Progress on catastrophic health spending in 133 countries: a retrospective observational study

Background The goal of universal health coverage (UHC) requires inter alia that families who get needed health care do not suffer undue financial hardship as a result. This can be measured by the percentage of people in households whose out-of-pocket health expenditures are large relative to their income or consumption. We aimed to estimate the global incidence of catastrophic health spending, trends between 2000 and 2010, and associations between catastrophic health spending and macroeconomic and health system variables at the country level. Methods We did a retrospective observational study of health spending using data obtained from household surveys. Of 1566 potentially suitable household surveys, 553 passed quality checks, covering 133 countries between 1984 and 2015. We defined health spending as catastrophic when it exceeded 10% or 25% of household consumption. We estimated global incidence by aggregating up from every country, using a survey for the year in question when available, and interpolation and model-based estimates otherwise. We used multiple regression to explore the relation between a country’s incidence of catastrophic spending and gross domestic product (GDP) per person, the Gini coefficient for income inequality, and the share of total health expenditure spent by social security funds, other government agencies, private insurance schemes, and non-profit institutions. Findings The global incidence of catastrophic spending at the 10% threshold was estimated as 9·7% in 2000, 11·4% in 2005, and 11·7% in 2010. Globally, 808 million people in 2010 incurred catastrophic health spending. Across 94 countries with two or more survey datapoints, the population-weighted median annual rate of change of catastrophic payment incidence was positive whatever catastrophic payment incidence measure was used. Incidence of catastrophic payments was correlated positively with GDP per person and the share of GDP spent on health, and incidence correlated negatively with the share of total health spending channelled through social security funds and other government agencies. Interpretation The proportion of the population that is supposed to be covered by health insurance schemes or by national or subnational health services is a poor indicator of financial protection. Increasing the share of GDP spent on health is not sufficient to reduce catastrophic payment incidence; rather, what is required is increasing the share of total health expenditure that is prepaid, particularly through taxes and mandatory contributions

Trypanosomiase humaine africaine : étude d'un score de présomption de diagnostic au Congo

Une enquête cas-témoins a été réalisée au Congo afin de définir une grille de score de présomption de la maladie du sommeil à #T.b. gambiense$, basée sur une sélection de critères cliniques et épidémiologiques de la trypanosomiase, utilisable par les structures sanitaires périphériques. L'enquête a été réalisée sur 163 cas et 326 témoins. Les signes cliniques et les symptômes retenus sont :fièvre, céphalées, prurit et lésions de grattage, diarrhée, oedèmes, adénopathies cervicales, troubles du sommeil, troubles de l'appétit, troubles sexuels, psychisme, signes neurologiques et autres troubles cliniques mineurs. Les autres critères retenus sont les antécédents de trypanosomiase humaine africaine (THA) et l'existence d'un cheptel dans la concession. L'analyse des résultats confirme qu'il n'existe pas de critère ou groupe de critères pathognomoniques. Aucun des critères sélectionnés n'est suffisamment discriminant pour permettre une sélection des trypanosomés parmi les consultants. Une grille de score de présomption semble donc de peu d'utilité au niveau périphérique; ceci est d'autant plus vrai si l'on considère l'augmentation de la charge de travail. Le faible pouvoir discriminant des signes cliniques et des symptômes ainsi que des autres paramètres de la trypanosomiase africaine met en évidence la difficulté de mise en place d'une stratégie d'intégration efficiente en tant qu'outil diagnostique précoce. (Résumé d'auteur

Progress on catastrophic health spending in 133 countries: a retrospective observational study

Background The goal of universal health coverage (UHC) requires inter alia that families who get needed health care do not suffer undue financial hardship as a result. This can be measured by the percentage of people in households whose out-of-pocket health expenditures are large relative to their income or consumption. We aimed to estimate the global incidence of catastrophic health spending, trends between 2000 and 2010, and associations between catastrophic health spending and macroeconomic and health system variables at the country level. Methods We did a retrospective observational study of health spending using data obtained from household surveys. Of 1566 potentially suitable household surveys, 553 passed quality checks, covering 133 countries between 1984 and 2015. We defined health spending as catastrophic when it exceeded 10% or 25% of household consumption. We estimated global incidence by aggregating up from every country, using a survey for the year in question when available, and interpolation and model-based estimates otherwise. We used multiple regression to explore the relation between a country’s incidence of catastrophic spending and gross domestic product (GDP) per person, the Gini coefficient for income inequality, and the share of total health expenditure spent by social security funds, other government agencies, private insurance schemes, and non-profit institutions. Findings The global incidence of catastrophic spending at the 10% threshold was estimated as 9·7% in 2000, 11·4% in 2005, and 11·7% in 2010. Globally, 808 million people in 2010 incurred catastrophic health spending. Across 94 countries with two or more survey datapoints, the population-weighted median annual rate of change of catastrophic payment incidence was positive whatever catastrophic payment incidence measure was used. Incidence of catastrophic payments was correlated positively with GDP per person and the share of GDP spent on health, and incidence correlated negatively with the share of total health spending channelled through social security funds and other government agencies. Interpretation The proportion of the population that is supposed to be covered by health insurance schemes or by national or subnational health services is a poor indicator of financial protection. Increasing the share of GDP spent on health is not sufficient to reduce catastrophic payment incidence; rather, what is required is increasing the share of total health expenditure that is prepaid, particularly through taxes and mandatory contributions

