Clinical Geriatrics

CASE PRESENTATION
A 74-year-old white male was referred to the ophthalmologist with a 3-week history of difficulty in reading and diminution of vision. He also complained of a right-sided headache, which was throbbing in nature and episodic, each episode lasting a few hours. On direct questioning his wife said that he had been getting progressively more tired over the past few weeks. There was no apparent loss of weight. He had no history of shoulder stiffness or joint pains or any other significant past medical history. Clinical examination revealed vision of 20/60 in each eye with glasses. No obvious acute ocular problem was identified. There was tenderness over the right temporal artery. Investigations revealed an elevated erythrocyte sedimentation rate (ESR) of 77 mm in the first hour. Based on a clinical diagnosis of temporal arteritis (TA), he was started on oral prednisolone 50 mg once daily. The ophthalmologist referred the patient to us for further management and follow-up of TA.

When seen in the outpatient clinic 1 month later, his symptoms had improved remarkably since the start of steroids. Clinical examination showed the patient in good health; he was afebrile and had mild hypertension. Temporal arteries were nontender and pulsatile. Systemic examination of chest, cardiovascular system, and abdomen was unremarkable. Further investigations showed complete blood count (CBC), liver function tests, renal function tests, and thyroid function tests to be normal. The ESR showed a decline from previous results. Oral steroids were continued and osteoporosis prophylaxis was initiated.

He was regularly followed in the outpatient clinic. Over the next 6 months, his steroid dose was gradually tapered in view of clinical improvement and fall in ESR. At the end of 6 months’ treatment, he had one relapse of his symptom of headache associated with a further rise in ESR. An increase in the steroid dose improved the symptoms.

Subsequently, about 9 months following his first visit, while still on steroids, he complained of loss of appetite and weight and low back pain but denied any headaches. Clinically, he had a mild cushingoid appearance. Chest examination revealed scattered crackles over bases and a firm hepatomegaly 4 cm below coastal margin. Investigations revealed normal CBC. The ESR was further elevated to 71 mm in the first hour. Chest x-ray showed multiple nodular lesions suggestive of metastatic lung disease. Ultrasound of the abdomen showed metastatic deposits in liver parenchyma. The histology of the liver lesions revealed poorly differentiated adenocarcinoma. On immunophenotyping, the tumor cells showed strong membrane expression of cytokeratin 7 and 20, which is commonly associated with pancreatic, nonperipheral cholangiocarcinoma and gastric adenocarcinoma. Further investigations to locate the primary cause were not undertaken. He was commenced on chemotherapy for metastatic malignancy. He is currently receiving palliative therapy with oral capecitabine.

DISCUSSION
Our case patient presented with typical clinical features of TA that, although not biopsy-proven, had a good clinical and laboratory response to high-dose steroids. Subsequently, he was found to have an underlying malignancy. This association prompted us to search the literature for any evidence of a relationship between TA and malignancy. Does this relationship exist? If so, what is the nature—is it causal or coincidental? Is TA a paraneoplastic manifestation or a premalignant condition? Is there any underlying common pathogenetic mechanism? How far should a patient with TA be investigated for occult malignancy?