7 research outputs found

    Hong Kong's domestic health spending—financial years 1989/90 through 2004/05

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    This report presents the latest estimates of Hong Kong’s domestic health spending between fiscal years 1989/90 and 2004/05, cross-stratified and categorised by financing source, provider and function on an annual basis. Total expenditure on health was HK67807millioninfiscalyear2004/05.Inrealerms,totalexpenditureonhealthshowedpositivegrowthaveraging7Thisincreasewaslargelydrivenbytheriseinpublicspending,whichrose9Ofthe67 807 million in fiscal year 2004/05. In real erms, total expenditure on health showed positive growth averaging 7% per annum hroughout the period covered in this report while gross domestic product grew t 4% per annum on average, indicating a growing percentage of health spending elative to gross domestic product, from 3.5% in 1989/90 to 5.2% in 2004/05. This increase was largely driven by the rise in public spending, which rose 9% er annum on average in real terms over the period, compared with 5% for private pending. This represents a growing share of public spending from 40% to 55% f total expenditure on health during the period. While public spending was the ominant source of health financing in 2004/05, private household out-of-pocket xpenditure accounted for the second largest share of total health spending (32%). he remaining sources of health finance were employer-provided group medical enefits (8%), privately purchased insurance (5%), and other private sources (1%). Of the 67 807 million total health expenditure in 2004/05, current xpenditure comprised 65429million(9665 429 million (96%) while 2378 million (4%) were apital expenses (ie investment in medical facilities). Services of curative care ccounted for the largest share of total health spending (67%) which were made p of ambulatory services (35%), in-patient curative care (28%), day patient ospital services (3%), and home care (1%). The next largest share of total health xpenditure was spent on medical goods outside the patient care setting (10%). Analysed by health care provider, hospitals accounted for the largest share (46%) and providers of ambulatory health care the second largest share (30%) f total health spending in 2004/05. We observed a system-wide trend towards ervice consolidation at institutions (as opposed to free-standing ambulatory linics, most of which are staffed by solo practitioner). In 2004/05, public expenditure on health amounted to 35247million(53.935 247 million (53.9% f total current expenditure), which was mostly incurred at hospitals (76.5%), hilst private expenditure (30 182 million) was mostly incurred at providers of mbulatory health care (54.6%). This reflects the mixed health care economy of ong Kong where public hospitals generally account for about 90% of total beddays nd private doctors (including Western and Chinese medicine practitioners) rovide 75% to 80% of out-patient care. While both public and private spending were mostly expended on personal ealth care services and goods (92.9%), the distributional patterns among functional ategories differed. Public expenditure was targeted at in-patient care (54.2%) and ubstantially less on out-patient care (24.5%), especially low-intensity first-contact are. In comparison, private spending was mostly concentrated on out-patient care (49.6%), whereas medical goods outside the patient care setting (22 .6%) and inpatient are (18.8%) comprised the majority of the remaining share. Compared to OECD countries, Hong Kong has devoted a relatively low percentage of gross domestic product to health in he last decade. As a share of total spending, public funding (either general government revenue or social security funds) was lso lower than in most comparably developed economies, although commensurate with its public revenue collection base.published_or_final_versio

    Next-generation sequencing with a myeloid gene panel in core-binding factor AML showed KIT activation loop and TET2 mutations predictive of outcome

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    Clinical outcome and mutations of 96 core-binding factor acute myeloid leukemia (AML) patients 18-60 years old were examined. Complete remission (CR) after induction was 94.6%. There was no significant difference in CR, leukemia-free-survival (LFS) and overall survival (OS) between t(8;21) (N=67) and inv(16) patients (N=29). Univariate analysis showed hematopoietic stem cell transplantation at CR1 as the only clinical parameter associated with superior LFS. Next-generation sequencing based on a myeloid gene panel was performed in 72 patients. Mutations in genes involved in cell signaling were associated with inferior LFS and OS, whereas those in genes involved in DNA methylation were associated with inferior LFS. KIT activation loop (AL) mutations occurred in 25 patients, and were associated with inferior LFS (P=0.003) and OS (P=0.001). TET2 mutations occurred in 8 patients, and were associated with significantly shorter LFS (P=0.015) but not OS. Patients negative for KIT-AL and TET2 mutations (N=41) had significantly better LFS (P<0.001) and OS (P=0.012) than those positive for both or either mutation. Multivariate analysis showed that KIT-AL and TET2 mutations were associated with inferior LFS, whereas age ⩾40 years and marrow blast ⩾70% were associated with inferior OS. These observations provide new insights that may guide better treatment for this AML subtype.published_or_final_versio

