RESUMO
OBJECTIVES: We investigated whether early worsening of cerebrospinal fluid (CSF) predicts the later paradoxical tuberculomas and is a potential predictive biomarker. METHODS: Patients of HIV-negative tuberculous meningitis fulfilling the inclusion criteria(n = 98) underwent clinical and CSF evaluation, together with repeated neuroimaging. We compared the baseline clinical data and continuous CSF of patients who did (n = 36) and did not (n = 62) develop paradoxical tuberculomas, and reported the changes associated with symptomatic tuberculomas. A logistic regression analysis was developed to reveal predictors for paradoxical tuberculomas. RESULTS: The proportion of worsening CSF parameters (WBC count and percent neutrophils) in the paradoxical tuberculomas group (27/36, 75.0%) was significantly higher than the non-paradoxical tuberculomas group (15/62, 24.2%). The logistic regression analysis revealed that worsening CSF parameters was the highest risk predictor for paradoxical tuberculomas. Most worsening CSF parameters (81.0%) occurred within two weeks after treatment (2-24 days, median 7 days), and paradoxical tuberculomas commonly happened two weeks later (12 days to 13 months, median 22 days). The period between worsening CSF parameters and paradoxical tuberculomas ranged from 6 to 383 days (median 21days). There were no significant differences in mortality and prognosis between the two groups. CONCLUSIONS: Early worsening of CSF parameters predicts subsequent development or progression of tuberculomas.
Assuntos
Antituberculosos/uso terapêutico , Tuberculoma/etiologia , Tuberculose Meníngea/complicações , Tuberculose Meníngea/tratamento farmacológico , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Líquido Cefalorraquidiano/química , Progressão da Doença , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos , Tuberculoma/líquido cefalorraquidiano , Tuberculose Meníngea/líquido cefalorraquidiano , Tuberculose Meníngea/microbiologia , Adulto JovemRESUMO
In vitro culture models of the blood-brain barrier (BBB) provide a useful platform to test the mechanisms of cellular infiltration and pathogen dissemination into the central nervous system (CNS). We present an in vitro mouse model of the BBB to test Mycobacterium tuberculosis (Mtb) dissemination across brain endothelial cells. One-third of the global population is infected with Mtb, and in 1%-2% of cases bacteria invade the CNS through a largely unknown process. The "Trojan horse" theory supports the role of a cellular carrier that engulfs bacteria and carries them to the brain without being recognized. We present for the first time a protocol for an in vitro BBB-granuloma model that supports the Trojan horse mechanism of Mtb dissemination into the CNS. Handling of bacterial cultures, in vivo and in vitro infections, isolation of primary astroglial and endothelial cells, and assembly of the in vitro BBB model is presented. These techniques can be used to analyze the interaction of adaptive and innate immune system cells with brain endothelial cells, cellular transmigration, BBB morphological and functional changes, and methods of bacterial dissemination. © 2020 Wiley Periodicals LLC. Basic Protocol 1: Isolation of primary mouse brain astrocytes and endothelial cells Basic Protocol 2: Isolation of primary mouse bone marrow-derived dendritic cells Support Protocol 1: Validation of dendritic cell purity by flow cytometry Basic Protocol 3: Isolation of primary mouse peripheral blood mononuclear cells Support Protocol 2: Isolation of primary mouse spleen cells Support Protocol 3: Purification and validation of CD4+ T cells from PBMCs and spleen cells Basic Protocol 4: Isolation of liver granuloma supernatant and determination of organ load Support Protocol 4: In vivo and in vitro infection with mycobacteria Basic Protocol 5: Assembly of the BBB co-culture model Basic Protocol 6: Assembly of the combined in vitro granuloma and BBB model.
