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  1. Article ; Online: Routine hematologic clinical tests as prognostic markers in patients with acute coronary syndromes.

    Turner, Samuel J / Ketch, Terry R / Gandhi, Sanjay K / Sane, David C

    American heart journal

    2008  Volume 155, Issue 5, Page(s) 806–816

    Abstract: Prognostic markers are needed to identify patients with acute coronary syndrome (ACS) who are at high risk for adverse events. Although the search for new biomarkers is quite active, prognostic information is available from routine hematologic tests, ... ...

    Abstract Prognostic markers are needed to identify patients with acute coronary syndrome (ACS) who are at high risk for adverse events. Although the search for new biomarkers is quite active, prognostic information is available from routine hematologic tests, such as the complete blood count. For example, elevated white blood cell counts during ACS are associated with increased risk of mortality, heart failure, shock, and left ventricular dysfunction. Anemia is associated with increased risk of mortality, whereas elevated platelet counts predict poorer clinical and angiographic outcomes. In this review, we summarize the literature regarding the use of clinical hematology tests including white blood cell count, hemoglobin and hematocrit values, and platelet count as prognostic markers in patients with ACS, and we describe potential mechanisms to explain these associations.
    MeSH term(s) Acute Coronary Syndrome/blood ; Acute Coronary Syndrome/diagnosis ; Biomarkers/blood ; Hematocrit ; Hemoglobins ; Humans ; Leukocytes ; Platelet Count ; Predictive Value of Tests ; Prognosis ; Risk Factors
    Chemical Substances Biomarkers ; Hemoglobins
    Language English
    Publishing date 2008-05
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 80026-0
    ISSN 1097-6744 ; 0002-8703
    ISSN (online) 1097-6744
    ISSN 0002-8703
    DOI 10.1016/j.ahj.2007.11.037
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Four faces of baroreflex failure: hypertensive crisis, volatile hypertension, orthostatic tachycardia, and malignant vagotonia.

    Ketch, Terry / Biaggioni, Italo / Robertson, RoseMarie / Robertson, David

    Circulation

    2002  Volume 105, Issue 21, Page(s) 2518–2523

    Abstract: Background: The baroreflex normally serves to buffer blood pressure against excessive rise or fall. Baroreflex failure occurs when afferent baroreceptive nerves or their central connections become impaired. In baroreflex failure, there is loss of ... ...

    Abstract Background: The baroreflex normally serves to buffer blood pressure against excessive rise or fall. Baroreflex failure occurs when afferent baroreceptive nerves or their central connections become impaired. In baroreflex failure, there is loss of buffering ability, and wide excursions of pressure and heart rate occur. Such excursions may derive from endogenous factors such as stress or drowsiness, which result in quite high and quite low pressures, respectively. They may also derive from exogenous factors such as drugs or environmental influences.
    Methods and results: Impairment of the baroreflex may produce an unusually broad spectrum of clinical presentations; with acute baroreflex failure, a hypertensive crisis is the most common presentation. Over succeeding days to weeks, or in the absence of an acute event, volatile hypertension with periods of hypotension occurs and may continue for many years, usually with some attenuation of pressor surges and greater prominence of depressor valleys during long-term follow-up. With incomplete loss of baroreflex afferents, a mild syndrome of orthostatic tachycardia or orthostatic intolerance may appear. Finally, if the baroreflex failure occurs without concomitant destruction of the parasympathetic efferent vagal fibers, a resting state may lead to malignant vagotonia with severe bradycardia and hypotension and episodes of sinus arrest.
    Conclusions: Although baroreflex failure is not the most common cause of the above conditions, correct differentiation from other cardiovascular disorders is important, because therapy of baroreflex failure requires specific strategies, which may lead to successful control.
    MeSH term(s) Autonomic Nervous System Diseases/diagnosis ; Baroreflex/physiology ; Blood Pressure ; Diagnosis, Differential ; Heart Rate ; Humans ; Hypertension/diagnosis ; Hypertension/etiology ; Hypertension/therapy ; Posture ; Tachycardia/diagnosis ; Tachycardia/etiology ; Tachycardia/therapy ; Vagus Nerve Diseases/diagnosis ; Vagus Nerve Diseases/etiology ; Vagus Nerve Diseases/therapy
    Language English
    Publishing date 2002-05-28
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S. ; Review
    ZDB-ID 80099-5
    ISSN 1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
    ISSN (online) 1524-4539
    ISSN 0009-7322 ; 0069-4193 ; 0065-8499
    DOI 10.1161/01.cir.0000017186.52382.f4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Assessment of O-methylated catecholamine levels in plasma and urine for diagnosis of autonomic disorders.

