S0001-600220080001 Acta Médica Costarricense Acta méd. costarric 0001-6002 Colegio de Médicos y Cirujanos de Costa Rica S0001-60022008000100001 Peritazgo Pacheco Mena Licda. Olga Martha ,Universidad de Costa Rica 03 2008 2008 50 4 4
S0001-600220080001 Acta Médica Costarricense Acta méd. costarric 0001-6002 Colegio de Médicos y Cirujanos de Costa Rica S0001-60022008000100002 Actualización en los mecanismos fisiopatológicos de la insuficiencia cardiaca Update in physiopathological mechanisms in heart failure Ulate-Montero Guido Ulate-Campos Adriana ,Universidad de Costa Rica 03 2008 2008 50 5 12

La insuficiencia cardiaca es uno de los síndromes clínicos más frecuentes en la práctica médica y se presenta cuando el corazón,a presiones normales de llenado,es incapaz de bombear la cantidad suficiente de sangre que requiere el metabolismo de los tejidos.Aquí se presenta una revisión de los datos más recientes sobre los mecanismos involucrados en la fisiopatología de la insuficiencia cardiaca,para que su conocimiento sea de utilidad en el manejo adecuado de esta entidad. En la insuficiencia cardiaca,como respuesta al gasto cardiaco insuficiente, se activan una serie de mecanismos neuroendocrinos sistémicos,que posteriormente, contribuyen al deterioro del cuadro clínico; es el caso del sistema simpático y el sistema renina-angiotensina-aldosterona, los cuales terminan produciendo daño endotelial, incremento de radicales libres, de la apoptosis, de la fibrosis cardiaca y generación de arritmias.También se observa un incremento en la liberación de péptidos natriuréticos, los cuales tienden a regular algunas de las respuestas neurohumorales exacerbadas, sin embargo, con el transcurso de la enfermedad su acción tiende a atenuarse.Celular y molecularmente se producen una serie de alteraciones en el manejo intracelular del Ca2+, así como en algunas de las corrientes iónicas que participan en la generación del potencial de acción de los miocitos cardiacos. La remodelación cardiaca precede al cuadro clínico de la insuficiencia y contribuye a su deterioro.Mensajeros químicos como la endotelina-1, la norepinefrina y la angiotensina II, que activan la cascada de las MAP quinasas, provocan hipertrofia cardiaca, lo que favorece la isquemia y la aparición de arritmias.El manejo farmacológico de la insuficiencia cardiaca debe dirigirse a los mecanismos fisiopatológicos afectados, es decir, al bloqueo de las acciones deletéreas de los sistemas neuroendocrinos sobreestimulados y a evitar la pérdida de miocitos, la generación de fibrosis y de arritmias cardiacas, para lo cual es indispensable el manejo apropiado de los niveles intracelulares de Ca2+.

Heart failure is one of the most frequent clinical syndromes in medical practice;it appears when the heart is unable to pump enough volume of blood to supply the tissue ’s requirements.This article reviews the most recent information regarding the mechanisms involved in the pathophysiology of heart failure,the main goal is to offer the knowledge necessary to understand and manage properly this condition.In heart failure,as a response to the low cardiac output,a series of neuroendocrine systemic mechanisms are activated,but they contribute to deteriorate the clinical status;this happens with the sympathetic and the renin-angiotensin-aldosterone systems,which end up producing endothelial damage,increase of oxidative radicals,apoptosis, cardiac fibrosis and generation of arrhythmias.Also there is an increase in the secretion of natriuretic peptides,which tend to regulate some of the exacerbated neuroendocrine responses, but with time their effect tend to diminish.At the cellular and molecular level a series of alterations occur in the regulation of intracellular Ca2+, as well as in some of the ionic currents that play a role in the generation of action potentials in cardiac myocytes.Cardiac remodeling precedes the clinical manifestations of heart failure and contributes to its deterioration.Chemical messengers like endothelin-1,norepinephrine and angiotensin II,activate the MAP kinases cascade and provoke cardiac hypertrophy favoring the development of ischemia and the appearance of arrhythmias.Pharmacological management of heart failure must aim the mechanisms affected,it must block the deleterious actions of the neuroendocrine systems,avoiding the loss of myocytes, the generation of fibrosis and the production of cardiac arrhythmias,in order to achieve this goal an appropriate management of intracellular levels of Ca2+ is required.