Assuntos
Barreira Hematoencefálica/metabolismo , Barreira Hematoencefálica/microbiologia , Modelos Animais de Doenças , Mycobacterium tuberculosis/imunologia , Tuberculoma/etiologia , Tuberculoma/metabolismo , Tuberculose do Sistema Nervoso Central/etiologia , Tuberculose do Sistema Nervoso Central/metabolismo , Animais , Astrócitos/imunologia , Astrócitos/metabolismo , Barreira Hematoencefálica/imunologia , Encéfalo/imunologia , Encéfalo/metabolismo , Encéfalo/microbiologia , Encéfalo/patologia , Técnicas de Cultura de Células , Separação Celular/métodos , Células Dendríticas/imunologia , Células Dendríticas/metabolismo , Células Endoteliais/imunologia , Células Endoteliais/metabolismo , Interações Hospedeiro-Patógeno/imunologia , Imunofenotipagem , Leucócitos Mononucleares/imunologia , Leucócitos Mononucleares/metabolismo , Camundongos , Tuberculoma/patologia , Tuberculose do Sistema Nervoso Central/patologiaRESUMO
Varón de 57 años con tuberculosis miliar que refirió pérdida visual por ojo derecho, al mes de iniciar un régimen antituberculoso de 4 fármacos. En la exploración se objetivó un edema papilar sectorial inferior que fue atribuido a etiología isquémica. Se le retiró el etambutol y se le administraron 60mg diarios de prednisona oral en pauta descendente. Al mes y medio, presentó una pérdida súbita de visión en el ojo izquierdo. En el fondo de ojo se observó un edema de papila acompañado de un desprendimiento neurosensorial de la fóvea, sin más signos uveíticos acompañantes. Le fue intensificado el tratamiento con moxifloxacino y se redujeron los corticoides, objetivándose una resolución del desprendimiento macular, pero con atrofia óptica. Es posible la afectación tuberculosa aislada del nervio óptico en el contexto de una tuberculosis miliar. En este caso, la actitud terapéutica adoptada ante la papilitis inicial, al ser interpretada como isquémica, pudo favorecer la aparición de la neurorretinitis en el ojo adelfo
A 57-year-old man with miliary tuberculosis reported visual loss in his right eye, a month after starting a four-drug antituberculous treatment regimen. On exploration, an inferior segmental optic disc edema was objectived and it was attributed to ischemic aetiology. Ethambutol was withdrawn and 60mg of oral prednisone daily were given with a tapering dosage. One and a half months later, he presented a sudden loss of vision in his left eye. In fundoscopy, a papillary edema accompanied by a foveal neurosensory detachment was observed but with no more accompanying uveitic signs. Treatment was intensified with moxifloxacin and corticosteroids were reduced, showing a resolution of the macular detachment but with optic atrophy. Isolated tuberculous involvement of the optic nerve may possible in the context of miliary tuberculosis. In this case, the adopted therapeutic approach to the initial papillitis, which was interpreted as ischemic, could favour the appearance of a neuroretinitis in the fellow eye
Assuntos
Humanos , Masculino , Pessoa de Meia-Idade , Papiledema/etnologia , Retinite/etiologia , Tuberculose Miliar/complicações , Tuberculose Ocular/etiologia , Antituberculosos/uso terapêutico , Quimioterapia Combinada , Moxifloxacina/uso terapêutico , Prednisona/uso terapêutico , Tuberculoma/etiologia , Tuberculose Miliar/tratamento farmacológicoRESUMO
A 57-year-old man with miliary tuberculosis reported visual loss in his right eye, a month after starting a four-drug antituberculous treatment regimen. On exploration, an inferior segmental optic disc edema was objectived and it was attributed to ischemic aetiology. Ethambutol was withdrawn and 60mg of oral prednisone daily were given with a tapering dosage. One and a half months later, he presented a sudden loss of vision in his left eye. In fundoscopy, a papillary edema accompanied by a foveal neurosensory detachment was observed but with no more accompanying uveitic signs. Treatment was intensified with moxifloxacin and corticosteroids were reduced, showing a resolution of the macular detachment but with optic atrophy. Isolated tuberculous involvement of the optic nerve may possible in the context of miliary tuberculosis. In this case, the adopted therapeutic approach to the initial papillitis, which was interpreted as ischemic, could favour the appearance of a neuroretinitis in the fellow eye.
