The Effect of Anticoagulant Therapy in Primary and Anorectic Drug-Induced Pulmonary Hypertension

CHEST Journal ◽  
1997 ◽  
Vol 112 (3) ◽  
pp. 714-721 ◽  
Author(s):  
Herbert Frank ◽  
Kurt Ruber ◽  
Johannes Mlczoch ◽  
Ernst Schuster ◽  
Hans Peter Gurtner ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Anticoagulant Therapy ◽  
Drug Induced ◽  
Anorectic Drug

Drug-Induced Pulmonary Hypertension in Newborns: A Review.

2007 ◽  
Vol 5 (2) ◽  
pp. 129-133 ◽  
Author(s):  
Paolo Silvani ◽  
Anna Camporesi
Keyword(s):  
Pulmonary Hypertension ◽  
Drug Induced

A CASE OF DRUG-INDUCED(?) PULMONARY HYPERTENSION

2009 ◽  
Vol 188 (1-6) ◽  
pp. 265-272 ◽  
Author(s):  
Jörgen Malmquist ◽  
Erik Trell ◽  
Alf Torp ◽  
Clas Lindström
Keyword(s):  
Pulmonary Hypertension ◽  
Drug Induced

An Uncommon Presentation of Adult Hemophagocytic Lymphohistiocytosis with Severe Pulmonary Hypertension

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 4734-4734
Author(s):  
Lauren Marie Gerard ◽  
Katharine He Xing ◽  
Christine M Cserti-Gazdewich
Keyword(s):  
Bone Marrow ◽  
Pulmonary Hypertension ◽  
Hemophagocytic Lymphohistiocytosis ◽  
Blood Film ◽  
Polymicrobial Sepsis ◽  
Severe Pulmonary Hypertension ◽  
Drug Induced ◽  
Off Label ◽  
Ebv Reactivation ◽  
Uncommon Presentation

Abstract Abstract 4734 Introduction: Adult hemophagocytic lymphohistiocytosis (HLH) is a rare and potentially life-threatening hyperinflammatory syndrome that presents both diagnostic and therapeutic challenges. HLH may be primary and related to an underlying genetic abnormality or secondary to infection, malignancy, or rheumatologic condition. We describe a case of HLH in a latently EBV-/CMV-/HBV-immune 52-year old male co-presenting with severe pulmonary hypertension and a novel heterozygous perforin missense exon mutation. He was intolerant of the HLH 2004 protocol but responded to salvage alemtuzumab therapy, which was then followed seven weeks later by a fatal polymicrobial sepsis. Case Presentation: This previously healthy 52 year-old male developed the insidious onset of acral paresthesia and exertional dsypnea over a two year period. Seven months prior to admission, he was treated as an outpatient for suspected H1N1 infection, followed by the development of spontaneously-resolving superior oblique nerve palsy, with the EMG/NCS correlate of demyelinating polyneuropathy and secondary axonal loss. His dyspnea progressed, and he presented to hospital with fevers, weight loss, and respiratory distress requiring mechanical ventilation. His course in the intensive care unit was complicated by nephrotic range azotemia (Cr >200 umol/L), cryptogenic hepatitis (transaminases >1000 IU/ml), and splenomegaly. Hematologic investigations initially revealed an isolated thrombocytopenia that was IVIg and steroid refractory, followed by hemolytic anemia with oxidative blood film abnormalities, and an initial bone marrow biopsy devoid of hemophagocytosis. Rheumatologic serologies (ANA, ENA, C3, C4, p-ANCA, c-ANCA, ds-DNA, anti-GBM) and microbiologic studies (HIV, Monospot, and indices of reactivation of HBV or CMV) were negative. Other causes of peripherally destructive cytopenias were also ruled out (DAT, PNH flow cytometry, APLA, ADAMTS13, methemoglobin, G6PD, PK normal). Four weeks after admission, worsening pancytopenia and unexplained fevers prompted a second bone marrow examination, which demonstrated hemophagocytosis with an EBV reactivation viral load of 7 × 105/ml. Meeting clinicopathologic diagnostic criteria for HLH, the HLH 2004 protocol was thus initiated. Within 7 days, treatment-limiting nephrotoxicity and hepatotoxicity developed, prompting discontinuation of cyclosporine and dose-reduction of etoposide. Hepatic biopsy revealed drug-induced sinusoidal necrosis without lymphohistiocytic infiltration. Worsening HLH prompted the next-line use of anti-CD52 monoclonal therapy (alemtuzumab), which associated with the onset of freedom from transfusion within 35 days. Over the six week course of therapy, clinical, biochemical, and hematologic manifestations continued to improve. In parallel with sildenafil, the pulmonary hypertension was also dramatically alleviated. He thus remained in a transfusion-free remission for 55 days until day 105 after diagnosis. Fevers then recurred, with polymicrobial sepsis complicated by disseminated intravascular coagulation, respiratory failure, and hematopathologic evidence of macrophage re-activation. The goals of care were changed to comfort measures and the patient succumbed. Autopsy revealed disseminated blastomycosis with relapsed HLH. Perforin gene sequencing identified a novel heterozygous exon missense single nucleotide polymorphism 1517A>C (His506Pro). Conclusion: This is an extraordinary case of adult EBV-reactivation-associated HLH presenting with severe pulmonary hypertension, a novel perforin gene mutation, intolerance towards the HLH-2004 protocol, and responsiveness to alemtuzumab. Fatal secondary infections, including the discovery of disseminated blastomycosis, presaged or provoked the concomitant relapse of HLH. The relevance of the unique perforin mutation or the co-infection with Blastomyces with respect to the atypical features of this HLH presentation remains unknown. Disclosures: Off Label Use: Alemtuzumab (anti-CD52) was used off-label in the salvage management of hemophagocytic lymphohistiocytosis (HLH).

