Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033377 (prolapse)
 11,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

2-(3,4-Dichlorobenzyl)-2-dimethylamino-1-propanol, hydrochloride (JO 1017) is a novel antidepressant drug. Its biochemical and pharmacological properties were investigated in mice, rats, dogs, rabbits and guinea pigs. In vitro, it selectively inhibited serotonin uptake and had a high affinity for the 3H-paroxetine and 3H-imipramine binding sites. Biochemical studies demonstrated the lack of MAO-A and MAO-B inhibition and the absence of marked affinity for muscarinic, histaminic or other conventional brain receptors. Chronic treatment with JO 1017 induced a decrease in the Bmax values for imipramine sites but did not modify the Bmax for beta-adrenergic and 5-HT2 receptors. The neuropsychopharmacological profile of JO 1017 is characterized by a decrease of the immobility times in behavioural despair tests with mice, a decrease of the escape failures in the rat learned helplessness test, a strong potentiation of L-5-HT P-induced head-twitches in mice and an antagonism of reserpine-induced ptosis in rabbits. It weakly antagonized oxotremorine-induced hypothermia and did not influence the hypothermia induced by apomorphine. In contrast to most other antidepressants, a high dose of JO 1017 induced hypermotility in mice placed in an activity meter without producing stereotyped behaviour and group toxicity. Unlike tricyclic antidepressants, JO 1017 was devoid of severe cardiotoxicity in guinea pigs and had no central anticholinergic nor antihistaminic properties. These results suggest that JO 1017 is a selective serotonin uptake inhibitor with a high safety margin. JO 1017 may have a potential clinical utility both in the treatment of depression and for indications where serotonin transmission is involved, e.g., anxiety, panic attack, obsessive compulsive disorder, obesity and alcohol consumption.
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PMID:Biochemical and pharmacological evaluation of the novel antidepressant and serotonin uptake inhibitor 2-(3,4-Dichlorobenzyl)-2-dimethylamino-1-propanol hydrochloride. 216 3

Panic disorder with or without agoraphobia is dominated by the occurrence of panic attacks. However, panic attacks are also reported to occur as part of the clinical picture in several medical conditions, notably thyroid disease, hypoglycemia, and pheochromocytoma. The authors examine these conditions, review the relevant literature, and offer an evaluation strategy. Routine screening is not recommended. Panic disorder is also associated with mitral-valve prolapse and temporal lobe seizures. The authors explore the possible consequences of this association and outline an evaluation strategy. Again, routine screening is not recommended.
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PMID:Medical evaluation of panic attacks. 330 23

Whether mitral valve prolapse (MVP) is more common in patients with panic disorder (PD) and agoraphobia with panic attacks (AgP) than in the normal population is controversial. A related issue is whether the presence of MVP in such patients has any clinical or biological significance. Echocardiograms were performed on 36 patients with PD/AgP and 22 normal controls. MVP was found to be more common in PD/AgP patients than in normal controls. However, MVP in the patients was mild and not associated with thickened mitral leaflets or small left ventricular size. Moderate or severe prolapse was uncommon in both groups. Patients with MVP had trends to higher heart rate and prolonged QTc interval on EKG, and reported more respiratory difficulty during panic attacks compared to patients without MVP. Lactate infusion did not affect patients with MVP differently than patients without MVP. The authors conclude that MVP is more common in patients with PD or AgP than in normal controls, but is of doubtful clinical significance.
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PMID:The mitral valve prolapse--panic disorder connection. 337 3

