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Manifestaciones Radiológicas de la TB y el HIV

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Manifestaciones radiológicas de la Tuberculosis Pulmonar y el HIV.

Manifestaciones radiológicas de la Tuberculosis Pulmonar y el HIV.

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  • In addition, HIV infection is the greatest known risk factor for reactivating latent tuberculosis infection. The estimated risk for developing tuberculosis in an HIV-infected tuberculin positive individual is 7 to 10 percent per year [8] . Incidence — Tuberculosis has become particularly prevalent in populations likely to be coinfected with HIV and M. tuberculosis, such as inner city minority populations, injection drug users, and immigrants from endemic countries. From 1985 through 1990, tuberculosis cases increased 55 percent in Hispanics and 27 percent in blacks. This increase was greatest in individuals aged 25 to 44 and was most pronounced in cities with a high incidence of HIV infection. In some inner city tuberculosis clinics, 40 percent of all patients with tuberculosis are infected with HIV [3] . The Centers for Disease Control and Prevention analyzed data from the U.S. National TB Surveillance System for the years 1993 through 2005 and found that reporting of HIV status among TB patients increased from 35 percent in 1993 to 68 percent in 2003 [9] . They also found that 9 percent of TB patients were HIV positive and TB patients at greater risk for HIV infection included injection drug users, non-injection drug users, homeless individuals, non-Hispanic blacks, correctional facility inmates, and alcohol abusers. Primary infection — HIV infection markedly increases the susceptibility for tuberculous infection to develop into active disease, which can be rapidly progressive. Consequently, a large number of epidemics of tuberculosis have been reported from facilities in which HIV-infected people are concentrated. Outbreaks have occurred in prisons, hospitals, HIV outpatient clinics, homeless shelters, and community living quarters [10-14] . Restriction fragment length polymorphism (RFLP) analysis has been a valuable tool when investigating outbreaks of tuberculosis. By providing a DNA "fingerprint" of isolates from different individuals, RFLP analysis allows identification of patients who have been infected with identical organisms. In one outbreak, the entry of an index case into an HIV residence facility was followed by 11 patients developing tuberculosis over a five-month period [13] . Analysis of the RFLP patterns from the organisms isolated from these patients suggested that the index case served as the source of transmission for the other 11 cases. On an AIDS ward in New York City, 15 patients developed tuberculosis with identical isolates identified by RFLP. The majority of patients developed active disease between one and three-and-a-half months following initial exposure to their contact cases [15] . Within the community at large, there has also been an increase in newly acquired primary tuberculosis, as opposed to secondary or reactivation disease. Patients infected with RFLP-identical isolates are considered to form a cluster, even if no contact between them can be identified by standard case investigation techniques. Such cases are considered to represent new infection and primary disease rather than reactivation of prior tuberculous infection. In a study of tuberculosis in the northern Bronx, 39 of 104 cases (37 percent) were found in clusters and considered to have primary disease [14] . Twenty-six of the 39 patients (66 percent) with primary infection were HIV-positive. Similar results were found in San Francisco, where one study showed that 31 percent of cases of tuberculosis were the result of primary infection, and that HIV infection was an important risk factor for primary disease [16] . These studies contrast with the traditional view that only 10 percent of tuberculosis in the United States is the result of recent infection [17] . Drug-resistant disease — Multidrug-resistant tuberculosis (MDR-TB), defined by resistance to both INH and RIF, has become prominent during the AIDS epidemic, and many of the outbreaks of tuberculosis in HIV-infected persons have involved MDR-TB [18,19] . In response to concerns regarding rising rates of MDR-TB, the World Health Organization (WHO) and the International Union Against Tuberculosis and Lung Disease, launched the Global Project on Anti-Tuberculosis Drug Resistance Surveillance in 1994 to determine the prevalence, patterns, and trends of drug resistance around the world. Data on drug susceptibility testing for isoniazid, rifampicin, ethambutol, and streptomycin were gathered from 1999 to 2002 from surveys in 79 countries with the following results [20] : The median prevalence of resistance to any of the four antituberculosis drugs in new cases of tuberculosis was 10 percent. The median prevalence of MDR-TB in new clinical cases was one percent, although in countries of the former Soviet Union and in some provinces of China, prevalence rates were as high as 6.5 percent. Hong Kong and the United States reported significant declines in MDR-TB. Epidemiologic investigation of tuberculosis outbreaks has been substantially improved by DNA fingerprinting techniques [21,22] . Use of restriction fragment length polymorphisms has shown that the development of multidrug resistance in patients infected with an originally sensitive organism can be due to either new infection with a resistant strain or the development of resistance in the original strain [21] . (See "Epidemiology and molecular mechanisms of drug-resistant tuberculosis").
