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Sergio Castillo
Sergio Castillo, Médico
Categoría: Medicina
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Experiencia:  Medicina de Urgencias, Ambulatoria y Hospitalaria
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Uso de nitrofurantoina

Pregunta del cliente

Mi hija (39 años y artritis reumatoidea) tiene Staphylococcus saprophyticus en orina resiste clindamicina y oxacilinat ; sensible a eritromicina, itrofurantoina,ciprofloxacina ,Trimetropina/sulfametatoxazol, Ceporexina. Fecha de parto 2º senana setiembre , su medico le indico nitrofurantoina y  viajó. El prospecto dice no usarse  el ultimo trimestre,como un paper publicado por Elseiver. Podria darme su opinion? Gracias Maria
Enviada: hace 5 año.
Categoría: Medicina
Experto:  Pablo Rodríguez escribió hace 5 año.
Hola María, gracias XXXXX XXXXX con nosotros, trataré de ayudarle con su problema médico:

Las contraindicaciones de ese antibiótico son:

Insuficiencia renal, insuficiencia hepática grave, neonatos, embarazo a término, deficiencia de G-6-P-deshidrogenasa, porfirias.

La contraindicación es cuando el embarazo está "a punto de terminar", en teoría se puede usar, habitualmente como médico de urgencias yo suelo usar la fosfomicina trometanol 3 g una vez al día durante 2 días, tiene un perfil de seguridad excelente en embarazadas y es muy efectivo en las infecciones de tracto urinario.

Espero que mi respuesta le resulte útil, si ha sido así le agradecería que la aceptase y siguiese preguntando sus dudas.

Un saludo!
Cliente: escribió hace 5 año.
He consultado bibliografia que indica que este antibiotico no tiene buena actividad para este microorganismo. Le agradezco pero no me satisfizo su respuesta . María

Experto:  Pablo Rodríguez escribió hace 5 año.
Si va a consultar bibliografía la mejor opción es la vancomicina intravenosa pero como se imaginará necesita administración intrahospitalaria, del resto de opciones la nitrofurantoína se puede usar puesto que el embarazo no está a término.

Le dejo la información actualizada a Enero de 2011 en base a la revisión de toda la evidencia científica en el tratamiento de los estafilococos coagulasa negativos (primero le dejo las conclusiones y luego el resto del documento, está en inglés pero no creo que tenga problema).



TREATMENT — The agent of choice for empiric treatment of infections due to coagulase-negative staphylococci is vancomycin. In the setting of infection due to CoNS that is known to be methicillin susceptible, the preferred agent is nafcillin or oxacillin.

Newer agents include quinupristin-dalfopristin, linezolid, daptomycin, tigecycline, and telavancin; these have largely been developed for and evaluated in the setting of MRSA infection. Quinupristin-dalfopristin has in vitro activity against multiple-resistant CoNS, although it does not have FDA approval for treatment of these organisms [43-45]. Linezolid has significant bacteriostatic activity versus methicillin-resistant CoNS in vitro and has been successfully used in infected patients, although it does not have FDA approval for treatment of methicillin-resistant CoNS infections [46-48].

Published clinical experience with daptomycin for the treatment of CoNS infections is limited; it appears to have high in vitro activity against clinical isolates, including bloodstream isolates obtained from bone marrow transplant patients with symptomatic bacteremia. Tigecycline has demonstrated in vitro activity against CoNS; there are little clinical data on its efficacy [49-51]. Telavancin is a new glycopeptide with excellent in vitro activity against staphylococci; there is limited clinical experience with its clinical efficacy [52]. Further discussion of efficacy and adverse effects of these agents is outlined in detail separately. (See "Treatment of invasive methicillin-resistant Staphylococcus aureus infections in adults".)

Alternative agents with possible efficacy include teicoplanin (a glycopeptide antibiotic), clindamycin, and the macrolides.

Investigational agents for treatment of MRSA may also prove effective against CoNS. (See "Treatment of invasive methicillin-resistant Staphylococcus aureus infections in adults", section on 'Investigational agents'.)

