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Anchorage, AL, United States

Jonas M.M.,Childrens Hospital Boston | Block J.M.,Hepatitis B Foundation | Haber B.A.,Childrens Hospital of Philadelphia | Karpen S.J.,Baylor College of Medicine | And 6 more authors.
Hepatology | Year: 2010

Chronic hepatitis B virus (HBV) infection in children presents a therapeutic challenge for the practitioner. Decisions regarding selection of patients who may benefit from treatment, appropriate timing of treatment, and the choice of antiviral therapy are complex and are compounded by the limited number of drugs that have been studied in children. An expert panel of nationally recognized pediatric liver specialists was convened by the Hepatitis B Foundation on August 11, 2009, to consider clinical practice relative to the therapeutic options available for children. A detailed account of these discussions is provided, and the opinions expressed are based on consensus of the experts, as well as on published evidence when available. The panel concludes that, at this time, there is no established benefit of treatment of children in the immune tolerant phase, and there is a very high risk of development of drug resistance. In addition, there is no indication for treatment of children in the inactive carrier state. For children in the immune active or reactivation phases, liver histology can help guide treatment decisions, and family history of liver disease, especially hepatocellular carcinoma, may argue for early treatment in some cases. Outside of clinical trials, interferon is the agent of choice in most cases. Nucleos(t)ide analogues are secondary therapies, and children who receive these agents require careful monitoring for development of resistance. There are a few situations when treatment is indicated regardless of HBV DNA or alanine aminotransferase levels. There is still much to be elucidated about the appropriate use of HBV therapy in children. Until more clinical data and therapeutic options are available, a conservative approach is warranted. Copyright © 2010 American Association for the Study of Liver Diseases. Source

Kelly H.W.,University of New Mexico | Sternberg A.L.,Johns Hopkins University | Lescher R.,Washington University in St. Louis | Lescher R.,Alaska Native Medical Center | And 7 more authors.
New England Journal of Medicine | Year: 2012

BACKGROUND: The use of inhaled glucocorticoids for persistent asthma causes a temporary reduction in growth velocity in prepubertal children. The resulting decrease in attained height 1 to 4 years after the initiation of inhaled glucocorticoids is thought not to decrease attained adult height. METHODS:We measured adult height in 943 of 1041 participants (90.6%) in the Childhood Asthma Management Program; adult height was determined at a mean (±SD) age of 24.9±2.7 years. Starting at the age of 5 to 13 years, the participants had been randomly assigned to receive 400 μg of budesonide, 16 mg of nedocromil, or placebo daily for 4 to 6 years. We calculated differences in adult height for each active treatment group, as compared with placebo, using multiple linear regression with adjustment for demographic characteristics, asthma features, and height at trial entry. RESULTS: Mean adult height was 1.2 cm lower (95% confidence interval [CI], -1.9 to -0.5) in the budesonide group than in the placebo group (P = 0.001) and was 0.2 cm lower (95% CI, -0.9 to 0.5) in the nedocromil group than in the placebo group (P = 0.61). A larger daily dose of inhaled glucocorticoid in the first 2 years was associated with a lower adult height (-0.1 cm for each microgram per kilogram of body weight) (P = 0.007). The reduction in adult height in the budesonide group as compared with the placebo group was similar to that seen after 2 years of treatment (-1.3 cm; 95% CI, -1.7 to -0.9). During the first 2 years, decreased growth velocity in the budesonide group occurred primarily in prepubertal participants. CONCLUSIONS: The initial decrease in attained height associated with the use of inhaled glucocorticoids in prepubertal children persisted as a reduction in adult height, although the decrease was not progressive or cumulative. (Funded by the National Heart, Lung, and Blood Institute and the National Center for Research Resources; CAMP ClinicalTrials.gov number, NCT00000575.) Copyright © 2012 Massachusetts Medical Society. All rights reserved. Source

Zhu A.Z.X.,University of Toronto | Renner C.C.,Alaska Native Medical Center | Hatsukami D.K.,University of Minnesota | Benowitz N.L.,University of California at San Francisco | Tyndale R.F.,University of Toronto
Addiction | Year: 2013

