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GLASGOW, SCOTLAND — Sulfasalazine should be added to the list of drugs that can interfere with assays of urinary catecholamines and their metabolites, Dr. Clive Kelly reported at the annual meeting of the British Society for Rheumatology.
Several medications—including tricyclic antidepressants, antipsychotics, and levodopa—can cause false-positive results when assays for normetanephrine and metanephrine are undertaken to rule out pheochromocytoma. The effect of sulfasalazine on the results of urinary catecholamine assays has not thus far been reported in the literature or to the manufacturers, according to Dr. Kelly, who heads the department of rheumatology, Queen Elizabeth Hospital, Gateshead, Tyne and Wear, England.
In one such case of a false-positive pheochromocytoma result, a 48-year-old man with well-controlled rheumatoid arthritis was admitted with a blood pressure reading of 210/130 mm Hg. He had been taking sulfasalazine for 6 years and was then on 1 g/day. His other medications included Calcichew D3 (calcium carbonate plus vitamin D3), cimetidine, and thyroxine. Initial investigations found nothing remarkable, Dr. Kelly said, but following a 24-hour urine collection, a high-performance liquid chromatography assay found significantly increased levels of normetanephrine at 60.8 μmol/day (the normal range is less than 3.2 μmol/day).
Three repeated analyses during the subsequent 5 months produced similar results, despite that neither MRI nor metaiodobenzylguanidine scintigraphy showed any evidence of a pheochromocytoma, Dr. Kelly wrote in a poster.
To further examine the influence of sulfasalazine on urine collections for fractionated metanephrines, he and his colleagues then prospectively recruited 10 rheumatoid arthritis patients on sulfasalazine who were not hypertensive and were not taking antihypertensive drugs, and 10 age- and sex-matched controls who also were not hypertensive but were not taking sulfasalazine. Both groups provided 24-hour urine collections, which were then analyzed using standard techniques.
The mean level of normetanephrine in the sulfasalazine group was 17.3 μmol/day, compared with 2.4 μmol/day in the control group. The pheochromocytoma false-positive rate was 80% in the sulfasalazine group and 20% in the control group, Dr. Kelly reported. Normetanephrine elevations were not dose dependent.
“We suspect that a metabolite of sulfasalazine forms a peak on the chromatogram close to the position of normetanephrine and is therefore easily misidentified,” he wrote. An alternative explanation is that sulfasalazine may increase endogenous loads of catecholamines or their metabolites.
GLASGOW, SCOTLAND — Sulfasalazine should be added to the list of drugs that can interfere with assays of urinary catecholamines and their metabolites, Dr. Clive Kelly reported at the annual meeting of the British Society for Rheumatology.
Several medications—including tricyclic antidepressants, antipsychotics, and levodopa—can cause false-positive results when assays for normetanephrine and metanephrine are undertaken to rule out pheochromocytoma. The effect of sulfasalazine on the results of urinary catecholamine assays has not thus far been reported in the literature or to the manufacturers, according to Dr. Kelly, who heads the department of rheumatology, Queen Elizabeth Hospital, Gateshead, Tyne and Wear, England.
In one such case of a false-positive pheochromocytoma result, a 48-year-old man with well-controlled rheumatoid arthritis was admitted with a blood pressure reading of 210/130 mm Hg. He had been taking sulfasalazine for 6 years and was then on 1 g/day. His other medications included Calcichew D3 (calcium carbonate plus vitamin D3), cimetidine, and thyroxine. Initial investigations found nothing remarkable, Dr. Kelly said, but following a 24-hour urine collection, a high-performance liquid chromatography assay found significantly increased levels of normetanephrine at 60.8 μmol/day (the normal range is less than 3.2 μmol/day).
Three repeated analyses during the subsequent 5 months produced similar results, despite that neither MRI nor metaiodobenzylguanidine scintigraphy showed any evidence of a pheochromocytoma, Dr. Kelly wrote in a poster.
To further examine the influence of sulfasalazine on urine collections for fractionated metanephrines, he and his colleagues then prospectively recruited 10 rheumatoid arthritis patients on sulfasalazine who were not hypertensive and were not taking antihypertensive drugs, and 10 age- and sex-matched controls who also were not hypertensive but were not taking sulfasalazine. Both groups provided 24-hour urine collections, which were then analyzed using standard techniques.
The mean level of normetanephrine in the sulfasalazine group was 17.3 μmol/day, compared with 2.4 μmol/day in the control group. The pheochromocytoma false-positive rate was 80% in the sulfasalazine group and 20% in the control group, Dr. Kelly reported. Normetanephrine elevations were not dose dependent.
“We suspect that a metabolite of sulfasalazine forms a peak on the chromatogram close to the position of normetanephrine and is therefore easily misidentified,” he wrote. An alternative explanation is that sulfasalazine may increase endogenous loads of catecholamines or their metabolites.
GLASGOW, SCOTLAND — Sulfasalazine should be added to the list of drugs that can interfere with assays of urinary catecholamines and their metabolites, Dr. Clive Kelly reported at the annual meeting of the British Society for Rheumatology.
Several medications—including tricyclic antidepressants, antipsychotics, and levodopa—can cause false-positive results when assays for normetanephrine and metanephrine are undertaken to rule out pheochromocytoma. The effect of sulfasalazine on the results of urinary catecholamine assays has not thus far been reported in the literature or to the manufacturers, according to Dr. Kelly, who heads the department of rheumatology, Queen Elizabeth Hospital, Gateshead, Tyne and Wear, England.
In one such case of a false-positive pheochromocytoma result, a 48-year-old man with well-controlled rheumatoid arthritis was admitted with a blood pressure reading of 210/130 mm Hg. He had been taking sulfasalazine for 6 years and was then on 1 g/day. His other medications included Calcichew D3 (calcium carbonate plus vitamin D3), cimetidine, and thyroxine. Initial investigations found nothing remarkable, Dr. Kelly said, but following a 24-hour urine collection, a high-performance liquid chromatography assay found significantly increased levels of normetanephrine at 60.8 μmol/day (the normal range is less than 3.2 μmol/day).
Three repeated analyses during the subsequent 5 months produced similar results, despite that neither MRI nor metaiodobenzylguanidine scintigraphy showed any evidence of a pheochromocytoma, Dr. Kelly wrote in a poster.
To further examine the influence of sulfasalazine on urine collections for fractionated metanephrines, he and his colleagues then prospectively recruited 10 rheumatoid arthritis patients on sulfasalazine who were not hypertensive and were not taking antihypertensive drugs, and 10 age- and sex-matched controls who also were not hypertensive but were not taking sulfasalazine. Both groups provided 24-hour urine collections, which were then analyzed using standard techniques.
The mean level of normetanephrine in the sulfasalazine group was 17.3 μmol/day, compared with 2.4 μmol/day in the control group. The pheochromocytoma false-positive rate was 80% in the sulfasalazine group and 20% in the control group, Dr. Kelly reported. Normetanephrine elevations were not dose dependent.
“We suspect that a metabolite of sulfasalazine forms a peak on the chromatogram close to the position of normetanephrine and is therefore easily misidentified,” he wrote. An alternative explanation is that sulfasalazine may increase endogenous loads of catecholamines or their metabolites.