    Oeltmann, Timothy / Carson, Robert / Shannon, John R / Ketch, Terry / Robertson, David

    Autonomic neuroscience : basic & clinical

    2004  Volume 116, Issue 1-2, Page(s) 1–10

    Abstract: The term 'metanephrines' is used to indicate the two catechol 3-O-methylated metabolites of epinephrine (E) and norepinephrine (NE): metanephrine and normetanephrine (NMN). The corresponding 3-O-methylated metabolite of dopamine is usually referred to as ...

    Abstract The term 'metanephrines' is used to indicate the two catechol 3-O-methylated metabolites of epinephrine (E) and norepinephrine (NE): metanephrine and normetanephrine (NMN). The corresponding 3-O-methylated metabolite of dopamine is usually referred to as 3-methoxytyramine rather than 3-methoxydopamine and is not generally considered a "metanephrine". O-Methylation occurs outside the sympathetic neuron and neuroeffector junction. Metanephrines are products of the enzyme catechol-O-methyltransferase (COMT). Subsequent conjugation with sulfate or deamination by monoamine oxidase (MAO) followed by reduction to vanilmandelic acid (VMA) facilitates urinary excretion. For the clinician, measurement of normetanephrine provides an index of norepinephrine released during sympathetic nervous system activity, whereas metanephrine concentration provides an indication of adrenal medullary metabolism of epinephrine prior to its discharge into the circulation. Plasma epinephrine concentration is the preferable index of adrenal medullary epinephrine discharge. Pheochromocytomas, with their protean clinical manifestations, may be diagnostic challenges, but assay of metanephrines, especially plasma metanephrine, can be particularly helpful in diagnosis. These COMT metabolites may also help in elucidation of still undiscovered genetic and acquired disorders of catecholamine metabolism.
    MeSH term(s) Animals ; Autonomic Nervous System Diseases/blood ; Autonomic Nervous System Diseases/diagnosis ; Autonomic Nervous System Diseases/urine ; Biomarkers/blood ; Biomarkers/urine ; Catechol O-Methyltransferase/physiology ; Catecholamines/metabolism ; Humans ; Metanephrine/blood ; Metanephrine/urine ; Models, Chemical ; Models, Neurological
    Chemical Substances Biomarkers ; Catecholamines ; Metanephrine (5001-33-2) ; Catechol O-Methyltransferase (EC 2.1.1.6)
    Language English
    Publishing date 2004-11-30
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S. ; Review
    ZDB-ID 2020105-9
    ISSN 1872-7484 ; 1566-0702
    ISSN (online) 1872-7484
    ISSN 1566-0702
    DOI 10.1016/j.autneu.2004.08.013
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: ABO blood types: influence on infarct size, procedural characteristics and prognosis.

    Ketch, Terry R / Turner, Samuel J / Sacrinty, Matthew T / Lingle, Kevin C / Applegate, Robert J / Kutcher, Michael A / Sane, David C

    Thrombosis research

    2008  Volume 123, Issue 2, Page(s) 200–205

    Abstract: Introduction: Patients with non-O blood groups have higher plasma von Willebrand factor (vWF) levels than those with type O. vWF mediates platelet adhesion, aggregation and thrombosis. These considerations likely explain the prior observations that non- ... ...