 Insuficiencia cardiaca remodelación cardiaca activación neurohumoral acople excitación-contracción arritmias apoptosis Heart failure cardiac remodeling neurohumoral activation excitation-contraction coupling arrhythmias apoptosis Minamisawa S Sato Y Cho MC Calcium cycling proteins in heart failure, cardiomyopathy and arrythmias Exp Mol Med 2004 36 Braunwald E Colucci W Grossman W Zipes DP Libby P Bonow RO Braunwald E Aspectos clínicos de la insuficiencia cardíaca: insuficiencia cardíaca de gasto alto; edema pulmonar Tratado de Cardiología Tratado de Cardiología 2005 Madrid Elsevier España S.A Hunt SA Abraham WT Chin MH Feldman AM Francis GS Ganiats TG ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure): Developed in Collaboration With the American College of Chest Physicians and the International Society for Heart and Lung Transplantation:Endorsed by the Heart Rhythm Society Circulation 2005 112 Opie LH The neuroendocrinology of congestive heart failure Cardiovasc J South Afr 2002 13 Wright DJ Tan LB The role of exercise testing in the evaluation and management of heart failure Postgrad Med J 1999 75 Jessup M Brozena S Heart Failure N Engl J Med 2003 348 Dávila DF Núñez TJ Odreman R Mazzei de Dávila CA Mechanisms of neurohormonal activation in chronic congestive heart failure: pathophysiology and therapeutic implications Int J Cardiol 2005 101 Brum PC Rolim N Bacurau A Medeiros A Neurohumoral activation in heart failure: the role of adrenergic receptors An Acad Bras Cienc 2006 78 Schrier RW Abraham WT Hormones and Hemodinamics in Heart Failure N Engl J Med 1999 341 Cleland JG Khand A Clark A The heart failure epidemic: exactly how big is it? Eur Heart J 2001 22 Farr MA Basson CT Sparking the Failing Heart N Engl J Med 2004 351 Ho KK Pinsky JL Kannel WB Levy D The epidemiology of heart failure: the Framingham study J Am Coll Cardiol 1993 22 Goldberg LR Jessup M Stage B Heart Failure Circulation 2006 113 Harrington D Anker SD Coats AJ Preservation of exercise capacity and lack of peripheral changes in asymptomatic patients with severely impaired left ventricular function Eur Heart J 2001 22 Berk BC Fujiwara K Lehoux S ECM remodeling in hypertensive heart disease J Clin Invest 2007 117 Weir R Mcmurray J Taylor J Brady A Heart Failure in Older Patients Br J Cardiol 2006 13 Birkeland JA Sejersted OM Taraldsen T Sjaastad I EC-coupling in normal and failing hearts Scand Cardiovasc J 2005 Leite-Moreira AF Current perspectives in diastolic dysfunction and diastolic heart failure Heart 2006 92 Zile MR Brutsaert D New concepts in diastolic dysfunction and diastolic heart failure: part I:diagnosis, prognosis and measurements of diastolic function Circulation 2002 105 Clark AL Origin of symptoms in chronic heart failure Heart 2006 92 Ulate G Ulate A El calcio en los miocitos cardiacos y su papel en las miocardiopatías Rev Costarr Cardiol 2006 8 Benjamin IJ Schneider MD Learning from failure:congestive heart failure in the postgenomic age J Clin Invest 2005 115 Iwanaga Y Hoshijima M Gu Y Iwatate M Dieterle T Ikeda Y Chronic phospholamban inhibition prevents progressive cardiac dysfunction and pathological remodeling alter infarction in rats J Clin Invest 2004 113 Sande JB Sjaastad I Hoen IB Bokenes J Tonnessen T Holt E Reduced level of serine phosphorylated phospholambn in the failing rat myocardium: A major contributor to reduced SERCA2 activity Cardiovasc Res 2002 53 Tappia PS Phospholipid-mediated signaling systems as novel targets for treatment of heart disease Can J Physiol Pharmacol 2007 85 Hunter JJ Chien KR Signaling pathways for cardiac hypertrophy and failure N Eng J Med 1999 341 Swynghedauw B Phenotypic plasticity of adult myocardium: molecular mechanisms J Exp Biol 2006 209 Berenji K Drazner MH Rothermel BA Hill JA Does load-induced ventricular hypertrophy progress to systolic heart failure? Am J Physiol Heart Circ Physiol 2005 289 Teunissen BE Jongsma HJ Bierhuizen MF Regulation of myocardial connexins during hypertrophic remodeling Eur Heart J 2004 25 Watanabe T Barker TA Berk BC Angiotensin II and the endothelium: diverse signals and effects Hypertension 2005 45 Dorn GW Force T Protein kinase cascades in the regulation of cardiac hypertrophy J Clin Invest 2005 115 Francis GS Benedict C Johnstone DE Kirlin PC Nicklas J Liang CS Comparison of neuroendocrine activation in patients with left ventricular dysfunction with and without congestive heart failure. 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Circ Res 2003 93 Communal C Singh K Sawyer DB Colucci WS Opposing effects of beta(1)-and beta(2)-adrenergic receptors on cardiac myocyte apoptosis: role of a pertussis toxin-sensitive G protein Circulation 1999 100 Xiao RP Zhu W Zheng M Chakir K Bond R Lakatta EG Subtype-specific beta-adrenoceptor signaling pathways in the heart and the potential clinical implications Trends Pharmacol Sci 2004 25 Zhao XL Gutierrez LM Chang CF Hosey MM The alpha 1-aubunit of skeletal muscle L-type Ca channels is the key target for regulation by A-kinase and protein phosphatase-1C Biochem Biophys Res Commun 1994 198 Gerhardstein BL Puri TS Chien AJ Hosey MM Identification of the sites phosphorylated by cyclic AMP-dependent protein kinase on the beta 2 subunit of L-type voltage-dependent calcium channels Biochemistry 1999 38 Simmerman HK Jones LR Phospholamban: protein structure, mechanism of action,and role in cardiac function Physiol Rev 1998 78 Sulakhe PV Vo XT Regulation of phospholamban and troponin-I phosphorylation in the intact rat cardiomyocytes by adrenergic and cholinergic stimuli: roles of cyclic nucleotides,calcium,protein kinases and phosphatases and depolarization Mol Cell Biochem 1995 149-150 Kunst G Kress KR Gruen M Uttenweiler D Gautel M Fink RH Myosin binding protein C,a phosphorylation-dependent force regulator in muscle that controls the attachment of myosin heads by its interaction with myosin S2 Circ Res 2000 86 Xiao RP Cell logic for dual coupling of a single class of receptors to G(s)and G(i)proteins Circ Res 2000 87 Sibley DR Strasser RH Benovic JL Daniel K Lefkowitz RJ Phosphorylation /dephosphorylation of the beta -adrenergic receptor regulates its functional coupling to adenylate cyclase and subcellular distribution Proc Natl Acad Sci USA 1986 83 Hausdorff WP Lohse MJ Bouvier M Liggett SB Caron MG Lefkowitz RJ Two kinases mediate agonist-dependent phosphorylation and desensitization of the beta 2-adrenergic receptor Symp Soc Exp Biol 1990 44 Ungerer M Bohm M Elce JS Erdmann E Lohse MJ Altered expression of beta-adrenergic receptor kinase and beta1-adrenergic receptors in the failing human heart Circulation 1993 87 Marx SO Reiken S Hisamatsu Y Jayaraman T Burkhoff D Rosemblit N PKA phosphorylation dissociates FKBP12.6 from the calcium release channel (ryanodine receptor):defective regulation in failing hearts Cell 2000 101 Reiken S Gaburjakova M Guatimosim S Gomez AM D 'Armiento J Burkhoff D Protein kinase A phosphorylation of the cardiac calcium release channel (ryanodine receptor)in normal and failing hearts.Role of phosphatases and response to isoproterenol J Biol Chem 2003 278 Wehrens XH Lehnart SE Marks AR Intracellular calcium release and cardiac disease Annu Rev Physiol 2005 67 Wehrens XH Marks AR Altered function and regulation of cardiac ryanodine receptors in cardiac disease Trends Biochem Sci 2003 28 Schwinger RH Munch G Bolck B Karczewski P Krause EG Erdmann E Reduced Ca(2+)-sensitivity of SERCA2a in failing human myocardium due to reduced serin-16 phospholamban phosphorylation J Mol Cell Cardiol 1999 31 Hajjar RJ Muller FU Schmitz W Schnabel P Bohn M Molecular aspects of adrenergic signal transduction in cardiac failure J Mol Med 1998 76 Roma G Catecholamine cardiotoxicity J Mol Cell Cardiol 1985 17 Mann DL Kent RL Parsons B Cooper GT Adrenergic affects on the biology of the adult mammalian cardiocyte Circulation 1992 85 Levine TB Francis GS Goldsmith SR Simon AB Cohn JN Activity of the sympathetic nervous system and renin-angiotensin system assessed by plasma hormone levels and their relation to hemodynamic abnormalities in congestive heart failure Am J Cardiol 1982 49 Hensen J Abraham WT Dürr J Schrier RW Aldosterone in congestive heart failure: analysis of determinants and role in sodium retention Am J Nephrol 1991 11 Chun TY Bloem LJ Pratt JH Aldosterone inhibits inducible nitric oxide synthase in neonatal rat Cardiomyocytes Endocrinology 2003 144 Fuller PJ Young MJ Mechanisms of 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S0001-600220080001 Acta Médica Costarricense Acta méd. costarric 0001-6002 Colegio de Médicos y Cirujanos de Costa Rica S0001-60022008000100003 El virus influenza y la gripe aviar Influenza virus and avian flu Herrero-Uribe Libia ,Universidad de Costa Rica 03 2008 2008 50 13 19

En este artículo se presenta una revisión del virus influenza,su biología,sus mecanismos de variación antigénica,las pandemias que ha producido y la prevención mediante las vacunas y medicamentos antivirales.Se analizan las razones por las cuales aparece el virus H5N1 que produce la fiebre aviar en humanos,la patogénesis de este virus y las estrategias para su prevención.Se informa sobre el plan de preparación para la pandemia en los niveles nacional e internacional.

This article presents a review of Influenza virus,its biology,its mechanism of antigenic variation and its prevention by vaccination and the use of antivirals.The pandemics produced by this virus through history are presented.The appearance of the avian flu virus H5N1 is analyzed and its pathogenesis and strategies of prevention are discussed.National and international information about pandemic preparedness is presented.

