RESUMO
BACKGROUND: Neoadjuvant chemotherapy with methotrexate-vinblastine-doxorubicin-cisplatin (MVAC) is the standard of care for muscle-invasive urothelial bladder cancer. Gemcitabine plus cisplatin (GC) shows similar efficacy with less toxicity in the metastatic setting and has therefore often been used interchangeably with MVAC. We report on the efficacy and safety of neoadjuvant GC in patients with locally advanced urothelial cancer. MATERIALS AND METHODS: We prospectively evaluated 87 patients in 2 centers. Their median age was 68 years. Treatment consisted of 3× GC prior to radical cystectomy. The primary endpoint was pathologic response. The secondary endpoints were safety, progression-free survival (PFS), and overall survival (OS). RESULTS: In all, 83 patients finished chemotherapy; 80 patients were evaluable for the primary endpoint. Pathologic complete response (pCR) was achieved in 22.5% and near pCR was seen in 33.7% of the patients. The 1-year PFS rate was 79.5% among those patients achieving ≤pT2 versus 100% among those patients achieving pCR or near pCR (p = 0.041). Five-year OS was 61.8% (95% CI 67.6 to NA). GC was well tolerated. Grade 3/4 toxicities occurred in 38% of the patients. There was no grade 3/4 renal toxicity, febrile neutropenia, or death. CONCLUSION: Neoadjuvant GC is a well-tolerated regimen. Although the pathologic response is lower than that reported with MVAC, our data support GC as a feasible option in the absence of a prospective randomized comparison, particularly for older patients, since its toxicity is lower than that of MVAC.
Assuntos
Carcinoma de Células de Transição/tratamento farmacológico , Cisplatino/uso terapêutico , Desoxicitidina/análogos & derivados , Terapia Neoadjuvante , Neoplasias da Bexiga Urinária/tratamento farmacológico , Adulto , Idoso , Idoso de 80 Anos ou mais , Protocolos de Quimioterapia Combinada Antineoplásica , Carcinoma de Células de Transição/patologia , Desoxicitidina/uso terapêutico , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Estudos Prospectivos , Resultado do Tratamento , Neoplasias da Bexiga Urinária/patologia , GencitabinaRESUMO
Osteoporosis is defined as a continuous loss of bone mineral density accompanied by an increased fracture risk in females and males. A fall of estrogen concentrations at the menopause and the consecutive rapid bone loss are an established pathogenic mechanism in female osteoporosis. Males do not have a menopause equivalent during which significant amounts of bone are lost. Several diseases, therapeutic strategies and nutritional deficiencies may also result in bone loss and reduced bone mineral density. Prostate cancer is the most common visceral malignancy in men. Suppression of endogenous androgen production as a therapeutic tool is commonly used in patients with non-metastatic prostate cancer and is associated with significant bone loss and an increased fracture risk. Androgen deprivation therapy is prescribed both for men with locally advanced or high-risk non-metastatic prostate cancer. Osteoclast inhibition with any of several bisphosphonates improves bone mineral density and reduces fracture risk. Denosumab (a monoclonal antibody against RANK ligand) and toremifene (a selective estrogen receptor modulator) recently have been shown to be effective to reduce vertebral fractures in patients with non-metastatic prostate cancer receiving androgen-deprivation therapy. This overview focuses on cancer-treatment-induced bone loss in patients with non-metastatic prostate cancer.
Assuntos
Antagonistas de Androgênios/efeitos adversos , Antagonistas de Androgênios/uso terapêutico , Antineoplásicos Hormonais/efeitos adversos , Antineoplásicos Hormonais/uso terapêutico , Osteoporose/induzido quimicamente , Neoplasias da Próstata/tratamento farmacológico , Idoso de 80 Anos ou mais , Anticorpos Monoclonais Humanizados/efeitos adversos , Anticorpos Monoclonais Humanizados/uso terapêutico , Densidade Óssea/efeitos dos fármacos , Conservadores da Densidade Óssea/efeitos adversos , Conservadores da Densidade Óssea/uso terapêutico , Denosumab , Difosfonatos/efeitos adversos , Difosfonatos/uso terapêutico , Hormônio Liberador de Gonadotropina/agonistas , Humanos , Masculino , Estadiamento de Neoplasias , Osteoclastos/efeitos dos fármacos , Osteoporose/tratamento farmacológico , Fraturas por Osteoporose/induzido quimicamente , Fraturas por Osteoporose/prevenção & controle , Neoplasias da Próstata/patologia , Ligante RANK/antagonistas & inibidores , Ensaios Clínicos Controlados Aleatórios como Assunto , Moduladores Seletivos de Receptor Estrogênico/efeitos adversos , Moduladores Seletivos de Receptor Estrogênico/uso terapêutico , Fraturas da Coluna Vertebral/induzido quimicamente , Fraturas da Coluna Vertebral/prevenção & controle , Toremifeno/efeitos adversos , Toremifeno/uso terapêuticoRESUMO
BACKGROUND: Many patients with cardiac implantable electronic devices (CIED) undergo magnetic resonance imaging (MRI); however, a relevant proportion have a CIED system that has not been classified as MRI-conditional because of generators and leads from different brands (mixed-brand group). The available data concerning the outcome of these mixed patients undergoing MRI is limited. METHODS: A retrospective single center study, including all patients with CIEDs undergoing MRI between January 2013 until May 2020, was performed. Primary endpoints were defined as death or any adverse event necessitating hospitalization or CIED revision. Secondary endpoints were the occurrence of any sign for beginning device or lead failure or patient discomfort during MRI. RESULTS: A total of 227 MRI examinations, including 10 thoracic MRIs, were carried out in 158 patients, with 1-9 MRIs per patient. Of the patients 38 underwent 54 procedures in the mixed-brand group and 89 patients underwent 134 MRIs in the MRI-conditional group. Of the patients 31 were excluded since the MRI conditionality could not be determined. No primary endpoints occurred within the mixed-brand group but in 2.2% of the MRI-conditional group (p = 1.000), with 2 patients developing new atrial fibrillation during MRI, of whom one additionally had a transient CIED dysfunction. No secondary endpoints were met in the mixed-brand group compared to 3.4% in the MRI-conditional group (p = 0.554). No complications occurred in the excluded patients. CONCLUSION: The complication rate of CIED patients undergoing MRI was low. Patients with a mixed CIED system showed no signs of increased risk of adverse events compared to patients with MRI-conditional CIED systems.