Combinations of antimicrobial agents are frequently used to treat CoNS prosthetic device infections (eg, prosthetic valve endocarditis) [53]. This approach is primarily based on clinical experience rather than clinical trials.




ast literature review version 19.1: January 2011 | This topic last updated: May 7, 2010 (More)


INTRODUCTION — Coagulase-negative staphylococci (CoNS) are common colonizers of the human skin and the most frequent constituent of the normal flora at this site [1]. Once considered relatively avirulent and usually a contaminant when isolated from a clinical specimen, these organisms have become increasingly recognized as agents of clinically significant nosocomial bloodstream infections.

Patients at risk include those with prosthetic devices, intravascular catheters, or other foreign bodies in place, and immunocompromised hosts. These infections are inherently difficult to treat given the frequent presence of foreign material and the often multiple drug resistant nature of the organisms.

Issues related to antimicrobial resistance in CoNS will be reviewed here. The microbiology, pathogenesis, epidemiology of CoNS and the clinical features, diagnosis, and treatment of specific infections caused by these organisms are discussed separately. (See "Microbiology, pathogenesis, and epidemiology of coagulase-negative staphylococci".)

ANTIBIOTIC RESISTANCE

Epidemiology — More than 80 percent of coagulase-negative staphylococcal isolates are resistant to methicillin and semisynthetic penicillins [2].

Although detailed epidemiologic studies describing the acquisition and spread of these resistant organisms are generally lacking, such studies have been performed in patients undergoing cardiac surgery. A common finding in each of these studies was that acquisition of resistant skin flora did not occur in the absence of antibiotic prophylaxis [3-7].

Preoperatively, cardiac surgery patients generally have skin isolates of CoNS that are susceptible to methicillin [3]. However, one study that utilized techniques to amplify the number of bacteria recovered was able to detect rare methicillin-resistant coagulase-negative staphylococci preoperatively from at least one site in almost three-quarters of patients [4]. After surgery, 17 of the 28 sites with preoperative low-level colonization contained high levels of methicillin-resistant staphylococci. Antibiograms and plasmid profile patterns suggested that these resistant organisms were derived from the small number of preoperative resistant organisms. This observation is consistent with the hypothesis that resistant clones emerged with the selective pressure of perioperative antibiotic prophylaxis.

Other studies have confirmed that patients who have undergone cardiac surgery have a postoperative skin flora composed primarily of methicillin-resistant CoNS. In one report, 91 percent of patients were colonized with organisms resistant to both methicillin and gentamicin by 10 days after surgery, a resistance pattern that was not present preoperatively [5,6]. However, plasmid pattern analysis revealed that pre- and postoperative isolates were distinct. Some of the nurses in the cardiothoracic intensive care unit were colonized with CoNS resistant to methicillin and gentamicin of the matching plasmid type [5].

Methicillin resistance — According to the NNIS survey, the incidence of methicillin resistance among CoNS rose from 20 to 60 percent between 1980 and 1989 [8]. Such isolates are often resistant to multiple classes of antibiotics in addition to beta-lactams. Because CoNS are commensal skin flora, they are frequently exposed to antibiotics used to treat infections at other sites. As a result, they may become antibiotic resistant and persist on the skin. The genes responsible for this resistance are often found on plasmids facilitating the horizontal exchange of resistance genes among strains.

The mecA gene encoding a low-affinity penicillin-binding protein (PBP 2a) is responsible for mediating methicillin or oxacillin resistance in coagulase-negative staphylococci as it is in S. aureus [9]. This resistance is heterotypic in both coagulase-negative and -positive strains, since only a minority of the bacterial population (as few as one in 10(3) or 10(6) organisms) expresses the resistant phenotype, making detection of resistance especially challenging [10]. (See "Microbiology of methicillin-resistant Staphylococcus aureus".)

