On 10 April 2017, a 77-year-old male was referred to our department for persistent hyperbilirubinaemia and symptoms, including jaundice, tea-coloured urinary ascites and bilateral leg swelling, approximately 3 months after a few trials of initiation, discontinuation, and switching of anti-TB treatment.
Physical examination 1 week prior (3 April 2017), the patient had undergone oesophago-gastro-duodenoscopy and was diagnosed with antral gastritis.
Concerning recent medical history, the patient had undergone a thorax CT (1 February 2017) showing widespread, scattered cystic bronchiectasis, and fibrosis in both lung fields affecting more the right apicoposterior, the lateral segment of the right middle lobe, and all segments in the right lower lobe, the left upper lobe, left inferior lingual, and the whole left lower lobe. Acalculous cholecystitis, multiple liver cysts, right exophytic simple renal cyst, and lumbar spondylosis were also observed.
Clinical and ultrasound follow-up (17 April 2017) showed a liver homogenously increased in echogenicity and smoothness (liver span measured 14.2 cm) and a well-defined anechoic lesion (1.5x1.3 cm) in segment II in keeping with the liver cyst. Biliary trees were not dilated, the gall bladder was well distended, and there was no calculus or wall thickening. The portal vein was patent and not dilated (7 mm in diameter), the pancreas was normal with no peripancreatic mass or collection, and the spleen was homogeneous with no focal lesions (9.5 cm in length). Moderate ascites in the upper abdomen were observed.
Regarding the anti-TB interventions, TB was initially treated as smear-negative pulmonary TB with an EHRZ regimen (1 January 2017), suspended the following month due to deranged liver enzyme activity. The treatment was then resumed with levofloxacin 500 mg once daily and changed to a regimen with streptomycin, ethambutol and moxifloxacin on 5 March 2017; 2 months later (26 April 2017), streptomycin therapy was disrupted and replaced by Augmentin 1.2 g three-times daily (TDS) a few days after. Within 3 weeks (22 May 2017), the treatment was stopped due to the severity of adverse drug reactions from medications.
At the physician's examination (10 April 2017), hepatomegaly was palpable and jaundice was present. The patient's whole clinical picture suggested that the clinical features were in keeping with fatty liver disease with a simple liver cyst, and biochemical abnormalities were suggestive of DILI due to anti-TB treatment. To manage liver enzyme activity, the patient was prescribed treatment with silymarin 140 mg TDS for 3 months (10 April to 3 July 2017) because no other treatment-suitable options were available, and the patient was not eligible for clinical trials due to his medical conditions.
In routine biochemical and liver function tests (Table 1), altered liver enzyme levels were progressively decreasing, and, at the follow-up visit (17 July 2018), AST and alkaline phosphatase (ALP) levels, in particular, were significantly reduced (Table 1).
The patient's clinical events are summarized in Table 2.