A 28 year old male student of Nepalese origin living in the United Kingdom for 3 years presented to the Accident and Emergency department with a 3 week history of increasing right hip pain, with associated fevers but no other symptoms and no history of trauma. 5 years previously, he had been treated for pulmonary tuberculosis with a 6 month course of chemotherapy. There was no positive family history. The remaining history was unremarkable.
On admission he was partially weight bearing on the affected side. On inspection there were no signs of inflammation. Flexion was limited to100 degrees; extension to 20 degrees; internal and external rotation were reduced to 10 degrees with normal adduction and abduction. There were no further positive findings on the remainder of physical examination or X-ray (figure 1).
Blood results on admission were haemoglobin 12.5 g/dl (12.5–18.0 g/dl), white cell count 6.47 (4.0–11.0 × 109/l), Platelets 378 (150–400 × 109/l), C reactive protein (CRP) 205 (<5 mg/l), Erythrocyte sedimentation rate (ESR) 96 (2–12 mm/1st hour). His biochemistry revealed an alkaline phosphatase (ALP) 342 (30–300 iu/L), bilirubin 15 (3–17 μmol/L), alanine aminotransferase (ALT) 45 (3–35 iu/L), aspartate transaminase (AST) 42 (3–35 iu/L), corrected calcium 2.82 (2.12–2.65 mmol/L), lactate dehydrogenase (LDH) 782 (iu/L). Renal function was normal.
An Ultrasound of the hip revealed a moderate right sided joint effusion. Magnetic resonance imaging (MRI) of the pelvis and hips (figure 2) confirmed the effusion with marked soft tissue swelling and synovial thickening. There was oedema in the proximal femur.
Our working diagnosis was septic arthritis, with tuberculosis of the hip as a differential, in view of his past medical history. He was thus managed accordingly with a washout and commenced on chemotherapy. Microbiology of the synovial fluid revealed no organisms; auramine tests were repeatedly negative, as was syphilis serology, Human Immunodeficiency Virus (HIV), Hepatitis and melioidosis.
There was little clinical response to treatment and inflammatory markers 2 weeks after admission were elevated at a CRP of 130 and ESR of 114.
He then developed an episode of diarrhoea and vomiting as an inpatient. Initial investigations for amoeba, cysts, ova, parasites were all negative. Colonoscopy was undertaken and revealed a stricture in the sigmoid colon. Multiple biopsies revealed a moderately to poorly differentiated adenocarcinoma on histological examination. An immunohistochemical panel showed the tissue to be cytokeratin 20 (CK-20) positive, cytokeratin 7 (CK-7) negative and villin negative, thus in keeping with a colorectal primary tumour. Carcinoembryonic antigen (CEA) was measured at 100.7. Genetic screening and microsatellite instability (MSI) testing on the tumour were negative.
The synovial fluid was re-examined for cytology following the histological diagnosis and this confirmed a malignant joint effusion.
A computerised tomogram (CT) revealed multiple para-aortic lymph nodes, with no evidence of metastases other solid organs. A bone scan (figure 3) revealed high uptake areas in the skull vault, spine, ribs, pelvis, proximal ends of both femurs and sternum; all in keeping with widespread metastatic disease.
In view of the advanced nature of the adenocarcinoma the primary tumour was not resected and he was commenced on Oxaliplatin 130 mg/m2 (day one of cycle) and Capecitabine 1.25 g/m2 (twice daily for fourteen days) for a planned eight cycles (each cycle of twenty-one days). He responded well initially with an improvement symptomatically after 2 cycles of chemotherapy, and objectively on computerised tomogram (CT) of his abdomen and pelvis with reduction in the size and number of significant lymph nodes. However was unable to tolerate more than 3 cycles and died 4 months after his initial presentation.