Reliable detection of methicillin resistance is critical to permit the initiation of appropriate antimicrobial therapy and to prevent the overuse of glycopeptides for the treatment of CoNS infections. Because many laboratories were detecting isolates that were mecA positive but testing susceptible to oxacillin by MIC or disk diffusion, breakpoints for determining the susceptibility of CoNS to oxacillin were revised by the Clinical and Laboratory Standards Institute (CLSI) [11,12].

The MIC breakpoints for CoNS (except S. lugdunensis) are ≤0.25 mcg/mL for susceptibility to oxacillin and ≥0.5 mcg/mL for resistance. This is in contrast to S. aureus (and S. lugdunensis), for which the oxacillin MIC breakpoints are ≤2 mcg/mL for susceptibility and ≥4 mcg/mL for resistance [11]. For disk susceptibility testing, the cefoxitin disk is the preferred method to detect CoNS oxacillin susceptibility [13].

Accurate detection of resistance in the clinical laboratory requires the use of measures to enhance expression of this phenotype, including [14]:

Incubation at a lower temperature (30 to 35ºC)Incubation for a prolonged period of time (24 to 48 hours)Medium with an increased sodium chloride content (2 percent NaCl)

If the results remain in doubt, one can pursue detection of the mecA gene using DNA hybridization or polymerase chain reaction techniques [15-17]. In addition, a latex agglutination test developed for detection of PBP 2a of methicillin-resistant S. aureus (MRSA-Screen, Denka Seiken Co., Niigata, Japan) has been investigated for its applicability in identifying methicillin resistance in a variety of species of CoNS [18-21]. This rapid assay has shown 98 percent sensitivity and high specificity in the hands of some investigators for S. epidermidis [18], although non-S. epidermidis strains occasionally yielded false-positive results.

An isolate determined to be methicillin-resistant should, regardless of the in vitro susceptibility results, be considered resistant to all beta-lactam antibiotics, including beta-lactamase inhibitor combinations, cephalosporins, and carbapenems [22].

Intermediate resistance to vancomycin — The emergence of S. aureus with intermediate resistance to vancomycin has received much attention. (See "Vancomycin-intermediate and vancomycin-resistant Staphylococcus aureus infections".)

Similarly, there have been several case reports of coagulase-negative staphylococci (CoNS) with reduced susceptibility to vancomycin: two in patients on continuous ambulatory peritoneal dialysis (CAPD) and one during empiric therapy for febrile neutropenia [23-25]. The minimum inhibitory concentrations (MICs) were 8 to 16 mg/L in these patients. One of these reports documented the emergence of relative vancomycin resistance (with a stepwise increase in the MIC from 2 to 8 mg/L) in a CAPD patient who was treated with vancomycin for S. haemolyticus peritonitis [23]. MIC cutoffs for CoNS vancomycin testing are: susceptible if ≤4 mg/L, intermediate if 8 to 16 mg/L, and resistant if ≥32 mg/L [11]. The vancomycin MIC breakpoints for S. aureus were modified by the CLSI in 2006 and differ from those of coagulase-negative staphylococci.

Because glycopeptide resistance, like methicillin resistance, appears to be due to heteroresistant subpopulations of staphylococci, its accurate detection in the laboratory can be problematic. As an example, one group reported the isolation of vancomycin-intermediate S. epidermidis (VISE) from peritoneal fluid specimens of a patient undergoing CAPD who developed peritonitis [26]. The primary isolate yielded a vancomycin MIC of 12 to 16 mcg/mL. However, upon subculture and testing by a variety of methods, the strains appeared to be susceptible to vancomycin. (See "Overview of antibacterial susceptibility testing", section on 'Heteroresistance'.)

The authors proposed that the phenotype of intermediate vancomycin resistance may have been expressed by only a small subpopulation of organisms in the original specimen, which may have been lost or diluted upon subculture, perhaps due to loss of selective pressure of the antibiotic. Some investigators have used induction methods, including an aztreonam disk placed on vancomycin-salt agar to demonstrate growth of satellite colonies, in order to screen for potential vancomycin resistance in CoNS [27].

