scholarly journals 577Inequalities in access to in vitro fertilisation treatment in France

2021 ◽  
Vol 50 (Supplement_1) ◽  
Author(s):  
Khaoula Ben Messaoud ◽  
◽  

Abstract Background In vitro fertilisation (IVF) treatment is one of the most expensive infertility treatments. Cost has been described as a substantial barrier to access. In France all infertility treatments, including IVF, are fully reimbursed, but are there other barriers to access? Methods Based on the French national health insurance database that exhaustively records reimbursed healthcare, this cohort study included all women aged 18–49 years unsuccessfully treated with ovarian induction (first-line infertility treatment) between January–August 2016. Outcome was IVF access within 24 months of starting first-line treatment. Univariate and multivariate regressions explored age, disadvantaged social status, driving time to nearest IVF centre, and deprivation index of area of residence. Results Over 20,000 women unsuccessfully received first-line treatment. Almost 80% did not access IVF within 24 months. After age 34, probability of access decreased. Disadvantaged social status and living in a disadvantaged area were associated with lower probability of accessing IVF. Driving time to the nearest IVF centre was not significantly associated with access. Conclusions Socio-economic barriers to access IVF exist despite full treatment reimbursement in France. To reduce health inequalities, we need to better understand the nature and patterns of these barriers among less socially advantaged people. Key messages After failure of first-line infertility treatment, only 20% of women access IVF although it is fully reimbursed in France. Age, but most importantly socio-economic status, is a key determinant of access to IVF treatment. Distance from nearest IVF centre does not appear significant in explaining access to treatment in France.

2015 ◽  
Vol 59 (8) ◽  
pp. 4417-4423 ◽  
Author(s):  
Tamalee Roberts ◽  
Stephen Bush ◽  
John Ellis ◽  
John Harkness ◽  
Damien Stark

ABSTRACTBlastocystisis the most common human enteric protist with controversial clinical significance. Metronidazole is considered a first-line treatment forBlastocystisinfection; however, there has been increasing evidence for the lack of efficacy of this treatment. Treatment failure has been reported in several clinical cases, and recentin vitrostudies have suggested the occurrence of metronidazole-resistant strains. In this study, we tested 12Blastocystisisolates from 4 commonBlastocystissubtypes (ST1, ST3, ST4, and ST8) against 12 commonly used antimicrobials (metronidazole, paromomycin, ornidazole, albendazole, ivermectin, trimethoprim-sulfamethoxazole [TMP-SMX], furazolidone, nitazoxanide, secnidazole, fluconazole, nystatin, and itraconazole) at 10 different concentrationsin vitro. It was found that each subtype showed little sensitivity to the commonly used metronidazole, paromomycin, and triple therapy (furazolidone, nitazoxanide, and secnidazole). This study highlights the efficacy of other potential drug treatments, including trimethoprim-sulfamethoxazole and ivermectin, and suggests that current treatment regimens be revised.


2019 ◽  
Vol 6 (Supplement_2) ◽  
pp. S309-S310 ◽  
Author(s):  
Christopher Longshaw ◽  
Masakatsu Tsuji ◽  
Meredith M Hackel ◽  
Daniel F Sahm ◽  
Yoshinori Yamano

Abstract Background DTR organisms are defined as nonsusceptible to all high-efficacy, low-toxicity antibiotics (penicillins, cephalosporins, carbapenems, and quinolones), leaving physicians with limited first-line treatment options. Analyses of electronic health records have shown that patients with DTR Gram-negative bacterial infections are more likely to receive inappropriate antibiotic therapy, have longer hospital stay and increased risk of mortality. CFDC is a novel parenteral siderophore cephalosporin with potent activity against aerobic Gram-negative pathogens, including carbapenem-resistant strains. We evaluated the in vitro activity of CFDC and comparators against DTR pathogens collected by the SIDERO-WT surveillance study. Methods A total of 30,459 clinical isolates of Gram-negative bacilli were systematically collected from United States, Canada, and 11 EU countries during 2014–2017. MICs were determined by broth microdilution for a panel of 7 antibiotics, including CFDC, ceftazidime–avibactam (CZA), ceftolozane–tazobactam (C/T), colistin (CST), cefepime (FEP), meropenem (MEM), and ciprofloxacin (CIP) according to CLSI guidelines. All antibiotics were tested in cation-adjusted Mueller–Hinton broth (CAMHB) except CFDC, for which iron-depleted CAMHB was used. Susceptibility was determined according to CLSI interpretive breakpoints except CST, where EUCAST breakpoints were used. DTR pathogens were defined as being nonsusceptible to FEP, MEM, and CIP according to CLSI breakpoints. Results Among 30,459 Gram-negative isolates collected between 2014 and 2017, 9.3% were nonsusceptible to FEP, MEM, and CIP and could be defined as DTR. DTR was most frequently observed in Acinetobacter spp. (55.5%), followed by Burkholderia spp. (19%), Pseudomonas aeruginosa (9.5%), and Enterobacterales (2.7%). Of the 1,173 Stenotrophomonas maltophilia tested, 97% had MEM MIC of ≥8 mg/L; however, only 2.9% could be defined as DTR. Cefiderocol was the most active antibiotic tested against DTR isolates with 94.5% DTR-Acinetobacter spp., 98.3% DTR-P. aeruginosa, and 99.8% DTR-Enterobacterales susceptible (Table 1). Conclusion CFDC demonstrated potent activity against DTR Gram-negative pathogens with limited first-line treatment options. Disclosures All authors: No reported disclosures.


Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 864-864 ◽  
Author(s):  
Steven Knapper ◽  
Alan K. Burnett ◽  
Jonathan Kell ◽  
Raj Chopra ◽  
Richard Clark ◽  
...  

Abstract Activating mutations of the receptor tyrosine kinase FLT3 are present in approximately one-third of cases of AML and are associated with an adverse prognosis. Activated FLT3 is also frequently expressed in wild type (WT) patients. The indolocarbazole derivative CEP701 (Cephalon Inc) has been shown to potently inhibit phosphorylation of both mutant and WT FLT3 in vitro causing cytotoxicity in primary AML blasts and prolonging survival in mouse AML models. We present results from the first phase II trial of CEP701 given as first line treatment in AML in patients aged over 70 years (or aged 60–69 with a poor performance score or cardiac toxicity) and not considered fit for intensive chemotherapy, irrespective of FLT3 mutation status. Patients with presenting white blood cell (WBC) count of over 30x109/l received hydroxycarbamide for up to 21 days to reduce the WBC to less than 10x109/l before starting CEP701. CEP701 was administered orally for 56 days, initially at a dose of 60mg bd with dose increase to 80mg bd from day 28. Response was assessed by BM and peripheral blood examination on days 14, 28 and 56. 24 patients entered the study: 12 male and 12 female with a median age of 73 (range 67–84). 5 are too early in treatment to assess response. 1 patient died from intracerebral haemorrhage and 2 were withdrawn due to toxicity (emesis) before response could be assessed. Of the sixteen fully evaluable patients 4 were FLT3 mutants (2 ITD, 2 point mutations) and the remaining 12 had WT FLT3. Bone marrow response (BMR) was defined as a greater than 50% reduction in bone marrow blasts without haematological recovery. Haematological response (HR) was defined as disappearance of blasts from the peripheral blood not attributable to hydroxycarbamide. 3 of the 4 FLT3 mutant cases responded to CEP701. A 72 year-old male point mutant (deletion 836) achieved a late HR with normalisation of counts lasting 6 months. A 74 year-old male point mutant (D835) continues CEP701 after achieving a HR on 60mg bd associated with transfusion independence and normalisation of counts. A 74 year-old female ITD mutant achieved a HR on 60mg bd followed by rapid disease progression after the drug was withdrawn due to profound fatigue. 3 of the 12 wild type cases responded including 1 BMR and 1 HR (both transient) on 80mg bd. A third wild type case had a transient BMR on 60mg bd and a further transient BMR following dose increase to 80mg bd. No patient achieved a conventional complete remission. 11 of the first 24 patients (46%) experienced grade 1/2 gastrointestinal toxicity. Cases have been further categorised by Affymetrix gene expression analysis to identify gene signatures associated with drug responsiveness. 2 clinical CEP701 responders among the first 10 cases analysed fit a previously-defined gene expression signature associated with high in vitro CEP701 responsiveness (Knapper et al. Blood 102:11). Flow cytometric surface FLT3 expression assay, MTS cytotoxicity assay and ex vivo surrogate bioassay of plasma FLT3 inhibitory activity show limited correlation with clinical response. The preliminary trial results suggest that CEP701 has haematological activity in both mutant and WT patients. In view of the modest response of WT cases it is proposed to amend the trial to assess sequential low dose cytarabine and CEP701 as a combined approach.


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