[Show abstract][Hide abstract] ABSTRACT: The in vitro gluten challenge test is an important diagnostic modality in celiac disease, especially in patients who begin treatment with a gluten-free diet before adequate diagnostic work-up or in cases with atypical celiac disease.
Available literature was reviewed regarding the accuracy of the in vitro gluten challenge test for celiac disease diagnosis.
Medline, SCOPUS, and Google scholar were searched and studies that used serology and bowel biopsy as the gold standard for diagnosis were included in our study. Data on authors, publication year, characteristics of the patient and control groups, patients' diet, duration of the gluten challenge test, histology findings, EMA and anti-TTG levels, CD markers, ICAM-1 and HLA antigens pre- and post-gluten challenge test were extracted.
Overall, 15 studies were included in this meta-analysis. Pooled sensitivity%/specificity% was 84/99 for EMA after the challenge, 52/96 for EMA without the challenge, 95.5/98.3 for anti-TTG after the challenge, and 95.1/98.3 for anti-TTG without the challenge test. Sensitivity/specificity for immunological markers were 89/97 for percentage of CD25+ -lamina propria lymphocytes, 96/91 for percentage of CD3+ -lamina propria lymphocytes, and 96.1/85.7 for percentage of ICAM-1-lamina propria lymphocytes. The factors that increased the sensitivity of EMA were longer test duration, evaluation of patients on a gluten containing diet or short-term gluten-free diet.
The in vitro gluten challenge test can be a useful part of the diagnostic work up of celiac disease, rather than only a model to evaluate its mechanisms.
Full-text · Article · Jul 2015 · Journal of pediatric gastroenterology and nutrition
[Show abstract][Hide abstract] ABSTRACT: Abstract The incidence and pattern of secondary neoplasms in patients with acute promyelocytic leukemia (APL) treated with ATRA-containing regimens is not well-described. We compared secondary neoplasms in 160 patients with APL treated with ATRA plus idarubicin (n=54), or ATRA plus arsenic trioxide (ATO) (n=106) for the incidence of secondary cancers per unit time of follow-up. Median follow-up times for the two cohorts were 136 and 29 months, respectively. Nine patients developed secondary cancers in the chemotherapy group. These included two breast cancers, three myelodysplastic syndromes/acute myeloid leukemia, one vulvar cancer, one prostate cancer, one colon cancer and one soft tissue sarcoma. A melanoma and one pancreatic cancer developed in the ATO group. We conclude that treatment of patients with APL using the non-chemotherapy regimen of ATRA plus ATO is not associated with a higher incidence of secondary cancers (p=0.29) adjusted for unit time of exposure.
No preview · Article · Aug 2014 · Leukemia and Lymphoma
[Show abstract][Hide abstract] ABSTRACT: Introduction:
The outcome of patients with CML who discontinue 2G-TKI initial therapy is unknown. We analyzed the characteristics of patients in whom treatment with first-line 2G-TKIs had failed.
Patients and methods:
A total of 218 patients with CML were treated with dasatinib (n = 101) or nilotinib (n = 117; 12 in AP). After a median follow-up of 23 months, 40 patients (18%) discontinued therapy: 25 initially treated with nilotinib (21% of all treated with nilotinib; 6 treated in AP) and 15 (15%) initially treated with dasatinib. Median age of the patients was 47 (range, 19-79) years, and they had received therapy for a median of 8 (range, 0-62) months.
Reasons for treatment discontinuation include: toxicity, 16 patients; resistance in CP, 5 patients; transformation to blast phase, 4 patients (2 treated in AP); and other reasons, 15 patients. Subsequent treatment was imatinib in 11 patients, nilotinib in 7, dasatinib in 4, ponatinib in 2, chemotherapy plus dasatinib in 3, stem cell transplant in 2, bafetinib in 1, and unknown or none in 8 patients. A complete cytogenetic response was achieved in 19 patients, including 17 with major molecular response. Fourteen of the patients who achieved a complete molecular response or major molecular response with subsequent TKIs were in CP at the time of 2G-TKI discontinuation.
We conclude that treatment failure after first-line therapy with 2G-TKIs is mostly associated with toxicity or patient preference, and these patients respond well to alternative TKIs.
No preview · Article · Jun 2013 · Clinical lymphoma, myeloma & leukemia
[Show abstract][Hide abstract] ABSTRACT: We conducted a phase 2 study of ruxolitinib in patients with relapsed/refractory leukemias. Patients with acceptable performance status (0-2), adequate organ function, and no active infection, received ruxolitinib 25 mg orally twice a day for 4 weeks (1 cycle). Response was assessed after every 2 cycles of treatment, and patients who completed 2 cycles were allowed to continue treatment until disease progression. Dose escalation to 50 mg twice daily was permitted in patients demonstrating a benefit. Thirty-eight patients, with a median age of 69 years (range, 45-88), were treated. The median number of prior therapies was 2 (range, 1-6). Twelve patients had JAK2V617F mutation. Patients received a median of 2 cycles of therapy (range, 1-22). Three of 18 patients with postmyeloproliferative neoplasm (MPN) acute myeloid leukemia (AML) showed a significant response; 2 achieved complete remission (CR) and one achieved a CR with insufficient recovery of blood counts (CRi). The responding patients with palpable spleens also had significant reductions in spleen size. Overall, ruxolitinib was very well tolerated with only 4 patients having grade 3 or higher toxicity. Ruxolitinib has modest antileukemic activity as a single agent, particularly in patients with post-MPN AML. The study was registered at www.clinicaltrials.gov as NCT00674479.
[Show abstract][Hide abstract] ABSTRACT: A subgroup of patients with core binding factor acute myeloid leukemias (AML) is characterized by the presence of the fusion gene CBFb-Myh11. At the cytogenetic level, most of these patients are identified by the presence of an inversion of chromosome 16 [inv(16)(p13q22)] and rarely by a translocation t(16;16)(p13;q22). The aim of this study is to describe the natural history of patients with t(16;16) [N = 6] treated at MD Anderson Cancer Center and compared them with a cohort of patients with inv(16)(p13q22) [n = 61]. In patients with t(16;16) the complete remission rate (CR) was 100% when treated with a combination of fludarabine and high-dose cytarabine. Median overall survival (OS) had not been achieved. There was no difference in response or OS or progression free survival between both groups. Presence of additional chromosomal abnormalities and molecular aberrations had no effect on prognosis. In conclusion, and consistent with previous reports, the natural history of patients with t(16:16)(p13;q22) is similar to that of classic patients with inv16 AML and therefore should be treated similarly.
Preview · Article · Mar 2012 · American Journal of Hematology