The mechanism of glycopeptide resistance among staphylococci appears to be associated with alterations in cell wall metabolism, including cell wall thickening [28-31]. Increased cell wall thickness has also been observed in various CoNS clinical strains that demonstrate heterogeneous resistance to vancomycin [32]. (See "Vancomycin-intermediate and vancomycin-resistant Staphylococcus aureus infections".)

Resistance to other antibiotics — Vancomycin has been the mainstay of treatment for methicillin-resistant coagulase-negative staphylococcal infections. Gentamicin or rifampin may be added for the treatment of some deep-seated infections, such as prosthetic valve endocarditis and central nervous system shunt infections.

Although gentamicin is rapidly bactericidal for CoNS, resistance to gentamicin has increased to 60 to 70 percent of isolates in some studies, limiting the clinical utility of this agent [33,34]. More than 90 percent of CoNS remain susceptible to rifampin [10], but this drug must be used in combination with another antibiotic since resistance develops rapidly if rifampin is used as a single agent [3,35].

Trimethoprim-sulfamethoxazole has been used to treat a variety of serious staphylococcal infections, including prosthetic joint infections, endocarditis, meningitis, and CSF shunt infections [36-39]. Unfortunately, approximately half of methicillin-resistant CoNS in the United States are also resistant to trimethoprim [10].

The widespread use of ciprofloxacin has resulted in an increase in fluoroquinolone resistance among CoNS, perhaps due to selective pressure on skin flora since the drug is excreted into sweat [40]. Some of the newer fluoroquinolones have greater activity than ciprofloxacin against staphylococci, but ciprofloxacin-resistant strains have reduced susceptibility to these other quinolones as well [41].

An outbreak of colonization with linezolid-resistant coagulase-negative staphylococci was reported among 16 ICU patients over a six month period. Such resistance is extremely rare. The resistant strains were isolated from several sites and contained the G2576T mutation conferring linezolid resistance. Nasal screening among ICU staff was negative. Institution and reinforcement of infection control procedures and restrictions on linezolid prescribing were successful in controlling the outbreak [42]