  • Epidemiologic investigation of tuberculosis outbreaks has been substantially improved by DNA fingerprinting techniques [21,22] . Use of restriction fragment length polymorphisms has shown that the development of multidrug resistance in patients infected with an originally sensitive organism can be due to either new infection with a resistant strain or the development of resistance in the original strain [21] . (See "Epidemiology and molecular mechanisms of drug-resistant tuberculosis").
  • HIV-infected patients are at increased risk of developing active TB from both reactivated latent and exogenous infection [ 2 ]. An HIV-seropositive status is also a risk factor for accelerated progression of TB, particularly in the setting of extensively drug-resistant (XDR) tuberculosis Likewise, TB has a negative impact on HIV disease [ 11 ]. TB infection is associated with significant increases in plasma HIV viremia [ 12 ]. This may result at least in part from one or more of the following mechanisms: Generalized immune activation, which increases the proportion of CD4 cells that are preferential targets for HIV [ 13 ]. Increased expression of the HIV coreceptors CCR5 and CXCR4 [ 14 ]. HIV viremia usually declines after initiation of successful TB treatment in patients residing in developed countries [ 15 ]. However persistently high levels of viremia have been observed in patients from Africa despite initiation of effect TB therapy [ 14,16 ]. This may be mediated by persistent elevated expression of the HIV coreceptors CCR5 and CXCR4 [ 14 ]. Why this occurs is not known.
  • Extrapulmonary disease  — AIDS patients with TB have a higher incidence of extrapulmonary and pleural disease. The risk of extrapulmonary TB is greater in patients with advanced immunosuppression [ 6,26 ]. Clinical indicators of severe disease, such as mycobacteremia and positive acid-fast smears, are also more common in patients with markedly depressed CD4 cell counts [ 6 ]. The most common sites of extrapulmonary involvement are blood and extrathoracic lymph nodes, followed by bone marrow, genitourinary tract, and the central nervous system [ 2,6 ]. Unusual complications, such as tracheoesophageal fistula and cutaneous disease, have also been reported [ 27,28 ].
  • mediastinal lymphadenopathy, cough, and retching or vomiting should alert clinicians treating HIV-infected patients to the possibility of tuberculous bronchoesophageal fistulae.
  • Chest radiographs showed the following: Patterns typical for primary TB — 36 percent. These findings included pleural effusion, intrathoracic lymphadenopathy (mediastinum and hilum), or middle or lower lobe consolidation without cavitation. Patterns compatible with post-primary (reactivation) TB — 29 percent. These findings included apical/posterior consolidation of the upper lobes or consolidation of the superior segments of the lower lobes (without adenopathy or effusion), endobronchial spread (acinar or 3-4 mm shadows, remote from a cavity or upper lobe consolidation), or bronchiectasis. A miliary pattern — 4 percent. Abnormalities atypical for TB, such as diffuse infiltrates suggestive of PCP — 13 percent. Minimal changes — 5 percent. Normal chest radiographs — 14 percent
  • Ensanchamiento mediastinal - adenopatía
  • 29 percent. These findings included apical/posterior consolidation of the upper lobes or consolidation of the superior segments of the lower lobes (without adenopathy or effusion), endobronchial spread (acinar or 3-4 mm shadows, remote from a cavity or upper lobe consolidation), or bronchiectasis.
  • tree-in-bud opacities (arrow) in the right upper lobe. Also note bronchiectasis and reticulation in the left upper lobe due to previous tuberculous infection.
  • cavitating nodule (arrow) in the left lower lobe, bilateral noncavitating nodules and tree-in-bud opacities.