 Influenza A gripe aviar pandemia H5N1 Influenza A avian influenza pandemia HN1 Webster RG Influenza: An Emerging Disease Emerg Infect Dis 1998 4 Murphy BR Webster RG Fields BN Orthomyxovirus Virology Virology 1996 Lippincott-Raven Publishers Kuiken T Holmes EC McCauley J Rimmelzwaan GF Williams C.S Grenfell B.T Host species barriers to Influenza Virus Infections Science 2006 312 Yamada Sh Suzuki Y Suzuqui T Le M Nidom ch Sakai Y Haemagglutinin mutations responsable for the binding of H5N1 influenza A virases to human-type receptors Nature 2006 444 Webster R.G Peiris M Chen H Guan Y H5N1 Outbreaks and Enzootic Influenza Emerg Infect Dis 2006 12 Palese P Making Better Influenza Virus Vaccines? Emerg Infect Dis 2006 12 Taubenberger JK Morens DM Influenza: the Mother of All Pandemics Emerg Infect Dis 1918 20 06 12 Johnson NP Mueller J Updating the accounts: global mortality of the 1918-1920 "Spanish "influenza pandemic Bull Hist Med 2002 76 Kobasa D Takada A Shinya K Hatta M Halfmann P Theriault S Enhanced virulence of Influenza A viruses with the haemagglutinin of the 1918 pandemic virus Nature 2004 431 Reid AH Fanning TG Hultin JV Taubenberger JK Origen and evolution of the 1918 "Spanish "influenza virus hemagglutinin gene Proc Nalt Acad Sci USA 1999 96 Kilbourne ED Influenza Pandemics of the 20 th Century Emerg Infect Dis 2006 12 Dowdle WR .Influenza Pandemic Periodicity,Virus Recycling and the Art of Risk Assessment Emerg Infect Dis 2006 12 Karasin AI Olsen CW Anderson GA Genetic characterization of an H1N2 influenza virus isolated from a pig in Indiana J Clin Microbiol 2000 38 Yeun KY Wong SSY Human Infection by avian influenza A H5N1 Hong Kong Med J 2005 11 Liu J Xiao H Lei F Zhu Q Qin K Zang X-W Highly Pathogenic H5N1!Influenza Virus Infection in Migratory Birds Science 2005 309 Webster R G Wet markets-continuing source of severe acute respiratory syndrome and Influenza? Lancet 2004 363 Halvorson S Avian Influenza Avian Influenza Luke CJ Subbaroa K Vaccines for Pandemic Influenza Emerg Infect Dis 2006 12 Kuiken T Rimmelzwaan G van Riel D van Amerongen G Baars M Fouchier R Avian H5N1 influenza in cats Science 2004 306 Shinyal K Ebina M Yamada Sh Ono M Kasai N Kawaoka Y Avian flu: Influenza virus receptors in the human airway Nature 2006 440 Olsen B Munster VJ Wallensten A Waldenstrom J Osterhaus ADME Fouchier RAM Global Patterns of Influenza A virus in Wild Birds Science 2006 312 Garcia-Sastre A Antiviral Response in Pandemic Influenza Viruses Emerg Infect Dis 2006 12 Thomas PG Keating R Hulse-Post DJ Doherty PC Cell-Mediated Protection in Influenza Infection Emerg Infect Dis 2006 12 Quirk M H5N1 genes show avian origins and drifting Emerg Infect Dis 2005 11 Stephenson I Bugarini R Nicholson KG Podda a Wood JM Zambon MC Katz JM Cross-Reactivity to highly Pathogenic Avian Influenza H5N1 Viruses after Vaccination with Nonadjuvant and MF59- Adjuvantes Influenza A/Duck/Singapore/97 (H5N3)Vaccine: A Potential Priming Strategy JID 2005 191 Yang ZY Wei ChJ Kong WP Wu L Xu L Smith D.F Nabel GJ Immunization by Avian H5 Influenza Hemagglutinin Mutants with Altered Receptor Binding Specificity Science 2007 317 Taubenberger JK Reid A.H Fanning TG Capturing a Killer Flu virus Scientific American 2005 Stephenson I Gust I Pervikov Y Kieny MP Development of vaccines against influenza H5 Lancet Infect Dis 2006 6 Influenza pandemic preparation -much still to be done Lancet Infect Dis 2006 6315 Stephenson I Gust I Pervikov Y Kieny MP Development of vaccines against influenza H5 Lancet Infect Dis 2006 6 Gani R Hughes H Fleming D Griffin T Medlock J Leach S Potential Impact of Antiviral Drug Use during Influenza Pandemic Emerging Infectious Diseases 2006 11 Katz JM Lim W Bridges CB Antibody response in individuals infected with avian influenza A (H5N1)viruses and detection of anti-H5 antibody among household and social contacts J Infect Dis 1999 180 Buxton Briges C Katz JM Seto WH Risk of influenza A (H5N1) infection among health care workers exposed to patients with influenza A (H5N1),Hong Kong J Infect Dis 2000 181 Seo SH Hoffmann E Webster RG Lethal H5N1 influenza viruses escape host anti-viral cytokine responses Nat Med 2002 8 Cheung CY Poon LL Lau AS Shortridge KF Gordon S Guan Y Induction of proinflammatory cytokines in human macrophages by influenza A (H5N1)viruses: a mechanism for the unusual severity of human disease? Lancet 2002 360 Peiris JS Yu WC Leung CW Cheung CY Ng WF Nicholls JM Re-emergence of fatal human influenza type A subtype H5N1 disease Lancet 2004 363 Bonn D Wild birds,poultry,and avian influenza Lancet Infect Dis 2006 6 Acciones Básicas ante una Pandemia de Influenza Boletín de Práctica Médica Efectiva Dici em br Yang Y Halloran ME Sugimoto J Longini,Jr IM Detecting human-to-human transmission of avian influenza A (H5N1) Detecting human-to-human transmission of avian influenza A (H5N1) Herrero L Alfaro W Virus Influenza circulantes en Costa Rica 1998 -2001.¿Cuándo vacunar? Acta Médica Pediátrica 2002 16 3
S0001-600220080001 Acta Médica Costarricense Acta méd. costarric 0001-6002 Colegio de Médicos y Cirujanos de Costa Rica S0001-60022008000100004 Tamaño de muestra en estudios clínicos Camacho-Sandoval Jorge ,UNA 03 2008 2008 50 20 21 Fernández P Determinación del tamaño muestral Cad Aten Primaria 2001 19 96 3 Gilete V Parés P Molet J Oliver B Tresserras P Bartumeus F Estimación del coste económico atribuible a la infección postoperatoria en neurocirugía Neurocirugía 1998 99 2 Sierra- Fernández HH Schultz- Faingezicht M Loaiza- Mendoza C Arguedas- Mohs A Otitis media: conceptos actuales Act Méd Costarric 2004 20 04 6 Wong-McClure R León-BBratti M Efecto de la terapia antirretroviral en la rehospitalización por enfermedad oportunista en Costa Rica Act Méd Costarric 2006 8 4
S0001-600220080001 Acta Médica Costarricense Acta méd. costarric 0001-6002 Colegio de Médicos y Cirujanos de Costa Rica S0001-60022008000100005 Mortalidad por causas accidentales en niños menores de 5 años en el Hospital Nacional de Niños "Dr. Carlos Sáenz Herrera", 2002-2004 Mortality due to accidental causes in children younger than 5 years of age at the Hospital Nacional de Niños "Dr. Carlos Sáenz Herrera", 2002-2004 Benavides-Lara Adriana Vargas-Salas Marco ,Instituto Costarricense de Investigación y Enseñanza en Nutrición y Salud (INCIENSA) ,Hospital Nacional de Niños 03 2008 2008 50 22 28

Las lesiones traumáticas por causas externas corresponden en Costa Rica a la segunda causa de muerte en niños menores de 5 años, con una tasa para 2004 de 9.23 x 100000 habitantes, y la primera causa de años de vida potencialmente perdidos (37%) para esta edad. El objetivo de esta investigación fue evaluar el impacto de este tipo de lesiones como causa de muerte en niños menores de 5 años, atendidos en el Hospital Nacional de Niños (HNN), y caracterizar esta población. Materiales y métodos: Se realizó un estudio caso control pareado, donde se incluyeron todos los niños menores de 5 años egresados del HNN desde diciembre de 2001 a diciembre de 2004, con diagnóstico de lesión no intencional por causas externas. Los casos los constituyeron los niños que egresaron fallecidos y para cada uno se eligió al azar un control de la misma edad y sexo que no hubiera fallecido por causa de la lesión traumática. Resultados: Hubo un total de 36 casos distribuidos igualmente por sexo.Las principales causas de muerte resultaron,en orden de importancia:los accidentes de tránsito y los ahogamientos.La mayoría de los casos provinieron de la provincia de San José.No se encontraron diferencias estadísticamente significativas en la mayoría de variables estudiadas entre casos y controles.La mayoría de muertes ocurrieron durante los meses de verano y típicos de vacaciones escolares; además,el 35%de estas ocurrieron durante el fin de semana.La mayoría de los niños ingresó al hospital durante el segundo turno (2pm-10pm)y la gran mayoría de las lesiones (64%)ocurrieron en la casa (p<0.05).La no supervisión figuró,dentro del estudio,como un factor de riesgo de ocurrencia de una lesión no intencional (p<0.05). Conclusiones: El registro de este tipo de lesiones es aún muy deficiente en Costa Rica,lo cual dificulta la realización de un estudio analítico sobre prevalencia y factores de riesgo de lesiones no intencionales por causas externas.

In Costa Rica unintentional injuries are the second cause of mortality in children under 5 years of age, with a ratio of 9.23 per 100000 inhabitants for the year 2004. hey are also the leading cause of loss of productive life years (337%)) for this age group. The objetive of this study was to determine the impact of this kind of injuries over the mortality of children under 5 years of age seen t the Hospital Nacional de Niños (HNN) and to characterize this population. Methods: We performed a case-ccontrol study pooling data on chilren aged 0-5 years who had been discharged from HNN with the diagnosis of unintentional injury from december 2001 to december 2004. All children who died from these injuries during this period constituded the cases and for each one we choose a control with the same age, sex and diagnosis discharged alive for this cause. Results: There were 36 cases (ddeaths from unintentional injuries) 50% of each sex. Motor vehicle related injuries and drownings were the leading causes of death. Most of them were from San José. There was no statatistical difference betwen cases and the controls in the mayority of variables. Most of the deaths were during the summer and vacational months, beside 35% of them ocurred on weekends. Most of the cases were admitted during the second shift (2pm-10pm) moreover the mayority of injuries (64%) took place at home (p<0.05). No supervision of children resulted to be risk factor for an unintentional injury ocurrence (p<0.05), but not for mortality. Conclusion: The Injury Registry in Costa Rica is still very deficient,which makes difficult to carry out analitycal sutdies of prevalence of risk factors of unintentional injuries.

