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Hydralazine
General information
Hydralazine is a direct vasodilator that acts on vascular smooth muscle to produce systemic vasodilatation. As a result there is baroreceptor-mediated activation of the sympathetic nervous system and the renin–angiotensin system.
Vasodilators (as monotherapy) are associated acutely with flushing, headache, dizziness, reflex tachycardia, and palpitation. Chronic treatment can be complicated by fluid retention.
Organs and systems
Cardiovascular
Aggravation of angina, presumably as a result of reflex tachycardia, has been reported with hydralazine.
Pericarditis has been attributed to hydralazine in a 75-year-old man who developed a full-blown hydralazine-induced autoimmune syndrome [ ]. The authors referred to a similar previously published case of late pericarditis after hydralazine treatment.
Respiratory
Hydralazine can cause a lupus-like syndrome and a fatal case of hydralazine-associated lupus pneumonitis has been reported [ ].
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A 36-year-old African–American woman developed fatigue, dyspnea on exertion, weakness, dizziness, and arthralgias. She had taken atenolol, clonidine, nifedipine, fosinopril, and hydralazine 100 mg/day for hypertension. Computed tomographic chest imaging 5 months before for an incidental bony abnormality had shown ground glass abnormalities in the lower lobes of both lungs. She was hypotensive and hypoxic. Her antihypertensive medications were withdrawn. Blood tests showed an inflammatory response and raised lactate dehydrogenase and serum transaminase activities. Further chest imaging showed bilateral alveolar infiltrates and small pleural effusions. Despite treatment with broad-spectrum antibiotics she required invasive ventilation by the third day of admission. In the absence of evidence of vasculitis or pulmonary hemorrhage, she was given methylprednisolone and underwent one cycle of plasmapheresis for presumed lupus pneumonitis. She died despite full intensive care support on the fourth hospital day. Post-mortem laboratory results confirmed the presence of antinuclear, antihistone, and anti-single stranded DNA antibodies. There was organized diffuse alveolar damage and evidence of pericarditis.
The authors acknowledged that a definite diagnosis of drug-induced lupus could not be made, as the patient had died before the effects of drug withdrawal could be known. However, several features of her presentation supported the presumed diagnosis, including a typical immune profile and no obvious renal involvement.
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