metabolismo , Capecitabina , Desoxicitidina/uso terapéutico , Dihidrouracilo Deshidrogenasa (NADP)/metabolismo , Femenino , Fluorouracilo/uso terapéutico , Humanos , Masculino , Persona de Mediana Edad , Neoplasias Pancreáticas/metabolismo , Farmacogenética , Análisis de Supervivencia , Timidina Fosforilasa/metabolismo , Resultado del Tratamiento , Gemcitabina
7.
World J Gastroenterol ; 13(39): 5277-81, 2007 Oct 21.
Artículo en Inglés | MEDLINE | ID: mdl-17876901

RESUMEN

Hypersensitivity reactions (HSR) to oxaliplatin in patients with colorectal cancer include facial flushing, erythema, pruritus, fever, tachycardia, dyspnea, tongue swelling, rash/hives, headache, chills, weakness, vomiting, burning sensations, dizziness, and edema. We report a patient with fever as the sole manifestation of initial HSR, review the literature and discuss the management of HSR. A 57-year-old female with T3N2M0 rectal adenocarcinoma received modified FOLFOX-6. She tolerated the first 8 cycles without any toxicities except grade 1 peripheral neuropathy and nausea. During 9th and 10th infusions, she developed fever to a maximum of 38.3 centigrade with stable hemodynamic status despite medications. During 11th infusion, she developed grade 3 HSR consisting of symptomatic bronchospasm, hypotension, nausea, vomiting, cough, and fever. On examination, she was pale, cyanotic, with a temperature of 38.8 centigrade, BP dropped to 95/43 mm Hg, pulse of 116/min and O(2) saturation of 88%-91%. She was hospitalized for management and recovered in 24 h. Fever alone is not a usual symptom of oxaliplatin HSR. It may be indicative that the patient may develop serious reactions subsequently, as did our patient who developed hypotension with the third challenge. Treatment and prevention consists of slowing the infusion rate, use of steroids and antagonists of Type 1 and 2 histamine receptor antagonists, whereas desensitization could help to provide the small number of patients who experience severe HSR with the ability to further receive an effective therapy for their colorectal cancer.


Asunto(s)
Adenocarcinoma/tratamiento farmacológico , Antineoplásicos/efectos adversos , Neoplasias Colorrectales/tratamiento farmacológico , Hipersensibilidad a las Drogas/diagnóstico , Fiebre/inducido químicamente , Compuestos Organoplatinos/efectos adversos , Antineoplásicos/uso terapéutico , Femenino , Fiebre/diagnóstico , Humanos , Hipotensión/inducido químicamente , Hipotensión/diagnóstico , Persona de Mediana Edad , Compuestos Organoplatinos/uso terapéutico , Oxaliplatino
8.
Ther Clin Risk Manag ; 3(1): 177-80, 2007 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-18360625

RESUMEN

BACKGROUND: Hyopkalemia is a listed toxicity in the capecitabine (Xeloda(R); Roche, Nutley, NJ) package insert. However, the incidence and severity of this toxicity is not known. METHODS: We performed a retrospective evaluation of hypokalemia in 77 patients, who received capecitabine for gastrointestinal malignancies between April 2002 and November 2004. Hypokalemia was defined as K(+) level <3.2 mEq/L. Patients with documented >/=grade 2 vomiting or diarrhea, diuretics, hypomagnesemia, hypokalemia, renal insufficiency, endocrine dysfunction (thyroid, adrenal, diabetic) were excluded. Hypokalemic patients were graded as: mild (grade 1: 3.0-3.2 mEq/L), moderate (grade 3: 2.5-2.9 mEq/L) and severe (grade 4: <2.5 mEq/L). We also reviewed the literature. RESULTS: Fifty-four patients met the above criteria. The most common cause of exclusion was >/= grade 2 diarrhea (23 patients; 30%). Overall, hypokalemia was encountered in 11 patients (20.4%). Among hypokalemic patients, 8 patients (73%) presented with mild/grade 1 hypokalemia (3.0-3.2 mEq/L), 2 patients (18.18%) with moderate/grade 3 hypokalemia (2.5-2.9 mEq/L) and 1 patient (9.09%) with severe/grade 4 hypokalemia (<2.5 mEq/L) 8 (73%). Dose of capecitabine ranged between 1000-2000 mg/m(2). Hypokalemia occurred after an average of 83.7 days of capecitabine administration. No cardiac or neuromuscular complications were noticed. Replacement of K(+) was required in 6 patients (2 intravenous and 4 oral), while 2 patients (3.7%) required oral supplements >4 weeks. No patient had to stop capecitabine due to hypokalemia. One patient had persistent hypokalemia even after stopping capecitabine. Normalization of K(+) levels was achieved in 91% of patients. Four patients were on K(+) sparing diuretics for ascites and never presented with hypokalemia. Mean urine K(+) was 28 mEq/L. Only 5.5% patients had >/=grade 3 hypokalemia in our study compared with 2% and 14% in two other studies. CONCLUSIONS: Although diarrhea being the most common cause of hypokalemia in patients on capecitabine, we postulate that hypokalemia may also be related to the effect of capecitabine on renal tubules suggested by the urine K(+) in some patients. Due to potential complications, hypokalemia in patients on capecitabine deserves special diagnostic and therapeutic attention.