Assuntos
Papiledema/etiologia , Retinite/etiologia , Tuberculose Miliar/complicações , Tuberculose Ocular/etiologia , Antituberculosos/uso terapêutico , Quimioterapia Combinada , Humanos , Masculino , Pessoa de Meia-Idade , Moxifloxacina/uso terapêutico , Prednisona/uso terapêutico , Tuberculoma/etiologia , Tuberculose Miliar/tratamento farmacológicoRESUMO
PURPOSE: As a result of multilateral migration and globalization in times of humanitarian crises, western countries face a possible increase in the incidence of central nervous system tuberculosis (CNS TB). The diagnosis of CNS TB is challenging and often delayed due to the manifold and often non-specific presentation of the disease. The aim of this review is to analyze and summarize imaging features and correlated clinical findings of CNS TB. METHODS: The different manifestations of CNS TB are explained and illustrated by characteristic neuroradiological as well as neuropathological findings. An overview on diagnostic and therapeutic approaches is provided. For clarity, tables summarizing the lesion patterns, differential diagnoses and diagnostic hints are added. RESULTS: The CNS TB can be manifested (1) diffuse as tuberculous meningitis (TBM), (2) localized as tuberculoma or (3) tuberculous abscess or (4) in extradural and intradural spinal infections. Information on clinical presentation, underlying pathology and the distinguishing features is demonstrated. The TBM is further described, which may lead to cranial nerve palsy, hydrocephalus and infarction due to associated arteritis of the basal perforators. The differential diagnoses are vast and include other infections, such as bacterial, viral or fungal meningoencephalitis, malignant causes or systemic inflammation with CNS. Complicating factors of diagnosis and treatment are HIV coinfection, multi-drug resistance and TB-associated immune reconstitution inflammatory syndrome (IRIS). CONCLUSIONS: Neurologists and (neuro-)radiologists should be familiar with the neuroradiological presentation and the clinical course of CNS TB to ensure timely diagnosis and treatment.
Assuntos
Tuberculose do Sistema Nervoso Central/complicações , Tuberculose do Sistema Nervoso Central/diagnóstico , Antituberculosos/uso terapêutico , Diagnóstico Diferencial , Feminino , Infecções por HIV/complicações , Infecções por HIV/diagnóstico , Humanos , Síndrome Inflamatória da Reconstituição Imune/diagnóstico , Imageamento por Ressonância Magnética , Masculino , Meningoencefalite/diagnóstico por imagem , Meningoencefalite/etiologia , Mycobacterium tuberculosis/isolamento & purificação , Neuroimagem , Doenças da Coluna Vertebral/diagnóstico por imagem , Doenças da Coluna Vertebral/etiologia , Tomografia Computadorizada por Raios X , Tuberculoma/diagnóstico por imagem , Tuberculoma/etiologia , Tuberculoma Intracraniano/diagnóstico por imagem , Tuberculoma Intracraniano/etiologia , Tuberculose do Sistema Nervoso Central/líquido cefalorraquidiano , Tuberculose do Sistema Nervoso Central/tratamento farmacológico , Tuberculose Meníngea/líquido cefalorraquidiano , Tuberculose Meníngea/diagnóstico , Tuberculose Meníngea/tratamento farmacológico , Tuberculose Meníngea/etiologia , Tuberculose Resistente a Múltiplos Medicamentos , Tuberculose Osteoarticular/diagnóstico por imagem , Tuberculose Osteoarticular/etiologiaRESUMO
TITLE: Tuberculomas optoquiasmaticos como reaccion paradojica al tratamiento de tuberculosis meningea.
