When the “Tree of Life” becomes a threat to life: A rare case of pulmonary embolism associated with Moringa oleifera

INTRODUCTION

Pulmonary embolism (PE) is a potentially life-threatening condition resulting from the obstruction of the pulmonary arteries by thrombotic material, most commonly originating from the deep veins of the lower limbs. It is a common cardiovascular emergency with significant morbidity and mortality and remains a leading cause of preventable in-hospital death. Classical risk factors include recent surgery, prolonged immobilization, malignancy, hormonal therapy, pregnancy, and inherited thrombophilia.

In recent years, there has been growing recognition of the role of complementary and alternative medicines, including herbal supplements, as possible contributors to thrombotic events. Moringa oleifera, commonly known as the “Tree of life” or “Miracle tree,” is widely consumed for its antioxidant, anti-inflammatory, and antidiabetic properties.^[1] Despite its reputation as a natural and safe supplement, in vitro studies have demonstrated that M. oleifera leaf extracts may have procoagulant effects, including the ability to hydrolyze fibrinogen and significantly shorten clotting time in human plasma. These biological actions raise concerns regarding its potential to predispose individuals to thromboembolic events.^[2] A previously reported case described a 63-year-old lady who developed bilateral PE following prolonged M. oleifera extract use, in the absence of other identifiable risk factors,^[3] further supporting the need for clinical vigilance.

CASE REPORT

A 77-year-old gentleman with a history of hypertension and type 2 diabetes mellitus presented to the emergency department with an acute onset of severe shortness of breath and profuse sweating lasting 1 h. He was a non-smoker and had no recent history of surgery, trauma, prolonged immobilization, or malignancy. On presentation, he was tachypneic with a respiratory rate of 44 breaths/min, hypoxic (SPO₂ 80% on room air), and hypotensive (blood pressure 80/50 mmHg), necessitating vasopressor support. The chest was clear on auscultation. Laboratory evaluation revealed an elevated alveolar-arterial gradient on arterial blood gas analysis, significant hypoxemia, and hypocapnia. Notably, D-dimer was markedly raised at 34,500 ng/mL, NT-pro B-type natriuretic peptide (BNP) at 856 pg/mL, and troponin I at 71.5 ng/L. Chest X-ray and electrocardiogram showed no abnormalities. Two-dimensional echocardiography demonstrated dilation of the right atrium and right ventricle with moderate right ventricular dysfunction. Computed tomography pulmonary angiography confirmed bilateral PE with right ventricular strain [Figure 1]. The patient was admitted to the intensive care unit for close hemodynamic monitoring. Due to hemodynamic compromise, systemic thrombolysis was administered with alteplase followed by anticoagulation therapy. Venous Doppler ultrasound of both lower limbs was negative for deep vein thrombosis. A detailed history revealed daily consumption of M. oleifera leaf extract supplements for the preceding 4 months for the purpose of weight loss and diabetes control. Indeed, he managed to achieve a weight loss of 8 kg over 4 months. There was no personal or family history of venous thromboembolism, and no other transient risk factors were identified. In the absence of alternative etiologies, M. oleifera use was considered the probable precipitant of this thrombotic event, prompting discontinuation of the supplement. The patient showed clinical improvement and was discharged after 72 h on maintenance anticoagulation. At the 3-month follow-up, he remained asymptomatic. He was assessed by hematology team and a detailed thrombophilia screen did not reveal any genetic or acquired risk factor to explain the thrombosis. Hence, the PE event was attributed to Moringa consumption, and the anticoagulation was stopped subsequently after 6 months.

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Figure 1: Computed tomography pulmonary angiography demonstrates hyperattenuation within the right main pulmonary artery and its main branches (yellow arrows).

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DISCUSSION

M. oleifera, commonly known as the “miracle tree,” is a medicinal and nutritional plant native to South Asia and widely cultivated across tropical and subtropical regions. Figure 2 here shows Moringa Leaves, Stem, and Roots.^[4] Various parts of the plant including the leaves, pods, bark, roots, flowers, seeds, gum, and seed oil have been used for centuries in traditional medicine and dietary practices owing to their significant therapeutic value. These components are utilized for nutritional supplementation and for managing conditions such as hypertension, anxiety, diarrhea, dysentery, colitis, inflammation, ulcers, infections, liver and kidney disorders, and malnutrition, with reported antihypertensive, anti-inflammatory, diuretic, and antioxidant properties. The leaves are particularly valued for their high vitamin, mineral, and antioxidant content and are commonly consumed as powders, teas, and health beverages, while other parts are used for wound healing, pain relief, and dermatological applications.^[1] Despite its widespread perception as a safe natural supplement, increasing consumption highlights the need for greater awareness of potential adverse effects and herb–drug interactions in clinical practice.

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Figure 2: (a) Moringa leaves, stem, and roots, (b) seeds with seed coat (6).

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However, its potential prothrombotic effects are underrecognized. In vitro studies have shown that leaf extracts can hydrolyze fibrinogen and accelerate clot formation, indicating a possible thrombogenic risk.^[5] In contrast, seed extracts have demonstrated anticoagulant activity, with evidence showing prolongation of prothrombin time and activated partial thromboplastin time. This divergence highlights the variable, part-dependent effects of M. oleifera, suggesting that while seeds may exert antithrombotic effects,^[6] leaf preparations could promote coagulation and contribute to thrombotic risk, providing a plausible mechanistic basis for the thrombotic manifestation observed in our case. Despite this, clinical evidence remains limited, and no regulatory guidelines currently address its safety in this context.

This case is significant due to the absence of inherited or acquired risk factors for PE, alongside a clear temporal relationship with recent Moringa use. Biological plausibility, supported by experimental data, strengthens the likelihood of causation. While causality cannot be confirmed without controlled studies, the pattern observed here is clinically compelling.

Given the widespread and often unsupervised use of herbal supplements, this case highlights the need for appropriate dose regulation and clear safety warnings to prevent potential complications associated with herbal supplementation. In this patient, the adverse event was attributed to the use of Moringa, allowing discontinuation of long-term anticoagulation therapy and thereby reducing the risk of potential bleeding complications.

CONCLUSION

This case illustrates a rare but important potential adverse effect of M. oleifera – PE. Healthcare providers should actively inquire about herbal supplement use in patients with thrombotic events of unknown etiology. Greater awareness, patient education, and further research are needed to evaluate the safety profile of M. oleifera and other commonly used herbal products.