Today at Morning Report, we had a case of recurrent pericardial effusion. The discussion lead to a broad differential. Here is a European Heart Journal article (2013) with a nice list of Infectious vs. Non-infectious causes of pericardial effusion:
|Viral (most common: Echovirus and Coxsackievirus (usual), Influenza, EBV, CMV, Adenovirus, Varicella, Rubella, Mumps, HBV, HCV, HIV, Parvovirus B19 and Human Herpes Virus 6 (increasing reports)|
|Bacterial [most common: tuberculous (4–5%), Coxiella burnetii, other bacterial rare may include Pneumo-, Meningo-, Gonococcosis, Haemophilus, Staphylococci, Chlamydia, Mycoplasma, Legionella, Leptospira, and Listeria]|
|Fungal (rare: Histoplasma more likely in immunocompetent patients, Aspergillosis, Blastomycosis, Candida more likely in immunosuppressed host)|
|Parasitic (very rare: echinococcus, toxoplasma)|
|Autoimmune and autoinflammatory|
|Systemic inflammatory diseases (more common in systemic lupus erythematosus, Sjögren syndrome, rheumatoid arthritis, systemic sclerosis, systemic vasculitides, Behçet syndrome, Sarcoidosis, Familial Mediterranean Fever)|
|Pericardial injury syndromes (post-myocardial infarction, post-pericardiotomy syndrome, post-traumatic)|
|Primary tumours (rare, especially pericardial mesothelioma)|
|Secondary metastatic tumours (lung, breast cancer, lymphomas, and melanoma)|
|Metabolic (Uraemia, Myxedema)|
|Direct injury (penetrating thoracic injury, oesophageal perforation, and iatrogenic)|
|Indirect injury (non-penetrating thoracic injury, and radiation injury)|
|Mediastinal radiation, recent, or remote|
|Drugs and toxins (rare): Procainamide, hydralazine, isoniazid, and phenytoin (lupus-like syndrome), Penicillins (hypersensitivity pericarditis with eosinophilia), Doxorubicin and daunorubicin (often associated with a cardiomyopathy, may cause a pericardiopathy). Minoxidil. Immunosuppressive therapies (e.g. methotrexate, cyclosporine)|
|Haemodynamic (heart failure, pulmonary hypertension, and hypoalbuminaemia)|
Our conversation lead us to: Drug-induced lupus. Here are a few highlights:
Epidemiology: 15,000 to 30,000 cases per year.
–> 15 to 20 percent of those taking procainamide, and 7 to 13 percent of those taking hydralazine, to as low as 2 per 1000 for those taking anti-tumor necrosis factor (TNF) agent, and 5 per 10,000 of those taking minocycline.
Pathogenesis: drug metabolism (eg, slow acetylators) and/or immunogenetic characteristics (drug acting as hapten/agonist to T cell, activating lymphocytes, abnormal thymus function)
–> especially patients with (HLA)-DR4, HLA-DR0301, and the complement C4 null allele, slow acetylators.
–> noted to be dose dependent (>100mg daily)
procainamide, hydralazine, minocycline, diltiazem, penicillamine, isoniazid (INH), quinidine, anti-tumor necrosis factor (TNF) alpha therapy (most commonly with infliximab and etanercept), interferon-alfa, methyldopa, chlorpromazine, and practolol. Several others probable+possible.
Diagnosis: history of taking one or more of known drugs for at least one month (often longer) and with the development of at least one clinical feature of SLE. Discontinuation of offending medication resolve symptoms within weeks but sometimes up to several months.
Asking one of our UTSW Rheumatology experts today, Dr. Guillermo Quiceno says that SLE features usually will show early, within the 1st month or months – not likely years. For those with persistent symptoms even after stopping the offending medication may require Plaquenil.
****and REMEMBER from a 2016 post:
Myocarditis: inflammation of the heart muscle
Pericarditis: the inflammation of the lining outside the heart.
Myopericarditis: elevated troponin in the setting of pericarditis without new onset of focal or diffuse depressed LV function by echo or MRI
Perimyocarditis: with new onset of focal or diffused depressed LV function
Remember: Acute pericarditis: dx by the presence of 2 or more: chest pain, pericardial friction rub, ECG changes (diffuse ST-segment elevation or PR depression) and pericardial effusion.
Typical ECG: initially diffuse ST elevation and PR depression, followed by normalization of ST and PR segments, and then diffuse T-wave inversions