    Abstract Introduction: Patients with non-O blood groups have higher plasma von Willebrand factor (vWF) levels than those with type O. vWF mediates platelet adhesion, aggregation and thrombosis. These considerations likely explain the prior observations that non-O patients have higher rates of arterial and venous thromboembolic events. However, the effect of blood group status on size of MI, procedural findings and outcomes after PCI for MI have not been reported.
    Methods: We analyzed 1198 patients who underwent percutaneous coronary intervention for acute myocardial infarction between 10/03 and 8/06, and who had ABO blood group status and clinical follow-up.
    Results and conclusions: Patients with O blood type were slightly older (62 +/- 13 vs. 60 +/- 13 years; p = 0.017) had a higher prevalence of hypercholesterolemia (67% vs. 58%; p = 0.002), and had a higher burden of atherosclerosis with more vascular disease (17% vs. 13%; p = 0.017) and higher prevalence of previous PCI (22% vs. 17%; p = 0.025). Non-O blood group patients had larger infarcts as measured by median peak troponin (33 vs. 24; p = 0.037), total CK (721 vs. 532; p = 0.012) and CK-MB (101 vs. 68; p = 0.010). At PCI, non-O patients had increased visible thrombus and reduced TIMI flow pre-procedure. However, there were no differences in procedural success, in-hospital blood transfusion or occurrence of MACE at 1 year follow-up. Our data demonstrate that non-O compared to O blood groups patients have higher thrombus burden despite less extensive atherosclerosis. Nevertheless, outcomes at 1 year were similar.
    MeSH term(s) ABO Blood-Group System ; Aged ; Angioplasty, Balloon, Coronary ; Atherosclerosis/epidemiology ; Female ; Follow-Up Studies ; Humans ; Hypercholesterolemia/epidemiology ; Male ; Middle Aged ; Myocardial Infarction/blood ; Myocardial Infarction/diagnosis ; Myocardial Infarction/therapy ; Myocardium/pathology ; Necrosis/pathology ; Prevalence ; Prognosis ; Survival Analysis ; Thrombolytic Therapy ; Time Factors ; Treatment Outcome ; von Willebrand Factor/metabolism
    Chemical Substances ABO Blood-Group System ; von Willebrand Factor
    Language English
    Publishing date 2008
    Publishing country United States
    Document type Journal Article
    ZDB-ID 121852-9
    ISSN 1879-2472 ; 0049-3848
    ISSN (online) 1879-2472
    ISSN 0049-3848
    DOI 10.1016/j.thromres.2008.02.003
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  5. Article ; Online: Derived fibrinogen compared with C-reactive protein and brain natriuretic peptide for predicting events after myocardial infarction and coronary stenting.

    Ketch, Terry R / Turner, Samuel J / Sacrinty, Matthew T / Lingle, Kevin C / Applegate, Robert J / Kutcher, Michael A / Sane, David C

    American heart journal

    2008  Volume 156, Issue 2, Page(s) 234–240

    Abstract: Background: After myocardial infarction (MI), biomarkers can be helpful to identify patients who might benefit from more intensive therapies. The prothrombin time-derived fibrinogen (PTDF) assay is widely available and relatively inexpensive. We ... ...

    Abstract Background: After myocardial infarction (MI), biomarkers can be helpful to identify patients who might benefit from more intensive therapies. The prothrombin time-derived fibrinogen (PTDF) assay is widely available and relatively inexpensive. We determined whether PTDF predicts events in patients with MI and compared this assay with brain natriuretic peptide (BNP) and C-reactive protein (CRP).
    Methods: We retrospectively analyzed data from 915 patients admitted with MI. Follow-up was collected at 1 year for major adverse cardiac events (MACE) defined as death from any cause, nonfatal MI or death, target vessel revascularization, or coronary artery bypass grafting.
    Results: Patients in the fourth quartile of PTDF were older and had more risk factors but fewer ST-elevation MI and lower peak troponin values. The fourth quartiles of PTDF, CRP, and BNP were associated with increased MACE compared with the first quartiles with hazard ratios of 2.08 (1.30-3.33), 1.94 (1.22-3.07), and 2.56 (1.57-4.18), respectively, findings that remained significant after adjustment. When outcomes by strata of PTDF were examined, CRP failed to add additional prognostic value. Higher BNP levels predicted MACE in the upper but not lower stratum of PTDF.
    Conclusion: In patients with MI, PTDF is a predictor of MACE at 1 year, with equivalent value compared to BNP and CRP. With low PTDF levels, neither BNP nor CRP adds prognostic value. At elevated PTDF values, higher BNP, but not CRP, identifies a higher-risk population. Therefore, PTDF can be substituted for CRP, with BNP being useful in the presence of elevated PTDF.
    MeSH term(s) Aged ; Angioplasty, Balloon, Coronary ; C-Reactive Protein/analysis ; Coronary Artery Bypass/statistics & numerical data ; Female ; Fibrinogen/analysis ; Follow-Up Studies ; Humans ; Kaplan-Meier Estimate ; Male ; Middle Aged ; Myocardial Infarction/blood ; Myocardial Infarction/mortality ; Myocardial Infarction/therapy ; Natriuretic Peptide, Brain/blood ; Prognosis ; Proportional Hazards Models ; Prothrombin Time ; Recurrence ; Retrospective Studies ; Risk Assessment/methods ; Stents
    Chemical Substances Natriuretic Peptide, Brain (114471-18-0) ; Fibrinogen (9001-32-5) ; C-Reactive Protein (9007-41-4)
    Language English
    Publishing date 2008-08
    Publishing country United States
    Document type Comparative Study ; Journal Article
    ZDB-ID 80026-0
    ISSN 1097-6744 ; 0002-8703
    ISSN (online) 1097-6744
    ISSN 0002-8703
    DOI 10.1016/j.ahj.2008.03.015
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  6. Article: Ageing and water homeostasis.