A recurrent p.Arg92Trp variant in steroidogenic factor-1 (NR5A1) can act as a molecular switch in human sex development

Cell lineages of the early human gonad commit to one of the two mutually antagonistic organogenetic fates, the testis or the ovary. Some individuals with a 46,XX karyotype develop testes or ovotestes (testicular or ovotesticular disorder of sex development; TDSD/OTDSD), due to the presence of the testis-determining gene, SRY Other rare complex syndromic forms of TDSD/OTDSD are associated with mutations in pro-ovarian genes that repress testis development (e.g. WNT4); however, the genetic cause of the more common non-syndromic forms is unknown. Steroidogenic factor-1 (known as NR5A1) is a key regulator of reproductive development and function. Loss-of-function changes in NR5A1 in 46,XY individuals are associated with a spectrum of phenotypes in humans ranging from a lack of testis formation to male infertility. Mutations in NR5A1 in 46,XX women are associated with primary ovarian insufficiency, which includes a lack of ovary formation, primary and secondary amenorrhoea as well as early menopause. Here, we show that a specific recurrent heterozygous missense mutation (p.Arg92Trp) in the accessory DNA-binding region of NR5A1 is associated with variable degree of testis development in 46,XX children and adults from four unrelated families. Remarkably, in one family a sibling raised as a girl and carrying this NR5A1 mutation was found to have a 46,XY karyotype with partial testicular dysgenesis. These unique findings highlight how a specific variant in a developmental transcription factor can switch organ fate from the ovary to testis in mammals and represents the first missense mutation causing isolated, non-syndromic 46,XX testicular/ovotesticular DSD in humans

Mutations involving the SRY-related gene SOX8 are associated with a spectrum of human reproductive anomalies

SOX8 is an HMG-box transcription factor closely related to SRY and SOX9. Deletion of the gene encoding Sox8 in mice causes reproductive dysfunction but the role of SOX8 in humans is unknown. Here, we show that SOX8 is expressed in the somatic cells of the early developing gonad in the human and influences human sex-determination. We identified two individuals with 46,XY disorders/differences in sex development (DSD) and chromosomal rearrangements encompassing the SOX8 locus and a third individual with 46,XY DSD and a missense mutation in the HMG-box of SOX8. In-vitro functional assays indicate that this mutation alters the biological activity of the protein. As an emerging body of evidence suggests that DSDs and infertility can have common etiologies, we also analyzed SOX8 in a cohort of infertile men (n = 274) and two independent cohorts of women with primary ovarian insufficiency (POI; n = 153 and n = 104). SOX8 mutations were found at increased frequency in oligozoospermic men (3.5%; p<0.05) and POI (5.06%; p=4.5x10-5) as compared to fertile/normospermic control populations (0.74%). The mutant proteins identified altered SOX8 biological activity as compared to the wild-type protein. These data demonstrate that SOX8 plays an important role in human reproduction and SOX8 mutations contribute to a spectrum of phenotypes including 46,XY DSD, male infertility and 46,XX POI

Pathogenic variants in the DEAH-box RNA helicase DHX37 are a frequent cause of 46,XY gonadal dysgenesis and 46,XY testicular regression syndrome

PURPOSE: XY individuals with disorders/differences of sex development (DSD) are characterized by reduced androgenization caused, in some children, by gonadal dysgenesis or testis regression during fetal development. The genetic etiology for most patients with 46,XY gonadal dysgenesis and for all patients with testicular regression syndrome (TRS) is unknown. METHODS: We performed exome and/or Sanger sequencing in 145 individuals with 46,XY DSD of unknown etiology including gonadal dysgenesis and TRS. RESULTS: Thirteen children carried heterozygous missense pathogenic variants involving the RNA helicase DHX37, which is essential for ribosome biogenesis. Enrichment of rare/novel DHX37 missense variants in 46,XY DSD is highly significant compared with controls (P value = 5.8 × 10-10). Five variants are de novo (P value = 1.5 × 10-5). Twelve variants are clustered in two highly conserved functional domains and were specifically associated with gonadal dysgenesis and TRS. Consistent with a role in early testis development, DHX37 is expressed specifically in somatic cells of the developing human and mouse testis. CONCLUSION: DHX37 pathogenic variants are a new cause of an autosomal dominant form of 46,XY DSD, including gonadal dysgenesis and TRS, showing that these conditions are part of a clinical spectrum. This raises the possibility that some forms of DSD may be a ribosomopathy

Financial Globalization and Economic Policies

We review the large literature on various economic policies that could help developing economies effectively manage the process of financial globalization. Our central findings indicate that policies promoting financial sector development, institutional quality and trade openness appear to help developing countries derive the benefits of globalization. Similarly, sound macroeconomic policies are an important prerequisite for ensuring that financial integration is beneficial. However, our analysis also suggests that the relationship between financial integration and economic policies is a complex one and that there are unavoidable tensions inherent in evaluating the risks and benefits associated with financial globalization. In light of these tensions, structural and macroeconomic policies often need to be tailored to take into account country specific circumstances to improve the risk-benefit tradeoffs of financial integration. Ultimately, it is essential to see financial integration not just as an isolated policy goal but as part of a broader package of reforms and supportive macroeconomic policies