The patient under consideration was diagnosed with postoperative acute gouty arthritis secondary to thiazide intake. Within 2 days, there was an improvement in the patient's condition after the immediate withdrawal of hydrochlorothiazide.

The patient had no history of early morning stiffness of small joints, fever or trauma, but she complained of bilateral knee pain for the past 3 years, dull aching and worsening on mild physical exertion. On further questioning, she gave a previous surgical history of lumbar vertebral disc prolapse 15 years ago, hysterectomy 5 years ago and incisional hernia below umbilicus 5 days ago. She had a history of hypertension which had been treated with hydrochlorothiazide for the past 3 years.

On examination, the patient was obese with a body mass index of 35 kg/m². She was a vegetarian and her appetite was good, and sleep was undisturbed. Bowel and bladder functions were normal and regular. Her pulse rate was 84 beats/min, blood pressure was 150/80mm Hg and cardiovascular, respiratory, central nervous systems and abdomen were found to be normal. On investigation, her biochemical parameters were within normal limits. Local examination revealed redness, swelling, and warmth in the dorsal aspect of the left foot and tenderness at the first metatarsophalangeal joint. Range of movement was found to be painful and restricted. In view of the patient's typical history and local examination findings, it was thought that she might have suffered from crystal arthritis secondary to prolonged intake of hydrochlorothiazide, and precipitated by surgical stress.

She was provisionally diagnosed as having postoperative acute gouty arthritis secondary to thiazide intake. The patient had a negative past history and family history of gout. Hydrochlorothiazide was immediately withdrawn following the attack and improvement of the patient's condition was noticed within 2 days. The patient was not commenced on any specific treatment for gout. Re-determination of blood uric acid level was performed after 2 weeks and it was found to be 0.25 mmol/L. On follow-up, there were no further complaints and the patient was discharged.

Gout is a clinical syndrome caused by deposition of monosodium urate mono-hydrate crystals in the synovial joints. Diuretics are the most common cause of secondary gout and it is being used in over 75% of the patients with late-onset gout. Thiazides contribute to an elevated serum urate level through a combination of volume depletion and decreased renal tubular secretion. Gouty arthritis can be precipitated by diverse factors such as trauma, surgery, infection, fever, dietary indiscretion and administration of drugs such as penicillin, sulfonamides and ergotamine. If the amount of synovial fluid increases due to trauma or edema, then urate levels within the joint may temporarily rise after re-absorption of water. The exact mechanism of postoperative gout attack is not clearly understood. It usually develops within 14 days of surgery and in this case, it was observed after 5 days.

Other clinical features of postoperative gout attacks include involvement of the lower extremity joints, particularly the first metatarsophalangeal joint. Most attacks are usually monoarticular with the number of affected joints correlating with the total number of previously involved joints. Although new joints may be involved, the site of attacks usually corresponds to previously affected sites. These clinical features are consistent with the features of gouty podagra the patient had suffered following her surgery.

The level of blood uric acid in this patient was determined to be 0.53 mmol/L. This was in accord with the findings from previous studies, which reported that the blood uric acid levels when symptoms of gout are present ranges from 0.32 to 0.71 mmol/L. In hyperuricemia patients, the serum urate levels exceed their solubility limit. Sodium concentration in the extracellular fluid is supersaturated by monosodium urate at concentrations greater than 0.37 mmol/L. Above this limit, there is a significant risk for crystallization of sodium urate in soft tissues and joints which forms deposits called tophi, causing an inflammatory reaction and acute gouty arthritis.

Gout is commonly seen in men but most of the patients who are newly diagnosed with gout in 60 years are women. This may be attributed to the key role played by estrogen in protecting pre-menopausal women from hyperuricemia and gout, by enhancing renal urate excretion. A strong association between female patients with gout and some pre-existing joint disorders, mainly, osteoarthritis has been determined. Our patient had complained of bilateral knee pain for the past 3 years, a dull ache which worsened with mild physical activities, also suggestive of osteoarthritis. Development of gout can also be attributed to obesity. Her BMI was estimated to be 35 kg/m². Several studies evaluating the risk factors for hyperuricemia and gout, not its association with obesity, possibly by increasing the production and decreasing the renal excretion of urate. Diet has also been suspected of affecting the serum uric acid level. A high purine-rich diet is reported to produce a small and transient increase in uric acid levels by 0.05–0.11 mmol/L. Our patient was a vegetarian and several studies suggest that while increased dietary consumption of meat and seafood are associated with high serum uric acid levels, intake of food from plant sources, dairy products and coffee are inversely associated with the risk of hyperuricaemia and gout. Moreover, the isocaloric diet during hospitalization should have a protective effect as it is known to reduce serum uric acid levels by 0.05–0.11 mmol/L when given for 7–10 days. 

Hypertension may also play an additive role in the development of gout. This condition itself is associated with reduced renal blood flow, increased renal and systemic vascular resistance and poor renal clearance of urate, leading to hyperuricaemia. However, the patient's renal parameters were found to be normal. The risk of drug-induced gout appears to be thiazide dose-related. Our patient was prescribed a total daily dose of 25 mg; thus, she had an increased risk of a gout attack. She was also taking other anti-hypertensive medications (telmisartan and amlodipine). Research shows that the risk of gout is increased when thiazide diuretics are combined with any other non-thiazide anti-hypertensive medication. Moreover, non-losartan angiotensin II receptor blockers such as telmisartan have also been found to be associated with an increased risk of gout, but to a lesser degree than diuretics. There are several agents available for the treatment of gout. However, our patient did not receive any specific treatment, as these treatments are only recommended for patients who have more than two to three gouty attacks per year.

Although catabolic events are known to precipitate gout, postoperative attacks of gout have rarely been reported, especially in patients with no prior history of gout. A classic podagra is also relatively uncommon. The present case has highlighted the importance of monitoring the blood uric acid level pre and postoperatively in an individual on thiazide diuretics. It also helps to create awareness of the various risk factors associated with gout.

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