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Clinical Aspects of Interstitial Lung Disease in Children
Published in Lourdes R. Laraya-Cuasay, Walter T. Hughes, Interstitial Lung Diseases in Children, 2019
A right middle and lower lobectomies were performed after an episode of massive hemoptysis. Pulmonary veno-occlusive disease was confirmed. The histologic picture simulated interstitial pneumonitis with interstitial infiltrates of lymphocytes and macrophages. The pulmonary muscular arteries and arterioles showed medial thickening and intimal fibrosis. No plexiform angiomatoid lesions were seen.
Clinical Diagnosis of Pulmonary Hemorrhage
Published in Philip T. Cagle, Timothy C. Allen, Mary Beth Beasley, Diagnostic Pulmonary Pathology, 2008
Pulmonary veno-occlusive disease is a rare cause of pulmonary hypertension that presents with dyspnea and syncope secondary to postcapillary obstruction of pulmonary capillaries. Occult alveolar hemorrhage may be a more common feature of this disease than previously recognized (22). The chest radiograph will usually show evidence of pulmonary hypertension and Kerley’s B lines may be visible. Alveolar infiltrates may be superimposed when alveolar hemorrhage occurs.
Overview of HIV Infection
Published in Mark J. Rosen, James M. Beck, Human Immunodeficiency Virus and the Lung, 1998
Factors resulting in increased pulmonary vascular resistance and pulmonary artery hypertension in patients diagnosed with PPH include vasoconstriction, vascular wall remodeling, and thrombosis in situ (2). Autopsies of these patients demonstrate specific features of pulmonary arteriopathy, including intimal fibrosis, medial hypertrophy, and aneurysmal dilations of pulmonary arterioles, known as plexiform lesions (2,5,7,8; Fig. 1). Weiss et al. (5) reviewed 23 patients with HIV infection and unexplained pulmonary hypertension for whom histological evaluation was available. With the exception of 1 patient who had evidence of pulmonary veno-occlusive disease, all had the typical findings of classic PPH described previously. Interestingly, there were no foreign body granulomas found in the intravenous drug users. This confirms another study reporting that patients with PPH did not have foreign body granulomas, unless crushed oral medications were injected (12). In fact, only 5% of drug abusers use drugs in this fashion (5,8,13).
A case of pulmonary arterial hypertension complicated by anti-neutrophil cytoplasmic antibody-associated vasculitis and systemic sclerosis
Published in Immunological Medicine, 2021
Hajime Yoshifuji, Sumika Kagebayashi, Hideyuki Kinoshita, Takao Fujii, Yoshiaki Okano, Masao Katsushima, Tsuneyo Mimori
The phenotype of limited cutaneous SSc, positive anti-centromere antibody, and poor response to GC in the present case were compatible with SSc-PAH. Especially, Sanchez et al. reported that PAH complicated by SSc did not respond to GC plus IVCY and those cases required pulmonary vasodilators [9]. Recent reports have suggested that the increased FVC/DLCO ratio is a specific finding of SSc-PAH and useful for predicting the diagnosis of SSc-PAH [17,18]. Since the VC/DLCO ratio was as high as 3.45 (≥ 1.6), it supported that PAH might be derived from SSc in the present case. Considering the low %DLCO (28.5%), it is possible that pulmonary veno-occlusive disease was also complicated in the present case. The present case also had SS. However, it seemed that the PAH was not associated with SS in the present case, because PAH associated with SS often responds to GC [16].
Pulmonary tumor thrombotic microangiopathy: A systematic review of the literature
Published in Canadian Journal of Respiratory, Critical Care, and Sleep Medicine, 2021
L. V. Morin-Thibault, D. Wiseman, P. Joubert, R. Paulin, S. Bonnet, S. Provencher
In the context of severe PH of unknown origin, few patients were anticoagulated (n = 39), received thrombolytics (n = 5) or were treated with PH-targeted treatments (n = 27) including phosphodiesterase-5 inhibitors (n = 15), endothelin receptor antagonists (n = 12), prostanoids (n = 11), stimulator of soluble guanylate cyclase (n = 1) and inhaled nitric oxide (n = 1) (Supplementary Table S2). One patient quickly developed hypoxic respiratory failure after the initiation of epoprostenol. Interestingly, on autopsy, this patient showed signs of pulmonary veno-occlusive disease. Of the 5 patients who received thrombolysis, one had a concomitant massive PE and one had a subsegmental PE and DVT. Reasons for thrombolysis in the three other cases are unknown. One intracranial bleed was reported.11 Among the 29 patients with an antemortem diagnosis of PTTM, 4 did not receive any treatment, 16 received anticoagulants, 11 were treated with PH-specific therapies and 10 received either oral or IV corticosteroids. Moreover, 1 patient underwent an oncological surgery, 1 patient received percutaneous cardiorespiratory support and 1 patient underwent a cardiopulmonary transplant. Finally, 21 patients received conventional chemotherapy and 6 patients received imatinib (Table 4).12–17
Diagnosis of chronic thromboembolic pulmonary hypertension: A Canadian Thoracic Society clinical practice guideline update
Published in Canadian Journal of Respiratory, Critical Care, and Sleep Medicine, 2019
Doug Helmersen, Steeve Provencher, Andrew M. Hirsch, Anne Van Dam, Carole Dennie, Marc De Perrot, Lisa Mielniczuk, Naushad Hirani, George Chandy, John Swiston, Dale Lien, Nick H. Kim, Marion Delcroix, Sanjay Mehta
The potential differential diagnosis for CTEPH includes a range of pulmonary vascular diseases such as: (i) central pulmonary artery thrombosis in the setting of dilated pulmonary arteries secondary to PAH, emphysema or congenital heart disease (ii) pulmonary artery sarcoma; (iii) extrinsic vascular compression such as from fibrosing mediastinitis; (iv) pulmonary veno-occlusive disease (PVOD); (v) large vessel pulmonary artery vasculitis; and (vi) congenital pulmonary artery branch stenosis.