A 48-year-old Chinese construction worker presented to the orthopaedic unit with a 1-month history of bilateral lower limbs weakness, numbness, pain, and progressive difficulty in walking. His past medical history included smear-negative pulmonary tuberculosis 2 years ago, for which he completed 6 months of anti-TB treatment. Four months prior to this presentation, he was diagnosed with right eye scleritis and 1 month later he diagnosed with "late onset of bronchial asthma" when he presented with recurrent cough and difficulty in breathing. He denied any history of alcohol consumption, recreational drug abuse, or use of traditional medication. He was a chronic smoker (20 packs per year), was married, and had 2 children.
Physical examination showed that he was afebrile, with the blood pressure of 130/80 mmHg. There were no oral ulcers, malar rash, or alopecia, but he had a vasculitic rash on his palms and feet. His left upper limb and both lower limbs appeared wasted, with bilateral foot drop. Cardiorespiratory examination revealed a systolic murmur at the left sternal edge and bronchial breath sounds bilaterally in the upper zones with no rhonchi. Results of abdominal examination were unremarkable.
Hemoglobin: 11.2 g/dl (14.0-17.0),
White cell count: 16.2x109/L (4.0-10.0),
Platelet: 752x109/L (150-400),
Eosinophil: 3.1x109/L (0.02-0.5),
Full blood count: 
Urea: 6.6 mmol/L (2.5-6.4),
Sodium: 131 mmol/L (135-150),
Potassium: 5.1 mmol/L (3.5-5.0),
Creatinine: 116 umol/L (62-106),
Calcium: 2.23 mmol/L (2.14-2.58),
Renal Profile: 
Total Protein: 72 g/L (67-88),
Albumin: 31 g/L (35-50),
Alkaline Phosphatase (ALP): 190 U/L (32-104),
Alalinetransaminase (ALT): 27 U/L (<44),
Erythrocyte Sedimentation Rate (ESR): 119 mm/hr.
Liver Function Test (LFT): 
His initial lab results were: 
His chest X-ray is shown in Figure 1.
He treated as having reactivation of pulmonary TB with possible spinal TB spine with involvement of L4/L5 nerve root compression with 4 anti-TB medications. However, he remained febrile in the ward and a CT scan of the thorax revealed a large cavity in the apical segment, measuring 4.9x4.8x3.5 cm, with an intracavitary lesion measuring 1.9x1.1 cm. (Figure 2).
There were multiple cystic air spaces in his right upper lobe, with thickened bronchial wall and traction fibrotic bands - cystic bronchiectasis and multiple nodules in the right middle lobe, the left upper lobe, and lower the lobe. The overall impression was of right apical old pulmonary TB changes with Mycetoma and cystic bronchiectasis. Oral itraconazole 200 mg bd was started. Aspergillus antibody was positive and bronchial alveolar lavage grew candida albicans.
Nerve conduction study revealed an axonal sensory-motor polyneuropathy over both lower limbs and a left ulnar neuropathy at the elbow. A diagnosis of chronic inflammatory demyelinating polyneuropathy secondary to possible vasculitis with multiorgan involvement was considered. Autoimmune screening showed a negative antinuclear antibody (ANA) and normal complement levels but positive rheumatoid factor. His eosinophilia was persistently elevated (3.1x109/L) and c-ANCA was positive. His urine analysis showed protein 1+ and blood 3+ with a 24-hour urine protein excretion of 1 g/day. Sural nerve biopsy was suggestive of vasculitis. The diagnosis of granulomatosis with polyangiitis involving nerves, lungs, and kidneys was considered. He was empirically treated with high-dose pulse methylprednisolone and a few sessions of plasma exchange as his kidney function progressively deteriorated. He also required intermittent hemodialysis. An urgent renal biopsy was planned but, unfortunately, he developed acute chest pain with an acute coronary syndrome. Echocardiogram demonstrated an ejection fraction of 20% with global hypokinetic walls, dilated chambers, moderate mitral regurgitation, and severe tricuspid regurgitation.
He was started on low-dose IV cyclophosphamide 200 mg due to concomitant respiratory infection and renal failure. He developed severe epigastric pain, dyspnea, and diarrhoea 3 hours after completion of IV cyclophosphamide, which resolved after 4 hours with symptomatic treatment. His liver enzymes showed a sudden elevation of alalinetransaminase (ALT) from 41 U/L to 336 U/L the next day and peaked at 568 U/L 4 days after administration of IV cyclophosphamide.
His anti-TB and antifungal medications were withheld and a liver ultrasound showed normal liver echotexture. Hepatitis B and C and HIV screening results were negative. His ALT improved to 104 U/L after 2 weeks of treatment and we proceeded with a second dose of IV cyclophosphamide 200 mg. He complained of similar symptoms following this and his ALT rose to 1253 U/L the next day. A diagnoses of cyclophosphamide-induced hepatitis was made. Cyclophosphamide was stopped. We were unable to perform a liver biopsy due to a coagulopathy. The trend of his liver enzyme (ALT) is shown in Figure 3. Subsequently, the patient developed hospital-acquired pneumonia and died due to another episode of acute coronary syndrome.