Assuntos
Antituberculosos/efeitos adversos , Interações Hospedeiro-Patógeno , Quiasma Óptico/patologia , Tuberculoma/etiologia , Tuberculose Meníngea/patologia , Adulto , Antituberculosos/uso terapêutico , Infarto Encefálico/etiologia , Erros de Diagnóstico , Progressão da Doença , Resistência Microbiana a Medicamentos , Substituição de Medicamentos , Etambutol/efeitos adversos , Etambutol/uso terapêutico , Feminino , Humanos , Isoniazida/efeitos adversos , Isoniazida/uso terapêutico , Imageamento por Ressonância Magnética , Meningite Viral/diagnóstico , Moxifloxacina/uso terapêutico , Mycobacterium tuberculosis/efeitos dos fármacos , Mycobacterium tuberculosis/isolamento & purificação , Neuroimagem , Quiasma Óptico/diagnóstico por imagem , Paresia/etiologia , Prednisona/uso terapêutico , Pirazinamida/efeitos adversos , Pirazinamida/uso terapêutico , Rifampina/efeitos adversos , Rifampina/uso terapêutico , Tálamo/irrigação sanguínea , Tuberculoma/patologia , Tuberculose Meníngea/líquido cefalorraquidiano , Tuberculose Meníngea/complicações , Tuberculose Meníngea/tratamento farmacológico , Transtornos da Visão/etiologiaRESUMO
Subretinal hypopyon is an uncommon entity which has been described in ocular infections and inflammations including endophthalmitis, acute retinal necrosis, and sympathetic ophthalmia. The authors report subretinal hypopyon in two cases of presumed tubercular uveitis which responded well to antitubercular therapy (ATT). The first case was a 47-year-old male with bilateral peripapillary chorioretinitis with a subretinal hypopyon. Tuberculosis was confirmed on biopsy of a cervical lymph node which revealed acid-fast bacilli. Case 2 was a 17-year-old male with unilateral involvement in the form of a choroidal granuloma with disc edema and retinitis. In addition, a subretinal hypopyon was evident. Both these cases showed dramatic anatomical improvement with ATT. A novel finding of subretinal hypopyon is described in these cases of presumed ocular tuberculosis. It may be prudent to start empirical ATT early on detection of a subretinal hypopyon along with other manifestations compatible with tubercular etiology.
Assuntos
Doenças da Coroide/etiologia , Infecções Oculares Bacterianas/complicações , Tuberculoma/etiologia , Tuberculose Ocular/complicações , Uveíte/complicações , Adolescente , Antituberculosos/uso terapêutico , Doenças da Coroide/diagnóstico , Doenças da Coroide/tratamento farmacológico , Diagnóstico Diferencial , Infecções Oculares Bacterianas/diagnóstico , Infecções Oculares Bacterianas/tratamento farmacológico , Humanos , Masculino , Pessoa de Meia-Idade , Tomografia de Coerência Óptica , Tuberculoma/diagnóstico , Tuberculoma/tratamento farmacológico , Tuberculose Ocular/diagnóstico , Tuberculose Ocular/tratamento farmacológico , Uveíte/diagnóstico , Uveíte/tratamento farmacológicoAssuntos
Anemia Hemolítica Autoimune/etiologia , Vacina BCG/efeitos adversos , Púrpura Trombocitopênica Idiopática/etiologia , Tuberculose/etiologia , Administração Intravesical , Idoso , Antituberculosos/uso terapêutico , Vacina BCG/uso terapêutico , Prótese Vascular/microbiologia , Carcinoma de Células de Transição/cirurgia , Carcinoma de Células de Transição/terapia , Terapia Combinada , Quimioterapia Combinada , Humanos , Masculino , Mycobacterium bovis/isolamento & purificação , Tuberculoma/etiologia , Tuberculoma/microbiologia , Tuberculose/tratamento farmacológico , Tuberculose/imunologia , Neoplasias da Bexiga Urinária/cirurgia , Neoplasias da Bexiga Urinária/terapiaAssuntos
Esclerite/diagnóstico , Tuberculoma/diagnóstico , Tuberculose dos Linfonodos/diagnóstico , Tuberculose Ocular/diagnóstico , Feminino , Humanos , Pessoa de Meia-Idade , Esclerite/etiologia , Esclerite/patologia , Tuberculoma/etiologia , Tuberculoma/patologia , Tuberculose dos Linfonodos/complicações , Tuberculose Ocular/etiologia , Tuberculose Ocular/patologiaAssuntos
Peritonite Tuberculosa/complicações , Tuberculose Gastrointestinal/complicações , Dor Abdominal/etiologia , Idoso , Antituberculosos/uso terapêutico , Colonoscopia , Feminino , Humanos , Imunocompetência , Laparotomia , Tuberculose Latente/complicações , Tuberculoma/etiologia , Redução de PesoRESUMO