  • Árbol en gemación
  • 29 percent. These findings included apical/posterior consolidation of the upper lobes or consolidation of the superior segments of the lower lobes (without adenopathy or effusion), endobronchial spread (acinar or 3-4 mm shadows, remote from a cavity or upper lobe consolidation), or bronchiectasis.
  • 29 percent. These findings included apical/posterior consolidation of the upper lobes or consolidation of the superior segments of the lower lobes (without adenopathy or effusion), endobronchial spread (acinar or 3-4 mm shadows, remote from a cavity or upper lobe consolidation), or bronchiectasis.
  • B: High-resolution computed tomography (CT) image (1-mm collimation) at the level of the great vessels shows airspace consolidation, ground-glass opacities, and numerous bilateral randomly distributed small nodules. C: CT image at the level of the distal left main bronchus demonstrates small nodules of random distribution, interlobular septal thickening, and patchy parenchymal opacities
  • Minimal changes — 5 percent. Normal chest radiographs — 14 percent
  • CD4 counts were available in 68 patients. Most of the patients with CD4 counts greater than 200 cells/mm3 showed post-primary patterns (55 percent). Only one such patient had a normal chest radiograph. In comparison, patients with fewer than 200 CD4 cells/mm3 were nearly as likely to have normal chest radiographs (21 percent) as they were to have post-primary patterns (23 percent). This trend has been documented in other studies and should be kept in mind when faced with a symptomatic patient who has a normal chest radiograph [ 6,23,25,32,33 ].
  • CD4 counts were available in 68 patients. Most of the patients with CD4 counts greater than 200 cells/mm3 showed post-primary patterns (55 percent). Only one such patient had a normal chest radiograph. In comparison, patients with fewer than 200 CD4 cells/mm3 were nearly as likely to have normal chest radiographs (21 percent) as they were to have post-primary patterns (23 percent). This trend has been documented in other studies and should be kept in mind when faced with a symptomatic patient who has a normal chest radiograph [ 6,23,25,32,33 ].
  • HIV-infected patients are at increased risk of developing active TB from both reactivated latent and exogenous infection [ 2 ]. An HIV-seropositive status is also a risk factor for accelerated progression of TB, particularly in the setting of extensively drug-resistant (XDR) tuberculosis Likewise, TB has a negative impact on HIV disease [ 11 ]. TB infection is associated with significant increases in plasma HIV viremia [ 12 ]. This may result at least in part from one or more of the following mechanisms: Generalized immune activation, which increases the proportion of CD4 cells that are preferential targets for HIV [ 13 ]. Increased expression of the HIV coreceptors CCR5 and CXCR4 [ 14 ]. HIV viremia usually declines after initiation of successful TB treatment in patients residing in developed countries [ 15 ]. However persistently high levels of viremia have been observed in patients from Africa despite initiation of effect TB therapy [ 14,16 ]. This may be mediated by persistent elevated expression of the HIV coreceptors CCR5 and CXCR4 [ 14 ]. Why this occurs is not known.
  • HIV-infected patients are at increased risk of developing active TB from both reactivated latent and exogenous infection [ 2 ]. An HIV-seropositive status is also a risk factor for accelerated progression of TB, particularly in the setting of extensively drug-resistant (XDR) tuberculosis Likewise, TB has a negative impact on HIV disease [ 11 ]. TB infection is associated with significant increases in plasma HIV viremia [ 12 ]. This may result at least in part from one or more of the following mechanisms: Generalized immune activation, which increases the proportion of CD4 cells that are preferential targets for HIV [ 13 ]. Increased expression of the HIV coreceptors CCR5 and CXCR4 [ 14 ]. HIV viremia usually declines after initiation of successful TB treatment in patients residing in developed countries [ 15 ]. However persistently high levels of viremia have been observed in patients from Africa despite initiation of effect TB therapy [ 14,16 ]. This may be mediated by persistent elevated expression of the HIV coreceptors CCR5 and CXCR4 [ 14 ]. Why this occurs is not known.
  • 180 patients had atypical radiographs (adenopathy, effusion, mid lower lung zone infiltrates) HIV infection was significantly associated with an atypical radiographic appearance. Cluster status, which is suggestive of recently acquired TB, was not a significant predictor of radiographic appearance.
