Pulmonary Alveolar Proteinosis and tuberculosis in a diabetic patient: a rare or a seldom diagnosed association

Pereira-Silva, J L; Marinho, M M M A; Veloso, Tavarela; Jc, Jaime-Pérez

doi:10.1590/s1413-86702002000400006

Cited by 16 publications

(19 citation statements)

References 40 publications

(48 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…103,104 The crazy-paving pattern is not pathognomonic of pulmonary alveolar proteinosis, and occurs in other infectious or non-infectious conditions. [104][105][106][107][108][109][110][111][112][113][114] The subacute or chronic clinical course, absence of architectural distortion, smooth 78 Cryptococcus neoformans 79,80 Mycobacterium tuberculosis [81][82][83][84] Mycobacterium avium-intracellulare 85,86 inter-lobular septal thickening, geographical distribution, and discordance between the clinical and radiological features help differentiate pulmonary alveolar proteinosis from other causes of crazy paving. In a study of 42 patients, Ishii et al 115 reported differences in the pattern and distribution of ground-glass opacity on high-resolution CT, which help to differentiate secondary from autoimmune pulmonary alveolar proteinosis.…”

Section: High-resolution Computed Tomographymentioning

confidence: 99%

Pulmonary Alveolar Proteinosis

Khan

Agarwal

2011

Respir Care

View full text Add to dashboard Cite

Section: High-resolution Computed Tomographymentioning

confidence: 99%

Pulmonary Alveolar Proteinosis

Khan

Agarwal

2011

Respir Care

View full text Add to dashboard Cite

“…Publications in the literature suggest that PAP predisposes to TB 5, 54, 55 . Most PAP is an autoimmune disease caused by neutralizing antibodies against GM-CSF.…”

Section: Introductionmentioning

confidence: 99%

Tuberculosis as a three-act play: A new paradigm for the pathogenesis of pulmonary tuberculosis

2016

View full text Add to dashboard Cite

Lack of access to human tissues with untreated tuberculosis (TB) has forced generations of researchers to use animal models and to adopt a paradigm that granulomas are the characteristic lesion of both primary and post primary TB. An extended search of studies of human lung tissues failed to find any reports that support this paradigm. We found scores of publications from gross pathology in 1804 through high resolution CT scans in 2015 that identify obstructive lobular pneumonia, not granulomas, as the characteristic lesion of developing post-primary TB. This paper reviews this literature together with other relevant observations to formulate a new paradigm of TB with three distinct stages: a three-act play. First, primary TB, a war of attrition, begins with infection that spreads via lymphatics and blood stream before inducing systemic immunity that contains and controls the organisms within granulomas. Second, post-primary TB, a sneak attack, develops during latent TB as an asymptomatic obstructive lobular pneumonia in persons with effective systemic immunity. It is a paucibacillary process with no granulomas that spreads via bronchi and accumulates mycobacterial antigens and host lipids for 1–2 years before suddenly undergoing caseous necrosis. Third, the fallout, is responsible for nearly all clinical post primary disease. It begins with caseous necrotic pneumonia that is either retained to become the focus of fibrocaseous disease or is coughed out to leave a cavity. This three-stage paradigm suggests testable hypotheses and plausible answers to long standing questions of immunity to TB.

show abstract

“…Concomitant mycobacterial infection can theoretically explain the pleural effusion in this immunocompromised state especially being reported from a high TB endemic population. 5 Neither we could find any evidence of mycobacterium tuberculosis or any other infective pathogen nor the presence of bilateral effusion was clinically in favour of tuberculosis. Nocardia and Aspergillus also have been reported with increased frequency in PAP.…”

mentioning

confidence: 69%