scholarly journals Pulmonary Hypertension Roundtable: Metabolic Disease and PH

2018 ◽  
Vol 17 (3) ◽  
pp. 115-120
Keyword(s):  
Metabolic Disease ◽  
Pulmonary Hypertension ◽  
Medical Center ◽  
Associate Professor ◽  
Clinical Database ◽  
Drug Induced ◽  
Methamphetamine Use ◽  
School Of Medicine ◽  
Pulmonary Arterial

On June 20, 2018, Guest Editor Anna Ryan Hemnes, MD, gathered a group of pulmonary hypertension specialists by telephone to talk about the role of metabolic disease in PH. Among the participants in the animated discussion was Roham Zamanian, MD, Director of the Adult Pulmonary Hypertension Program at Stanford University Medical Center. He directs the Vera Moulton Wall Center clinical database and biobank and focuses his research on clinical characterization and impact of novel risk factors such as methamphetamine use, and biomarkers such as insulin resistance in pulmonary arterial hypertension. Readers will recall his participation in the previous issue's roundtable on drug-induced PH. Joining Dr Zamanian were Ioana Preston, MD, Pulmonary Function Lab Director; Director, Pulmonary Hypertension Center; and Associate Professor, Tufts University School of Medicine; and Advances in Pulmonary Hypertension editor-in-chief Harrison W. Farber, MD.

scholarly journals Drug-induced Pulmonary Hypertension?

BMJ ◽  
1971 ◽  
Vol 1 (5743) ◽  
pp. 265-266 ◽  
Author(s):  
F. Follath ◽  
F. Burkart ◽  
W. Schweizer
Keyword(s):  
Pulmonary Hypertension ◽  
Drug Induced

scholarly journals Real-life data of direct anticoagulant use, bleeding risk and venous thromboembolism recurrence in chronic thromboembolic pulmonary hypertension patients: an observational retrospective study

2020 ◽  
Vol 10 (1) ◽  
pp. 204589401987354 ◽  
Author(s):  
Sert Sena ◽  
Mutlu Bulent ◽  
Kocakaya Derya ◽  
Kaptan Deniz ◽  
Ataş Halil ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Venous Thromboembolism ◽  
Anticoagulant Therapy ◽  
Major Bleeding ◽  
Real Life ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Bleeding Events ◽  
Warfarin Group ◽  
Thromboembolic Pulmonary Hypertension ◽  
Recurrent Vte

