Search PubMed⌕ Search

PubMed · 1959378

Hyperadrenergic states.

Abstract

OBJECTIVE: To review the physiologic and pathophysiologic hyperadrenergic states and the pharmacologic use of sympathomimetic agents. DATA SOURCES: Pharmacologic and physiologic studies in experimental animals and humans. DATA EXTRACTION/SYNTHESIS: Plasma catecholamines are increased in a variety of clinical situations. Following major injury, catecholamines act to support vital organ perfusion and mobilize fuel substrates. However, with surgical trauma and during acute medical illnesses, such as myocardial infarction, catecholamine-induced physiologic changes can interact with underlying disease processes to result in clinically significant complications. Exogenous catecholamines are used to treat a variety of medical conditions, including anaphylaxis and various shock states. Available sympathomimetic agents differ in their availability to stimulate different subpopulations of adrenergic receptors. These differences permit the astute clinician to achieve specific physiologic end-points. Finally, plasma catecholamines are increased in patients with pheochromocytoma. This latter condition provides insights into the long-term effects of catecholamine excess. CONCLUSIONS: Based on knowledge of the pharmacology of sympathomimetic agents and the physiologic consequences of adrenergic receptor stimulation, it is possible to prevent undesirable catecholamine effects and to utilize these agents to achieve desired therapeutic goals.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

M J Breslow, B Ligier. 1991. Hyperadrenergic states.. https://doi.org/10.1097/00003246-199112000-00021

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Treatment of neuroblastoma-related opsoclonus-myoclonus-ataxia syndrome with high-dose dexamethasone pulses.

Opsoclonus-myoclonus-ataxia-syndrome (OMS) represents a rare neuroblastoma-associated paraneoplastic syndrome that commonly results in neurologic deficits despite tumor resection and immunosuppressive therapy. We describe the response of five such children to high-dose dexamethasone pulses including two patients in whom previous glucocorticoids, rituximab, and cytostatic drugs were not successful. All patients had MYCN non-amplified tumors that were detected 1 to 7 months after the onset of the OMS or ataxia. This treatment resulted in a good partial response in three and in complete remission in two patients. Our results show that dexamethasone pulses are likely to be useful for both, first-line- and salvage-therapy for OMS-patients.

Adrenal Gland Neoplasms↗

Malignant paragangliomas associated with mutations in the succinate dehydrogenase D gene.

INTRODUCTION: Malignant paragangliomas have been well described in carriers of mutations of the succinate dehydrogenase B (SDHB) gene, but have rarely been associated with mutations in the succinate dehydrogenase D (SDHD) gene. AIM: The aim of the study was to report the different clinical expression patterns of malignant paragangliomas in five patients with SDHD (D92Y) mutations observed in approximately 200 SDHD (D92Y) mutation carriers followed in our institution. RESULTS: Metastasis and/or local tumor invasion was documented 0 (n=2), 1, 18, and 30 yr after the initial diagnosis of paraganglioma. Malignancy was proven by paraganglioma bone metastases (n=2), intrathoracic paraganglioma with lymph node metastases, locally invasive head-and-neck paraganglioma with destruction of the petrosal bone, and locally invasive paraganglioma of the bladder with lymph node metastases. Four of the five patients developed catecholamine excess during follow-up due to intraadrenal paraganglioma (pheochromocytoma) (n=1), extra adrenal paraganglioma (n=2), and presumed subclinical disease (n=1). CONCLUSION: SDHD mutations (D92Y) are associated with malignant paragangliomas and catecholamine excess with remarkable interindividual variations despite the same mutation. We estimate that the prevalence of malignancy in carriers of D92Y mutations is at least 2.5%.

Adrenal Gland Neoplasms↗