  • HIV-infected patients are at increased risk of developing active TB from both reactivated latent and exogenous infection [ 2 ]. An HIV-seropositive status is also a risk factor for accelerated progression of TB, particularly in the setting of extensively drug-resistant (XDR) tuberculosis Likewise, TB has a negative impact on HIV disease [ 11 ]. TB infection is associated with significant increases in plasma HIV viremia [ 12 ]. This may result at least in part from one or more of the following mechanisms: Generalized immune activation, which increases the proportion of CD4 cells that are preferential targets for HIV [ 13 ]. Increased expression of the HIV coreceptors CCR5 and CXCR4 [ 14 ]. HIV viremia usually declines after initiation of successful TB treatment in patients residing in developed countries [ 15 ]. However persistently high levels of viremia have been observed in patients from Africa despite initiation of effect TB therapy [ 14,16 ]. This may be mediated by persistent elevated expression of the HIV coreceptors CCR5 and CXCR4 [ 14 ]. Why this occurs is not known.
  • The role of computed tomography (CT) in the diagnosis of mediastinal tuberculous lymphadenitis was evaluated retrospectively in 25 human immunodeficiency virus (HIV)-infected patients (19 had AIDS). In all cases, the diagnosis of tuberculosis was established by mycobacterial culture and/or histologic evaluation. The most characteristic CT finding was the presence of low-density mediastinal and hilar lymph nodes in 16 of 19 (84 percent) patients with AIDS and four of six (67 percent) HIV-seropositive patients without AIDS. Marked enhancement of the periphery of nodes was identified in five cases, all in patients with documented AIDS. In most cases, lymphadenopathy proved to be massive, presenting as extensive, heterogenous soft-tissue lesions, presumably the result of coalescence of groups of matted nodes. We conclude that low-density mediastinal and/or hilar lymph nodes on CT, while not pathognomonic, is sufficiently characteristic for tuberculosis to warrant empiric antituberculosis therapy pending results of cultures.
  • One study of 176 patients found no difference in the smear-positivity rate between HIV-seropositive and HIV-seronegative patients (60 versus 57 percent) [ 39 ]. There was no variation among the subgroups of the seropositive patients with different CD4 counts. Similar findings have been noted in other reports, one of which found no correlation of smear positivity with the radiographic findings [ 27 ]. These two studies also found no difference in the rate of smear-positivity between patients with drug-sensitive and those with drug-resistant disease [ 27,39 ]. In a nationwide survey, however, the CDC found the rate of smear-positivity to be higher in patients with multidrug-resistant (MDR) TB (76 versus 50 percent in drug-sensitive TB) [ 40 ]. Another report identified a different subgroup with a higher rate of smear-positivity: patients having CD4 counts less than 200 and disseminated disease [ 6 ]. In patients infected with HIV, a positive smear for acid-fast bacilli (AFB) is very specific for Mycobacterium tuberculosis (MTB), even in a setting with a high incidence of Mycobacterium avium complex (MAC). At San Francisco General Hospital, for example, 248 of 271 (92 percent) expectorated sputum samples that were positive for AFB grew MTB on culture [ 41 ]. This value is comparable to that found in HIV-negative patients.
  • Patients with HIV and CD4 count < 50, 50 to 200, and > 200 had positive acid-fast smear rates of 58 percent, 60 percent, and 56 percent, respectively; HIV-infected patients with drug-resistant organisms had 65 percent positive smears. Smear positivity was 96 percent in patients with HIV infection and disseminated MTB, CONCLUSIONS: Positive acid-fast sputum smears in culture-proven MTB occur with similar frequency in patients with and without HIV. The absence of cavitary disease did not significantly reduce the frequency of positive acid-fast smears. For patients with HIV, the likelihood of a positive smear was also independent of CD4 cell counts and drug resistance. Patients with HIV and disseminated MTB had positive sputum smears in nearly all cases.
  • In this setting, the predictive value of the acid-fast bacilli smear for Mycobacterium tuberculosis was 92% for expectorated sputum specimens, 71% for induced sputum specimens, and 71% for bronchoalveolar lavage specimens. When multiple specimens collected from the same patient were excluded from the data base, the predictive values were 87%, 70%, and 71%, respectively. Smears of sputum samples were positive at the same rate for patients with tuberculosis who had AIDS and for patients with tuberculosis who did not have AIDS.