    Robertson, David / Jordan, Jens / Jacob, Giris / Ketch, Terry / Shannon, John R / Biaggioni, Italo

    Novartis Foundation symposium

    2002  Volume 242, Page(s) 265–75; discussion 275–8

    Abstract: This review outlines current knowledge concerning fluid intake and volume homeostasis in ageing. The physiology of vasopressin is summarized. Studies have been carried out to determine orthostatic changes in plasma volume and to assess the effect of ... ...

    Abstract This review outlines current knowledge concerning fluid intake and volume homeostasis in ageing. The physiology of vasopressin is summarized. Studies have been carried out to determine orthostatic changes in plasma volume and to assess the effect of water ingestion in normal subjects, elderly subjects, and patients with dysautonomias. About 14% of plasma volume shifts out of the vasculature within 30 minutes of upright posture. Oral ingestion of water raises blood pressure in individuals with impaired autonomic reflexes and is an important source of noise in blood pressure trials in the elderly. On the average, oral ingestion of 16 ounces (473ml) of water raises blood pressure 11 mmHg in elderly normal subjects. In patients with autonomic impairment, such as multiple system atrophy, strikingly exaggerated pressor effects of water have been seen with blood pressure elevations greater than 75 mmHg not at all uncommon. Ingestion of water is a major determinant of blood pressure in the elderly population. Volume homeostasis is importantly affected by posture and large changes in plasma volume may occur within 30 minutes when upright posture is assumed.
    MeSH term(s) Aging/metabolism ; Homeostasis ; Humans ; Vasopressins/metabolism ; Water/metabolism
    Chemical Substances Water (059QF0KO0R) ; Vasopressins (11000-17-2)
    Language English
    Publishing date 2002
    Publishing country England
    Document type Journal Article ; Review
    ISSN 1528-2511
    ISSN 1528-2511
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: Postural pseudoanemia: posture-dependent change in hematocrit.

    Jacob, Giris / Raj, Satish R / Ketch, Terry / Pavlin, Boris / Biaggioni, Italo / Ertl, Andrew C / Robertson, David

    Mayo Clinic proceedings

    2005  Volume 80, Issue 5, Page(s) 611–614

    Abstract: Objective: To determine the magnitude of posture-related changes in blood components.: Subjects and methods: Twenty-eight healthy subjects were studied between 1995 and 2004 at the Vanderbilt Autonomic Dysfunction Center, Nashville, Tenn. Lying and ... ...

