Metanephrines for Evaluating Palpitations and Flushing

Hannah‐Shmouni, Fady; Pacák, Karel; Stratakis, Constantine A.

doi:10.1001/jama.2017.5926

Cited by 13 publications

(7 citation statements)

References 8 publications

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“…Coupled with persistent HTN, the elevated metanephrine levels in our patient prompted consideration into whether pheochromocytoma or paraganglioma, rare catecholamine-secreting tumors that can cause extreme HTN [ 24 , 25 ], was contributing to her symptoms. Other causes of elevated catecholamines that were considered included use of medications such as tricyclic antidepressants, antipsychotic agents, serotonin-reuptake and norepinephrine-reuptake inhibitors, and levodopa [ 26 ], use of stimulants such as caffeine and nicotine [ 27 ], and use of substances such as cocaine and its derivatives [ 28 ]. Mercury poisoning has also been reported to cause elevations in metanephrines [ 29 ].…”

Section: Discussionmentioning

confidence: 99%

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Hypertensive Crisis in a Pediatric Patient Experiencing Clonidine Withdrawal

Cao

Lorenz

Sojka

et al. 2022

Case Reports in Pediatrics

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Background. Clonidine, a central alpha-adrenoreceptor agonist, was initially developed as an antihypertensive. Though no longer commonly used for its original indication due to rebound hypertension after discontinuation, it is currently widely prescribed as a treatment for many pediatric indications including sleep disorders, behavioral concerns, and attention deficit hyperactivity disorder. Case Report. We describe a girl who developed prolonged symptoms of clonidine withdrawal, including hypertension and elevated serum metanephrines. Discussion. Clonidine withdrawal in pediatric patient can present with hypertensive urgency and other signs of sympathetic stimulation. Withdrawal can also lead to dramatic elevation in serum metanephrines. Treatment with a clonidine taper will reduce development of withdrawal symptoms. Conclusion. Given the rise in clonidine use in pediatric patients, clinicians should be aware of the risk of clonidine withdrawal and how to recognize and avoid its development.

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Section: Discussionmentioning

confidence: 99%

“…Mercury poisoning has also been reported to cause elevations in metanephrines [ 29 ]. Lastly, withdrawal from clonidine, ethanol, and benzodiazepines has also been associated with elevations in catecholamines [ 28 ].…”

Section: Discussionmentioning

confidence: 99%

Hypertensive Crisis in a Pediatric Patient Experiencing Clonidine Withdrawal

Cao

Lorenz

Sojka

et al. 2022

Case Reports in Pediatrics

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“…For this reason, the patient should be placed in a supine position with venipuncture performed 20-30 minutes before biochemical labs are obtained – as both non-supine position and venipuncture may lead to catecholamine release ( 32 ). Medications that can artifactually increase plasma or urinary fractionated metanephrines include acetaminophen, α-methyldopa, tricyclic antidepressants, monoamine oxidase inhibitors, sympathomimetics, catecholamine reuptake inhibitors, mesalamine/sulfasalazine, phenoxybenzamine, levodopa, anesthetics, neuromuscular blockers, antiemetics, linezolid, peptide hormones, steroids, cocaine, and opioids ( 17 , 39 ). Glucocorticoids potentiate catecholamine biosynthetic enzymes and should be avoided in patients with PPGL due to risk of causing PCC crisis ( 40 ).…”

Section: Biochemical Foundationsmentioning

confidence: 99%

Pediatric Metastatic Pheochromocytoma and Paraganglioma: Clinical Presentation and Diagnosis, Genetics, and Therapeutic Approaches