 Lesiones traumáticas causas externas accidentes de tránsito trauma en niños traumatic lesions external causes traffic accidents children trauma Estadísticas de Salud de las Américas Estadísticas de Salud de las Américas 1998 4 Organización Panamericana de la Salud Defunciones por accidentes de tránsito en países seleccionados de las Américas, 1985-2001 OMS Boletín Epidemiológico 2004 25 Scholer S Hickson G Ray W Sociodemographic factors indentify US infants at high risk of injury mortality Pediatrics 1999 103 Scholer S Mitchel E Ray W Predictors of injury mortality in early childhood Pediatrics 1997 100 Wayne R Prevention or Household and Recreational injuries in children Canadian Task Force on the Periodic Health Examination Canadian Task Force on the Periodic Health Examination 1994 : Health Canada Guyer B Ellers B Childhood injuries en the United States: mortality, morbidity and cost Am Dis Child 1990 144 Waller AE Bake SP Szocka A Childhood injury deaths: national analysis and geographic variations Am J Public Health 1989 79 Peclet MH Newman KD Eichelberger MR Gotschall K Guzzetta P Anderson K Patterns of injury in children J Pediatr Surg 1990 25 Morison A Unintentional childhood injury mortality in Europe 1984-93: a report from the EURORISC Working Group Inj Prev 1999 5 Plan de atención a la salud de las personas: PASP 2001-22006 Plan de atención a la salud de las personas: PASP 2001-22006 2001 Edición 2001 San José Caja Costarricense del Seguro Social Lobo F Vernon M Quesada A González M Accidentes de tránsito en niños: aspectos médicos y epidemiológicos Act Méd Costarric 1991 34 Quirós Intoxicaciones atendidas en el Hospital Nacional de Niños durante 1990-1996 Acta Mediát Cost 1998 12 Vargas M Moraga M Chacón F Elizondo I Trauma mayor severo: Unidad de Trauma Hospital Nacional de Niños Act Méd Costarric 1999 Bianchini S Espinoza D Centeno C Quemaduras infantiles y sus aspectos sociales Revista Médica del Hospital Nacional de Niños Dr. Carlos Sáenz Herrera 1984 19 Wintemute G Childhood drowning and near-ddrowning in the United States Am Dis Child 1990 144 Quan L Gore EJ Wantz K Ten year study of pediatric drowning and near-dorwning: lessons in injury prevention Pediatrics 1989 83 McMillan J DeAngelis C Modena Hoover Wilson: Injury prevention and control Oski ’s Pediatrics: principles and practice Oski ’s Pediatrics: principles and practice 1999 Third ^ePhiladelphia Lippincot Williams & Wilkins Kohen D Soubhi H Porminder R A canadian picture of maternal report of childhood injuries A canadian picture of maternal report of childhood injuries 1999 British Columbia Research for Children and Women Health Barlow Niemirska M Gandhi R Ten years experience with falls from eight in hildren J Pediatr Surg 1983 18 Bourguet CC Mc Artur RE Unintentional injuries. Risk factors in preschool children Am Dis Child 1989 143 Runyan CW Risk factors for fatal residential fires N Engl J Med 1992 27 Kopjar B Wickizer T How safe are day care centers? Day care versus home injuries among children in Norway Pediatrics 1996 97 Cummings P Theis MK Mueller BA Rivara F Infant injury death en Washington State, 1981 through 1990 Arch Pediátr Adolesc Med 1994 48 Wicklund K Moss S Frost F Effects of maternal education, age and parity on fatal infant accidents Am J Public Health 1984 74 Nersesian W Petit M Shaper R Lemieux D Naor E Childhood death and poverty: a study of all childhood deaths in Maine, 1976 to 1980 Pediatrics 1988 75 Scholer SJ Hickson GB Mitchel EF Ray WA Persistently increased injury mortality rates in high-rrisk young children Arch Pediatr Adolesc Med 1997 51
S0001-600220080001 Acta Médica Costarricense Acta méd. costarric 0001-6002 Colegio de Médicos y Cirujanos de Costa Rica S0001-60022008000100006 Incidencia de diabetes tipo 2 en un área urbano marginal de Costa Rica Type 2 diabetes in a peripheral-urban area in Costa Rica Laclé-Murray Adriana Valero-Juan Luis F ,C.C.S.S ,Universidad de Salamanca 03 2008 2008 50 29 34

Justificación y objetivo: La "diabetes mellitus" tipo 2 se considera actualmente como una pandemia que afecta tanto a países desarrollados como en vías de desarrollo, por lo cual es necesario conocer su prevalencia,incidencia y factores asociados para planificar estrategias para su prevención. En Costa Rica se dispone de una estimación de su prevalencia en el área metropolitana (7-8%),pero no se tiene dato alguno de su incidencia.El presente estudio tuvo como objetivo conocer la prevalencia de personas en riesgo de desarrollar diabetes en una comunidad urbano marginal,sus factores de riesgo y la incidencia de diabetes en esa población. Materiales y métodos: De las 7039 personas de 20 años y más con expediente activo en 4 EBAIS del área 3 de Desamparados en el año 2000,4228 tenían al menos un criterio de riesgo para desarrollar diabetes según los criterios de la Asociación Americana de Diabetes del 2000. Esta cohorte fue seguida durante 4 años para determinar la tasa de incidencia de desarrollar diabetes. Resultados: La prevalencia de personas en riesgo fue del 60.1%;sus factores de riesgo más prevalentes fueron:la dislipidemia (67.3%),el índice de masa corporal <IMG SRC="../img/menor_igual.JPG" WIDTH=11 HEIGHT=12>27 (60,8%),edad <IMG SRC="file:///C:/SciELO/serial/amc/v50n1/img/menor_igual.JPG" WIDTH=11 HEIGHT=12>45 años (41,8%),familiares con DM (34.9%)e hipertensión arterial (19.7%).La incidencia acumulada de diabetes fue de 4.77%con un promedio anual de 1.19%.La tasa de incidencia fue de 1.62 por 100 personas-año (IC95%:1.38-1.86).La tasa de incidencia por 100 personas-año según sexo fue de 1.5 para las mujeres y de 1.93 para hombres,sin diferencia significativa por sexo. Conclusión: Los resultados obtenidos en este estudio han permitido disponer de la primera estimación de la Incidencia de Diabetes tipo 2 en una población de riesgo en Costa Rica.La incidencia estimada fue de 1.62%;por lo tanto podemos esperar 16 diabéticos nuevos por año por cada 1000 personas en riesgo sin presentar diferencias por sexo.Este indicador permitirá al área de Salud estudiada medir la carga de la enfermedad y el impacto que tiene sobre su población la atención de salud prestada y sus programas preventivos.

Justification and Objective:Diabetes is now a global epidemic.Once thought to be a disease primarily affecting developed nations,diabetes is growing rapidly and exponentially in developing nations,seriously impacting the health systems and environments of these countries.Costa Rica has collected some diabetes prevalence data,but little is known of its incidence.Epidemiological studies of prevalence and incidence of diabetes are needed for the planning of prevention strategies in Costa Rica.This study was conducted to determine the percentage of the population at risk of developing diabetes within a health district located in a poor,urban marginal community of Costa Rica and to estimate the incidence rate of diabetes type 2. Methodology: Of the 7039 persons 20 years or older receiving primary care in four marginal urban primary health care centers of Desamparados 3 of Costa Rica in the year 2000, 4228 (60%)had at least one risk factor for developing diabetes using the 1997 ADA risk criteria.This cohort was followed for 4 years and the incidence rate of diabetes was determined,using the ADA 2000 criteria for diabetes with fasting plasma glucose to identify new cases. Results: Approximately sixty percent of the reference population had at least one risk factor for diabetes.Among these,the most prevalent risk factors were dyslipidemia (67.3%),Body Mass Index <IMG SRC="file:///C:/SciELO/serial/amc/v50n1/img/menor_igual.JPG" WIDTH=11 HEIGHT=12>27 (60,8%),age <IMG SRC="file:///C:/SciELO/serial/amc/v50n1/img/menor_igual.JPG" WIDTH=11 HEIGHT=12>45 years (41,8%),family with diabetes (34.9%),and hypertension (19.7%)The crude cumulative incidence for diabetes in four years was 4.77%(IC95%:4.09%- 5.45%)with an average of 1.19%per year.The incidence rate was 1.62 per 100 person-years (IC95%:1.38-1.86);for women 1.5 and for men 1.93.There were no significant differences between the genders. Conclusion:This study provides Costa Rica with its first glance at the incidence rate of diabetes, being between the range of 1-2%per year in an urban marginal community.The prevalence of obesity,dyslipidemia and hypertension are very high in this community.All these risk factors can be modified with lifestyle interventions that promote proper diet and physical activity.The studied Health Area, Desamparados 3, now has a baseline measurement to evaluate its outcomes in future preventive nterventions

