Tuberc Respir Dis.  2011 Mar;70(3):251-256. 10.4046/trd.2011.70.3.251.

A Case of Prothionamide Induced Hepatitis on Patient with Multi-Drug Resistant Pulmonary Tuberculosis

Affiliations
  • 1Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea. pms70@yuhs.ac
  • 2The Institute of Chest Diseases, Yonsei University College of Medicine, Seoul, Korea.
  • 3Department of Pathology, Yonsei University College of Medicine, Seoul, Korea.

Abstract

The prevalence of multi-drug resistant tuberculosis (MDR-TB), which is resistant to isoniazid and rifampin, has been increasing in Korea. And the side effects of 2nd line anti-tuberculosis medications, including drug-induced hepatitis, are well known. Although prothionamide (PTH) is one of the most useful anti-TB medications and although TB medication-induced acute hepatitis is a severe complication, there are only a few published case reports about prothionamide induced hepatitis. In this case report, a 22 year old male was diagnosed with pulmonary MDR-TB and was administered 2nd line anti-TB mediations, including PTH. Afterwards, he had a spiking fever and his liver enzymes were more than 5 times greater than the upper limit of the normal range. He was then diagnosed with drug-induced hepatitis by liver biopsy. His symptoms and liver enzyme elevation were improved after stopping PTH. Accordingly, we report this case of an association between PTH and acute hepatitis.

Keyword

Tuberculosis, Multidrug-Resistant; Hepatitis; Prothionamide

MeSH Terms

Biopsy
Drug-Induced Liver Injury
Fever
Hepatitis
Humans
Isoniazid
Korea
Liver
Male
Prevalence
Prothionamide
Reference Values
Rifampin
Tuberculosis, Multidrug-Resistant
Tuberculosis, Pulmonary
Isoniazid
Prothionamide
Rifampin

Figure

  • Figure 1 (A) Chest PA was performed 8 monthe ago. (B) Chest PA showed progression of consolidation in the left apex compared to previous.

  • Figure 2 Chest CT scans showed necrotizing pneumonia at left lower lobe superior segment (A) and bronchogenic dissemination to the basal segment of left lower lobe (B). It was likely reactive pulmonary tuberculosis.

  • Figure 3 Pathologic findings showed lobular hepatitis presenting severe necroinflammatory activity with perivenular confluent necrosis (A, H&E stain, ×100), prominent eosinophilic infiltration and loose periportal fibrosis (B, H&E stain, ×400). It was consistent with drug induced hepatitis.

  • Figure 4 Flowchart of AST/ALT. There was no change of AST/ALT after taking SM, LFX, CS and PAS, but AST and ALT were increased after taking PTH. SM: streptomycin; LFX: levofloxacine; CS: cycloserine; PAS: paraaminosalicylic acid; PTH: prothionamide.


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