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18. Horstkotte MA, Knobloch JK, Rohde H, Mack D. Rapid detection of methicillin resistance in coagulase-negative staphylococci by a penicillin-binding protein 2a-specific latex agglutination test. J Clin Microbiol 2001; 39:3700.
19. Zbinden R, Ritzler M, Ritzler E, Berger-Bächi B. Detection of penicillin-binding protein 2a by rapid slide latex agglutination test in coagulase-negative staphylococci. J Clin Microbiol 2001; 39:412.
20. Hussain Z, Stoakes L, Garrow S, et al. Rapid detection of mecA-positive and mecA-negative coagulase-negative staphylococci by an anti-penicillin binding protein 2a slide latex agglutination test. J Clin Microbiol 2000; 38:2051.
21. Udo EE, Mokadas EM, Al-Haddad A, et al. Rapid detection of methicillin resistance in staphylococci using a slide latex agglutination kit. Int J Antimicrob Agents 2000; 15:19.
22. Chambers HF. Methicillin-resistant staphylococci. Clin Microbiol Rev 1988; 1:173.
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24. Sanyal D, Johnson AP, George RC, et al. Peritonitis due to vancomycin-resistant Staphylococcus epidermidis. Lancet 1991; 337:54.
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26. Dunne WM Jr, Qureshi H, Pervez H, Nafziger DA. Staphylococcus epidermidis with intermediate resistance to vancomycin: elusive phenotype or laboratory artifact? Clin Infect Dis 2001; 33:135.
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28. Hanaki H, Kuwahara-Arai K, Boyle-Vavra S, et al. Activated cell-wall synthesis is associated with vancomycin resistance in methicillin-resistant Staphylococcus aureus clinical strains Mu3 and Mu50. J Antimicrob Chemother 1998; 42:199.
29. Cui L, Ma X, Sato K, et al. Cell wall thickening is a common feature of vancomycin resistance in Staphylococcus aureus. J Clin Microbiol 2003; 41:5.
30. Sieradzki K, Tomasz A. Gradual alterations in cell wall structure and metabolism in vancomycin-resistant mutants of Staphylococcus aureus. J Bacteriol 1999; 181:7566.
31. Sieradzki K, Pinho MG, Tomasz A. Inactivated pbp4 in highly glycopeptide-resistant laboratory mutants of Staphylococcus aureus. J Biol Chem 1999; 274:18942.
32. Nunes AP, Teixeira LM, Iorio NL, et al. Heterogeneous resistance to vancomycin in Staphylococcus epidermidis, Staphylococcus haemolyticus and Staphylococcus warneri clinical strains: characterisation of glycopeptide susceptibility profiles and cell wall thickening. Int J Antimicrob Agents 2006; 27:307.
33. Archer GL, Johnston JL. Self-transmissible plasmids in staphylococci that encode resistance to aminoglycosides. Antimicrob Agents Chemother 1983; 24:70.
34. Archer GL, Scott J. Conjugative transfer genes in staphylococcal isolates from the United States. Antimicrob Agents Chemother 1991; 35:2500.
35. Mandell GL, Moorman DR. Treatment of experimental staphylococcal infections: effect of rifampin alone and in combination on development of rifampin resistance. Antimicrob Agents Chemother 1980; 17:658.
36. Stein A, Bataille JF, Drancourt M, et al. Ambulatory treatment of multidrug-resistant Staphylococcus-infected orthopedic implants with high-dose oral co-trimoxazole (trimethoprim-sulfamethoxazole). Antimicrob Agents Chemother 1998; 42:3086.
37. Levitz RE, Quintiliani R. Trimethoprim-sulfamethoxazole for bacterial meningitis. Ann Intern Med 1984; 100:881.
38. Markowitz N, Quinn EL, Saravolatz LD. Trimethoprim-sulfamethoxazole compared with vancomycin for the treatment of Staphylococcus aureus infection. Ann Intern Med 1992; 117:390.
39. Frame PT, McLaurin RL. Treatment of CSF shunt infections with intrashunt plus oral antibiotic therapy. J Neurosurg 1984; 60:354.
40. Høiby N, Jarløv JO, Kemp M, et al. Excretion of ciprofloxacin in sweat and multiresistant Staphylococcus epidermidis. Lancet 1997; 349:167.
41. Thomson KS, Sanders CC, Hayden ME. In vitro studies with five quinolones: evidence for changes in relative potency as quinolone resistance rises. Antimicrob Agents Chemother 1991; 35:2329.
42. Kelly S, Collins J, Maguire M, et al. An outbreak of colonization with linezolid-resistant Staphylococcus epidermidis in an intensive therapy unit. J Antimicrob Chemother 2008; 61:901.
43. Aldridge KE, Schiro DD, Varner LM. In vitro antistaphylococcal activity and testing of RP 59500, a new streptogramin, by two methods. Antimicrob Agents Chemother 1992; 36:854.
44. Eliopoulos GM. Antimicrobial agents for treatment of serious infections caused by resistant Staphylococcus aureus and enterococci. Eur J Clin Microbiol Infect Dis 2005; 24:826.
45. Rubinstein E, Bompart F. Activity of quinupristin/dalfopristin against gram-positive bacteria: clinical applications and therapeutic potential. J Antimicrob Chemother 1997; 39 Suppl A:139.
46. Rybak MJ, Cappelletty DM, Moldovan T, et al. Comparative in vitro activities and postantibiotic effects of the oxazolidinone compounds eperezolid (PNU-100592) and linezolid (PNU-100766) versus vancomycin against Staphylococcus aureus, coagulase-negative staphylococci, Enterococcus faecalis, and Enterococcus faecium. Antimicrob Agents Chemother 1998; 42:721.
47. Chien JW, Kucia ML, Salata RA. Use of linezolid, an oxazolidinone, in the treatment of multidrug-resistant gram-positive bacterial infections. Clin Infect Dis 2000; 30:146.
48. Antony SJ, Diaz-Vasquez E, Stratton C. Clinical experience with linezolid in the treatment of resistant gram-positive infections. J Natl Med Assoc 2001; 93:386.
49. Kratzer C, Rabitsch W, Hirschl AM, et al. In vitro activity of daptomycin and tigecycline against coagulase-negative staphylococcus blood isolates from bone marrow transplant recipients. Eur J Haematol 2007; 79:405.
50. Sader HS, Streit JM, Fritsche TR, Jones RN. Antimicrobial susceptibility of gram-positive bacteria isolated from European medical centres: results of the Daptomycin Surveillance Programme (2002-2004). Clin Microbiol Infect 2006; 12:844.
51. Fritsche TR, Kirby JT, Jones RN. In vitro activity of tigecycline (GAR-936) tested against 11,859 recent clinical isolates associated with community-acquired respiratory tract and gram-positive cutaneous infections. Diagn Microbiol Infect Dis 2004; 49:201.
52. Saravolatz LD, Stein GE, Johnson LB. Telavancin: a novel lipoglycopeptide. Clin Infect Dis 2009; 49:1908.
53. Baddour LM, Wilson WR, Bayer AS, et al. Infective endocarditis: diagnosis, antimicrobial therapy, and management of complications: a statement for healthcare professionals from the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in the Young, and the Councils on Clinical Cardiology, Stroke, and Cardiovascular Surgery and Anesthesia, American Heart Association: endorsed by the Infectious Diseases Society of America. Circulation 2005; 111:e394.
Experto:  fernando cruzado escribió hace 5 año.
de los antibióticos probados en el antibiograma, la opción más razonable es Nitrofurantoina. otra opcion totalmente segura sería Amoxicilina/clavulánico 500/125 (Augmentine) 1c/8h 8 dias, pero no está probado en su antibiograma
Experto:  Sergio Castillo escribió hace 5 año.
Saludos Maria,