 Diabetes mellitus tipo 2 factores de riesgo incidencia urbano marginal diabetes mellitus type 2 risk factors incidence urban marginal Zimmet P McCarty D The NIDDM Epidemic: global estimates and projections-a look into the crystal ball IDF Bull 1995 40 Zimmet P Alberti KGMM Shaw J Global and societal implication of the diabetes epidemic Nature 2001 414 Vaughan P Gilson L Mills A Diabetes in the developing countries: its importance for public health Health police planning 1989 4 King H Aubert RE Herman WH Global burden of diabetes,1995-2025: prevalence,numerical estimates,and projections Diabetes Care 1998 21 Prevention of Diabetes mellitus Prevention of Diabetes mellitus 1994 WHO Wild S Roglic G Green A Sicree R King H Global Prevalence of Diabetes,Estimates for the Year 2000 and Projections for 2030 Diabetes Care 2004 27 Melton LjIII Palumbo Pj Chu C-P Incidence of diabetes mellitus by clinical type Diabetes Care 1983 6 Morales PA Mitchell BD Valdez Ra Hazuda HP Stern MP Haffner SM Incidence of NIDDM and impaired glucose tolerance in hypertensive subjects: the San Antonio Heart Study Diabetes 1993 42 Leibson CL O ’Brien PC Atjinson E Palumbo PJ Melton LJ Relative contribution of incidence and survival to increasing pervalence of adult-onset diabetes mellitus: a population-bbased study Am J Epidemiol 1997 146 Edelstein SL Knowler WC Bain RP Anres R Barrett-Connor EL Dowse GK Predictors of Progression from Impairred Glucose Tolerance to NIDDM,an Analysis of six Prospective Studies Diabetes 1997 46 Burke JP Williams K Gaskill SP Hazuda HP Haffner SM Stern MP Rapid rise in the incidence of type 2 diabetes form 1987-1996: results from the San Antonio Heart Study Arch Intern Med 1999 159 Motala AA Pirie FJ Gouws E Amod A Omar MA High incidence of Type 2 diabetes mellitus in South African Indians: a 10-year follow-up study Diabet Med 2003 20 Lorenzo C Okoloise M Wiliams K The Metabolic Sindrome as predictor of Type 2 Diabetes: The San Antonio Heart Study Diabetes Care 2003 26 Soderberg S Zimmet P Tuomilehto J de Courten M Dowse GK Chitson P High incidence of type 2 diabetes and increasing conversion rates from impaired fasting glucose and impaired glucose tolerance to diabetes in Mauritius J Intern Med 2004 256 Bonora E Kiechl S Willeit J Oberhollenzer F Egger G Meigs JB Bonadonna RC Muggeo M Population-based incidence rates and risk factors for type 2 diabetes in white individuals: the Bruneck study Diabetes 2004 J ul 53 D ´ágostino RB Hamman RF Karter AJ Mykkanen L Wagenknecht LE Haffner SM Cardiovascular Risk Factors predict the development of Type 2 diabetes: the insulin resistance Atherosclerosis Study Diabetes Care 2004 27 Morice A Situación de las enfermedades crónicas no transmisibles en Costa Rica Situación de las enfermedades crónicas no transmisibles en Costa Rica 1998 Tres Ríos Ministerio de Salud,Inciensa, CCSS,OPS Morice A Roselló M Araúz AG Sanchez G Padilla G Diabetes Mellitus en Costa Rica: un análisis interdisciplinario.Capitulo IV: Prevalencia de Diabetes Mellitus en Costa Rica Diabetes Mellitus en Costa Rica: un análisis interdisciplinario.Capitulo IV: Prevalencia de Diabetes Mellitus en Costa Rica Agos to 1 Serie de Documentos Técnicos.Instituto de Investigación y Enseñanza en Nutrición y Salud Laclé A Perfil del Paciente Diabético Tipo 2 de 55 y más años de una Clínica Periférica de la C.C.S.S Act Méd Costarric 1999 41 Informe de la Encuesta Multinacional de Diabetes mellitus,Hipertensión Arterial y Factores de Riesgo asociados del Área Metropolitana del 2004 Informe de la Encuesta Multinacional de Diabetes mellitus,Hipertensión Arterial y Factores de Riesgo asociados del Área Metropolitana del 2004 2005 San José screening for type 2 diabetes Diabetes Care 2000 23 Guías de detección,diagnóstico y tratamiento de las dislipidemias para el primer nivel de atención Guías de detección,diagnóstico y tratamiento de las dislipidemias para el primer nivel de atención 2005 San José Report of the Expert Comitee on the Diagnosis and Classification of diabetes mellitus Diabetes Care 1998 21 Tuomilehto J Lindstrom J Eriksson JG Valle TT Hamalainen H Ilanne-Parikka Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance N Engl J Med 2001 344 Knowler WC Barrett-Connor E Fowler SE Hamman RF Lachin JM Walker EA Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin N Engl J Med 2002 7, 346 Lee ET Welty TK Cowan LD Wang W Devereux R Go O Incidence of diabetes in American Indians of Three Geographic Areas, the Strong Heart Study Diabetes Care 2002 25 Meigs JB Muller DC Nathan DM Blake DR Anres R The Natural History of Progression from Normal Glucose Tolerance to Type 2 diabetes in the Baltimore Longitudinal Study of Aging Diabetes 2003 52 Uauy R Albala C Kain J Obesity trends in Latin America: transiting from under-to overweight J Nutr 2001 M ar 131
S0001-600220080001 Acta Médica Costarricense Acta méd. costarric 0001-6002 Colegio de Médicos y Cirujanos de Costa Rica S0001-60022008000100007 Diagnóstico molecular de la enfermedad de Huntington en Costa Rica Molecular diagnosis of Huntington´s disease in Costa Rica Vásquez-Cerdas Melissa Morales-Montero Fernando Fernández-Morales Húbert el Valle-Carazo Gerardo Fornaguera-Trías Jaime Cuenca-Berger Patricia ,UCR ,Hospital Dr.Rafael A. Calderón Guardia ,Laboratorio de Neurofisiología Neurolab ,UCR 03 2008 2008 50 35 41

Justificación y objetivo. Este estudio representa un esfuerzo para establecer por primera vez en Costa Rica el diagnóstico molecular de la enfermedad de Huntington; esto favorecerá un mejor manejo clínico de los pacientes y podrá ser traducido en un incremento de la calidad de vida de las familias. Se pretende determinar el número de repeticiones CAG en personas con la enfermedad de Huntington y familiares mediante el diagnóstico molecular,con el fin de ofrecerles asesoramiento genético decuado y oportuno. Métodos:El estudio se realizó en 7 pacientes con diagnóstico clínico de Huntington y 31 familiares en riesgo. Para determinar el número de repeticiones CAG se utilizó la reacción en cadena e polimerasa a posterior electroforesis sobre geles de agarosa y poliacrilamida. Resultados:Se obtuvo el diagnóstico molecular de los 38 individuos.Se confirmó el diagnóstico clínico en las 7 personas afectadas, se encontraron 11 con la mutación que permanecían asintomáticas y 20 sin la mutación. Se observó una correlación negativa entre la edad de inicio y el número de repeticiones, así como inestabilidad intergeneracional, tanto vía materna como paterna. No hay diferencias en el número de repeticiones, según el sexo del progenitor transmisor. Conclusión: Los análisis moleculares mostraron un perfil de repeticiones similar al de otras poblaciones.Hemos identificado las primeras familias portadoras de enfermedad de Huntington en Costa Rica, permitiendo dar a los pacientes y su familia asesoramiento genético adecuado y oportuno basado en información confiable.