et al. 2022

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Although pediatric pheochromocytomas and paragangliomas (PPGLs) are rare, they have important differences compared to those in adults. Unfortunately, without timely diagnosis and management, these tumors have a potentially devastating impact on pediatric patients. Pediatric PPGLs are more often extra-adrenal, multifocal/metastatic, and recurrent, likely due to these tumors being more commonly due to a genetic predisposition than in adults. This genetic risk results in disease manifestations at an earlier age giving these tumors time to advance before detection. In spite of these problematic features, advances in the molecular and biochemical characterization of PPGLs have heralded an age of increasingly personalized medicine. An understanding of the genetic basis for an individual patient’s tumor provides insight into its natural history and can guide clinicians in management of this challenging disease. In pediatric PPGLs, mutations in genes related to pseudohypoxia are most commonly seen, including the von Hippel-Lindau gene (VHL) and succinate dehydrogenase subunit (SDHx) genes, with the highest risk for metastatic disease associated with variants in SDHB and SDHA. Such pathogenic variants are associated with a noradrenergic biochemical phenotype with resultant sustained catecholamine release and therefore persistent symptoms. This is in contrast to paroxysmal symptoms (e.g., episodic hypertension, palpitations, and diaphoresis/flushing) as seen in the adrenergic, or epinephrine-predominant, biochemical phenotype (due to episodic catecholamine release) that is commonly observed in adults. Additionally, PPGLs in children more often present with signs and symptoms of catecholamine excess. Therefore, children, adolescents, and young adults present differently from older adults (e.g., the prototypical presentation of palpitations, perspiration, and pounding headaches in the setting of an isolated adrenal mass). These presentations are a direct result of genetic determinants and highlight the need for pediatricians to recognize these differences in order to expedite appropriate evaluations, including genetic testing. Identification and familiarity with causative genes inform surveillance and treatment strategies to improve outcomes in pediatric patients with PPGL.

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“…However, if not promptly recognized and treated, PGLs are associated to increased cardiovascular morbidity and mortality risk [3][4][5]. In non-syndromic cases, in fact, patients affected by PGLs can report a wide range of symptoms, including high blood pressure (BP) and uncontrolled paroxysmal hypertension episodes, accompanied by heart palpitations, headache, excessive sweating, facial pallor or flushing during the attack, and chest and/or abdominal pain [6][7][8].…”

Section: Introductionmentioning

confidence: 99%

Pelvic and Bladder Catecholamine-Producing Tumors: A Review of the Literature

Petramala¹,

Bisogni²,

Olmati³

et al. 2019

Preprint

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Background Although PGLs may arise at any site where physiologic paraganglionic tissue exists, pelvic origins are not frequent (about 2%), and the most common localization is the retroperitoneal space, whereas bladder PGLs account for less than 0.06% of all bladder neoplasms and less than 1% of all PGLs. Starting from the description of two interesting our cases, we wondered to review the literature on pelvic and bladder paragangliomas (PGLs) with the aim of illustrating clinical characteristics and current management, and enlightening the needed of a prompt diagnosis to avoid the onset of several complications.Methods We herein performed a brief review of the literature about pelvic PGLs in the PubMed library, conducted according to the PRISMA statement, including studies published from 1954 to 2019. We also discuss clinical presentation, morphologic appearance, and management of two cases of pelvic PGL, both of them characterized by a history of paroxysmal high blood pressure episodes uncontrolled by antihypertensive therapy associated with disabling symptoms, misdiagnosed for many years.Results Overall, we evaluated 108 case reports. The majority were females, presenting typical signs and symptoms, such as arterial hypertension (54.2%), hematuria (35.1%), and headache (33.6%). After treatment, the clinical and biochemical remission was showed in only 55% of analyzed cases.Conclusions For their singular localization, pelvic and bladder PGLs often might be misdiagnosed. The resulting delay in the proper treatment could be responsible for the relative low percentage of complete clinical and biochemical remission.

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Metanephrines for Evaluating Palpitations and Flushing

Cited by 13 publications

References 8 publications

Hypertensive Crisis in a Pediatric Patient Experiencing Clonidine Withdrawal

Hypertensive Crisis in a Pediatric Patient Experiencing Clonidine Withdrawal

Pediatric Metastatic Pheochromocytoma and Paraganglioma: Clinical Presentation and Diagnosis, Genetics, and Therapeutic Approaches

Pelvic and Bladder Catecholamine-Producing Tumors: A Review of the Literature

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