Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe a patient with a suprarenal pheochromocytoma that had a complex course with electrocardiographic findings characteristic of diffuse myocardial damage, normal findings on coronary angiography, and left intraventricular thrombus complicated by embolic stroke.
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PMID:[Acute myocardial ischemia and ventricular thrombus associated with pheochromocytoma]. 1589 4

Although clinical conditions associated with dysfunction of the ad-renal gland are often subtle, even insidious, in their presentation,and diagnosis and treatment usually are confined to outpatient clinics and offices, there are several situations that warrant the attention of emergency physicians. Recognition of the spectrum of presentations of pheochromocytoma, adrenal insufficiency, and pituitary apoplexy, and the sequelae of corticosteroid therapy and withdrawal, are critically important areas to emergency medicine. Prompt diagnosis with appropriate treatment and referral will reduce morbidity and mortality in many patients each year. A related topic pertinent to emergency physicians is the management of incidental adrenal masses that are discovered on abdominal radio-logic imaging.
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PMID:Recognition and management of adrenal emergencies. 1598 41

A 52-year-old woman with a right adrenal pheochromocytoma had repetitive attacks of symptomatic hypotension/shock with systolic blood pressure (SBP)<50 mmHg followed by hypertension/hypertensive crises with SBP>300 mmHg. A non-invasive recording of beat-to-beat SBP, diastolic blood pressure (DBP), heart rate (HR), stroke volume (SV), cardiac output (CO) and total peripheral resistance (TPR) was collected for 346 min. Twenty hemodynamic cycles occurred during this time, lasting 17 min on average, with the most dramatic changes of TPR. The ratio of the highest to the lowest observed values was nearly 12:1 for TPR, over 6:1 for both SBP and DBP, over 4:1 for CO, and nearly 4:1 for SV and 2:1 for HR. The fluctuations of TPR preceded changes of all other hemodynamic variables.
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PMID:Adrenal pheochromocytoma associated with dramatic cyclic hemodynamic fluctuations. 1609 6

Neurodegenerative disorders and chronic disability due to stroke in the brain or spinal cord afflict a large sector of the population. To investigate the mechanism involved in ischemic stroke and to develop neuroprotective drugs/therapies, in vivo and in vitro, pharmacological models are needed. To investigate the cellular and molecular neuroprotective mechanisms of nerve growth factor (NGF), a member of the nervous system neurotrophin family of growth factors, under ischemia, we used an oxygen-glucose-deprivation (OGD) device and pheochromocytoma PC12 cells exposed to a paradigm of ischemic insult. Pretreatment of the cultures with 50 ng/mL of NGF, 18 h prior to OGD insult, conferred 30% of neuroprotection. Time-course experiments showed marked activation of the ERK, JNK, and p-38 MAPK isoforms during the OGD phase, but not during OGD reperfusion. Pretreatment of the cultures with 50 ng/mL of NGF, 18 h prior to OGD insult, resulted in 50% attenuation of OGD-induced activation of JNK 1, and 20% and 50% attenuation of OGD-induced activation of p-38 alpha and beta, respectively. The effect of NGF on gene expression in the PC12 ischemic model using Affymatrix Rat DNA-Microarray technology indicates that only 6% of the genes are differentially regulated (induced/suppressed) by OGD insult and/or NGF. These findings support the notion that pretreatment with NGF confers neuroprotection from OGD insult, a phenomenon coincidentally related to differential inhibition of MAPK stress kinase isoforms and differential gene expression. This ischemic model may be useful to investigate molecular mechanisms of OGD-induced neurotoxicity and NGF-induced neuroprotection, and to generate novel therapeutic concepts for stroke treatment.
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PMID:Neuroprotection by NGF in the PC12 in vitro OGD model: involvement of mitogen-activated protein kinases and gene expression. 1617 11

Astrocytes are thought to be critical to neurons' surviving damage caused by ischemic stroke or other injury. Plasminogen activator inhibitor-1 is one of the active soluble factors released by astrocytes and regulates plasminogen activator-plasmin proteolytic sequence in the CNS as a serpin. In this study, we show that plasminogen activator inhibitor-1 can promote neurite outgrowth and survival of rat pheochromocytoma cells in serum-deprived conditions, and that this neuroprotective activity is correlated with enhanced activation of both extracellular signal-regulated kinases following a direct phosphorylation of nerve growth factor receptor, Trk A, and of c-Jun. Our results suggest that plasminogen activator inhibitor-1 can act as a neurotrophic factor, protecting neurons from serum deprivation-induced neuron death not only by compensating for nerve growth factor functions, but also by activating the c-Jun/activating protein-1 pathway.
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PMID:Plasminogen activator inhibitor-1 aids nerve growth factor-induced differentiation and survival of pheochromocytoma cells by activating both the extracellular signal-regulated kinase and c-Jun pathways. 1667 72