La nitrofurantoina es un antibiotico (bacteriostatico en realidad) cuyo efecto no es totalmente conocido. Pero se sabe que practicamente no tiene efecto sistemico, se concentra en la orina y es en la orina donde ejerce su efecto antibiotico (por este motivo no se utiliza para infecciones sistemicas como una pielonefritis aguda, en cambio si se usa para una infeccion urinaria baja como una cistitis). Por este motivo la nitrofurantoina es segura durante el embarazo y le sugiero que la use sin recelo.

Los farmacos se clasifican segun su seguridad de uso durante el embarazo desde A que es totalmente seuguro hasta el X que es probadamente teratogenico. Nitrofunratoina es B quiere decir que es probablemente seguro (http://www.cfnavarra.es/salud/PUBLICACIONES/Libro%20electronico%20de%20temas%20de%20Urgencia/22.Ginecologicas/Farmacos%20y%20embarazo.pdf).

Tener una infeccion urinaria es mas peligroso que tratarla, ya que una infeccion de orina no tratada aumenta el riesgo de parto prematuro, aborto y muerte fetal.

La practica clinica a traves de años (no por mi experiencia, sino que por la de mis profesores) ha demostrado que la nitrofurantoina es un farmaco seguro de usar durante el embarazo. Los estudios actuales no pueden ser perfectos ya que no es etico ni legal experimentar con embarazadas para determinar si un farmaco es seguro o no, por lo tanto debe mirar con ojos criticos y entrenados estas publicaciones.

Cliente: escribió hace 5 año.
Recien hoy pude conyactarme y agradezco su intervención. Mi hija consultó a otro obstetra casado con una nefróloga. El obstetra reconoció que era lógica su preocupación al haber sido medicada con algo que ha generado opiniones controvertidas y en decisión conjunta con la nefróloga le indicaron amoxicilina sin clavulanico dos veces por dia, no recuerdo la dosis, por ocho dias, luego realizar un nuevo cultivo y evaluar los pasos ha seguir. Me interesaria su opinion al respecto ( no la del primer medico, Rodriguez). Gracias Marìa
Experto:  Sergio Castillo escribió hace 5 año.
Saludos XXXXX XXXXX

Me alegro que se ha tranquilizado.


