Measurements of plasma metanephrines and methoxytyramine provide a sensitive test for diagnosis of pheochromocytoma/paraganglioma. False-positive results remain a problem, particularly in patients taking norepinephrine reuptake-blocking drugs. Therefore, in this retrospective observational study, we measured plasma metanephrines and methoxytyramine in 61 patients taking norepinephrine reuptake blockers (tricyclic antidepressants or serotonin–norepinephrine reuptake inhibitors) and 17 others taking selective serotonin reuptake inhibitors, all without pheochromocytoma/paraganglioma. We highlight a singular case with strongly elevated plasma normetanephrine and methoxytyramine concentrations associated with norepinephrine reuptake blockade. Data were compared to results from 252 and 1804 respective patients with and without tumors. Plasma normetanephrine was 40% higher (P < 0.0001) in patients on norepinephrine reuptake blockers and methoxytyramine was 127% higher (P = 0.0062) in patients taking tricyclic antidepressants compared to patients not taking uptake blockers and without tumors. The corresponding false-positive rates rose (P < 0.0001) from 4.8% to 23.0% for normetanephrine and from 0.9% to 28.6% for methoxytyramine. Selective serotonin reuptake inhibitors did not increase plasma concentrations of metabolites. In the highlighted case, plasma normetanephrine and methoxytyramine were elevated more than six times above upper reference limits. A pheochromocytoma/paraganglioma, however, was excluded by functional imaging. All biochemical test results normalized after discontinuation of norepinephrine reuptake blockers. These findings clarify that norepinephrine reuptake blockers usually result in mild elevations of normetanephrine and methoxytyramine that, nevertheless, significantly increase the number of false-positive results. There can, however, be exceptions where increases in normetanephrine and methoxytyramine reach pathological levels. Such exceptions may reflect failure of centrally mediated sympathoinhibition that normally occurs with the norepinephrine reuptake blockade.

血浆变肾上腺素和甲氧基酪胺的测量为嗜铬细胞瘤/副神经节瘤的诊断提供了灵敏的测试。假阳性结果仍然是一个问题，特别是对于服用去甲肾上腺素再摄取阻断药物的患者。因此，在这项回顾性观察研究中，我们测量了 61 名服用去甲肾上腺素再摄取阻滞剂（三环类抗抑郁药或 5-羟色胺-去甲肾上腺素再摄取抑制剂）的患者和另外 17 名服用选择性 5-羟色胺再摄取抑制剂的患者的血浆变肾上腺素和甲氧基酪胺，所有患者均未患有嗜铬细胞瘤/副神经节瘤。我们重点介绍一个与去甲肾上腺素再摄取阻断相关的血浆去甲肾上腺素和甲氧基酪胺浓度大幅升高的奇异病例。将数据与分别来自 252 名和 1804 名患有和不患有肿瘤的患者的结果进行比较。与未服用去甲肾上腺素再摄取阻滞剂且无肿瘤的患者相比，服用去甲肾上腺素再摄取阻滞剂的患者血浆去甲肾上腺素升高 40%（P < 0.0001），服用三环类抗抑郁药的患者血浆去甲酪胺升高 127%（ P  = 0.0062）。去甲肾上腺素的相应假阳性率从 4.8% 上升至 23.0%，甲氧基酪胺从 0.9% 上升至 28.6%（P < 0.0001）。选择性血清素再摄取抑制剂不会增加代谢物的血浆浓度。在突出显示的病例中，血浆去甲肾上腺素和甲氧基酪胺升高超过参考上限六倍以上。然而，功能成像排除了嗜铬细胞瘤/副神经节瘤。停用去甲肾上腺素再摄取阻滞剂后，所有生化测试结果均恢复正常。这些发现阐明，去甲肾上腺素再摄取阻滞剂通常会导致去甲肾上腺素和甲氧基酪胺轻度升高，然而，这会显着增加假阳性结果的数量。然而，也有例外情况，即去甲肾上腺素和甲氧基酪胺的增加达到病理水平。这种异常可能反映了中枢介导的交感神经抑制的失败，这种抑制通常伴随去甲肾上腺素再摄取阻断而发生。