Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a sample of 114 patients, 6 patients developed hypertension while taking tricyclic antidepressants. All these patients were diagnosed as having panic disorder, with or without major depression. Half of the 6 patients had a previous diagnosis of hypertension, which had been well controlled by antihypertensive drugs for years. A comparison group of patients with major depression, who had never had panic attacks, had no cases of hypertension induced by these antidepressants. These findings raise the possibility that patients who have panic disorder may experience cardiovascular disregulation that increases their risk for antidepressant-induced hypertension.
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PMID:Systemic hypertension associated with tricyclic antidepressant treatment in patients with panic disorder. 144 82

In order to examine the validity of the distinction between generalized anxiety disorder (GAD) and panic disorder (PD) we compared 41 subjects with GAD and 71 subjects with PD. The GAD subjects had never had panic attacks. In contrast to the symptom profile in PD subjects suggestive of autonomic hyperactivity, GAD subjects had a symptom pattern indicative of central nervous system hyperarousal. Also, subjects with GAD had an earlier, more gradual onset of illness. In terms of coexisting syndromes, GAD subjects more often had simple phobias, whereas PD subjects more commonly reported depersonalization and agoraphobia. GAD subjects more frequently had first-degree relatives with GAD, whereas PD subjects more frequently had relatives with PD. A variety of measures indicated that our GAD subjects had a milder illness than those with PD. Also, fewer GAD subjects gave histories of major depression than did PD subjects. Among GAD subjects, coexisting major depression was associated with simple phobia and thyroid disorders and among PD subjects, comorbid depression was associated with social phobia and hypertension. Our findings indicate that the separation of GAD from PD is a valid one. They also indicate that, within disorders, unique patterns of comorbidity may exist that are important both clinically and theoretically.
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PMID:Generalized anxiety disorder vs. panic disorder. Distinguishing characteristics and patterns of comorbidity. 143 31

An hypothesis is proposed that there exists a subgroup of African-American hypertensive patients whose hypertension could have been prevented by the early detection and treatment of easily recognizable symptoms that signal the initiation of the pathophysiologic processes that lead to essential hypertension.A pilot study of 31 patients with elevated blood pressure revealed that 41.9 percent had isolated sleep paralysis, 35.5 percent had panic attacks, and 9.7 percent had panic disorder. These proposed hyperadrenergic phenomena may be related to the development of hypertension in certain individuals.
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PMID:The relationship of isolated sleep paralysis and panic disorder to hypertension. 335 70

Episodic elevation of blood pressure was evaluated in two middle-aged men by assessing home, clinic, and 24-hour ambulatory values following exclusion of secondary forms of hypertension. Both individuals had normotensive home and clinic readings. The 24-hour blood pressure was 125/85 +/- 12/9 mm Hg in patient 1 and 119/84 +/- 13/13 mm Hg in patient 2; however, both patients experienced large, sustained rises in blood pressure associated with panic attacks that were not abolished with prophylactic benzodiazepine therapy. Episodic blood pressure elevations were not associated with concomitant increases in heart rate. Patient 1 underwent extensive psychological investigation that diagnosed a panic disorder, and he underwent therapy that reduced the frequency and intensity of his panic-related hypertensive episodes. Because patient 2 demonstrated hypertensive readings at work, he was given a beta-blocking agent that ultimately controlled his blood pressure during episodes of anxiety and panic. These findings suggest that patients with panic attacks may present with episodic hypertension and that ambulatory blood pressure monitoring is useful in the diagnosis of this disorder and in assessment of treatment outcome.
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PMID:Episodic hypertension secondary to panic disorder. 371

Panic disorder is a specific psychiatric entity with specific and successful treatments. A parturient patient with sudden hypertension, hyperreflexia and headache was diagnosed with pre-eclampsia and treated with magnesium sulphate. Further attacks after discharge were recognized as panic attacks, and resolved with the anti-depressant imipramine.
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PMID:Panic disorder masquerading as pre-eclampsia. 828 46

Citalopram is a chiral antidepressant drug. Its eutomer, S-citalopram (escitalopram), has recently been introduced as an antidepressant. In an open pilot study, four outpatients and two inpatients with a major depressive episode (ICD-10), and who were nonresponders to a 4-week pretreatment with 40-60 mg/day citalopram, were comedicated for another 4-week period with carbamazepine (200-400 mg/day). Some of the patients suffered also from comorbidities: Phobic anxiety disorder with panic attacks (n=2), generalised anxiety disorder, alcohol abuse, dependent personality disorder, hypertension (n=1). After a 4-week augmentation therapy with carbamazepine, a significant (P<0.03) decrease of the plasma concentrations of S-citalopram and R-citalopram, by 27 and 31%, respectively, was observed. Apparently, the probable induction of CYP3A4 by carbamazepine results in a nonstereoselective increase in N-demethylation of citalopram. Moreover, there was a significant (P<0.03) decrease of the ratio S/R-citalopram propionic acid derivative, the formation of it being partly regulated by MAO-A and MAO-B. Already, within 1 week after addition of carbamazepine, there was a slight but significant (P<0.03) decrease of the MADRS depression scores, from 27.0+/-7.7 (mean+/-S.D.) to 23.3+/-6.6, and the final score on day 56 was 18.8+/-10.9. The treatment was generally well tolerated. There was no evidence of occurrence of a serotonin syndrome. After augmentation with carbamazepine, treatment related adverse events were: Nausea in one case, diarrhea in one case, and rash in two cases. In conclusion, the results of this pilot study suggest that carbamazepine augmentation of a citalopram treatment in previous nonresponders to citalopram may be clinically useful, but that in addition carbamazepine can lead to a decrease of the plasma concentrations of the active enantiomer escitalopram.
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PMID:Carbamazepine augmentation in depressive patients non-responding to citalopram: a pharmacokinetic and clinical pilot study. 1200 77

