“Phenytoin-induced acute hypersensitivity pneumonitis” Lung India 2015 Nov-Dec; 32(6): 631–634.
Lungs are target organs for toxic effects of various drugs due to many reasons. Diphenylhydantoin (DPH) is reported to have many extrapulmonary side effects. We are presenting a case of acute hypersensitivity pneumonitis (HP) secondary to DPH, presenting with respiratory failure. Acute HP with respiratory failure is an uncommon drug side effect of the DPH therapy and is a diagnosis of exclusion. It requires detailed workup and exclusion of other causes along with evidence of improvement in the patient’s condition after withholding DPH.
The lungs remain common targets for toxic effects of drugs due to their large surface area and elaborate dual circulation from pulmonary and bronchial arterial systems. The number of drugs causing lung disease is increasing and more than 380 drugs have been reported to cause lung disease.[1] Diphenylhydantoin (DPH) use is reported to result in various extrathoracic complications.[2] Mediastinal lymphadenopathy is the commonest intrathoracic manifestation while lung parenchymal involvement is rare. Drug hypersensitivity secondary to DPH is well-known to present as rashes, lymphadenopathy, and fever but interstitial pneumonitis is rarely seen.[2]
We are reporting a case of acute hypersensitivity pneumonitis (HP), secondaryto the DPH therapy.
CASE REPORT
A 38-year-old man, nonsmoker, presented with a history of progressive breathlessness for 2 weeks, along with low-grade fever and cough with minimal expectoration. He was on antiepileptics (phenytoin- 100 mg TDS and levetiracetam- 750mg BD) since the past 6 months, for an episode of generalized tonic-clonic seizure (GTCS). Results of the magnetic resonance imaging (MRI) and electroencephalogram (EEG) of brain done then were normal. He had no significant family history. He had no history of exposure to environmental, domestic, or agricultural pollutants or allergic diathesis or drug hypersensitivity reaction in the past.
On examination, the patient was of average built, moderately nourished, with no anemia, icterus, clubbing, cyanosis, peripheral lymphadenopathy, or skin rashes. There was no abnormality on general physical examination. His pulse rate was 90/min, rate of respiration patient was Tachypnoic 24 breaths/min, blood pressure was 110/70 mmHg, and body temperature was 37.4 celcius. His resting oxygen saturation was 88% on room air. Examination of respiratory system revealed bilateral vesicular breath sound with few basal inspiratory crackles. Results of other systemic examinations were unremarkable.
Hematology and biochemistry profile was within normal limits. Hematology and biochemistry profile was withinnormal limits. Chest X-ray(CXR) revealed bilateral diffuse haziness with prominent interstitial markings in the mid and lower zones [Figure 1]. His electrocardiogram (ECG) report was normal ECHO was done, which revealed an ejection fraction of 50% and left ventricular(LV) diastolic dysfunction grade 1. Results of serological tests for human immunodeficiency virus(HIV), hepatitis B surface antigen(HBsAg), hepatitis C virus(HCV), and fever profile were negative. Serum precipitins were negative to molds.