Despite the growing worldwide burden of dengue fever, the global economic impact of dengue illness is poorly documented. Using a common protocol, we present the first multicountry estimates of the direct and indirect costs of dengue cases in eight American and Asian countries. We conducted prospective studies of the cost of dengue in five countries in the Americas (Brazil, El Salvador, Guatemala, Panama, and Venezuela) and three countries in Asia (Cambodia, Malaysia, and Thailand). All studies followed the same core protocol with interviews and medical record reviews. The study populations were patients treated in ambulatory and hospital settings with a clinical diagnosis of dengue. Most studies were performed in 2005. Costs are in 2005 international dollars (I$). We studied 1,695 patients (48% pediatric and 52% adult); none died. The average illness lasted 11.9 days for ambulatory patients and 11.0 days for hospitalized patients. Among hospitalized patients, students lost 5.6 days of school, whereas those working lost 9.9 work days per average dengue episode. Overall mean costs were I$514 and I$1,394 for an ambulatory and hospitalized case, respectively. With an annual average of 574,000 cases reported, the aggregate annual economic cost of dengue for the eight study countries is at least I$587 million. Preliminary adjustment for under-reporting could raise this total to $1.8 billion, and incorporating costs of dengue surveillance and vector control would raise the amount further. Dengue imposes substantial costs on both the health sector and the overall economy.
The rates of whole body nitric oxide (NO) synthesis, plasma arginine flux, and de novo arginine synthesis and their relationships to urea production, were examined in a total of seven healthy adults receiving an L-amino acid diet for 6 days. NO synthesis was estimated by the rate of conversion of the ['5N] indicating that -11% of the plasma arginine flux originates via conversion of plasma citrulline to arginine. Thus, the fraction of the plasma arginine flux associated with NO and also urea synthesis in healthy humans is small, although the plasma arginine compartment serves as a significant precursor pool (54%) for whole body NO formation. This tracer model should be useful for exploring these metabolic relationships in vivo, under specific pathophysiologic states where the L-arginine-NO pathway might be altered.Arginine serves various important metabolic functions, including roles in protein synthesis, nitrogen transport and elimination (1, 2), and as the precursor of nitric oxide (NO), which is a current area of considerable research interest (3-5). Oxidation of arginine by a homodimeric group of nitric oxide synthases yields citrulline and nitric oxide in stoichiometric amounts, with each containing a nitrogen atom derived from the guanidino moiety of arginine. NO undergoes oxidative degradation to the stable end products nitrite (NO-) and nitrate (NO-). In the in vivo system, NO-is readily oxidized to NO{ via hemoglobin, and so NO is eventually detected in plasma or urine as NOK (5) and its measurement has been used to estimate the rate of whole body NO synthesis.It has been suggested that therapeutic modulation of nitric oxide production may be achieved by supplying the precursor arginine (6-9) or by inhibiting NO production with L-arginine analogs (10-12). However, before profound changes in exogenous arginine intake levels or a pharmacologic inhibition of NO formation can be safely recommended, it is desirable to gain a better understanding of the regulation of whole body arginine metabolism in human subjects and its quantitative interrelationships with the L-arginine-NO pathway.In our previous studies, using stable isotopic tracer techniques, we have investigated whole body arginine metabolism and the use of arginine for NO synthesis, by measurement of the transfer of the guanidino nitrogen of plasma arginine to urinary NO-. These studies have been carried out in healthy humans receiving variable levels of arginine intake (13-15), and in infants with pulmonary hypertension (16). We have now extended these earlier investigations of whole body arginine homeostasis and the metabolism of urea cycle intermediates by examining the kinetics of arginine metabolism throughout a continuous 24-35-hr period. Using this design, it has been possible, for the first time to our knowledge, to determine the in vivo rate of conversion of [15N]guanidino arginine to [15N]ureido citrulline and NO, presumably due to the NO synthase reaction. We compared this estimate with the rate of transfer of the guanidino nitroge...
In an effort to attain earlier diagnoses in children with hemophagocytic lymphohistiocytosis (HLH), the International Histiocyte Society has now broadened their diagnostic criteria to no longer differentiate primary (HLH) and secondary hemophagocytic lymphohistiocytosis (SHLH). Five of the following eight diagnostic criteria needed to be met: 1) fever, 2) cytopenia of two lines, 3) hypertriglyceridemia and/or hypofibrinogenemia, 4) hyperferritinemia (>500 microg/L), 5) hemophagocytosis, 6) elevated soluble interleukin-2 receptor (CD25), 7) decreased natural killer-cell activity, and 8) splenomegaly can also commonly be found in patients with sepsis, systemic inflammatory response syndrome (SIRS), multiorgan dysfunction syndrome (MODS), and macrophage activation syndrome (MAS). Nevertheless, the therapeutic options for these are radically different. Chemotherapy and bone marrow transplant have been used for treatment of HLH/SHLH, whereas antibiotics and supportive treatment are used in severe sepsis/SIRS and MODS. MAS is treated with limited immune suppression. Outcomes are also different, SHLH has a mortality rate around 50%, whereas pediatric septic shock and MODS have a mortality of 10.3% and 18%, respectively, and severe sepsis in previously healthy children has a mortality rate of 2%. MAS has a mortality rate between 8% and 22%. Because SHLH and severe sepsis/SIRS/MODS/MAS share clinical and laboratory inflammatory phenotypes, we recommend extreme caution when considering applying HLH therapies to children with sepsis/SIRS/MODS/MAS. HLH therapies are clearly warranted for children with HLH; however, a quantitative functional estimate of cytotoxic lymphocyte function may be a more precise approach to define the overlap of these conditions, better identify these processes, and develop novel therapeutic protocols that may lead to improved treatments and outcomes.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2025 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.