Mycobacterium tuberculosis, the causative agent of tuberculosis, drives the formation of granulomas, structures in which both immune cells and the bacterial pathogen cohabit. The most abundant cells in granulomas are macrophages, which contribute as both cells with bactericidal activity and as targets for M. tuberculosis infection and proliferation during the entire course of infection. The mechanisms and factors involved in the regulation and control of macrophage microenvironment-specific polarization and plasticity are not well understood, as some granulomas are able to control bacteria growth and others fail to do so, permitting bacterial spread. In this issue of the European Journal of Immunology, Venkatasubramanian et al. [Eur. J. Immunol. 2016. 46: 464-479] show that mice lacking the tissue factor gene in myeloid cells have augmented M. tuberculosis growth and increased inflammation in the lungs. This suggests that tissue factor, an initiator of coagulation, is important for the generation of fibrin, which supports granuloma formation. This article demonstrates for the first time the involvement of tissue factor in inducing effective immunity against M. tuberculosis, and sheds new lights on the complex interplay between host inflammatory response, the coagulation system, and the control of M. tuberculosis infection.
Assuntos
Bacteriemia/imunologia , Coagulação Sanguínea , Macrófagos/imunologia , Mycobacterium tuberculosis/imunologia , Pneumonia/imunologia , Tromboplastina/metabolismo , Tuberculoma/imunologia , Tuberculose Pulmonar/imunologia , Animais , Bacteriemia/etiologia , Diferenciação Celular , Fibrina/metabolismo , Interações Hospedeiro-Patógeno , Humanos , Imunidade Inata/genética , Pulmão/metabolismo , Pulmão/patologia , Macrófagos/microbiologia , Camundongos , Camundongos Knockout , Mycobacterium tuberculosis/crescimento & desenvolvimento , Pneumonia/etiologia , Tromboplastina/genética , Tuberculoma/etiologia , Tuberculose Pulmonar/complicaçõesRESUMO
Tissue factor (TF) is a transmembrane glycoprotein that plays an essential role in hemostasis by activating coagulation. TF is also expressed by monocytes/macrophages as part of the innate immune response to infections. In the current study, we determined the role of TF expressed by myeloid cells during Mycobacterium tuberculosis (M. tb) infection by using mice lacking the TF gene in myeloid cells (TF(Δ) ) and human monocyte derived macrophages (MDMs). We found that during M. tb infection, a deficiency of TF in myeloid cells was associated with reduced inducible nitric oxide synthase (iNOS) expression, enhanced arginase 1 (Arg1) expression, enhanced IL-10 production and reduced apoptosis in infected macrophages, which augmented M. tb growth. Our results demonstrate that a deficiency of TF in myeloid cells promotes M2-like phenotype in M .tb infected macrophages. A deficiency in TF expression by myeloid cells was also associated with reduced fibrin deposition and increased matrix metalloproteases (MMP)-2 and MMP-9 mediated inflammation in M. tb infected lungs. Our studies demonstrate that TF expressed by myeloid cells has newly recognized abilities to polarize macrophages and to regulate M. tb growth.
Assuntos
Bacteriemia/imunologia , Macrófagos/imunologia , Mycobacterium tuberculosis/imunologia , Pneumonia/imunologia , Tromboplastina/metabolismo , Tuberculoma/imunologia , Tuberculose Pulmonar/imunologia , Animais , Bacteriemia/etiologia , Coagulação Sanguínea , Diferenciação Celular , Feminino , Fibrina/genética , Fibrina/metabolismo , Interações Hospedeiro-Patógeno , Humanos , Imunidade Inata/genética , Pulmão/metabolismo , Pulmão/patologia , Macrófagos/microbiologia , Camundongos Endogâmicos C57BL , Camundongos Knockout , Mycobacterium tuberculosis/crescimento & desenvolvimento , Pneumonia/etiologia , Tromboplastina/genética , Tuberculoma/etiologia , Tuberculose Pulmonar/complicaçõesRESUMO
Major histocompatibility complex (MHC) class II deficiency is a primary immunodeficiency disease characterized by abnormality of MHC class II molecules surface expression on peripheral blood lymphocytes and monocytes. Clinical manifestations include extreme susceptibility to viral, bacterial, and fungal infections but the immunodeficiency is not as severe as SCID (severe combined immunodeficiency), as evidenced by failure to develop disseminated infection after BCG vaccination. Therefore, MHC II deficiency with BCGosis, that is disseminated BCGitis, is not reported commonly. We report an interesting case of BCGosis after vaccination that was diagnosed to have probable MHC II deficiency.