  • patients with pleural TB [ 45 ]. A pleural biopsy should be performed to make the diagnosis more rapidly in patients suspected of having a tuberculous pleural effusion who do not have a coagulopathy or thrombocytopenia. Biopsies show AFB in 69 percent of patients and granulomata in 88 percent [ 45 ]. ( See "Tuberculous pleural effusions in HIV-infected patients" ).
  • Hoy se conoce que la Rifampicina puede emplearse en TB-VIH, con lo ARV del tipo de Efavirens, Ritonavir y con triple nucleosidos (142). Recordar además, que otros medicamentos frecuentemente empleadas en pacientes VIH tienen interacción con la Rifampicina, que podrían requerir ajuste de dosis, como son hormonas contraceptivas, dapsone, ketoconazol, fluconazol, itraconazol, anticoagulantes, corticosteroides, aminoglucosidos, hipoglicemiantes, diazepan, betabloqueadores, anticonvulsivantes y teofilina.   Además de lo anterior, es aconsejable en lo posible, no suministrar simultáneamente los tratamientos antituberculosos con los antirretrovirales, por el alto número de fármacos que necesitaría ingerir el paciente, y lo difícil para individualizar los efectos secundarios de ambos regímenes. Expertos recomiendan iniciar con el tratamiento de la TB, y posteriormente los fármacos contra el VIH. Esa conducta (A-III) se apoya en varios hechos: a) la TB es la única infección transmisible de las que complican el SIDA, b) curando la TB disminuye la progresión del VIH y, c) evita, por la circunstancia de interacción, tener que prescindir de una medicación tan potente como la rifampicina para el tratamiento de la TB en un paciente VIH, ya que su ausencia ha sido ligada con altas recaídas y mortalidad.   Cuando no se pueda usar Rifampicina simultáneamente con algunos ARV, se puede suministrar un esquema de H-Z-S-E, diaria por 48 dosis, y luego continuar con H-E diaria por 10 meses con estricto DOT, por la posibilidad de recaída o fracaso, debido a la ausencia de rifampicina. Es aconsejable la coordinación con los servicios locales del Programa VIH, para el manejo de estos pacientes.   Ha sido descrito que, ocasionalmente los pacientes VIH bajo tratamiento antituberculoso presentan exacerbación de los síntomas y de las imágenes radiológicas, lo cual se ha atribuido a una recuperación de la respuesta de hipersensibilidad retardada, reacción paradojal (143). Esas reacciones consisten en fiebre prolongada, adenomegalias y empeoramiento de las lesiones radiologicas, pero ellas no están asociadas con cambios en la bacteriología y generalmente los pacientes se sienten relativamente bien, sin signos de toxicidad. Raramente es necesario cambiar la terapia antituberculosa o antiviral. Si las adenomegalias u otras manifestaciones son severas, continuar con las terapias y administrar esteroides por corto tiempo, buscando suprimir esa respuesta inmune aumentada.   No es obligatoria la práctica de serología para VIH en todo paciente con TB, y solamente si existen factores de riesgo evidentes (homosexualidad, promiscuidad, etc) debe solicitarse el examen, previa asesoría pre-test, obteniendo la autorización del paciente después de brindarle suficiente información.     La vacunación con BCG no es recomendada en pacientes VIH severamente deprimidos < 200 CD4, por la posibilidad de siembra hematógena del bacilo vivo que contiene la vacuna (145) (D-II) , sin embargo, la vacunación con BCG es apoyada por la OMS (146) a niños con VIH asintomáticos (C-III).   La reinfección exógena, que podría presentarse varios años después de haber sido tratada exitosamente una tuberculosis, es producida por cepas de bacilos tuberculosos diferentes al primer episodio. El esquema de manejo para esa reinfección exógena, es similar al exitosamente usado en el primer tratamiento.   Si se presenta fracaso al tratamiento de la TB en los coinfectados, se debe utilizar el esquema ya conocido, que se emplea en pacientes no VIH. Si se documenta multirresistencia, debe remitirse al tercer nivel para manejo especializado
  • Patients who are not candidates for HAART — We recommend use of the standard six month rifampin-based antituberculous regimen for HIV-positive patients who are not candidates for antiretroviral therapy [43] . (See "Patients who are not candidates for HAART" above, and see "General principles of the treatment of tuberculosis").
