Carbamazepine
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Reactions 1355 - 11 Jun 2011 S Carbamazepine Agammaglobulinaemia and diffuse panbronchiolitis: case report A 61-year-old man developed agammaglobulinaemia and diffuse panbronchiolitis during treatment with carbamazepine for seizures. The man’s medical history was notable for removal of a meningioma and surgery for a postoperative epidural abscess 2 years prior to admission with respiratory symptoms. He had experienced several seizures perioperatively and carbamazepine had been started with excellent seizure control [dosage and route not stated]. He presented with a 3-month history of exertional dyspnoea and productive cough. Physical examination revealed a BP of 136/67mm Hg, a pulse of 110/min, fever (38.3°C) and coarse crackles bilaterally on chest auscultation. Investigations detected marked decreases in serum immunoglobulin levels (IgG, IgA and IgM 46, < 5 and < 5 mg/dL, respectively), CD4 T cell lymphopenia, an abnormal CD4:CB8 T cell ratio and a complete absence of CD19 B cells. His carbamazepine concentration was in the therapeutic range. Lung and brain CT showed multiple centrilobular lesions and maxillary sinusitis, respectively. Sputum cultures grew Haemophilus influenzae. Arterial blood gas analysis showed PCO2 and PO2 values of 37.4 and 74.6mm Hg, respectively, and lung function testing showed an obstructive pattern. Diffuse panbronchiolitis was diagnosed. Valproic acid was substituted for carbamazepine, which was considered the most likely cause of agammaglobulinaemia. The man received gammaglobulin supplementation (targeting a serum IgG level > 500 mg/dL) as well as a 10-day course of cefotaxime. He was afebrile by hospital day 8 and was discharged on day 28. Long-term therapy with clarithromycin was started on completing the cefotaxime course and supplemental gammaglobulin was continued. His serum IgG normalised while his IgA and IgM levels remained low 5 months after stopping carbamazepine. Six months postdiscontinuation, repeat lung CT showed resolution of the centrilobular lesions. Author comment: "In the present case, humoral immunodeficiency could have increased susceptibility to the H influenza infection responsible for inflammation centred on the respiratory bronchiole and adjacent centrilobular regions." Hoshino C, et al. Carbamazepine-induced agammagloblinaemia clinically mimicking diffuse panbronchiolitis. BMJ Case Reports : 2011. Available from: URL: http://dx.doi.org/10.1136/bcr.11.2010.3535 - Japan 803055469 1 Reactions 11 Jun 2011 No. 1355 0114-9954/10/1355-0001/$14.95 © 2010 Adis Data Information BV. All rights reserved
Transcript of Carbamazepine
Reactions 1355 - 11 Jun 2011
SCarbamazepine
Agammaglobulinaemia and diffusepanbronchiolitis: case report
A 61-year-old man developed agammaglobulinaemiaand diffuse panbronchiolitis during treatment withcarbamazepine for seizures.
The man’s medical history was notable for removal of ameningioma and surgery for a postoperative epiduralabscess 2 years prior to admission with respiratorysymptoms. He had experienced several seizuresperioperatively and carbamazepine had been started withexcellent seizure control [dosage and route not stated]. Hepresented with a 3-month history of exertional dyspnoeaand productive cough. Physical examination revealed a BPof 136/67mm Hg, a pulse of 110/min, fever (38.3°C) andcoarse crackles bilaterally on chest auscultation.Investigations detected marked decreases in serumimmunoglobulin levels (IgG, IgA and IgM 46, < 5 and< 5 mg/dL, respectively), CD4 T cell lymphopenia, anabnormal CD4:CB8 T cell ratio and a complete absence ofCD19 B cells. His carbamazepine concentration was in thetherapeutic range. Lung and brain CT showed multiplecentrilobular lesions and maxillary sinusitis, respectively.Sputum cultures grew Haemophilus influenzae. Arterialblood gas analysis showed PCO2 and PO2 values of37.4 and 74.6mm Hg, respectively, and lung functiontesting showed an obstructive pattern. Diffusepanbronchiolitis was diagnosed.
Valproic acid was substituted for carbamazepine, whichwas considered the most likely cause ofagammaglobulinaemia. The man received gammaglobulinsupplementation (targeting a serum IgG level > 500 mg/dL)as well as a 10-day course of cefotaxime. He was afebrile byhospital day 8 and was discharged on day 28. Long-termtherapy with clarithromycin was started on completing thecefotaxime course and supplemental gammaglobulin wascontinued. His serum IgG normalised while his IgA and IgMlevels remained low 5 months after stoppingcarbamazepine. Six months postdiscontinuation, repeatlung CT showed resolution of the centrilobular lesions.
Author comment: "In the present case, humoralimmunodeficiency could have increased susceptibility to theH influenza infection responsible for inflammation centred onthe respiratory bronchiole and adjacent centrilobular regions."Hoshino C, et al. Carbamazepine-induced agammagloblinaemia clinicallymimicking diffuse panbronchiolitis. BMJ Case Reports : 2011. Available from:URL: http://dx.doi.org/10.1136/bcr.11.2010.3535 - Japan 803055469
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Reactions 11 Jun 2011 No. 13550114-9954/10/1355-0001/$14.95 © 2010 Adis Data Information BV. All rights reserved