The authors aimed to determine whether hypertensive patients with panic attacks or panic disorder have a larger white coat effect (difference between clinic blood pressure measured under standard conditions and mean daytime ambulatory blood pressure) than hypertensive patients without panic attacks. White coat effect was compared in a hospital hypertension clinic between 24 patients with panic attacks in the previous 6 months (12 with panic disorder) and 23 hypertensive controls. There were no significant differences between cases and controls in clinic blood pressure, mean daytime ambulatory blood pressure, or white coat effect (18/3 vs. 19/6 mm Hg; difference for systolic, -1.9 mm Hg; 95% confidence interval, -15.8 to +12.0; difference for diastolic, -3.0 mm Hg; 95% confidence interval, -10.2 to +4.3). Comparing only patients with panic disorder with controls, there were again no significant differences in clinic blood pressure, mean daytime ambulatory blood pressure, or white coat effect. This study provides no evidence for an exaggerated white coat effect in hypertensive patients who have experienced panic attacks or panic disorder. However, only larger studies could exclude differences in white coat effect <12/4 mm Hg, or an exaggerated white coat effect in a minority of patients with panic attacks.
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PMID:No evidence that panic attacks are associated with the white coat effect in hypertension. 1267 28

Approximately one quarter of patients who present to physicians for treatment of chest pain have panic disorder. Panic disorder frequently goes unrecognized and untreated among patients with chest pain, leading to frequent return visits and substantial morbidity. Panic attacks may lead to chest pain through a variety of mechanisms, both cardiac and noncardiac in nature, and multiple processes may cause chest pain in the same patient. Panic disorder is associated with elevated rates of cardiovascular diseases, including hypertension, cardiomyopathy, and, possibly, sudden cardiac death. Furthermore, patients with panic disorder and chest pain have high rates of functional disability and medical service utilization. Fortunately, panic disorder is treatable; selective serotonin reuptake inhibitors, benzodiazepines, and cognitive-behavioral psychotherapy all effectively reduce symptoms. Preliminary studies have also found that treatment of patients who have panic disorder and chest pain with benzodiazepines results in reduction of chest pain as well as relief of anxiety.
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PMID:Panic Disorder and Chest Pain: Mechanisms, Morbidity, and Management. 1501 45

The aim of the present study was to evaluate the efficacy and safety of zolpidem in elderly subjects with disorders of sleep and comorbidities. The patients of this study had to present the following requirements: age over 70 years, reported disorders of sleep such as insomnia, and they had to be affected with diabetes and arterial hypertension. Patients presenting diseases that could interfere with sleep, i.e., anxiety, depression, panic attacks,alcohol abuse, some drugs were excluded from the study. All the jobs potentially causing insomnia carried out in the past from the patients were considered, too. A questionnaire of sleep was administered to all the patients (World Psychiatric Association: WPA, 1971).Insomnia, whenever present, was classified according to the criteria of the American Sleep Disorders (ASD) Society and the American Professional Sleep Society (APSS). The following scales were also administered: instrumental activities of daily living scale (IADL),activities of daily living (ADL), geriatric depression scale (GDS), cumulative illness rating scale (CIRS), short portable mental status questionnaire (SPMSQ), mini nutritional assessment (MNA), disease medical index (DMI), sleep questionnaire, social and environmental status. Two groups of patients were evaluated. Group A: 50 patients, 35 women and 15 men, mean age 78.9 years, with a history of insomnia, and Group B 30 patients, 20 women and 10 men, mean age 78.4 years, with onset of insomnia in the last three weeks. The two groups were further divided into three subgroups, diabetic, hypertensive and healthy patients. Zolpidem showed to be effective and well tolerated in both groups of patients.
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PMID:Use of zolpidem in over 75-year-old patients with sleep disorders and comorbidities. 1520 2

The ability of serotonin (5-HT) to facilitate or attenuate autonomic, endocrine, and behavioral responses to stressful stimuli has received much attention. The effects of 5-HT on physiologic and behavioral responses to stressful stimuli seem to depend on the brain region where it is released and the effector system it acts upon. This and the distinct morphology and topographic organization of subpopulations of serotonergic neurons have led to the hypothesis that subpopulations of serotonergic neurons are functionally distinct. Serotonin's role as a modulator of the "fight-or-flight" response is mediated in part by 5-HT release in the dorsolateral periaqueductal gray (DLPAG) and in the rostral ventrolateral medulla (RVLM), an area that contains sympathoexcitatory C1 adrenergic (A) neurons. The release of 5-HT in either region inhibits stress-induced sympathetic activity in part via actions on 5-HT(1A) receptors. In addition, 5-HT release in the DLPAG inhibits fight-or-flight or "Go" behaviors. The origin of endogenous 5-HT in the DLPAG and RVLM seems to be a subpopulation of serotonergic neurons within the ventrolateral PAG, a region implicated in "freezing" or "No Go" behaviors. These serotonergic neurons are located in the lateral "wings" of the dorsal raphe nucleus (DRN) a region also referred to as the ventrolateral DRN. The existence of a functional subpopulation of serotonergic neurons capable of inhibiting sympathoexcitation and fight-or-flight behavioral responses may be clinically relevant for explaining in part the efficacy of serotonergic drugs in the treatment of hypertension and panic attacks in panic disorder patients.
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PMID:A functional subset of serotonergic neurons in the rat ventrolateral periaqueductal gray implicated in the inhibition of sympathoexcitation and panic. 1524 Mar 52


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