Pericardial and pleural effusions associated with sirolimus and discussion of possible mechanisms
Sirolimus, a mammalian target of rapamycin inhibitor, is an increasingly used immunosuppressant in solid-organ transplantation. There are an increasing number of reports of unusual oedematous adverse effects associated with this drug, including lymphoedema, ascites and pleural effusions, and a few reports of pericardial effusions. No pathophysiological explanation for these phenomena has been disclosed. We report a 33-year-old sirolimus-treated kidney transplant recipient with chronic pericardial and pleural effusions identified nine years after transplantation. He was initially treated for a presumed tuberculous pericarditis, even though cultures for Mycobacterium tuberculosis were negative. After 12 months of antitubercular therapy, visceral effusions persisted. Pericardial effusion was drained and stabilised. After exclusion of other causes, sirolimus toxicity was considered the most likely cause. Two months after discontinuation of sirolimus, visceral effusions disappeared. Interaction of mammalian target of rapamycin inhibitors with mediators of lymphangiogenesis may be a common link in oedematous states associated with sirolimus.
| Main Authors: | , , , , , , |
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| Format: | Digital revista |
| Language: | English |
| Published: |
Sociedade Portuguesa de Nefrologia
2012
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| Online Access: | http://scielo.pt/scielo.php?script=sci_arttext&pid=S0872-01692012000200005 |
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| Summary: | Sirolimus, a mammalian target of rapamycin inhibitor, is an increasingly used immunosuppressant in solid-organ transplantation. There are an increasing number of reports of unusual oedematous adverse effects associated with this drug, including lymphoedema, ascites and pleural effusions, and a few reports of pericardial effusions. No pathophysiological explanation for these phenomena has been disclosed. We report a 33-year-old sirolimus-treated kidney transplant recipient with chronic pericardial and pleural effusions identified nine years after transplantation. He was initially treated for a presumed tuberculous pericarditis, even though cultures for Mycobacterium tuberculosis were negative. After 12 months of antitubercular therapy, visceral effusions persisted. Pericardial effusion was drained and stabilised. After exclusion of other causes, sirolimus toxicity was considered the most likely cause. Two months after discontinuation of sirolimus, visceral effusions disappeared. Interaction of mammalian target of rapamycin inhibitors with mediators of lymphangiogenesis may be a common link in oedematous states associated with sirolimus. |
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