Elevated urinary catecholamines and adrenal haemorrhage mimicking phaeochromocytoma

Wordsworth, Simon; Thomas, Ben; Agarwal, Neera; Hoddell, Kate; Davies, Sara

doi:10.1136/bcr.01.2010.2612

Cited by 5 publications

(3 citation statements)

References 11 publications

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“…Evidence of elevated urinary excretion of metanephrine or normetanephrine, the MRI and MIBG images, and histological confirmation indicative of pheochromocytoma are lacking. Other differential diagnosis includes adrenal infarction and haemorrhage revealing pseudopheochromocytoma followed by adrenal failure as reported in a patient with antiphospholipid syndrome [9]. However, our patient is unlikely to have the lupus anticoagulant (Table 1), signs of microthrombi, and adrenal failure.…”

Section: Discussionmentioning

confidence: 55%

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Vanishing of ruptured adrenal mass with takotsubo cardiomyopathy

2018

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A 45-year-old male suddenly experienced left-flank abdominal pain. Echocardiography revealed akinesis of the 'takotsubo cardiomyopathy' type. He experienced a sudden haemodynamic collapse (blood pressure, 324/154 mmHg; pulse rate, 180 beats/min) during emergency cardiac catheterisation. An abdominal computed tomography (CT) revealed expansion of a soft tissue mass 64 × 33 mm in dimension in the left adrenal region, with accumulation of fluid surrounding the left pararenal space. Three days after the attack, his urinary catecholamine concentrations were slightly elevated. We suspected the patient as having a pheochromocytoma followed by acute haemorrhagic rupture, based on signatures of adrenal mass, 'takotsubo cardiomyopathy', and the hypertensive crisis. Over the next few weeks, he recovered well as an outpatient, and his blood pressure remained around 110/60 mmHg without medication. Three weeks after the attack, an abdominal CT showed shrinkage of the ruptured adrenal mass (to a diameter of 30 mm) and absorption of the retroperitoneal hematoma. On day 190 after the attack, abdominal CT did not detect any left adrenal mass. This is the first report of the case showing a complete vanishing of ruptured adrenal mass with takotsubo cardiomyopathy. Although surgical approaches for ruptured adrenal mass involve either emergency or elective surgery, the patients did not need even the elective surgery. Accumulation of the similar cases may unravel clinical factors predicting self-limiting of the ruptured adrenal mass to avoid unnecessary risky surgery.

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Section: Discussionmentioning

confidence: 55%

“…Therefore, we cannot rule out the possibility that our patient experi-enced rupture of the cortisol-secreting adrenal adenoma. Anyway, there is no reported case of the vanishing adrenal mass in association with adrenal infarction, adrenal haemorrhage, and Cushing's syndrome [9][10][11].…”

Section: Discussionmentioning

confidence: 99%

Vanishing of ruptured adrenal mass with takotsubo cardiomyopathy

2018

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“…• During stress, catecholamine release in procoagulant environment causes vasoconstriction in adrenal veins resulting in venous thrombosis [21].…”

Section: Catecholamine Excess In Pheochromocytomamentioning

confidence: 99%

Thrombotic Tendencies in Excess Catecholamine States

Nambiar¹,

Chalappurath²

2019

Biogenic Amines in Neurotransmission and Human Disease

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Catecholamines are neurotransmitters distributed throughout the body including adrenal glands, chromaffin tissues and other tissues innervated by post ganglionic adrenergic neurons. The rate of release of medullary hormones is responsible for the control of serum catecholamines. Thrombogenicity of catecholamines are due various mechanisms including hypercoagulable states, endothelial damage, blood stasis and platelet aggregation. Oxidative stress generated by catecholamine excess causes coronary spasm, ultrastructural cell damage and arrhythmias. Elevated plasminogen activator inhibitor-1 during catecholamine excess causes hypercoagulability by hypofibrinosis. During stress, Catecholamines released in procoagulant environment causes vasoconstriction in adrenal veins resulting in venous thrombosis. Catecholamines generate moderately elevated levels of platelet count which enhances the risk of thrombosis. Hypercoagulability results in formation of coronary thrombus, rupture of atherosclerotic plaque and plaque progression due to gradual fibrinogen accumulation in the vessel walls. High levels of circulating catecholamines produce elevated levels thrombomodulin, the biomarkers of endothelial cell damage. In patients with hypertension in catecholamine excess, resistance to blood flow and damage to the integrity of blood vessels lead to atherosclerosis. A case report has been discussed which suggests an association of thrombotic tendency and catecholamine excess.

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