Justification and Aim.This study represents an effort to establish the molecular diagnosis of Huntington ’s disease in Costa Rica. This would improve the clinical management of the patients and that could be translated into better quality of life for them and their families. Aim: to determine the number of CAG repeats in affected individuals and their relatives by molecular diagnosis in order to offer them adequate genetic counseling. Methods:The study involved 7 patients with clinical diagnosis of this disease and 31 relatives at risk. To determine the number of repeats we used the polymerase chain reaction and electrophoresis on agarose and polyacrylamide gels. Results:We obtained the molecular diagnosis in all of the individuals. The clinical diagnosis was confirmed in the 7 affected individuals,11 remained asymptomatic but carrying the mutation and 20 were found without the mutation. A negative correlation was observed between the age of onset and the repeat size. We also observed intergenerational instability, both through the maternal and paternal side. There were no differences in the number of repeats according to sex of the progenitor transmitter. Conclusions: Our molecular analyses showed a profile of repeats similar to other populations. We have identified for the first time families carrying a CAG expansion in Costa Rica,which will allow us to give adequate and opportune genetic counseling to the patients and their families, based on reliable information.

 Costa Rica diagnóstico molecular enfermedad de Huntington inestabilidad genética mutaciones inestables tripleta repetida CAG Costa Rica molecular diagnosis Huntington disease genetic instability instable mutations AG repeat triplets Harper PS The epidemiology of Huntington ’s disease Hum Genet 1992 889 Burguera JA Solís P Salazar A Estimación de la prevalencia de la enfermedad de Huntington por el método captura-recaptura en la comunidad valenciana eurología 97 Deus Y J Pujol J Espert R Deterioro neurosicológico en la enfermedad e Huntington eurología 997 25 Myers RH Vonsattel JP Stevens TJ Cupples LA Richardson EP Martin JB Clinical and Neuropathological assessment of severity in Huntington’s disease Neurology 1988 38 Gusella J Young AB Conneally M Huntington ’s Disease Molecular Basis of Neurology Molecular Basis of Neurology 1993 Boston Blackwell Scientific Publications A novel gene containing a trinucleotide repeat that is expanded and unstable on untington’s disease chromosomes Cell 1993 72 Myers RH Marans KS MacDonald ME Wells RD Warren ST Huntington ’s disease Genetic Instabilities and Hereditary Neurological iseases Genetic Instabilities and Hereditary Neurological iseases 1999 ^ealifornia Academic Cuenca P Morales F Mutaciones inestables: causa de algunas enfermedades neurológicas hereditarias Acta Méd Costarric 1999 41 Potter NT Spector EB Prior TW Technical Standards and Guidelines for Huntington isease Testing Genet Med 2004 6 Schilling G Sharp A Loev S Wagster M Hua-Li S Colin O Expression of the Huntington ’s disease (IIT15) protein product in HD patients Hum Mol Genet 1995 4 Martín-Aparicio E Lucas JJ Bases moleculares de la enfermedad de Huntington y posibles mecanismos patogénicos Neurología 2002 35 Straus WM Ausubel FM Brent R Kinston RE Preparation of genomic DNA from mammalian tissue Current protocols in molecular biology Current protocols in molecular biology 1988 ^eNew York Wiley Warner JP Barron LH Brock DJH A new polymerase chain reaction (PCR) assay for the trinucleotide repeat that is unstable and expanded on Huntington ’s disease chromosome Mol Cell Probes 1993 77 Morera B Barrantes R Marín-Rojas R Gene Admixture in the Costa Rican Population Ann Hum Genet 2003 67 Andrew SE Goldberg YP Kremer B Telenius H Theilmann J Adam S The relationship between trinucleotide (CAG) repeat length and clinical features of Huntington ´sdisease Nat Genet 1993 44 Whitefield JE Williams L Snow K Dixon J Winship I Stapleton PM Molecular analysis of the Huntington ´sdisease gene in New Zealand NZ Med 1996 109 Sánchez A Castellvi-Bel S Mila M Genis D Calopa M Jiménez D Huntington ´s disease: confirmation of diagnosis and presymptomatic testing in spanish families by genetic analysis J Neurol Neurosurg Psychiatry 1996 61 Alonso ME Yescas P Cisneros B Martínez C Silva G Ochoa A Analysis of the (CAG)n repeat causing Huntington ´sdisease in a Mexican population Clin Genet 1997 51 Lima e Silva T Guerra H Bertuzzo C Lopes I Molecular diagnosis of Huntington disease in Brazilian patients Arq Neuropsiquiatr 2000 58 Saleem Q Roy S Murgood U Saxena R Verma IC Anand A Molecular analysis of Huntington ´sdisease and linked polymorphisms in the Indian population Acta Neurol Scand 2003 108 Akbas F Erginel-Unaltuna N DNA testing for Huntington disease in the Turkish opulation Eur Neurol 2003 50 Wexler N The U.S.-Venezuela Collaborative Research Project. Venezuelan kindreds reveal that genetic and environmental factors modulate Huntington ’s disease age of onset Proc Nat Acad Sci 2004 101 Laccone F Christian W A recurrent expansion of a maternal allele with 36 CAG repeats causes Huntington Disease in two sisters Am J Hum Genet 2000 66 Kremer B Almqvist E Theilmann J Spence N Telenius H Goldberg YP Sex-dependent mechanisms for expansions and contractions of the CAG repeat on affected Huntington disease chromosomes Am J Hum Genet 1995 57 Sánchez A Mila M Castellvi-Bel S Rosich M Jiménez D Badenas C Maternal transmission in sporadic Huntington ´sdisease J Neurol Neurosurg Psychiatry 1997 62 Cannella M Gellera C Maglione V Giallonardo P Cislaghi G Muglia M The gender effect in juvenile Huntington disease patients of Italian origin Am J Med Genet B Neuropsychiatr Genet 2004 1125 Duyao M Ambrose C Myers R Novelletto A Persichetti F Frontali M Trinucleotide repeat length instability and age of onset in Huntington ´s disease Nat Genet 1993 4 Telenius H Almqvist E Kremer B Spencer N Squitieri F Nichol K Somatic mosaicism in sperm is associated with intergenerational (CAG)n changes in Huntington disease Hum Mol Genet 1995 44 Bates GP The molecular genetics of Huntington disease-a history Nat Rev Genet 2005 6 Petersén A Mani K Brundin P Recent Advances on the Pathogenesis of Huntington ’s Disease Exp Neurol 1999 157
S0001-600220080001 Acta Médica Costarricense Acta méd. costarric 0001-6002 Colegio de Médicos y Cirujanos de Costa Rica S0001-60022008000100008 Brote de varicela en el Servicio de Oncología de hombres del Hospital San Juan de Dios, febrero-abril de 2004, San José, Costa Rica Chicken pox outbreak in the male Oncology Ward at he Hospital San Juan de Dios Hospital, febrero-abril de 2004 Vargas-Naranjo Sócrates Espinoza-Aguirre Azálea ,Hospital San Juan de Dios ,Ministerio de Salud 03 2008 2008 50 42 46

Justificación y objetivo:La infección intrahospitalaria por varicela en adultos es infrecuente, a pesar de ser una enfermedad altamente contagiosa. Es reconocido que en adultos se presentan las tasas de letalidad más altas y por ello es importante analizar las características del presente brote y así determinar cuáles factores contribuyeron a que ocurriera, para recomendar acciones dirigidas a la prevención de un brote similar. Métodos: Se diseñó un estudio de casos y controles para identificar los factores asociados al brote por varicela en el hospital. La prueba de U de Mann-Whitney se utilizó para valorar diferencias entre casos y controles según edad, contacto entre pacientes, estancia hospitalaria y grupo de cama. El cálculo de los Odds Ratio ayudó a determinar la posible asociación entre las variables y la presentación de la enfermedad. Se recomendó la cuarentena del Servicio. Resultados:El primer caso de varicela ocurrió en febrero, al tercer día de su ingreso al hospital. Posteriormente, se presentaron 5 casos más. Al analizar las variables estudiadas, la curva epidémica y el período de incubación, la variable contacto entre los pacientes fue la más importante para mantener la existencia del brote p < 0,05; R = 25; [IC95%]=2,3 - 275,7). Conclusión:Se confirmó la transmisión persona-persona de la varicela como fuente principal de contagio en el hospital. Si bien la cuarentena permitió detener el brote, se deben tomar medidas más prácticas y menos costosas, que prevengan la aparición de un brote similar.

