Pulmonary arterial hypertension associated with interferon beta treatment for multiple sclerosis: a case report

2009 ◽  
Vol 15 (7) ◽  
pp. 885-886 ◽  
Author(s):  
AH Ledinek ◽  
SŠ Jazbec ◽  
I Drinovec ◽  
U Rot
Keyword(s):  
Multiple Sclerosis ◽  
Case Report ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Respiratory Symptoms ◽  
Interferon Beta ◽  
Experimental Models ◽  
Interferon Treatment ◽  
Pulmonary Arterial ◽  
Stimulation Of

A 23-year-old woman with multiple sclerosis developed respiratory symptoms 3 years after introduction of interferon beta-1b. The diagnosis of pulmonary arterial hypertension (PAH) was established. The patient partially responded to sildenafil and bosetan treatment. This is the first report of PAH, associated with interferon beta therapy. As shown in experimental models, interferon treatment can induce PAH by stimulation of thromboxane cascade and secretion of various inflammatory mediators.

Pulmonary arterial hypertension associated with interferon-beta treatment for multiple sclerosis. Case report and literature review

2019 ◽  
Vol 28 ◽  
pp. 273-275 ◽  
Author(s):  
Eftychia Demerouti ◽  
Panagiotis Karyofyllis ◽  
George Athanassopoulos ◽  
George Karatasakis ◽  
Dimitrios Tsiapras ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Case Report ◽  
Pulmonary Arterial Hypertension ◽  
Literature Review ◽  
Arterial Hypertension ◽  
Interferon Beta ◽  
Multiple Sclerosis Case ◽  
Pulmonary Arterial

035 Interferon beta induced thrombotic microangiopathy in multiple sclerosis: a clinical-pathological report

2018 ◽  
Vol 89 (6) ◽  
pp. A15.1-A15 ◽  
Author(s):  
Charmaine Yam ◽  
Anthony Fok ◽  
Catriona McLean ◽  
Ernest Butler ◽  
Peter Kempster
Keyword(s):  
Multiple Sclerosis ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Renal Biopsy ◽  
Thrombotic Microangiopathy ◽  
Interferon Beta ◽  
Pulmonary Arterial ◽  
Multiple Sclerosis Patients ◽  
Dose Dependent

IntroductionThrombotic microangiopathy (TMA) has been described with long-term interferon-beta (IFN-β). We report a case of biopsy-proven TMA in a patient with multiple sclerosis (MS) who had been having IFN-β−1a injections for twenty years. These biopsy findings were similar to previously described lung histological changes in IFN β- induced pulmonary arterial hypertension (PAH).CaseA 57 year old woman with relapsing-remitting multiple sclerosis had been administering IFN-β−1a injections for twenty years. Her BMI was 21 and she was on a dose of 44 mcg three times per week. She presented with acute pulmonary oedema, renal failure, malignant hypertension, micro-angiopathic haemolytic anaemia and thrombocytopenia after one week of increasing dyspnoea. A renal biopsy showed malignant hypertensive nephropathy and microangiopathy consistent with TMA. Alternative TMA syndromes including haemolytic uraemic syndrome and thrombotic thrombocytopenic purpura were excluded. Renal function stabilised after the IFN was ceased but never returned to the baseline level.ResultsHer renal biopsy showed glomerular capillary thrombus deposition, endothelial reactivity, vessel necrosis and wall duplication with luminal thrombus. Fibromuscular proliferation, focal fibrinoid necrosis and luminal thrombus was also present within arterioles. These microvascular histopathological findings resemble vessel changes observed seen in lung biopsies in human IFN β mediated PAH, and those described in transgenic mouse models engineered to overproduce Type 1 IFN.1 2 Our patient was on treatment for twenty years at a dose exceeding 50 mcg per week. Both are postulated risk factors for the development of TMA.2ConclusionOur report highlights similarities between microvascular changes seen in IFN-induced TMA and those observed in pulmonary arterial hypertension associated with IFN therapy. This suggests a shared pathophysiological mechanism. Kavanagh et al had described a dose-dependent spectrum of renal microvascular disease in his mouse model.2 The duration and high dosage for weight of IFN Β supports a cumulative drug toxicity effect.References. Fok A, Williams T, McLean C, Butler E. Interferon beta- 1a long-term therapy related to pulmonary arterial hypertension in multiple sclerosis patients. Mult Scler2016Oct;22(11):1495–1498.. Kavanagh D, McGlasson S, Jury A, et al. Type I interferon causes thrombotic microangiopathy by a dose-dependent toxic effect on the microvasculature. Blood2016Aug;05–715987.

scholarly journals Pregnancy and pulmonary arterial hypertension: a case report

2021 ◽  
pp. 100135
Author(s):  
Ana Dias ◽  
Ana Mineiro ◽  
Luísa Pinto ◽  
Filipa Lança ◽  
Rui Plácido ◽  
...  
Keyword(s):  
Case Report ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Pulmonary Arterial

Bosentan therapy for pulmonary arterial hypertension: a case report of a 16-month-old boy

2007 ◽  
Vol 23 (sup2) ◽  
pp. S103-S107
Author(s):  
Y. Dulac ◽  
R. Bassil ◽  
V. Gressin ◽  
S. Bonnet ◽  
E. Costello ◽  
...  
Keyword(s):  
Case Report ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Pulmonary Arterial

Pulmonary arterial hypertension: a disease of tethers, SNAREs and SNAPs?

2007 ◽  
Vol 293 (1) ◽  
pp. H77-H85 ◽  
Author(s):  
Pravin B. Sehgal ◽  
Somshuvra Mukhopadhyay
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Membrane Trafficking ◽  
Experimental Models ◽  
Electron Microscopic ◽  
Surface Receptors ◽  
Arterial Lesions ◽  
Microscopic Studies ◽  
Pulmonary Arterial ◽  
Membrane Tethers

Histological and electron microscopic studies over the past four decades have highlighted “plump,” “enlarged” endothelial, smooth muscle, and fibroblastic cellular elements with increased endoplasmic reticulum, Golgi stacks, and vacuolation in pulmonary arterial lesions in human and in experimental (hypoxia and monocrotaline) pulmonary arterial hypertension. However, the contribution of disrupted intracellular membrane trafficking in the pathobiology of this disease has received insufficient attention. Recent studies suggest a pathogenetic role of the disruption of intracellular trafficking of vasorelevant proteins and cell-surface receptors in the development of this disease. The purpose of this essay is to highlight the molecular regulation of vesicular trafficking by membrane tethers, SNAREs and SNAPs, and to suggest how their dysfunction, directly and/or indirectly, might contribute to development of pulmonary arterial hypertension in experimental models and in humans, including that due to mutations in bone morphogenetic receptor type 2.

Reversible Interferon-Induced Pulmonary Arterial Hypertension in a Patient With Multiple Sclerosis

2017 ◽  
Vol 53 (10) ◽  
pp. 596-597 ◽  
Author(s):  
Alberto García Ortega ◽  
Raquel López Reyes ◽  
Ana Torrents Vilar ◽  
Enrique Zaldivar Olmeda ◽  
Marcos Prado Barragan
Keyword(s):  
Multiple Sclerosis ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Pulmonary Arterial

Undiagnosed Pulmonary Arterial Hypertension at 33 Weeks’ Gestation: A Case Report

2010 ◽  
Vol 30 (2) ◽  
pp. 45-52
Author(s):  
Maureen A. Seckel ◽  
Carol Gray ◽  
Megan B. Farraj ◽  
Gerald O’Brien
Keyword(s):  
Case Report ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Pulmonary Arterial
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