Assuntos
Vacina BCG/administração & dosagem , Encéfalo/microbiologia , Síndromes de Imunodeficiência/diagnóstico , Pulmão/microbiologia , Mycobacterium bovis/imunologia , Pneumonia/diagnóstico , Tuberculoma/diagnóstico , Antituberculosos/administração & dosagem , Vacina BCG/efeitos adversos , Encéfalo/imunologia , Feminino , Genes MHC da Classe II/genética , Humanos , Síndromes de Imunodeficiência/complicações , Lactente , Pulmão/imunologia , Mycobacterium bovis/isolamento & purificação , Pneumonia/complicações , Pneumonia/etiologia , Tuberculoma/etiologia , Tuberculoma/prevenção & controleAssuntos
Vacina BCG/efeitos adversos , Carcinoma de Células de Transição/terapia , Linfadenite/etiologia , Doenças do Mediastino/etiologia , Tuberculoma/etiologia , Tuberculose dos Linfonodos/etiologia , Neoplasias da Bexiga Urinária/terapia , Administração Intravesical , Adulto , Antituberculosos/uso terapêutico , Vacina BCG/administração & dosagem , Vacina BCG/uso terapêutico , Carcinoma de Células de Transição/secundário , Diagnóstico Diferencial , Radioisótopos de Flúor , Fluordesoxiglucose F18 , Humanos , Linfadenite/diagnóstico por imagem , Masculino , Doenças do Mediastino/diagnóstico por imagem , Doenças do Mediastino/tratamento farmacológico , Neoplasias do Mediastino/diagnóstico , Imagem Multimodal , Tomografia por Emissão de Pósitrons , Compostos Radiofarmacêuticos , Tomografia Computadorizada por Raios X , Tuberculoma/diagnóstico por imagem , Tuberculoma/tratamento farmacológico , Tuberculose dos Linfonodos/diagnóstico por imagem , Tuberculose dos Linfonodos/tratamento farmacológicoAssuntos
Anticorpos Monoclonais Humanizados/efeitos adversos , Produtos Biológicos/efeitos adversos , Peritonite Tuberculosa/etiologia , Tuberculoma/etiologia , Adalimumab , Adenocarcinoma/complicações , Anticorpos Monoclonais Humanizados/uso terapêutico , Antituberculosos/uso terapêutico , Ascite/etiologia , Produtos Biológicos/uso terapêutico , Carcinoma/diagnóstico , Carcinoma/secundário , Neoplasias Colorretais/complicações , Diagnóstico Diferencial , Humanos , Hospedeiro Imunocomprometido , Masculino , Pessoa de Meia-Idade , Neoplasias Peritoneais/diagnóstico , Neoplasias Peritoneais/secundário , Peritonite Tuberculosa/diagnóstico , Peritonite Tuberculosa/tratamento farmacológico , Espondiloartropatias/complicações , Espondiloartropatias/tratamento farmacológico , Tuberculoma/diagnóstico , Tuberculoma/tratamento farmacológico , Tuberculose Pulmonar/complicações , Tuberculose Pulmonar/tratamento farmacológicoRESUMO
Primary mycobacterial infections in the musculoskeletal system are rare with a limited number of published case reports. This report describes a case involving a primary musculoskeletal tuberculous abscess. A 62-year-old male patient who had a right total hip arthroplasty performed 8 years earlier, using metal-on-metal articulation presented with a 1-year history of non-tender masses on his right thigh. Initially, it was assumed he had metallosis. Intraoperatively, an incision into the mass was conducted which resulted in draining of a whitish-grey pus like fluid. A diagnosis of tuberculosis was confirmed with both microscopic and histological examination. The patient was treated over a course of six months with an anti-tuberculosis medication regimen following the confirmation of a solitary soft tissue tuberculosis infection. At the 24 month follow-up, the patient was asymptomatic with no relapse of the mass.