Background and aims: Gene variants in CHRNA5-A3-B4, which encode for the α5, α3 and β4 nicotinic receptor subunits, are associated with altered smoking behaviors in European Americans. Little is known about CHRNA5-A3-B4 and its association with smoking behaviors and weight in Alaska Native people, which is a population with high prevalence but low levels of tobacco consumption, extensive smokeless tobacco use and high rates of obesity. We investigated CHRNA5-A3-B4 haplotype structure and its association with nicotine intake and obesity in Alaska Native people. Design, setting and participants: A cross-sectional study of 400 Alaska Native individuals, including 290 tobacco users. Measurements: CHRNA5-A3-B4 genotype, body weight and tobacco consumption biomarkers such as plasma cotinine and urinary total nicotine equivalents (TNE). Findings: Alaska Native people have a distinct CHRNA5-A3-B4 haplotype structure compared with European/African Americans. In 290 Alaska Native tobacco users the 'G' allele of rs578776, which tagged a 30kb haplotype in CHRNA5-A3-B4, was prevalent (16%) and associated significantly with nicotine intake (20% higher plasma cotinine, P<0.001, 16% higher TNE, P=0.076), while rs16969968 was not associated with nicotine intake. Rs578776 acted in combination with CYP2A6, the main nicotine-metabolizing enzyme, to increase nicotine intake by 1.8-fold compared with the low-risk group (P<0.001). Furthermore, rs2869950, a single nucleotide polymorphism 5′ to CHRNB4, was associated significantly with increased body mass index (P<0.01) in the tobacco users even after controlling for differences in nicotine intake (P<0.01). Conclusions: Genetic variants in CHRNA5-A3-B4 alter nicotine intake and body mass index in a population of Alaska Native people, who have a distinct haplotype structure, smoking behaviors and prevalence of obesity. © 2013 Society for the Study of Addiction. Source

Bruce M.G.,Centers for Disease Control and Prevention | Zulz T.,Centers for Disease Control and Prevention | DeByle C.,Centers for Disease Control and Prevention | Singleton R.,Alaska Native Medical Center | And 6 more authors.
Emerging Infectious Diseases | Year: 2013

Before introduction of Haemophilus influenzae type b (Hib) vaccines, rates of Hib disease in Alaska's indigenous people were among the highest in the world. Vaccination reduced rates dramatically; however, invasive H. influenzae type a (Hia) disease has emerged. Cases of invasive disease were identified through Alaska statewide surveillance during1983-2011. Of 866 isolates analyzed for serotype, 32 (4%) were Hia. No Hia disease was identified before 2002; 32 cases occurred during 2002-2011 (p<0.001). Median age of case-patients was 0.7 years; 3 infants died. Incidence of Hia infection (2002-2011) among children <5 years was 5.4/100,000; 27 cases occurred in Alaska Native children (18/100,000) versus 2 cases in non-Native children (0.5/100,000) (risk ratio = 36, p<0.001). From 12/2009 to 12/2011, 15 cases of Hia disease occurred in southwestern Alaska (in children <5 years, rate = 204/100,000). Since introduction of the Hib conjugate vaccine, Hia infection has become a major invasive bacterial disease in Alaska Native children. Source

Zafren K.,Alaska Native Medical Center | Zafren K.,Stanford University
Travel Medicine and Infectious Disease | Year: 2014

High altitude illness - Acute Mountain Sickness (AMS), High Altitude Cerebral Edema (HACE) and High Altitude Pulmonary Edema (HAPE) - can be prevented or limited in severity by gradual ascent and by pharmacologic methods. The decision whether to use pharmacologic prophylaxis depends on the ascent rate and an individual's previous history of altitude illness. This review discusses risk stratification to determine whether to use pharmacologic prophylaxis and recommends specific drugs, especially acetazolamide, dexamethasone and nifedipine. This review also evaluates non-recommended drugs. In addition, this review suggests non-pharmacologic methods of decreasing the risk of severe altitude illness. There are also brief sections on how to decrease sleep disturbance at high altitude, travel to high altitude for patients with pre-existing illness and advice for travelers ascending to high altitude. © 2013 Published by Elsevier Ltd. Source

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