  • The immune reconstitution inflammatory syndrome usually occurs in immunosuppressed patients who were recently initiated on antituberculosis medications and HAART. This phenomenon presumably results from partial reconstitution of the host immune response and a transient increase in inflammation. Among patients with TB, immune reconstitution inflammatory syndrome has been described in 10 to 35 percent of patients [25,51,53] . The risk is increased in patients with an initial CD4 count below 100/microL [25] and in patients with a significant reduction in viral load and a larger increase in CD4 count [53] . (See "Immune reconstitution inflammatory syndrome", section on IRIS associated with mycobacterial infections). Paradoxical responses are self-limited and therefore do not require alteration or interruption of the antituberculous or antiretroviral regimens. The addition of a short course of corticosteroids has been recommended if paradoxical responses cause significant symptoms, but such treatment should be undertaken only after a thorough evaluation to exclude other potential causes of clinical deterioration (eg, TB treatment failure).
  • Transcript

    • 1. Tuberculosis y VIH Julián Ramírez Medicina Interna UdeA Marzo de 2009
    • 2. Datos epidemiológicos
      • Relación peligrosa  aumento de incidencia de TB.
      • 1/3 de todos los casos TB, tienen concomitantemente VIH.
      • Con el SIDA:
        • Incrementaron casos de TB primaria
        • Incrementaron los casos de TB multi-resistente
      N Engl J Med. 2008
    • 3.
      • VIH es el más importante factor de riesgo para la reactivación de TB.
      • Más prevalente en: minorías étnicas, drogadictos.
      • CDC  TB y VIH
        • 35% 1993
        • 68% 2003
      MMWR Morb Mortal Wkly Rep. 2007 Oct 26
    • 4.
      • Incremento en la TB primaria a comparación de reactivación.
      • 31% de tuberculosis son el resultado de infección primaria.
      • La infección por VIH es un importante factor de riesgo para enfermedad primaria.
      • Otros estudios  10% de TB resulta de infección reciente.
      • Coinfectado  50% más de posibilidades de desarrollar TB
      • No VIH: riesgo de TB 5 – 10% en toda la vida.
      • VIH: riesgo de TB 10%/año de vida.
      N Engl J Med 1994 330(24)
    • 5.
      • TBMR  más prevalente en pacientes con VIH.
      • 10% de resistencia a alguno de los 4 mctos de primera línea
      • Prevalencia de TB MR en nuevos casos  1% - 6% (China)
      • Transmisión de TBMR  Infección con germen resistente – Resistencia de la cepa origina.
      N Engl J Med 1993; 328(16)
    • 6. Interacciones TB y VIH
      • CD4 disminuyen  activación bacilos latentes  diseminación hematógena
      • TB se asocia con incremento de viremia
        • Activación inmune, incrementa proporción CD4, vulnerables a VIH
        • Se incrementa correceptores VIH CCR5 y CXCR4
      • Viremia declina luego de tratamiento para TB.
      • HIV aumenta riesgo de desarrollar TB activa por reactivación ó infección exógena.
      Clin Exp Immunol 2001; 123:233
    • 7.  
    • 8. Síntomas
      • Similares a otros pacientes con TB.
      • Síntomas pulmonares
      • Síntomas inespecíficos: pérdida de peso, fiebre de origen desconocido, o malestar.
      Am J Respir Crit Care Med 161:1376
    • 9. Enfermedad extra pulmonar
      • Pacientes con VIH, alta incidencia de enfermedad pulmonar y extrapulmonar.
      • A mayor inmunocompromiso, mayor riesgo
      • A mayor depresión de conteo de CD4, más probabilidad de micobacteremia y BK +
      • Sitios más comúnes: sangre, nódulos linfáticos extratorácicos, médula ósea, TGU, SNC. Hay también complicaciones inusuales.
    • 10. Tuberculous bronchoesophageal fistulae in patients infected with the human immunodeficiency virus: three case reports and review.
      • AU Porter JC; Friedland JS; Freedman AR SO
      Clin Infect Dis 1994 Nov;19(5):954-7
      • <30 pacientes descritos.