Diagnosis and management of endocrine crises in adulthood. The homeostasis of the body is regulated by concerted action of the endocrine, nervous and immune systems. An imbalance in this equilibrium, as a consequence of disease or endocrine failure, may lead to crisis, characterized by sudden onset and severe symptoms. The classical endocrine emergencies are rare but life-threatening conditions. Prompt and aggressive treatment significantly reduces mortality. Immediate therapy might be necessitated in cases of suspected endocrine emergencies, even prior to laboratory confirmation. These patients generally require admittance to an intensive care unit. In the present review only the most severe forms of life-threatening endocrine emergencies, including acute adrenal insufficiency, pituitary apoplexy, pheochromocytoma crisis, thyroid storm and myxedema coma will be discussed.
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PMID:[Diagnosis and management of endocrine crises in adulthood]. 1720

Transient left ventricular dysfunction associated with apical ballooning at echocardiography or angiography has been described in many overlapping clinical settings: neurological disorders, such as subarachnoid haemorrhage and stroke, pheochromocytoma, and the recent takotsubo syndrome. We describe the case of an elderly woman presenting with syncope, chest pain, electrocardiographic abnormalities, mild enzymatic release, and transient left ventricular apical ballooning, mimicking an anterior wall acute coronary syndrome with shock, following a subarachnoid haemorrhage that could not be detected upon admission.The pathophysiological mechanisms of myocardial damage during catecholamine surge cannot be completely explained by epicardial coronary vasoconstriction or microvascular spasm and subsequent ischaemia; also direct catecholamine-mediated myocyte injury may play a role in myocardial stunning.
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PMID:Syncope in a patient presenting to the emergency room with chest pain, shock, and neurological disorders. 1766 38

A thunderclap headache is a sudden and severe headache and is sometimes a sign of a medical emergency such as aneurysmal subarachnoid hemorrhage and pituitary apoplexy. We report a case of pheochromocytoma in the urinary bladder in a 37-year-old man who presented with recurrent thunderclap headache after voiding and exercises. Bladder pheochromocytoma should be included in the differential diagnosis of recurrent thunderclap headache after micturition or exercises.
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PMID:Thunderclap headache after micturition in bladder pheochromocytoma. 1854 75

Plasminogen activator inhibitor-1 (PAI-1), a member of the serpin gene family, is the primary inhibitor of urokinase-type and tissue-type PAs. PAI-1 plays an important role in the process of peripheral tissue remodeling and fibrinolysis through the regulation of PA activity. This serpin is also produced in brain tissues and may regulate the neural protease sequence in the central nervous system (CNS), as it does in peripheral tissues. In fact, PAI-1 mRNA is up-regulated in mouse brain after stroke. The serpin activity of PAI-1 helps to prevent tissue-type PA-induced neuron death. However, we have previously found that PAI-1 has a novel biological function in the CNS: the contribution to survival of neurites on neurons. In neuronally differentiated rat pheochromocytoma (PC-12) cells, a deficiency of PAI-1 in vitro caused a significant reduction in Bcl-2 and Bcl-X(L) mRNAs and an increase in Bcl-X(S) and Bax mRNAs. The change in the balance between mRNA expressions of the anti- and pro-apoptotic Bcl-2 family proteins promoted the apoptotic sequence: caspase-3 activation, cytochrome c release from mitochondria and DNA fragmentation. Our results indicate that PAI-1 has an anti-apoptotic role in neurons. PAI-1 prevented the disintegration of the formed neuronal networks by maintaining or promoting neuroprotective signaling through the MAPK/ERK pathway, suggesting that the neuroprotective effect of PAI-1 is independent of its action as a protease inhibitor. This review discusses the neuroprotective effects of PAI-1 in vitro, together with the relevant data from other laboratories. Special emphasis is placed on its action on PC-12 cells.
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PMID:Anti-apoptotic roles of plasminogen activator inhibitor-1 as a neurotrophic factor in the central nervous system. 1913 24

Pheochromocytoma (Pheo) is a rare tumor that develops in the core of a chromaffin cell. This article will focus on pheochromocytoma and its affect on the heart. Because the signs and symptoms of a pheochromocytoma are those of the sympathetic nervous system, this tumor is hard to detect and might not be considered early on. In addition, there are many common deferential diagnoses that may lead to a delay of the correct diagnosis of a pheochromocytoma. Uncontrollable hypertension is one of the primary effects of pheochromocytoma. A severe increase in blood pressure (hypertensive crisis) may occur and this can be a life threatening condition that leads to stroke or arrhythmias. African-Americans are disproportionately affected by hypertension and they often go undiagnosed because of a lack of resources or access to care. This tumor is difficult to detect and its effects often mimic many other diagnoses, which often leads to this tumor being a late consideration. The long-term effects of a pheochromocytoma can lead to damage to the heart muscle, congestive heart failure (CHF), increased risk of diabetes, and even death. Nurses need to be aware of the key signs and symptoms of a pheochromocytoma, and to know when testing for this tumor what symptoms should be considered. Patients who suffer from a diagnosis of this tumor need a lot of emotional support and they must follow a strict diet and medication regimen. Nurses can play a vital role in raising awareness in our community about this tumor as well as being a patient advocate.
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PMID:Pheochromocytoma induced hypertension. 2151 25


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