Introduction Lifelong anticoagulation is the cornerstone of the chronic thromboembolic pulmonary hypertension (CTEPH) treatment regardless of the additional pulmonary endarterectomy, balloon pulmonary angioplasty, or medical treatment alone. Aim of this study was to evaluate the rate of oral anticoagulant preferences and document direct oral anticoagulants’ (DOACs’) safety, efficacy in the CTEPH population. Methods Patients’ demographic data obtained from database between September 2011 and April 2018. In-hospital events, death, venous thromboembolism (VTE) recurrence, bleeding events and anticoagulant therapy transition were recorded. Results We reviewed 501 CTEPH patients who observed 9.0 ± 8.5 years. All-cause death, all bleeding, recurrent VTE was observed in 15.6%, 31% and 12%. Forty-one patients (8.2%) were diagnosed as inoperable. Of all, 15.2% of operable patients remained as residual. All-cause mortality rates were 13.8% (57 pts.) in the warfarin group as compared with 9.7% (13 pts.) in rivaroxaban group (HR: 1.61, 95% CI, 0.89–2.99; p: 0.11). Higher bleeding events occurred with warfarin group (27.1%) as compared with rivaroxaban (24.6%; HR: 1.28, 95% CI, 0.86–1.88; p: 0.22). Major bleeding was significantly higher with warfarin group (HR: 1.94, 95% CI, 1.05–3.62; p: 0.03). Subgroup analysis of all-cause death revealed that this significance dominated by the rate of death according to bleeding events; warfarin versus those seen with rivaroxaban (4.85% vs. 2.2%; HR: 4.75, 95% CI: 1.12–20.16; p = 0.03). The rate of recurrent VTE was found 8.9% in the rivaroxaban group, 10.9% in warfarin group (HR: 1.21, 95% CI, 0.64–2.23; p: 0.55). Conclusion DOACs could be a safe and effective alternative for lifelong anticoagulant therapy in CTEPH patients. Rivaroxaban produced similar rates of thromboembolism and non-relevant bleeding compared to those associated with warfarin. The main difference was found with major bleeding that it was mainly associated with the death rate according to major bleeding. Using DOACs might be a more reasonable way to prevent bleeding events without increasing thromboembolic risk.

scholarly journals March Of Medicine

2003 ◽  
Vol 3 (1) ◽  
pp. 39-44
Author(s):  
No Author
Keyword(s):  
Anticoagulant Therapy ◽  
Intellectual Development ◽  
Oral Polio Vaccine ◽  
Oral Contraception ◽  
Primary Dentition ◽  
Drug Induced ◽  
Polio Vaccine ◽  
In Pregnancy

Report on Long-term Anticoagulant Therapy to the M.R.C. (1964) Brit. med. J.,1964, 2, 837Discoloration of Primary Dentition after Tetracycline Therapy In Pregnancy. Swallow. J.N. Lancet 1964, 2, 611Undernutrition in Infancy and Intellectual Development. Stoch M.B. & Smythe P.M. Arch. Dis. Childh., 1963, 38, 546.Oral Polio Vaccine Communications. JAMA, 1964. 190:41.Tetanus Prophylaxis. Cox. C. A., Knowelden.J. & Sharrard. W.J.H. Brit. med. J., 1963, 2, 1360.Eight Years' Experience with Oral Contraception. Tyler. E. T. Brit. med. J. 1964, 2, 843.Drug induced Blood Dyscrasias. JAMA, 1964. 188 :817 JAMA, 1964. 188: 531.

Drug-Induced Lung Disease

Chest Imaging ◽  
2019 ◽  
pp. 403-407
Author(s):  
Travis S. Henry ◽  
Brent P. Little
Keyword(s):  
Pulmonary Hypertension ◽  
Hypersensitivity Reaction ◽  
Bronchiolitis Obliterans ◽  
Diffuse Alveolar Damage ◽  
Alternative Therapies ◽  
Eosinophilic Pneumonia ◽  
Organizing Pneumonia ◽  
Drug Reactions ◽  
Drug Induced ◽  
Pulmonary Abnormalities