Aim: Varicella ’s infection is not common in adults ’ hospital, in spite of being a highly contagious illness. Since in adults, death rates are higher, it is important to analyze the characteristics of the present outbreak. We tried to determine risk factors that contributed to its existence in order to recommend measures to prevent future varicella outbreaks. Methods:A case and contols study was designed to identify factors associated to a varicella outbreak in the hospital. The U test of Mann-Whitney valued differences between cases and controls according to age, contact among patients hospital stay and bed group. Odds Ratio determined the possible association between the variables and the presentation of the illness. Service quarantine as recommended. Results: The first case of chickenpox happened in February,at the third day of hospitalization. Later on 5 more cases were identified.When the variables were analyzed the epidemic curve and the period of incubation, contact among the patients was the most important to maintain outbreak existence (p < 0,005; R = 25; IC95%2,3 - 275.7). Conclusion: Person to person transmission of varicella was confirmed to be the main source of infection in the hospital. Although quarantine stopped the outbreak, more practical and less expensive mesures should be taken to prevent the appearance of future outbreak.

 brote odds ratio transmisión varicela chicken pox transmission odds ratio and outbreak Ponce de León S. R Manual de prevención y control de infecciones intrahospitalarias Manual de prevención y control de infecciones intrahospitalarias 2000 Editorial OPS-OMS Malagón G Esquivel G Libardo QF Infecciones hospitalarias Infecciones hospitalarias 1995 Bogotá Editorial Médica Panamericana Mandell G. L Bennett J. E Dolin R Principles and Practice of infection Diseases Principles and Practice of infection Diseases 2000 2 Quinta ^ePhiladelphia Churchill Livingstone Adhami N Arabi Y Races A Al-Shimeneri A Ur-Rahman M Memish Z. A Effect of corticosteroides on adult varicella pneumonia: Cohor study and literature review Respirol 2006 11 Stride P. J Coulter C Campher M. J. J Duhig E. E Geary J.M Adult chichenpox complicated by fatal necrotising pneumonia BMJA 2004 181 Venkatesh S. K Lo L. L CT appearance of Varicella Zoster lesions in liver and spleen in an innunocompetent patient J Clin Virol 2006 6 Robertson S Newbigging K Carman W Jones G Isles C Fulminating varicella despite prophylactic immune globulin and intravenous acyclovir in a renal transplant recipient: should renal patients be vaccinated against VZV before transplantation? Clin transplant 2006 20 Chin James El control de las enfermedades transmisibles El control de las enfermedades transmisibles 2001 Décima Washington D.C. SA Jones A.M Wilkins E.G.L Outcome of varicella pneumonitis in imnunocompetent adults requiring treatment in a high dependency unit Infect 2001 3 Etzioni A Eidenschenk C Katz R Beck R Casanova J Pollack S Fatal varicella associated with selective natural killer cell deficiency J Pediatr 2005 146 Zhou F Santoli J Messonier M.L Yusuf H.L Shefer A Chu S. Y Rodewald L Harpaz R Economic Evaluation of the 7-Vaccine Route Childhood Immunization Schedule in the United States, 2001 Arch Pediatr Adolesc Med 2005 159 Zhou F Harpaz R Jumaan A.O Winston C.A Shefer A Impact of Varicella Vaccination on Health Care Utilization JAMA 2005 294
S0001-600220080001 Acta Médica Costarricense Acta méd. costarric 0001-6002 Colegio de Médicos y Cirujanos de Costa Rica S0001-60022008000100009 El médico en procesos judiciales Flores-Sandí Grettchen ,Poder Judicial San José 03 2008 2008 50 47 50

La opinión del médico como perito es requerida comúnmente en los procesos judiciales como evidencia. Uno de los fundamentos más importantes de la efectividad de su labor es comprender el proceso y mantener una conducta ética. También los médicos que proveen peritajes deben tener conocimientos actualizados y experiencia en el área en que se pronunciaran. Hay reglas básicas que el perito médico debe siempre tener presente cuando comparece juicio.

Medical expert opinion is commonly required by courts as evidence, and one of the most important fundamentals of effective expert testimony is to understand the process, and to maintain an ethical behavior. Also, physicians who provide expert testimony should have recent and substantive experience and knowledge in the area in which they testify. There are several basic rules the expert witness should consider when testifying.

 perito médico ética peritaje juicio expert medical witness ethics expert testimony trial Butler-SSloss E Hall A Expert witnesses, courts and the law J R Soc Med 2002 95 Rojas JD La pericia médica ( noción y contenido) Med leg Costa Rica 1999 16 Cárdenas LM Becerra AM La prueba. U.S. Inter-Affairs La prueba. U.S. Inter-Affairs Ryan M The adversarial court system and the expert medical witness: The truth the whole truth and nothing but the truth? Emerg Med 2003 5 Vinen J The problem facing the expert medical witness: Does the tail wag the dog? Emerg Med 2003 J un 15 Franco E La necropsia como peritazgo médico Revista Médico-Legal on-lline 2000 1 Castillo N Guzmán Mora F Franco Delgadillo E Rosselli Cock DS Peritazgos Médicos La práctica de la medicina y la ley La práctica de la medicina y la ley 1999 Colombia Biblioteca Juridica Dike Schofferman J Opinions and Testimony of Expert Witnesses and Independent Medical Evaluators Pain Med 2007 4
S0001-600220080001 Acta Médica Costarricense Acta méd. costarric 0001-6002 Colegio de Médicos y Cirujanos de Costa Rica S0001-60022008000100013 Costa Rica en el exterior , 03 2008 2008 50 50 50
S0001-600220080001 Acta Médica Costarricense Acta méd. costarric 0001-6002 Colegio de Médicos y Cirujanos de Costa Rica S0001-60022008000100010 Confirmación por laboratorio de leptospirosis: laboratory confirmation Leptospirosis Valverde-Jiménez María De los Ángeles Brenes-Esquivel Roberto Sequeiro-Soto Jorge ,Centro Nacional de Referencia de Leptospirosis del INCIENSA ,UACA 03 2008 2008 50 51 54

Se presenta el caso de un joven de quince años de edad que consulta a un hospital privado por enfermedad febril aguda de origen desconocido, asociada a elevación discreta de transaminasas y otras alteraciones inespecíficas de los exámenes de laboratorio. Fue referido para observación a un hospital de la Caja Costarricense de Seguro Social, donde se le maneja como cuadro de dengue clásico. La atención en la clínica privada se restableció luego de su egreso, se confirmó el diagnóstico de leptospirosis por parte del laboratorio del Centro Nacional de Referencia de Leptospirosis del iNCIENSA y se manejó con antibióticos hasta su resolución. El artículo enfatiza la importancia del diagnóstico de la leptospirosis mediante un alto grado de sospecha, una historia clínica precisa, un buen examen fisico y la confirmación diagnóstica por laboratorio con el fin de tratarla apropiadamente.

A case of a 15 year old young man is presented, who consulted at a private hospital for acute fever, initially of unknown origin, associated with mild elevation of transaminases and other unspecific alterations of laboratory tests. He was referred for observation to a Hospital, where he was treated as a case of classic dengue fever. Afier his discharge his case was re-taken by a private practitioner, his diagnosis of leptospirosis was confirmed by the laboratory of the National Leptospirosis Referal Center in the INCIENSA, and he was properly treated with antibiotics until complete resolution of his episode. This article emphasizes the importance of a high level of suspicion, a precise and thorough clinical history, as well as a meticulous physical examination, followed by laboratory evidence, in order to diagnose and treat this illness in a proper way.

