Observational study of hand-foot syndrome events from XELOX therapy for metastatic colorectal cancer.
Ontology highlight
ABSTRACT:
DISEASE(S): Metastatic Colorectal Cancer
PROVIDER: 2622604 | ecrin-mdr-crc |
REPOSITORIES: ECRIN MDR
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Project description:Interventions: 12 weeks /Application of aluminium chloride ointment once a day and application of wound dressing after the presentation of grade 1 hand-foot syndrome
Primary outcome(s): Incidence of Grade 3 HFS
Study Design: Single arm Non-randomized
| 2647838 | ecrin-mdr-crc
Project description:Interventions: Effectiveness of prevention of hand-foot syndrome associated with Regorafenib by using aluminum chloride and wound dressing
Primary outcome(s): Incidence of Grade 3 HFS
Study Design: single arm study, open(masking not used), historical control, single assignment, prevention purpose
| 2613973 | ecrin-mdr-crc
Project description:Colorectal cancer (CRC) is the third most common cancer and the second leading cause of malignancy-related mortality. Capecitabine has been approved for the treatment of colorectal cancer as first-line therapy. About 50%-68% of patients who take capecitabine develop Hand-foot syndrome. Hand-foot syndrome (HFS) is the most common adverse event of capecitabine-based chemotherapy. Initial symptoms of HFS are dysesthesia, tingling in the palms, fingers, and soles of the feet, and erythema, which may progress to an extremely painful and debilitating condition without prompt management. These symptoms can potentially lead to a worsened quality of life in patients taking capecitabine-based chemotherapy. Moreover, the adverse reaction necessitates dose-reduction or withdrawal of the chemotherapeutic agent. The mechanisms of HFS are still unknown, and there are limited data available on how to prevent them or manage them. However, different hypotheses of capecitabine-induced HFS pathogenesis have been suggested. One of the hypotheses stated that HFS is a kind of inflammation mediated by cyclooxygenase’s (COX-2) over expression in palm and feet by capecitabine and its metabolites causing elevation of inflammatory markers as tumor necrosis factor alpha (TNF-α). COX-2 enzyme plays a main role in inflammation and pain. Therefore, celecoxib which is selective (COX-2) inhibitor may have a key role in the HFS treatment plan. A retrospective study and two prospective studies showed that combining capecitabine with celecoxib, a selective COX-2 inhibitor, can significantly reduce capecitabine-related HFS in colorectal cancer patients. Those studies were dependent on HFS grading only without measuring any markers. So, in our study we assess possible protective effect of celecoxib against capecitabine induced HFS and measure inflammatory marker as tumor necrosis factor alpha (TNF-α), oxidative stress marker as Malondialdehyde (MDA), and cyclooxygenase-2 (COX-2) enzyme to show whether capecitabine induced HFS is caused by COX-2 mediated inflammation or not.
| 2718708 | ecrin-mdr-crc
Project description:Importance:Hand-foot syndrome (HFS) is a common adverse effect of capecitabine treatment. Objective:To compare the incidence and time to onset of grade 2 or greater HFS in patients receiving pyridoxine vs placebo and to identify biomarkers predictive of HFS. Design, Setting, and Participants:This single-center, randomized double-blind, placebo-controlled phase 3 trial conducted at National Cancer Centre Singapore assessed whether oral pyridoxine could prevent the onset of grade 2 or higher HFS in 210 patients scheduled to receive single-agent capecitabine chemotherapy for breast, colorectal, and other cancers. Interventions:Patients were randomized to receive concurrent pyridoxine (200 mg) or placebo daily for a maximum of 8 cycles of capecitabine, with stratification by sex and use in adjuvant or neoadjuvant vs palliative setting. Patients were withdrawn from the study on development of grade 2 or higher HFS or cessation of capecitabine. Main Outcomes and Measures:Primary end point was the incidence of grade 2 or higher HFS in patients receiving pyridoxine. Secondary end points included the time to onset (days) of grade 2 or higher HFS and identification of biomarkers predictive of HFS, including baseline folate and vitamin B12 levels, as well as genetic polymorphisms with genome-wide arrays. Results:In this cohort of 210 patients (median [range] age, 58 [26-82] years; 162 women) grade 2 or higher HFS occurred in 33 patients (31.4%) in the pyridoxine arm vs 39 patients (37.1%) in the placebo arm (P?=?.38). The median time to onset of grade 2 or higher HFS was not reached in both arms. In univariate analysis, the starting dose of capecitabine (odds ratio [OR], 1.99; 95% CI, 1.32-3.00; P?=?.001), serum folate levels (OR, 1.27; 95% CI, 1.10-1.47; P?=?.001), and red blood cell folate levels (OR, 1.25; 95% CI, 1.08-1.44; P?=?.003) were associated with increased risk of grade 2 or higher HFS. In multivariate analyses, serum folate (OR, 1.30; 95% CI, 1.12-1.52; P?<?.001) and red blood cell folate (OR, 1.28; 95% CI, 1.10-1.49; P?=?.001) were the only significant predictors of grade 2 or higher HFS. Grade 2 or higher HFS was associated with 300 DNA variants at genome-wide significance (P?<?5?×?10-8), including a novel DPYD variant (rs75267292; P?=?1.57?×?10-10), and variants in the MACF1 (rs183324967, P?=?4.80?×?10-11; rs148221738, P?=?5.73?×?10-10) and SPRY2 (rs117876855, P?<?1.01?×?10-8; rs139544515, P?=?1.30?×?10-8) genes involved in wound healing. Conclusions and Relevance:Pyridoxine did not significantly prevent or delay the onset of grade 2 or higher HFS. Serum and red blood cell folate levels are independent predictors of HFS. Trial Registration:clinicaltrials.gov Identifier: NCT00486213.