Almost any medication may result in a reaction within the lungs. These reactions are often variable and include diffuse alveolar damage, organizing pneumonia, eosinophilic pneumonia, hypersensitivity reaction, interstitial pneumonitis/fibrosis, alveolar hemorrhage, pulmonary vasculitis/pulmonary hypertension, bronchiolitis obliterans, or a sarcoid-like reaction. Because these reactions may mimic their idiopathic counterparts, yet may respond to drug cessation or alternative therapies, suspicion must be high in patients with pulmonary findings who are on certain medications. This chapter will focus on the spectrum of drug reactions with the lungs. Amiodarone-related pulmonary abnormalities will also be discussed.

scholarly journals Pulmonary hypertension in patients with chronic myeloproliferative disorders

2015 ◽  
Vol 24 (137) ◽  
pp. 400-410 ◽  
Author(s):  
Yochai Adir ◽  
Davide Elia ◽  
Sergio Harari
Keyword(s):  
Pulmonary Hypertension ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Major Complication ◽  
Myeloproliferative Disorders ◽  
Clinical Classification ◽  
Drug Induced ◽  
Myeloproliferative Diseases ◽  
Thromboembolic Pulmonary Hypertension ◽  
Haematological Disorders ◽  
Chronic Myeloproliferative Diseases

Pulmonary hypertension (PH) is a major complication of several haematological disorders. Chronic myeloproliferative diseases (CMPDs) associated with pulmonary hypertension have been included in group five of the clinical classification for pulmonary hypertension, corresponding to pulmonary hypertension for which the aetiology is unclear and/or multifactorial. The aim of this review is to discuss the epidemiology, pathogenic mechanism and treatment approaches of the more common forms of pulmonary hypertension in the context of CMPD's: chronic thromboembolic pulmonary hypertension, precapillary pulmonary hypertension and drug-induced PH.

scholarly journals Predictors of Chronic Thromboembolic Pulmonary Hypertension

Kardiologiia ◽  
2018 ◽  
Vol 58 (12) ◽  
pp. 60-65
Author(s):  
M. R. Kuznetsov ◽  
I. V. Reshetov ◽  
B. B. Orlov ◽  
A. A. Khotinsky ◽  
A. A. Atayan ◽  
...  
Keyword(s):  
Risk Factors ◽  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Anticoagulant Therapy ◽  
Vena Cava ◽  
Significant Risk ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Thromboembolic Pulmonary Hypertension ◽  
Group 2 ◽  
Group 1

Purpose:to elucidate predictors of development of chronic thromboembolic pulmonary hypertension (CTEPH) after acute pulmonary artery thromboembolism (PTE).Material and methods. We included in this study 210 patients hospitalized with diagnosis of submassive and massive PTE from 2013 to 2017. In 1 to 3 years after initial hospitalization these patients were invited for control examination. According to results of this examination patients were divided into two groups: with (group 1, n=45) and without (group 2, n=165) signs of CTEPH. Severity of pulmonary artery vascular bed involvement was assessed by multislice computed tomography (MSCT) angiography and lung scintigraphy. For detection of thrombosis in the inferior vena cava system we used ultrasound angioscanning.   Examination also included echocardiography.Results.In the process of mathematical analysis, the following risk factors for the development of CTEPH embolism were determined: duration of thrombotic history (group 1 – 13.70±2.05 days, group 2– 16.16±1.13 days, p=0.015), localization of venous thrombosis in the lower extremities (the most favorable – shin veins, popliteal, and common femoral veins, unfavorable – superficial femoral vein). The choice of the drug for thrombolytic and anticoagulant therapy: streptokinase and urokinase were significantly more effective than alteplase, rivaroxaban was superior to the combination of unfractionated or low molecular weight heparins with warfarin. Also, risk factors for the development of CTEPH were the initial degree of pulmonary hypertension and tricuspid insufficiency, as well as the positive dynamics of these indicators at the background of thrombolytic or anticoagulant therapy. Of concomitant diseases, significant risk factors for development of CTEPH were grade 3 hypertensive disease, diabetes mellitus, post­infarction cardiosclerosis. On the other hand, age, gender, degree of severity at the time of admission, presence of infarction pneumonia, surgical prevention of recurrent pulmonary embolism, number of pregnancies and deliveries, history of trauma and malignancies, cardiac arrhythmias produced no significant impact on the development of CTEPH.

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