Assuntos
Desfibriladores Implantáveis , Marca-Passo Artificial , Eletrônica , Humanos , Imageamento por Ressonância Magnética/efeitos adversos , Imageamento por Ressonância Magnética/métodos , Estudos RetrospectivosRESUMO
PURPOSE: The purpose of this report is to describe a case of lipemia retinalis due to decompensating hyperlipidemia that occurred during chemotherapy in a patient with metastatic colon carcinoma. METHODS: Retrospective case report. RESULTS: A 55-year-old non-insulin-dependent diabetic man with well-controlled hyperlipidemia presented himself with temporarily blurred vision in both eyes occurring during chemotherapy. He was found to have lipemia retinalis in his both eyes. Blood tests revealed elevated cholesterol and triglyceride levels exceeding 8,200 mg/dL. He received six cycles of FOLFIRI/bevacizumab and accompanying dexamethasone because of colon cancer with pulmonary metastases. Lipemia retinalis had resolved after a 6-week follow-up when chemotherapy was finished, and the patients' triglyceride and glucose levels decreased to normal values. CONCLUSION: Lipemia retinalis associated with visual impairment may occur during chemotherapy under accompanying treatment with dexamethasone. Even if patients with hyperlipidemia are metabolically well-controlled with oral medication, treatment with dexamethasone can potentially lead to decompensation of hyperlipidemia causing secondary lipemia retinalis.
Assuntos
Glucocorticoides , Hiperlipidemias , Doenças Retinianas , Carcinoma/tratamento farmacológico , Neoplasias do Colo/tratamento farmacológico , Glucocorticoides/efeitos adversos , Humanos , Hiperlipidemias/induzido quimicamente , Masculino , Pessoa de Meia-Idade , Doenças Retinianas/induzido quimicamente , Estudos RetrospectivosRESUMO
Although it is well known that body mass index (BMI) and bone mineral density (BMD) are positively correlated, the mechanisms by which adiposity reduces the risk of osteoporotic fractures are not fully understood. The present study was initiated to gain deeper insight into the mechanisms underlying the osteoprotective effect of adiposity, and to assess particularly the relevance that BMI-associated changes in circulating hormone levels could have for the build-up of additional bone mineral density. Using data from a previous study on a large cohort of healthy adult Austrians, we analyzed correlations of BMI with (i) BMD at sites in the lumbar spine and hip region, (ii) bone resorption and formation markers, (iii) circulating levels of vitamin D, parathyroid hormone, testosterone and estrogen, and (iv) rates of daily vitamin D and calcium intake. After adjustment for age, positive correlations between BMI and BMD were highly significant (P<0.0001) at all skeletal sites across the entire study cohort. Associations were stronger in post-menopausal women than in pre-menopausal women and in men. In absolute values, the gain in BMD at the lumbar spine from an incremental rise of BMI in post-menopausal women was 1.5-fold higher than in pre-menopausal women, and three times of that observed in men (P<0.05). Inverse relations between BMI and ß-crosslaps were consistently found in men (P<0.01) and in women before and after menopause (P<0.01 and P<0.05, respectively), suggesting that inhibition of osteoclastic bone resorption is responsible at least in part for the positive effect of high BMI on BMD. Sub-group analysis revealed that increasing BMI was associated with a significant fall of testosterone in men (P<0.05), and of 25-(OH)D in pre- and post-menopausal women (P<0.001 and P<0.05, respectively), but with a significant rise in PTH (P<0.01) in women before menopause. Since all these hormonal changes would cause bone loss, this excludes their playing any role in the osteoprotective effect of adiposity.