      • 3 pacientes  fístula esofagomediastinal en VIH/TB.  Adenopatías mediastinales.
      • Todas las fístulas mejoraron con tratamiento antituberculoso – alimentación nasogástrica, sin cirugía.
      • Adenopatías mediastinales + tos + vómito  pte con VIH  Fístula broncoesofágica tuberculosa.
    • 11. Frecuencia de los sitios de enfermedad extrapulmonar más común en VIH
      • En una serie de 75 pacientes con SIDA y TB, hemocultivos para micobacterias fueron positivos en 22 (29%).
      • La prevalencia aumentó a 49% en aquellos con recuento de CD4 <100 céls/ml.
      • Nódulos linfáticos extratorácicos  18 – 22%. Los más comunes son los cervicales (84%) y axilares (18%)
      • TB pleural más común en pacientes con SIDA (11% vs 6%)
      Am Rev Respir Dis 1993; 148:1292
    • 12. Active pulmonary tuberculosis in patients with AIDS: spectrum of radiographic findings
      • Greenberg SD, Frager D, Suster B, Walker S
      Radiology. 1994 Oct;193(1):115-9. 133 pacientes con SIDA + esputo positivo /LBA/Cultivos. Correlación imágenes con conteo CD4, baciloscopias y sensibilidad a los antituberculosos. Definieron varios patrones así:
    • 13.
      • Derrame pleural
      • Linfadenopatía intratorácica
      • Consolidación del espacio aéreo en lóbulo medio ó inferior sin cavitación
    • 14.  
    • 15.  
    • 16.
      • Consolidación apical/posterior de lóbulos superiores
      • Consolidación lóbulos inferiores sin adenopatías ó derrame pleural
      • Diseminación endobronquial (sombras acinares 3-4 mm)
      • Bronquiectasias
    • 17.  
    • 18.  
    • 19.  
    • 20.  
    • 21.  
    • 22.
      • Infiltrados difusos ó reticulares
      • Infiltrados similares a PJ (áresas simétricas y difusas de vidrio esmerilado ó consolidación
      • Infiltrados multilobares de predominio medio/inferior.
    • 23.  
    • 24.  
    • 25.  
    • 26. CD4 y patrones radiológicos Radiology. 1994 Oct;193(1):115-9.
    • 27. CD4 y patrones radiológicos Radiology. 1994 Oct;193(1):115-9.
    • 28. Relación entre positividad de BK y Rx Radiology. 1994 Oct;193(1):115-9.
    • 29. Sensibilidad microbiológica y hallazgos radiológicos Radiology. 1994 Oct;193(1):115-9.
    • 30.  
    • 31. Clinical and radiographic correlates of primary and reactivation tuberculosis: a molecular epidemiology study.
      • Geng E, Kreiswirth B, Burzynski J.
      JAMA. 2005 Jun 8;293(22):2740-5 Los infiltrados atípicos de TB en VIH, corresponden a reactivación? Ó corresponden a primoinfección? Estudio retrospectivo. 456 pacientes. 180 pacientes  radiografías atípicas HIV se asoció a frecuencia de imágenes radiológicas atípicas. TB recientemente adquirida, no fue predictor radiológico
    • 32. Características radiológicas en pacientes con TB pulmonar y VIH JAMA. 2005 Jun 8;293(22):2740-5
    • 33. Predictores de cambios radiológicos típicos JAMA. 2005 Jun 8;293(22):2740-5
    • 34. Intrathoracic adenopathy associated with pulmonary tuberculosis in patients with human immunodeficiency virus infection.
      • Pastores SM, Naidich DP, Aranda CP
      Chest. 1993 May;103(5):1433-7 Qué papel tiene la TC en la linfadenitis tuberculosa? 25 pacientes con VIH. Imagen más característica: adenopatías hiliares y mediastinales hipodensa con respecto a tejidos blandos (84%). Estas características aunque no patognomónicas, si suficientes para terapia empírica
    • 35.  
    • 36. Tuberculina
      • Problemático! Guía el recuento de CD4.
      • > 300  la mayoría harán reacción > 5 mm
      • < 100  prácticamente ninguno hará reacción
      • Cuando se excluye TB activa, un test positivo indica tratamiento con Isoniazida.