 Leptospira Leptospirosis serología confirmación diagnóstica Enfermedad de Weil fiebre de origen desconocido Dengue fiebre Dengue hemorrágica leptospira Leptospirosis serology diagnostic confirmation Weil disease fever of unknown origin Dengue Dengue hemorrhagic fever Stefos A Georgiadou SP Gioti C Loukopoulos A Ioannou M Pournaras S Leptospirosis and pancytopenia: two case reports and review of the literature J Infect 2005 51 Erdinc FS Koruk ST Hatipoglu CA Kinikli S Demiroz AP Three cases of anictcric leptospirosis from Turkey: Mild to severo complications J lnfect 2006 52 Farrar Wc Mandeil GL Bennett JE Dolin R Leptospira species (leptospirosis) Principies and practice of infectious diseases Principies and practice of infectious diseases 1995 ^eNew York Churchill Livingstone Feigin RD Anderson DC Human leptospirosis Crit Rev Clin Lab Sci 1975 5 Fiannery B Pereira M Freitas L Carvalho C Góes L De Saboia G Referal pattem of leptospirosis cases during a large urban epidemic of dengue Am J Trop Med Hyg 2001 65 Bruce M Sanders E Leake J Zaidel O Bragg 5 Aye T Leptospirosis among patients presenting with dengue-like illncss in Puerto Rico Acta Trop 2005 96 Homem y Heinemann M Moraes Z Vasconcellos S Ferreira F Ferreira N Estudo epidemiológico da leptospirose bovina e humana na Amazónia oriental brasileira Rev Soc Bras Med Trop 2001 34 Vado I Cardenas M Jiménez B Alzina A Laviada H Suarez V Clinical-epidemiological study of leptospirosis in humans and reservoirs in Yucatán, Mexico Rev Inst Med Trop S Paulo 2002 44 Katz A Ansdell V Effler P Middleton C Sasaki O Leptospirosis in Hawaii, 1974-1998: epidemiologic analysis of 353 laboratory-confirmed cases Am J Trop Med Hyg 2002 66
S0001-600220080001 Acta Médica Costarricense Acta méd. costarric 0001-6002 Colegio de Médicos y Cirujanos de Costa Rica S0001-60022008000100011 Mielolipoma, una lesión quirúrgica poco frecuente de la glándula adrenal Myelolipoma, an infrequent surgical lesion of the adrenal gland Álvarez-Pertuz Humberto Arroyo-Martínez Laura Acuña-Calvo Jorge ,Caja Costarricense de Seguro Social 03 2008 2008 50 54 57

El mielolipoma es un tumor benigno poco frecuente, compuesto de tejido adiposo maduro y elementos hematopoyéticos diversos, histológicamente similares a la médula ósea normal. Estos tumores se pueden localizar comúnmente en las glándulas adrenales, pero también en sitios extra adrenales. Puede encontrarse como tumor único o múltiple, y es hormonalmente inactivo.¹ El origen del mielolipoma es desconocido y se han propuesto varias teorías. Los mielolipomas muestran una gran variedad de manifestaciones clínicas, tales como: sangrado digestivo, hematuria, dolor abdominal en los flancos, masa abdominal y pérdida de peso, entre otras. La incidencia de estos tumores en autopsias es del 0,08 al 0,2 %, gracias al US, la TAC y la RM, su hallazgo es mas frecuente hoy.² El diagnóstico es generalmente por exclusión, habiéndose descartado otras entidades suprarrenales. Entre los métodos diagnósticos figuran: la TAC, el US y la RM. La resección quirúrgica es el tratamiento de elección, cuando haya sintomatología; de lo contrario, un manejo conservador con controles periódicos del paciente será más que suficiente.³ Se presenta el caso de una paciente de 55 años, hipertensa, obesa y con un trastorno depresivo-ansioso, quien consultó por dolor abdominal, náuseas y vómitos.

Myelolipoma is a non functioning benign tumor of the adrenal gland which is formed by hematopoietic and adipose tissue. The tumor was first described by Gierke in 1905, and named by Oberling in 1929. Most series consist of myelolipomas discovered incidentally at autopsy. They are generally located in the adrenal gland, although they can occur in other organs. Endocrine and/or metabolic disorders associated with AML include obesity, Type II Diabetes, congenital adrenal hyperplasia due to 21 or 17 alpha-hydroxylase deficiency, Cushing’s disease, Conn’s syndrome, pheochromocytoma and polycystic ovarian disease. Myelolipomas are asymptomatic, but they may cause pain secondary to bleeding, hematuria or mass; when symptomatic, the most consistent complaint is abdominal pain caused by hemonhage within the tumor. Ultrasound combined with computed tomography is useful in diagnosis. Definitive diagnosis and treatment are accomplished by simple excision and histological repon; radical surgery is unneceSSary. We present here the case of a 55 years oId female who came in with abdominal pain, nausea and vomiting. After an abdominal ultrasound, an abdominal CI scan and eventually, surgical removal, an adrenal myelolipoma was found. She did well after surgery and remains asymptornatic.

 mielolipoma sangrado digestivo glándula adrenal tumor benigno tejido hematopoyético laparotomía exploratoria myelolipoma G.1 bleeding adrenal gland bening tumor hematopoietic tissue exploratory laparotomy Silva, Ortiz José Virgilio, Hernández Rubén Fonseca, Morales José Belmonte, Montes Carlos Magaña, Sánchez Ignacio Cough, Molina Jorge Mielolipoma adrenal: informe de dos pacientes Cir Gen 2000 22 Terry M Mónica, Ochoa V Carlos, Tamayo C Nahum, Siu Ting Ch Gloria, Terry Eduardo Palomino, D Victoria Mielolipoma adrenal: Reporte de un caso Rev Soc Peruana Med Int 2003 16 Han M Burnett A, L Fishman E, K Marshall F, F The natural history and treatment of adrenal myelolipoma J Urol 1997 157 Filobbos S.A Seddon J. A Myelolipoma of the adrenal Br J Surg 1980 67 Goldman H, B Howard, R C Patterson A,L Spontaneous retroperitoneal hemorrhage from a giant adrenal myelolipoma J Urol 1996 115 Pagana J Timothy MD Karasick J Steven MD Karasick, David MD Stahlgren, Leroy MD Myelolipoma of the adrenal gland Am J Sur 1981 141 A, Bhansali RJ Dash SK Singh A Behra P Singh, BD Radotra Adrenal Myelolipoma: profile of six patients with a brief review of literature Int J Endocrinol Metab 2003 1 Han M Burnett A, L Fishman, Marshall F,F The Natural history and treatment of adrenal myelolipoma J Urol 1997 Noble J Mark MD Montague, Drogo K Levin, Howard S Myelolipoma: an unusual surgical lesion of the adrenal gland Cancer 1982 49
S0001-600220080001 Acta Médica Costarricense Acta méd. costarric 0001-6002 Colegio de Médicos y Cirujanos de Costa Rica S0001-60022008000100012 Insuficiencia renal aguda asociada a picadura de abeja africanizada Acute renal failure secondary to africanized bee stings Huertas-Franco Verny Bucknor-Masís Jorge ,Hospital San Juan de Dios San José Costa Rica 03 2008 2008 50 57 60

Se presenta el caso de un adulto mayor diabético tipo 2, que sufrió un ataque masivo de abejas africanizadas, y llegó a la sala de emergencias tres horas después del inicio del ataque. El paciente presentó insuficiencia renal aguda por combinación de factores, y se recuperó con tratamiento de diálisis temprana. Se discuten los problemas que refieren estos pacientes, y cuál sería el manejo ideal de tales casos.

This is the case of an elderly patient who suffered multiple Africanized bee stings. He developed acute renal failure as a complication. He however recovered completely after treatment with peritoneal dialysis and hemodialysis.

 Abeja africanizada abeja africana insuficiencia renal aguda diálisis peritoneal hemodiálisis Africanized bee african bee acute renal failure peritoneal dialysis hemodialysis Kerr WE The history of the introduction of African bees to Brazil S Afr Bee J 1967 39 Kim KT Oguro J Update on the status of Africanized honey bees in the western states West J Med 1999 170 Sherman RA What Physicians should know about Africanized honey bees? West J Med 1995 163 Schumacher MJ Schmidt JO Egen Nb Lowy JE Quantity, analysis and lethality of European and Africanizad bee venoms Am J Trop Med Hyg 1990 43 De Melo MH da Silva EA Natal D Africanized bees in a metropolitan area of Brazil: shelters and climatic influences Rev Saude Publica 2003 37 Mejia G Arbelaez M Henao JE Sus AA Arango JL Acute renal failure due to Multiple Stings by Africanized bees Ann of Int Med 1986 104 Kolecki P Delayed toxic reaction following massive bee envenomation Ann Emerg Med 1999 33 Franca FO Benvenutti LA Fan HW Dos Santos DR Hain SH Picchi MFR Severe and fatal mass attacks by killer bees in Brazil > Clinicopathological studies with measurement of serum venom concentrations Q J Med 1994 87 Dos Reis MA Costa RS Coimbra TM Teixeira VP Acute renal failure in experimental envenomation with Africanized bee venom Ren Fail 1998 20 Schumacher MJ Egen NB Tanner D Neutralization of bee venom lethality by immune antibodies AM J Trop Hyg 1996 55 Musso CG Liakopoulos V Iannidis I Eleftheriadis T Stefanidis I Acute renal failure in the elderly: particular characteristics Int Urol Nephrol 2006 38