La amoxicilina es un antibiotico de tipo betalactamico, estos antibioticos actuan directamente en la pared celular de las bacterias que es una estructura presente solo en las bacterias (ninguna celula humana tiene pared celular) por lo que es un farmaco muy seguro de usar durante el embarazo. Si le han indicado amoxicilina dos veces al dia la dosis adecuada es 1gramo cada 12hrs. Me parece una buena alternativa, ya que Amoxicilina tambien es efectiva con E. Coli.
Sergio Castillo, Médico
Categoría: Medicina
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  • Me siento satisfecha y más orientada con estas respuestas, pienso ir al especialista cuanto antes.... Martínez Buenos Aires, Argentina
  • El tiempo de respuesta es excepcional, de menos de 6 minutos. La pregunta se respondió con profesionalidad y con un alto grado de compasión. Inés Santander
  • Quedé muy satisfecho con la rapidez y la calidad de los consejos que recibí. Me gustaría añadir que puse en práctica los consejos y que funcionaron la primera vez y siguen haciéndolo. Luis Málaga
 
 
 

Conozca a los expertos:

 
 
 
  • Dr. Maldonado

    Dr. Maldonado

    Médico

    Clientes satisfechos:

    6210
    Especialista en medicina familiar. Mas de 12 años de experiencia. Tutor de residentes.
  • http://ww2.justanswer.com/uploads/IS/ismaelmd/2011-4-27_175820_lafoto.64x64.JPG Avatar de Dr. Maldonado

    Dr. Maldonado

    Médico

    Clientes satisfechos:

    6210
    Especialista en medicina familiar. Mas de 12 años de experiencia. Tutor de residentes.
  • http://ww2.justanswer.com/uploads/AG/AGUEDA2011/2011-2-26_1305_CongresoSevillaMarzo2008019.64x64.jpg Avatar de AGUEDA2011

    AGUEDA2011

    Médico.

    Clientes satisfechos:

    801
    Licenciada en Medicina y Cirugía con la Especialidad en Ginecología y Obstetricia.
  • http://ww2.justanswer.com/uploads/TU/tuurologo/2011-4-17_212323_Dr.E.A..64x64.jpg Avatar de Enrique Artozqui

    Enrique Artozqui

    Médico

    Clientes satisfechos:

    300
    Licenciado en Medicina y Cirugía.Especialista en Endocrinología y Nutrición.Especialista en Urología.
  • http://ww2.justanswer.com/uploads/DS/dspalma/2012-10-18_23912_facebook14920836141.64x64.jpg Avatar de Dra. Debora Palma

    Dra. Debora Palma

    Postdoctorado

    Clientes satisfechos:

    201
    doctora en medicina con especialidad en cirugia general
  • http://ww2.justanswer.com/uploads/JU/juancarlosvillanueva/2013-3-7_9363_Dr.JCVillanueva.64x64.JPG Avatar de juancarlosvillanueva

    juancarlosvillanueva

    Médico

    Clientes satisfechos:

    56
    Licenciado en Medicina y Cirugía Universidad de Valencia año 1983
  • http://ww2.justanswer.com/uploads/PA/pablo.rdt/2013-3-14_17142_IMG0614.64x64.JPG Avatar de Pablo Rodríguez

    Pablo Rodríguez

    Licenciatura

    Clientes satisfechos:

    11179
    Médico adjunto de Servicio de Urgencias Hospitalarias. Consulta de Medicina Familiar y Comunitaria
  • http://ww2.justanswer.com/uploads/DR/drgamboa/2015-4-8_1861_foto.64x64.jpg Avatar de Dr. Jorge Gamboa

    Dr. Jorge Gamboa

    Especialidad Medicina Integrada

    Clientes satisfechos:

    1106
    Especialista en Enfermedades Crónicas de los Adultos
 
 
 

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