9.
Clin Colorectal Cancer ; 5(5): 354-8, 2006 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-16512995

RESUMEN

BACKGROUND: The extent and complications of the interaction between capecitabine and warfarin are not fully known. PATIENTS AND METHODS: A retrospective study of 77 patients who received capecitabine was performed to analyze coagulation abnormalities with or without warfarin. RESULTS: Twenty-one patients received warfarin with capecitabine. Twelve were on an average warfarin dosage of 19.4 mg per week (range, 7-35 mg) before capecitabine treatment, with a stable international normalized ratio (INR; range, 0.9-3.3). The dose of capecitabine ranged from 1.6 g/m2 to 2 g/m2 per day. Thirteen patients (11 on warfarin) had an INR > 3 (range, 3.23-11.5), resulting in a probability of an INR > 3 of 32% in the warfarin group versus 4% for those not on warfarin (P = 5.1 x 10(-14)) at 130 days. Six patients required a warfarin dose reduction (1-2.5 mg decrease). There were 7 episodes of bleeding (all gastrointestinal; 5 with warfarin). Seven patients who experienced bleeding had INRs ranging from 1.06 to 8 (average, 3.31) at the time bleeding occurred. Of the 7 bleeding episodes, 5 patients required transfusions, averaging 3.25 units of red blood cells and 2.4 units of fresh frozen plasma. The incidence of bleeding at 130 days of treatment with capecitabine was 18% with warfarin versus 2% without (P = 4 x 10(-13)). Bleeding episodes were not significantly different between patients with or without liver involvement (4 of 40 episodes vs. 3 of 37 episodes, respectively; P = 0.12). Patients with an INR > 3 were evenly distributed between those with or without liver involvement (6 of 40 patients vs. 7 of 37 patients, respectively). No INR increases persisted after discontinuation of capecitabine. CONCLUSION: This study confirms a clinically significant interaction between warfarin and capecitabine-based chemotherapy akin to that already known for 5-fluorouracil. In addition to altered coagulation parameters, bleeding can be a complication. These events occurred in patients with and without liver metastases. We recommend weekly monitoring of coagulation parameters for all patients receiving concomitant warfarin and capecitabine, with an appropriate adjustment of warfarin dose. The nature and extent of this interaction requires further investigation.


Asunto(s)
Anticoagulantes/efectos adversos , Antimetabolitos Antineoplásicos/efectos adversos , Trastornos de la Coagulación Sanguínea/inducido químicamente , Desoxicitidina/análogos & derivados , Hemorragia Gastrointestinal/inducido químicamente , Warfarina/efectos adversos , Adulto , Anciano , Anciano de 80 o más Años , Anticoagulantes/administración & dosificación , Anticoagulantes/farmacología , Antimetabolitos Antineoplásicos/administración & dosificación , Antimetabolitos Antineoplásicos/farmacología , Capecitabina , Desoxicitidina/administración & dosificación , Desoxicitidina/efectos adversos , Desoxicitidina/farmacología , Interacciones Farmacológicas , Femenino , Fluorouracilo/análogos & derivados , Humanos , Masculino , Persona de Mediana Edad , Neoplasias/complicaciones , Neoplasias/tratamiento farmacológico , Polifarmacia , Estudios Retrospectivos , Warfarina/administración & dosificación , Warfarina/farmacología
12.
J Am Acad Dermatol ; 48(2 Suppl): S31-2, 2003 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-12582381

RESUMEN

We describe a case of melanonychia induced by PUVA. This phenomenon likely is more common than the few reports in the literature indicate.


Asunto(s)
Dermatitis/tratamiento farmacológico , Enfermedades de la Uña/etiología , Terapia PUVA/efectos adversos , Trastornos de la Pigmentación/etiología , Femenino , Humanos , Persona de Mediana Edad
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