      Am Rev Respir Dis 1993; 148:1292
    • 37. Baciloscopias
      • Rendimiento entre un 50 – 60% de tinción de esputo.
      • Cultivo: 85 – 100%
      • Existe diferencia entre la positividad de la BK entre HIV positivos y HIV negativos?
      • Qué tan específico es el BK para MT?
    • 38. Factors affecting the yield of acid-fast sputum smears in patients with HIV and tuberculosis.
      • Smith RL; Yew K; Berkowitz KA
      Chest 1994 Sep;106(3):684-6. BK (+) en 100 pacientes HIV + y 76 sin VIH. 60% vs 57 %. La presencia ó ausencia de cavitación en ambas poblaciones no influyó en la positividad de las BK. Recuento de CD4 <50  58% 50 – 200  60% > 200  56% 96% si HIV y diseminación.
    • 39. High predictive value of the acid-fast smear for Mycobacterium tuberculosis despite the high prevalence of Mycobacterium avium complex in respiratory specimens.
      • Yajko DM; Nassos PS; Sanders CA; Madej JJ
      Clin Infect Dis 1994 Aug;19(2):334-6. Alta prevalencia de M. Avium Complex. Realizado en un Hospital donde aislamiento de MAV es alto! VPP de BK para MT: 92% (expectoración) – 71% (esputo inducido) – 71% (LBA) Las muestras fueron positivas a una tasa similar entre pacientes con TB con/sin VIH.
    • 40. Inducción del esputo
      • Controvertida sensibilidad y VP.
      • Un estudio de San Francisco: menor VPP para esputo inducido.
      • Un estudio de Brasil: 98% de concordancia entre esputo inducido vs espontáneo y 86% de concordancia entre cultivo de esputo inducido vs obtenido por LBA.
      • Esputo inducido puede ser + en cultivo, hasta en 50% de pacientes con DP.
      Am J Respir Crit Care Med 2000 dec;162(6):2238-40
    • 41. Pruebas Invasivas
      • Cuando los estudios no invasivos no dan respuesta inmediata.
      • Broncoscopia  Dx inmediato en 50%. La sensibilidad de los cultivos es del 100%.
      • Derrame Pleural  Toracentesis – Biopsia pleural. Cultivos 91% - Granulomas 88%
      .
    • 42.
      • Estado inmunológico del paciente, requerimento de terapia HAART y reacciones medicamentosas potenciales
      • ATS/CDC
      • GUIAS COLOMBIANAS
    • 43. Esquema convencional
      • 6 meses: 4 fármacos primera línea x 2 meses; fase bisemanal x 4 meses.
        • Trisemanal si CD4 < 100
        • No negativización al finalizar la primera fase  prolongar tratamiento por 9 meses.
      • Rifampicina: Sino se decide usar.
        • 48 dosis: HZSE; HE/diaria x 10 meses.
    • 44. Infección Tuberculosa Latente
      • Todo paciente con VIH con tuberculina > 5 mm.
      • Isoniacida por 9 meses ó
      • Rifampicina + Pirazinamida por 2 meses.
      • Tuberculina negativa/anergia  No está indicado tratamiento
    • 45. HAART
      • Considerar interacciones medicamentosas.
      • Régimen basado en Rifabutina (primera línea, 6 meses), concomitante con IP’s.
      • Efavirenz puede reducir concentraciones de rifabutina. Incrementar dosis de ésta última.
    • 46. Candidatos a HAART
      • Riesgo de síndrome de reconstitución inflamatoria inmune.
      • Si HAART + anti TB juntos  toxicidad  responsable?
      • Si se suspende HAART  oportunistas.
      • CD4 < 100  HAART dos semanas después de anti TB.
      • CD4 > 100  HAART dos meses después de anti TB.
    • 47. No Candidatos a HAART
      • Régimen estandar de 6 meses, basado en la rifampicina.
    • 48. Seguimiento
      • Esputo mensual.
      • Después del último negativo  al menos uno durante el tiempo restante de la terapia.
      • Si al 3er mes no es negativo  cultivos.
      • Fiebre  resuelve en un mes.
      • Mejoría radiológica  3 meses.
      • Nuevos signos con terapia apropiada  otra infección.

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