Pathology of Pulmonary Fibrosis, Including Chronic Pulmonary Sarcoidosis

Mallory, Tracy B.

doi:10.1148/51.4.468

Cited by 51 publications

(5 citation statements)

References 1 publication

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Cruickshank (1957Cruickshank ( , 1959 found interstitial pneumonia in fiveof 100 autopsies on rheumatoidsubjects, whereas none was found in 200 autopsies on subjects with ankylosing spondylitis. This differ-ence was significant (x2 = 7-35; P < 0 01), and significantly different from the figures of Mallory (1948) who found sixteen examples in 6,000 unselectedautopsies(x2 = 51-18;P < 0-001). Rheumatoid granulomata were present in the lungs of 10 per cent.…”

Section: Validity Of Associationcontrasting

confidence: 62%

Diffuse interstitial pulmonary fibrosis and rheumatoid arthritis.

Walker¹,

Wright²

1969

Annals of the Rheumatic Diseases

View full text Add to dashboard Cite

Section: Validity Of Associationcontrasting

confidence: 62%

Diffuse interstitial pulmonary fibrosis and rheumatoid arthritis.

Walker¹,

Wright²

1969

Annals of the Rheumatic Diseases

View full text Add to dashboard Cite

“…Furthermore, right ventricular failure was recognized as an explanation for dyspnea, cyanosis and death in patients with advanced lung disease. In 1948, for example, Mallory described six patients with granulomatous pneumonitis consistent with sarcoidosis, and parenchymal fibrosis [18]. In this report, the author presented evidence of invasion and thrombosis of the pulmonary vasculature.…”

Section: Historymentioning

confidence: 71%

Pulmonary Hypertension Caused by Sarcoidosis

Diaz-Guzman

Farver

Parambil

et al. 2008

Clinics in Chest Medicine

View full text Add to dashboard Cite

Pulmonary hypertension is an uncommon complication of sarcoidosis, but in severe pulmonary disease it occurs frequently. It is an important cause of cryptogenic dyspnea in sarcoidosis patients, and can occur despite the absence of pulmonary fibrosis. The true prevalence is unknown. With the advent of specific therapies for pulmonary hypertension, there has been a resurgence of interest in the pathophysiology, diagnosis, and treatment of sarcoidosis-associated pulmonary hypertension. This article reviews the status of the current epidemiologic, pathophysiologic and therapeutic knowledge regarding this entity.

show abstract

“…Studies of the pathology of pulmonary hypertension in sarcoidosis have shown in the majority of cases only the small and medium-sized arteries to be clearly affected. Lesions consist of generally incomplete thrombosis provoked by either peribronchovascular fibrosis or granulomatous invasion of the vascular walls (Mallory, 1948;Longcope and Freiman, 1952;Thompson, 1966;Turiaf et al, 1973). Thromboembolism may be superimposed in some cases.…”

Section: Methodsmentioning

confidence: 99%

Chronic cor pulmonale in pulmonary sarcoidosis.

Battesti¹,

Georges²,

Basset³

et al. 1978

Thorax

View full text Add to dashboard Cite

pulmonale in pulmonary sarcoidosis. Right-heart overload happens relatively rarely in sarcoidosis, even with fibroemphysematous changes. Of 21 cases that we studied, six (28%) had clinical and/or electrocardiographic features of cor pulmonale. The cause of cor pulmonale often evoked is an invasion of the walls of pulmonary vessels by sarcoid granulomas or their compression by the fibrotic process. Pathological studies in one patient showed compression of large pulmonary arteries associated with specific sarcoid lesions in small and medium-sized arteries.The development of chronic cor pulmonale due to pulmonary hypertension has rarely been described in pulmonary sarcoidosis, even in chronic fibroemphysematous forms. The mechanisms often evoked to explain the occurrence of pulmonary hypertension are based on histological findings, the perivascular occurrence of granulomas with the fibrosis which sometimes results, and the possibility of thrombosis or invasion of arterial and vein walls by granulomas. Material and methodsTwenty-one cases of chronic sarcoidosis were studied.The diagnosis was made using clinical, radiological, pathological (bronchial biopsy), and immunological (Kveim test, tuberculin anergy) findings. Such a diagnosis was confirmed in life by these methods even in the two cases (2 and 5) where no definite evidence of sarcoidosis was found at necropsy many years later.The radiographic classification was based on postero-anterior and lateral views, occasionally confirmed by tomography.Evidence of right-sided heart involvement was based upon clinical examination and six electrocardiographic criteria (Schaub, 1966): 1 QRS vector angle in the frontal plane (angle a)>+900.2 Negative T wave in S2 and S3 or S, and ca. +900.3 S wave in V, and V >07 mV.4 R wave in V,+S wave in V5>1 mV.5 QRS direction to the right and posterior:rS of V1 to V4, sometimes rS or Qs of V1 to V6 with positive or flattened T waves.6 Incomplete right bundle-branch block: rS R' in V1 with R' in V1>10 mV. Radiological measurement of the size of the right heart chambers and the diameter of the pulmonary arteries was in most cases impossible because of the perihilar pulmonary opacities which obscured the cardiac and arterial contours. Thus radiological criteria were not taken into account.

show abstract

Pathology of Pulmonary Fibrosis, Including Chronic Pulmonary Sarcoidosis

Cited by 51 publications

References 1 publication

Diffuse interstitial pulmonary fibrosis and rheumatoid arthritis.

Diffuse interstitial pulmonary fibrosis and rheumatoid arthritis.

Pulmonary Hypertension Caused by Sarcoidosis

Chronic cor pulmonale in pulmonary sarcoidosis.

Contact Info

Product

Resources

About