    Next-Generation Sequencing with a 54-Gene Panel Identifies Unique Mutational Profile and Prognostic Markers in Chinese Patients with Myelofibrosis

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    634. Myeloproliferative Syndromes: Clinical: Poster I: no. 1638Introduction and objectives: Myelofibrosis (MF) has the worst outcome amongst various myeloproliferative neoplasms. Its prognosis is determined by clinicopathologic features and mutations in key driver genes. An increasing number of gene mutations involving various biological pathways in myeloid malignancies has been discovered. The prognostic significance of these mutations have not been clearly defined. In this study, we aim to describe the genomic characteristic in a large cohort of MF patients and identify clinical and molecular predictors of outcome. Methods: We evaluated the genetic profile of 101 patients with MF (primary, N=70; secondary, N=30) using next-generation sequencing with a 54-gene panel comprising: ABL1, ASXL1, ATRX, BCOR, BCORL1, BRAF, CALR, CBL, CBLB, CBLC, CDKN2A, CEBPA, CSF3R, CUX1, DNMT3A, ETV6, EZH2, FBXW7, FLT3, GATA1, GATA2, GNAS, HRAS, IDH1, IDH2, IKZF1, JAK2, JAK3, KDM6A, KIT, KMT2A, KRAS, MPL, MYD88, NOTCH1, NPM1, NRAS, PDGFRA, PHF6, PTEN, PTPN11, RAD21, RUNX1, SETBP1, SF3B1, SMC1A, SMC3, SRSF2, STAG2, TET2, TP53, U2AF1, WT1, ZRSR2. Multivariate cox regression analysis was used to determine prognostic factors for overall survival (OS) and leukemia-free survival (LFS). Results: We identified mutations in 39 genes implicated in myeloid malignancies (Figure 1A). 96 patients (95%) with MF had a mutation in 1 or more genes: 14 patients (13.9%) had 1 mutation, 38 patients (37.6%) had 2 mutations, 18 patients (17.8%) had 3 mutations, 15 patients (14.9%) had 4 mutations, 7 patients (6.9%) had 5 mutations and 4 patients (4%) had 6 or more mutations. TET2/JAK2V617F (16 patients, 15.9%), ASXL1/JAK2V617F (12 patients, 11.9%) and ASXL1/CALR (10 patients, 9.9%) were the most frequently co-mutated genes (Figure 1B). Other JAK2 variants occurred concomitantly with JAK2V617F in 10 patients (9.9%) and CALR mutations in 4 patients (4%) mutations. Other frequently concomitant mutations included CUX1/JAK2V617F (6 patients, 5.9%), EZH2/JAK2V617F (6 patients, 5.9%), RUNX1/JAK2V617F (5 patients, 5%), SF3B1/JAK2V617F (5 patients, 5%), SETBP1/JAK2V617F (4 patients, 4%) and ZRSR2/JAK2V617F (4 patients, 4%). The median follow-up of the cohort was 49 (1-256) months. The 5-year and 10-year OS were 66.3% and 35.4%. The 5-year and 10-year LFS of were 84% and 63.3%. There were no statistically significant differences in OS and LFS between primary and secondary MF. Significant negative prognostic indicators were identified on multivariate analysis, including male gender (P=0.044), age > 65 years (P=0.044), Hb < 10g/dL (P=0.001), mutated CUX1 (P=0.003) and mutated TP53 (P=0.043) for OS, and Hb < 10g/dL (P=0.007), mutated TP53 (P=0.043) and mutated IDH2 (P=0.001) for LFS. In primary MF, inferior prognostic indicators included male gender (P=0.031), Hb < 10g/dL (P=0.002), platelet count < 100 x 109/L (P=0.021), mutated TET2 (P=0.011) and mutated CUX1 (P=0.011) for OS; and Hb < 10g/dL (P=0.027), mutated RUNX1 (P=0.019) and mutated DNMT3A (P=0.004) for LFS. In JAK2V617F positive MF, inferior prognostic indicators included mutated ASXL1 (P=0.006) and mutated SRSF2 (P<0.001) for OS; and mutated U2AF1 (P=0.037) for LFS. Conclusion: Our study demonstrated unique molecular profiles and prognostic predictors of outcome in Chinese patients with MF
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