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Table of Contents
CASE REPORT
Year : 2019  |  Volume : 7  |  Issue : 3  |  Page : 82-83

A case of pulmonary thromboembolism secondary to hyperhomocysteinemia


Department of General Medicine, MR Medical College, Kalaburagi, Karnataka, India

Date of Submission16-Oct-2018
Date of Decision18-Dec-2018
Date of Acceptance25-Feb-2019
Date of Web Publication15-Jul-2019

Correspondence Address:
Dr. Rishika Reddy
Department of General Medicine, M R Medical College, Kalaburagi, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/AJIM.AJIM_19_19

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  Abstract 

Hyperhomocysteinemia (HHcy) affects hemostasis and shifts its balance in favor of thrombosis. HHcy can be a potential cause of unprovoked pulmonary thromboembolism, which may be a sole manifestation rather than typical multisystem involvement of the disease. Here, we report a rare case of a 56-year-old male presented with sudden onset of breathlessness, unexplained tachycardia, hypoxemia, who was diagnosed as a case of pulmonary embolism secondary to HHcy without any evidence of deep vein thrombosis.

Keywords: Deep vein thrombosis, hyperhomocysteinemia, thromboembolism


How to cite this article:
Reddy R, Biradar S, Rakesh M. A case of pulmonary thromboembolism secondary to hyperhomocysteinemia. APIK J Int Med 2019;7:82-3

How to cite this URL:
Reddy R, Biradar S, Rakesh M. A case of pulmonary thromboembolism secondary to hyperhomocysteinemia. APIK J Int Med [serial online] 2019 [cited 2019 Aug 19];7:82-3. Available from: http://www.ajim.in/text.asp?2019/7/3/82/262745




  Introduction Top


High levels of homocysteine increase the risk of deep vein thrombosis (DVT), pulmonary embolism (PE), ischemic heart[1],[2] disease, and stroke. Few cases of hyperhomocysteinemia (HHcy) complicating DVT and pulmonary[3] embolism have been reported in literature. DVT with PE may present with a similar clinical, radiological, and laboratorial characteristics of community-acquired pneumonia, presenting a diagnostic challenge to the physician, especially in its difficulty in the differential diagnosis during the treatment[4] process. However, reported cases of PE in the absence of[5] DVT are very rare. Here, we report a rare case of pulmonary thromboembolism (PTE) secondary to HHcy masquerading as pneumonia.


  Case Report Top


A 56-year-old previously healthy male, smoker, and alcoholic, presented with sudden onset breathlessness, and dry cough. There was no history of chest pain, orthopnea, paroxysmal nocturnal dyspnea, no history of palpitation, syncope, no history of hemoptysis. On examination, the patient was tachypneic, with 85% saturation on room air, with decreased air entry into the right infra axillary area no added sounds. Chest X-ray appeared normal; computed tomography (CT) thorax was showing bilateral minimal effusion with right basal consolidation. The patient was admitted under general surgery for right-sided hydrocele, 24 h following, the procedure medical consultation was seeked with above-mentioned complains. The patient was treated with antibiotics for 3 days as a case of the right lower lobe pneumonia, later due to deterioration of the general condition and with persistent tachypnea, tachycardia, and hypoxia diagnosis was reconsidered. Therefore, in view of PTE, D-dimer, and CT pulmonary angiography (CTPA) was advised. CTPA showed thrombus in the right pulmonary artery [Figure 1], there were elevated d-dimer levels up to 8000 ng/mL (normal value - <500 ng/mL); there was no evidence of superficial or deep venous thrombosis by lower limb Doppler study. Further hematological workup revealed elevated homocysteine levels-28 micromol/L (normal value <15 ng/L), other hypercoagulable states such as Protein C and S deficiency, antithrombin III deficiency, and factor V Leiden mutation were negative. The patient was started on subcutaneous low molecular weight heparin (LMWH) according to weight, then, oral anticoagulant - tablet acitrom 3 mg was overlapped with LMWH on day 3. There was clinical improvement in the patient's general condition with improving saturation and reduction in tachypnea, tachycardia and was discharged.
Figure 1: CT Pulmonary angiogram

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CT pulmonary angiogram (CTPA)-An arrow demonstrates filling defect suggestive of thrombus in segmental branch of the right pulmonary artery in the right upper lobe, main pulmonary trunk diameter 26.6mm, with bilateral minimal pleural effusion.


  Discussion Top


Clinically, features of PE are of consolidation/effusion, and diagnosis may be delayed in[6] mild cases and often mistaken for pneumonia. PE can present with cough, fever, chest pain, hemoptysis, creative protein elevation, and pulmonary opacity so that bacterial pneumonia could represent a confounding[7] diagnosis. Noninfectious diseases should also be suspected and included in the differential diagnosis of patients with presumptive diagnosis of pneumonia but who present with treatment failure or disease progression, especially young patients or those without comorbidities. HHcy has been identified as an independent risk factor of atherosclerotic and thromboembolic disease. It can result from either genetic or nutritional disturbances. Elevations of homocysteine of 16–30, 31–100, and >100 μmol/L are classified as mild, moderate, and severe HHcy, respectively. In our patient, homocysteine levels were 28 μmol/L (normal value <15 ng/L). Toxic effect of homocysteine on vascular endothelium is one of the hypotheses on the mechanism by which HHcy causes thrombosis.

N. Radovanović et al. performed a study on HHcy in patients with PE; this study enrolled 70 patients with PTE and 50 healthy controls, results from this study confirm that HHcy represents a risk factor for the occurrence of PE. In order to clarify the HHcy role in specific VTE categories, such as unprovoked thromboses, further studies with a larger group of patients are required.


  Conclusion Top


A high index of suspicion in an unprovoked case of PTE and diligent evaluation for the same can lead to an unusual cause like HHcy.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Ueland PM, Refsum H, Beresford SA, Vollset SE. The controversy over homocysteine and cardiovascular risk. Am J Clin Nutr 2000;72:324-32.  Back to cited text no. 1
    
2.
Selhub J, Jacques PF, Bostom AG, D'Agostino RB, Wilson PW, Belanger AJ, et al. Association between plasma homocysteine concentrations and extracranial carotid-artery stenosis. N Engl J Med 1995;332:286-91.  Back to cited text no. 2
    
3.
Dani SI, Thanvi S, Shah JM, Prajapti J, Jain S, Joshi H. Hyperhomocysteinemia masquerading as pulmonary embolism. J Assoc Physicians India 2003;51:914-5.  Back to cited text no. 3
    
4.
Alves dos Santos JW, Torres A, Michel GT, de Figueiredo CW, Mileto JN, Foletto VG Jr., et al. Non-infectious and unusual infectious mimics of community-acquired pneumonia. Respir Med 2004;98:488-94.  Back to cited text no. 4
    
5.
Caldera A, Mora J, Kotler M, Eiger G. Pulmonary embolism in a patient with pernicious anemia and hyperhomocysteinemia. Chest 2002;122:1487-8.  Back to cited text no. 5
    
6.
Hampson NB. Pulmonary embolism: Difficulties in the clinical diagnosis. Semin Respir Infect 1995;10:123-30.  Back to cited text no. 6
    
7.
Rosendaal FR. Thrombosis in the young: Epidemiology and risk factors. A focus on venous thrombosis. Thromb Haemost 1997;78:1-6.  Back to cited text no. 7
    


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