    Abstract Objective: To determine the magnitude of posture-related changes in blood components.
    Subjects and methods: Twenty-eight healthy subjects were studied between 1995 and 2004 at the Vanderbilt Autonomic Dysfunction Center, Nashville, Tenn. Lying and standing plasma volume (PV) and hematocrit (Hct) values were determined for each subject.
    Results: Individual PV decreases on standing ranged from 6% to 25%. The absolute mean +/- SD PV shift was 417+/-137 mL (range, 149-717 mL). The mean +/- SD change in Hct was from 37.7%+/-2.8% while supine to 41.8%+/-3.2% within 30 minutes of standing. This absolute increase in Hct of 4.1%+/-1.3% represents a relative increase of 11.0%+/-3.6% from lying to standing.
    Conclusions: Changes in posture can lead to substantial changes in Hct, which may be attributed mistakenly to blood loss or acute anemia and result in a cascade of unnecessary diagnostic costs. In reality, these changes represent postural pseudoanemia, a normal physiological response to a change in position from standing to lying (and vice versa).
    MeSH term(s) Adult ; Anemia/blood ; Anemia/physiopathology ; Coloring Agents/administration & dosage ; Evans Blue/administration & dosage ; Female ; Follow-Up Studies ; Hematocrit ; Humans ; Injections, Intravenous ; Male ; Plasma Volume/physiology ; Posture/physiology ; Radiopharmaceuticals/administration & dosage ; Reference Values ; Retrospective Studies ; Serum Albumin, Radio-Iodinated/administration & dosage
    Chemical Substances Coloring Agents ; Radiopharmaceuticals ; Serum Albumin, Radio-Iodinated ; Evans Blue (45PG892GO1)
    Language English
    Publishing date 2005-05
    Publishing country England
    Document type Comparative Study ; Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 124027-4
    ISSN 1942-5546 ; 0025-6196
    ISSN (online) 1942-5546
    ISSN 0025-6196
    DOI 10.4065/80.5.611
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  8. Article ; Online: Chronic kidney disease and dipstick proteinuria are risk factors for stent thrombosis in patients with myocardial infarction.

    Lambert, Nathan D / Sacrinty, Matthew T / Ketch, Terry R / Turner, Samuel J / Santos, Renato M / Daniel, Kurt R / Applegate, Robert J / Kutcher, Michael A / Sane, David C

    American heart journal

    2009  Volume 157, Issue 4, Page(s) 688–694

    Abstract: Background: Kidney failure (stage 5 chronic kidney disease [CKD]) is an independent risk factor for stent thrombosis (ST). Moderate (stage 3-4) CKD and proteinuria are both associated with adverse cardiovascular events, including worse outcomes after ... ...

    Abstract Background: Kidney failure (stage 5 chronic kidney disease [CKD]) is an independent risk factor for stent thrombosis (ST). Moderate (stage 3-4) CKD and proteinuria are both associated with adverse cardiovascular events, including worse outcomes after myocardial infarction (MI). Whether moderate CKD and proteinuria increase the risk of ST after MI is not known. This study evaluated the risk of ST associated with moderate CKD and dipstick proteinuria.
    Methods: We retrospectively analyzed clinical and laboratory data from 956 non-stage 5 CKD patients who were admitted with MI and received intracoronary stenting. Clinical follow-up was collected at 1 year for definite or probable ST, as well as for all-cause mortality, nonfatal MI or death, and target vessel revascularization or coronary artery bypass graft surgery.
    Results: After adjustment for multiple clinical and biochemical covariates, patients with both estimated glomerular filtration rate (GFR) of 15 to 59 mL min(-1) 1.73 m(-2) and > or =30 mg/dL dipstick proteinuria had increased cumulative incidence of ST (hazard rate [HR] 3.69, 95% CI 1.54-8.89), all-cause mortality (HR 2.68, 95% CI 1.34-5.37), and nonfatal MI or death (HR 3.20, 95% CI 1.77-5.81) at 1 year. In addition, estimated GFR of 15 to 59 mL min(-1) 1.73 m(-2) was a significant independent predictor of ST (HR 2.61, 95% CI 1.33-5.10). Dipstick proteinuria > or =30 mg/dL was associated with a trend toward increased risk for all outcomes.
    Conclusions: In an acute MI population, moderate CKD was identified as a novel prognostic marker for ST. In addition, patients with both decreased GFR and proteinuria had higher incidences of all-cause mortality and nonfatal MI or death than patients with either condition alone.
    MeSH term(s) Aged ; Cause of Death ; Coronary Restenosis/complications ; Coronary Restenosis/epidemiology ; Coronary Restenosis/urine ; Female ; Follow-Up Studies ; Humans ; Incidence ; Kidney Failure, Chronic/epidemiology ; Kidney Failure, Chronic/etiology ; Kidney Failure, Chronic/urine ; Male ; Middle Aged ; Myocardial Infarction/complications ; Myocardial Infarction/diagnosis ; Myocardial Infarction/surgery ; Myocardial Revascularization/instrumentation ; North Carolina/epidemiology ; Prognosis ; Proteinuria/epidemiology ; Proteinuria/etiology ; Proteinuria/urine ; Retrospective Studies ; Risk Factors ; Stents ; Urinalysis/methods
    Language English
    Publishing date 2009-04
    Publishing country United States
    Document type Comparative Study ; Journal Article
    ZDB-ID 80026-0
    ISSN 1097-6744 ; 0002-8703
    ISSN (online) 1097-6744
    ISSN 0002-8703
    DOI 10.1016/j.ahj.2009.01.009
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  9. Article: Genetic basis of clinical catecholamine disorders.