| S-EPMC5710192 | biostudies-literature
Project description:Primary outcome(s): To study the effect of Structured Teaching module (STM) on incidence and severity of Hand Foot syndrome among patients receiving Capecitabine based chemotherapy for colorectal cancer at a Tertiary Cancer Care CentreTimepoint: 2 year
| 2577989 | ecrin-mdr-crc
Project description:Hand-foot-genital syndrome (HFGS) is a rare, dominantly inherited condition affecting the distal limbs and genitourinary tract. A nonsense mutation in the homeobox of HOXA13 has been identified in one affected family, making HFGS the second human syndrome shown to be caused by a HOX gene mutation. We have therefore examined HOXA13 in two new and four previously reported families with features of HFGS. In families 1, 2, and 3, nonsense mutations truncating the encoded protein N-terminal to or within the homeodomain produce typical limb and genitourinary abnormalities; in family 4, an expansion of an N-terminal polyalanine tract produces a similar phenotype; in family 5, a missense mutation, which alters an invariant domain, produces an exceptionally severe limb phenotype; and in family 6, in which limb abnormalities were atypical, no HOXA13 mutation could be detected. Mutations in HOXA13 can therefore cause more-severe limb abnormalities than previously suspected and may act by more than one mechanism.
| S-EPMC1287077 | biostudies-literature
Project description:The some biomarkers can be found by pairwise comparison. They can distinguish between extremely severe Hand,foot and mouth disease and mild Hand,foot and mouth disease,moreover,they can applied to diagnose extremely severe Hand,foot and mouth disease mild Hand,foot and mouth disease vs.control; extremely severe Hand,foot and mouth disease vs.control; extremely severe Hand,foot and mouth disease vs.mild Hand,foot and mouth disease,verification by qRT-PCR
2013-11-27 | E-GEOD-52780 | biostudies-arrayexpress
Project description:Hand-foot syndrome (HFS) is a relatively frequent dermatologic toxic reaction to certain anti-cancer chemotherapies. The syndrome can evolve into a distressing condition that limits function and affects quality of life. Pyridoxine (vitamin B6) has been used empirically for the prevention of HFS caused by anti-cancer therapy. However, evidence of its efficacy remains controversial.Systematic literature searches were conducted on the Cochrane Library, PUBMED, EMBASE, LILACS, CBM, CNKI, VIP, WANFANG and the U.S. ClinicalTrials.gov website. We included all related randomized controlled trials (RCTs) irrespective of language. Reviewers from different professions independently assessed all potential studies and extracted data. Subgroup analysis was planned according to dose of pyridoxine. 5 RCTs involving 607 patients were contributed to the meta-analysis. No significant differences were found between patients receiving pyridoxine and placebo for prevention of incidence of HFS and grade 2 or worse HFS (relative risk (RR) 0.96, 95%confidence interval (CI) 0.86-1.06; RR0.95, 95%CI 0.73-1.24, respectively). Similarly, no significant improvement in quality of life was detected among patients. However, significant difference was found for prevention of grade 2 or worse HFS with pyridoxine 400 mg daily compared to 200 mg (RR0.55, 95%CI 0.33-0.92).There is inadequate evidence to make any recommendation about using pyridoxine for prevention of HFS caused by chemotherapy. However, pyridoxine 400 mg may have some efficacy. Further studies of large sample sizes are needed to evaluate the efficacy and safety of pyridoxine, especially at high dose, in comparison with placebo.
| S-EPMC3748123 | biostudies-literature
Project description:Hand-Foot-Genital Syndrome (HFGS) is a dominantly inherited condition and one of the rarest cases encountered in clinical practice. It might be presented with a wide variety of limb malformations and urogenital defects manifestations. In this report, a unique and novel case of HFGS accompanied with Embryonal Rhabdomyosarcoma of the urinary bladder is described in a two-year-old male. The patient was admitted to the hospital in order to investigate a progressively enlarging mass in the lower abdomen. During hospitalization, oliguria was noted by resident physicians. However, hypospadias and dysmorphic abnormalities, demonstrated upon physical examination, were the cornerstone in the diagnosis of HFGS. An accurate visual examination of the abdomen showed dilated superficial veins, and abdominal rigidity appeared through palpation. Furthermore, the radiologic evaluation showed delayed ossification of carpal bones, and abdominal CT scan revealed a necrotic mass in the hypogastric region measuring 12 × 10 cm. A biopsy was performed through which the mass was confirmed as Embryonal Rhabdomyosarcoma of the urinary bladder. The kidney function follow-up showed normal results. Neoadjuvant chemotherapy was started to diminish the tumor size. However, the patient eventually passed away during the treatment phase. This report emphasizes the need for a high index of suspicion to establish early detection of Embryonal Rhabdomyosarcoma in each newborn diagnosed with Hand-Foot-Genital Syndrome (HFGS) to avoid potential fatal consequences.
| S-EPMC7820788 | biostudies-literature
Project description:Hyaline Fibromatosis Syndrome (HFS) is a rare genetic disorder caused by loss-of-function mutations in the gene CMG2. Patients develop subcutaneous nodules and painful joint contracture. CMG2 is a transmembrane protein of poorly understood physiological function. To understand better the pathogenesis of HFS and the role of CMG2 in this disease, we compared by mass-spectrometry the composition of nodular and matching non-nodular tissues. Two tissue pairs were analyzed, both obtained after surgical resection of nodules from a HFS patient. Our shotgun proteomics analysis showed that nodules were enriched in serum protein, which correlated with previous descriptions of blood vessel leakage in these tissues. Importantly, we also observed a clear accumulation of collagen VI in nodules. Collagen VI accumulation was caused by CMG2 loss-of-function and is the main cause of the nodule formation.
2017-07-07 | PXD006268 | Pride