Assuntos
Artroplastia de Quadril/efeitos adversos , Infecções Relacionadas à Prótese/microbiologia , Tuberculoma/microbiologia , Humanos , Masculino , Pessoa de Meia-Idade , Coxa da Perna , Tuberculoma/etiologiaRESUMO
Formation of tuberculoma is a rare response of neurotuberculosis in patients regularly and adequately treated with anti-tuberculous drugs. We report a 13-year-old girl with two tuberculomas which formed in the dorsal part of the medulla oblongata during chemotherapy for tuberculous meningitis. The tuberculomas were both removed via a suboccipital midline approach and were demonstrated by pathological findings but the girl died of cardiac arrest that was thought to be caused by postoperative medulla oblongata oedema. In combination with a literature review, we discuss the clinical features and treatment options of brainstem tuberculomas.
Assuntos
Antituberculosos/uso terapêutico , Encefalopatias/diagnóstico , Encefalopatias/etiologia , Tuberculoma/diagnóstico , Tuberculoma/etiologia , Tuberculose Meníngea/tratamento farmacológico , Adolescente , Antituberculosos/efeitos adversos , Edema Encefálico/etiologia , Quimioterapia Combinada , Evolução Fatal , Feminino , Parada Cardíaca/etiologia , Humanos , Isoniazida/administração & dosagem , Bulbo/patologia , Bulbo/cirurgia , Pirazinamida/administração & dosagem , Rifampina/administração & dosagem , Tuberculoma/patologia , Tuberculoma/cirurgia , Tuberculose Meníngea/complicaçõesRESUMO
Molecular factors of pathogenesis of the eosinophilic blood reaction under pulmonary tuberculosis are analyzed in the article. It has been established that the key cytokine providing the development of hemic eosinophilia in patients with pulmonary tuberculosis is IL-5. IL-5 plasma concentration turned out to be increased only in patients with eosinophilia. Increase of eotaxin was determined in patients with tuberculosis despite of the presense of eosinophilia. One-directional nature of the defined changes in eotaxin concentration might be explained by dual properties of this chemokine: on the one hand, eotaxin mediates long-term presence of eosinophils in blood; on the other hand, it initiates the process of adhesion of eosinophilic leucocytes to vascular endothelium with their further migration to the focus of granulomatous inflammation. The established increase in number of IL-5R-positive eosinophils presents one more mechanism which explains the basis of long-term presence of eosinophils in peripheral blood in patients with pulmonary tuberculosis.
Assuntos
Quimiocina CCL11/metabolismo , Eosinofilia , Eosinófilos/metabolismo , Interleucina-5/metabolismo , Tuberculose Pulmonar , Adulto , Fenômenos Fisiológicos Celulares , Eosinofilia/sangue , Eosinofilia/etiologia , Feminino , Humanos , Inflamação/sangue , Inflamação/etiologia , Masculino , Pessoa de Meia-Idade , Monitorização Fisiológica , Tempo , Tuberculoma/sangue , Tuberculoma/etiologia , Tuberculose Pulmonar/sangue , Tuberculose Pulmonar/complicações , Tuberculose Pulmonar/fisiopatologiaRESUMO
Tumor necrosis factor α antagonist therapies represent an increased risk of reactivation of tuberculosis. We report two cases of life-threatening disseminated tuberculosis in patients undergoing treatment with infliximab for Crohn's disease including one case of a patient with cerebral tuberculomas. We discuss the implication of tumor necrosis factor α in the genesis of tuberculosis infection and the features of tuberculosis under infliximab. Tuberculosis screening and eventually preventive chemotherapy should become the standard of care for individual undergoing tumor necrosis factor α antagonist therapies.