    Garland, Emily M / Hahn, Maureen K / Ketch, Terry P / Keller, Nancy R / Kim, Chun-Hyung / Kim, Kwang-Soo / Biaggioni, Italo / Shannon, John R / Blakely, Randy D / Robertson, David

    Annals of the New York Academy of Sciences

    2002  Volume 971, Page(s) 506–514

    Abstract: Norepinephrine and epinephrine are critical determinants of minute-to-minute regulation of blood pressure. Here we review the characterization of two syndromes associated with a genetic abnormality in the noradrenergic pathway. In 1986, we reported a ... ...

    Abstract Norepinephrine and epinephrine are critical determinants of minute-to-minute regulation of blood pressure. Here we review the characterization of two syndromes associated with a genetic abnormality in the noradrenergic pathway. In 1986, we reported a congenital syndrome of undetectable tissue and circulating levels of norepinephrine and epinephrine, elevated levels of dopamine, and absence of dopamine-beta-hydroxylase (DBH). These patients appeared with ptosis and severe orthostatic hypotension and lacked sympathetic noradrenergic function. In two persons with DBH deficiency, we identified seven novel polymorphisms. Both patients are compound heterozygotes for a variant that affects expression of DBH protein via impairment of splicing. Patient 1 also has a missense mutation in DBH exon 2, and patient 2 carries missense mutations in exons 1 and 6. Orthostatic intolerance is a common syndrome affecting young women, presenting with orthostatic tachycardia and symptoms of cerebral hypoperfusion on standing. We tested the hypothesis that abnormal norepinephrine transporter (NET) function might contribute to its etiology. In our proband, we found an elevated plasma norepinephrine with standing that was disproportionate to the increase in levels of dihydroxphenylglycol, as well as impaired norepinephrine clearance and tyramine resistance. Studies of NET gene structure revealed a coding mutation converting a conserved alanine residue in transmembrane domain 9 to proline. Analysis of the protein produced by the mutant cDNA demonstrated greater than 98% reduction in activity relative to normal. The finding of genetic mutations responsible for DBH deficiency and orthostatic intolerance leads us to believe that genetic causes of other autonomic disorders will be found, enabling us to design more effective therapeutic interventions.
    MeSH term(s) Catecholamines/genetics ; Catecholamines/physiology ; DNA, Complementary/metabolism ; Dopamine/biosynthesis ; Dopamine beta-Hydroxylase/deficiency ; Dopamine beta-Hydroxylase/genetics ; Exons ; Heterozygote ; Humans ; Models, Biological ; Models, Chemical ; Mutation ; Mutation, Missense ; Norepinephrine Plasma Membrane Transport Proteins ; Symporters/metabolism ; Syndrome
    Chemical Substances Catecholamines ; DNA, Complementary ; Norepinephrine Plasma Membrane Transport Proteins ; SLC6A2 protein, human ; Symporters ; Dopamine beta-Hydroxylase (EC 1.14.17.1) ; Dopamine (VTD58H1Z2X)
    Language English
    Publishing date 2002-10
    Publishing country United States
    Document type Case Reports ; Journal Article ; Review
    ZDB-ID 211003-9
    ISSN 1749-6632 ; 0077-8923
    ISSN (online) 1749-6632
    ISSN 0077-8923
    DOI 10.1111/j.1749-6632.2002.tb04515.x
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