Psychosomatics 49:84-85, January-February 2008
doi: 10.1176/appi.psy.49.1.84
© 2008 Academy of Psychosomatic Medicine
Pneumonitis Related to Venlafaxine
M. José Martín Vázquez, M.D., and
Blanca Carretero Quevedo, M.R.
Received February 4, 2006; revised February 22, 2007; accepted February 28, 2007. From the Hospital Son LLatzer, Dept. of Psychiatry, Carretera de Manacor, km 4, 07198, Palma de Mallorca. e-mail: mjmvmnc{at}telefonica.net; mjmartin@hsll.es
© 2008 The Academy of Psychosomatic Medicine
Between 2% and 5% of inpatients in general hospitals need treatment because of adverse reactions to medication. Drugs can cause eosinophilic pneumonitis or hypersensitivity pneumonia after exposure, with improvement of symptoms after stopping exposure. We report a case of a patient with pulmonary and hepatic effects secondary to treatment with venlafaxine. A woman, age 51 years, who was allergic to penicillin but had no toxic exposure, was admitted to the hospital because of 6 months of progressive dyspnea, dry coughing, respiratory sibilances, and pleuritic pain. She had been diagnosed with a depressive anxiety disorder 1 year earlier and was being given antidepressant treatment (mirtazapine, venlafaxine, benzodiazepines) and levothyroxine because of subclinical hypothyroidism. The findings during physical examination were oxygen saturation of 93%, impairment of vesicular murmur, sibilances, tachypnea, and rasping breathing. Follow-up examinations at admission were normal except for increases in gamma-GT (galactosyl transferase) and lactate dehydrogenase (LDH). Although treatment was begun with bronchodilators, corticoids, and levofloxacine, clinic response was minimal. The appearance of important hepatic cytolysis and cholestasis, and pronounced asthenia, lassitude, and erratic pain in the left hemithorax were observed. A pattern of bilateral mosaicism was found in thoracic angioTAC, with altered ventilation/perfusion index and small peripheral subpleural condensations. The respiratory pattern was suggestive of bronchial hyperactivity. Bronchoscopy revealed an increase of lymphocytes, and a low CD4/CD8 index was also found.
Hepatic cytolysis and cholestasis emerged during admission and disappeared when venlafaxine and levofloxacine were discontinued. Hepatitis A, B, and C and HIV serologies, as well as connective-tissue pathology exams were performed with no positive results. The discharge diagnosis was probable pneumonitis related to venlafaxine, with an improvement of mosaic pattern in lung images when treatment was withdrawn. Three months after discharge the patient was examined without pathologic findings.
The patient was evaluated during admission by a liaison psychiatrist because she had been treated for 1 year for depression with a predominance of somatic symptoms. Before discharge, the patient improved noticeably, with a total remission of physical symptoms and mood state.
Our patient’s unspecific pneumonitis had begun after 1 year of treatment with venlafaxine at a dosage of 300 mg per day. An eosinophilic pneumonia with respiratory failure and interstitial pneumonitis with heart failure had been previously reported with venlafaxine treatment.1,2 The causal mechanism can be secondary pulmonary hypertension due to a decrease in serotonin reuptake.3,4 Pulmonary hypertension associated with potent serotonergic drugs has been reported, and this could produce lung fibrosis over time. Metabolism occurs in the respiratory tract, where the venlafaxine concentration could increase, not only because of overdose, but also because of metabolic disorder. The administration of venlafaxine to slow CYP2D6 metabolizers would increase the risk of toxicity. Reactions and interactions between drugs that inhibit cytochrome P450 can cause adverse reactions at usual doses. What is more, drug concentrations in the respiratory tract can be higher than those in plasma, which can also take place with levofloxacine.
Idiopathic lung fibrosis has been connected to previous use of antidepressants, more with tricyclic antidepressants than with selective serotonin reuptake inhibitors (SSRIs), nefazodone, or venlafaxine.
Discontinuing the medication early in these cases would significantly reduce the risk of irreversible fibrosis, although diagnosis can be complicated because symptoms are unspecific. There must be a temporal relationship between clinical presentation and drug administration and an improvement after discontinuing the medication. There are no specific tests to diagnose this lung disorder.
In addition to this syndrome, liver damage appeared in this patient during admission, when levofloxacine was added to treatment, increasing the adverse reaction of the liver to the venlafaxine medication. Hepatitis remitted after discontinuing both drugs. Two cases of hepatitis related to venlafaxine had previously been described,5 and reversible as well as fatal hepatitis have been previously reported with levofloxacine.
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REFERENCES
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- Fleisch MC, Blauer F, Gubler JGH, et al: Eosinophilic pneumonia and respiratory failure associated with venlafaxine treatment. Eur Respir J 2000; 15:205–208[Abstract]
- Drent M, Singh S, Gorgels AP, et al: Drug-induced pneumonitis and heart failure simultaneously associated with venlafaxine. Am J Respir Crit Care Med 2003; 167:958–961[Abstract/Free Full Text]
- Reeve HL, Nelson DP, Archer SL, et al: Effect of fluoxetine, phentermine, and venlafaxine on pulmonary arterial pressure and electrophysiology. Am Rev Respir Dis 1989; 139:247–249[Medline]
- MacLean Margaret R: Endothelin-1 and serotonic mediators of primary and secondary pulmonary hypertension. J Lab Clin Med 1999; 134:105–114[CrossRef][Medline]
- Horsmans Y, De Clercq M, Sempoux C: Venlafaxine-associated hepatitis (letter). Ann Intern Med 1999; 130:944[Free Full Text]
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