Pulmonary Vascular Disease: Student/Resident Case Report Poster - Pulmonary Vascular Disease I |

Rituximab: Friend or Foe for PAH? FREE TO VIEW

Shaiva Meka, DO; Eva Otoupalova, MD; Vishal Patel, MD; Ashley Cichewicz, PA; Bhavinkumar Dalal, MD
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Beaumont Hospital, Warren, MI

Copyright 2016, American College of Chest Physicians. All Rights Reserved.

Chest. 2016;150(4_S):1215A. doi:10.1016/j.chest.2016.08.1324
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SESSION TITLE: Student/Resident Case Report Poster - Pulmonary Vascular Disease I

SESSION TYPE: Student/Resident Case Report Poster

PRESENTED ON: Tuesday, October 25, 2016 at 01:30 PM - 02:30 PM

INTRODUCTION: Rituximab is a monoclonal antibody that has recently shown promise as a treatment modality for pulmonary arterial hypertension (PAH) caused by connective tissue diseases such as systemic sclerosis. But can rituximab cause PAH?

CASE PRESENTATION: A sixty eight year old male with a history of recurrent lymphoplasmacytic lymphoma treated with rituximab presented to the emergency room for progressive dyspnea and fatigue in the last month. He was hypoxic and physical exam demonstrated trace bilateral lower extremity edema. An echocardiogram showed an elevated right ventricular systolic pressure (RVSP) of 72mmHg. Pulmonary embolism was ruled out and an extensive infectious and rheumatologic workup was negative. A right heart catheterization (RHC) was performed, which revealed a right ventricular pressure of 74/7mmHg and pulmonary artery pressure (PAP) of 74/28mmHg with a mean of 49mmHg. The pulmonary capillary wedge pressure was 13mmHg with a pulmonary vascular resistance of 6 Woods units. Saturation study did not reveal any shunts. With adenosine administration during vasodilator testing, the PAP decreased to 52/22mmHg with a mean of 39mmHg and Cardiac output went from 5.9 to 5.75 liters per minute (L/min). Of note, the PAP from a RHC performed a year prior to this presentation was 39/20mmHg. The patient was subsequently started on nifedipine, which improved his symptoms and oxygen requirement.

DISCUSSION: In summary, this case presents rapid progression of PAH within the timespan of a year. Common causes of PAH such as obstructive lung disease or chronic left heart failure typically result in a much slower disease course and rarely cause such elevated PAP. Hence, the best explanation for the rapidity and severity of PAH in this case can be attributed to a drug-effect from rituximab, which he had received in the preceding months. Another learning point is that vasodilator testing during a RHC can provide a potential treatment option, which is valuable for a disease such as PAH where options tend to be limited. Although cardiac output declines from 5.9 to 5.75 L/min, this was not felt to be significant and the vasodilator test was still considered to be positive.

CONCLUSIONS: Pulmonary arterial hypertension (PAH) as a result of rituximab therapy is extremely rare and has only been reported in one case so far. However, clinicians should remain vigilant of rapidly-progressive PAH as a possible adverse effect as this medication becomes more commonly used.

Reference #1: Montrone, D et al. Pulmonary arterial hypertension in a chronic lymphocytic leukemia patient in treatment with rituximab. J Cardiovasc Med. 2015; 16(suppl1):S65.

Reference #2: “Rituximab for Treatment of Systemic Sclerosis-Associated Pulmonary Arterial Hypertension (SSc-PAH)”. Clinicaltrials.gov. Identifier: NCT01086540. Accessed March 31, 2016.

Reference #3: Tonelli, AR, Alnuaimat H and Mubarak K. Pulmonary vasodilator testing and use of calcium channel blockers in pulmonary arterial hypertension. Resp Med.2010; 104: 481-96.

DISCLOSURE: The following authors have nothing to disclose: Shaiva Meka, Eva Otoupalova, Vishal Patel, Ashley Cichewicz, Bhavinkumar Dalal

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