Mitral valve prolapse, the most common inherited cardiovascular condition, has been associated with a variety of signs, symptoms and electrocardiographic abnormalities, but the true spectrum of the mitral prolapse syndrome remains in doubt because clinical findings often contribute to patient identification and their prevalence in patient groups may be overstated because of ascertainment bias. Accordingly, clinical findings in 88 patients with echocardiographic mitral prolapse were compared with those in 81 of their adult first degree relatives with mitral prolapse (a group free of ascertainment bias) and in two control groups without mitral prolapse: 172 first degree relatives and 60 spouses. Comparison of relatives with and without mitral prolapse demonstrated true associations between mitral prolapse and clicks or murmurs, or both (67 versus 9%, p less than 0.001), thoracic bony abnormalities (41 versus 16%, p less than 0.001), systolic blood pressure less than 120 mm Hg (53 versus 31%, p less than 0.001), body weight 90% or less of ideal (31 versus 14%, p less than 0.005) and palpitation (40 versus 24%, p less than 0.01). In contrast, relatives with mitral prolapse showed no significant increase over normal relatives or spouses without mitral prolapse in prevalence of chest pain, dyspnea, panic attacks, high anxiety or repolarization abnormalities, but these features were all more common in women than in men (p less than 0.01 to less than 0.001). Thus, the true spectrum of the mitral prolapse syndrome encompasses a midsystolic click and late systolic murmur, thoracic bony abnormalities, low body weight and blood pressure and palpitation. Other suggested clinical features, including nonanginal chest pain, dyspnea, panic attacks and electrocardiographic abnormalities, have appeared to be associated with mitral valve prolapse because of ascertainment bias and an erroneous classification of differences between men and women as being due to mitral valve prolapse.
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PMID:Relation between clinical features of the mitral prolapse syndrome and echocardiographically documented mitral valve prolapse. 376 Mar 52

One explanation for the association between mitral valve prolapse (MVP) and panic attacks in clinic populations is that panic attacks represent a set of symptoms caused by mitral prolapse. Since mitral prolapse is often familial, this hypothesis predicts a higher incidence of panic attacks in relatives of persons with prolapse than the general population and the incidence of panic attacks in the relatives should be independent of panic attacks in the proband. We interviewed 50 probands with mitral prolapse and obtained family history data on panic attacks in their first degree relatives. The incidence of panic attacks in these relatives was 4.5 +/- 1.4% which is consistent with control rates which we have reported in previous studies. Twelve MVP probands also had panic attacks. The incidence of panic attacks in their relatives (15.7 +/- 5.1%) was significantly higher than the rate found among relatives of 38 probands without panic attacks (1.2 +/- 0.8%). These findings are consistent with the hypothesis that mitral prolapse and panic attacks are segregating independently in these families.
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PMID:Panic attacks in families of patients with mitral valve prolapse. 621 90

In 25 patients with panic attacks the prevalence of mitral valve prolapse was 8%, close to that in the general population. The higher rates in previous reports may be due to differences in prolapse criteria, sampling techniques, or the samples' sex ratios.
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PMID:Low prevalence of mitral valve prolapse in patients with panic disorder. 669 4

It has been reported that panic attacks might cause mitral valve prolapse (MVP) via haemodynamic or indirect effects. Such prolapse can be classified as being physiological (benign course) or pathological (poor course). It is therefore important to consider whether panic attacks, as a risk factor for MVP, are associated with its physiological or pathological type. Our study sample consisted of two groups of patients with panic disorder (PD), one having onset within 1 year (n=24) and the other with a history of more than 10 years (n=21). Demographic data, symptom presentations, auscultatory and echocardiographic findings of both groups were compared, but no significant difference was found except with regard to anticipatory anxiety. It is concluded that panic attack exerts no significant effect on mitral valve prolapse.
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PMID:The effect of panic attack on mitral valve prolapse. 942 35

The adenosine A2a receptor (A2aAR) is thought to be implicated in the pathogenesis of panic disorder because caffeine, a potent antagonist for A2aAR, can precipitate panic attacks, and because disruption of the A2aAR gene increased anxiety-behaviors in mice. Recent studies demonstrated that the A2aAR 1976T > C genetic variant confers susceptibility to panic disorder though not by all studies. The present study tested the hypothesis that the A2aAR 1976T > C genetic variant confers susceptibility to panic disorder using a Chinese population of 104 panic disorder patients and 192 normal controls. We also tested whether the A2aAR 1976T > C polymorphism relates to the age of onset or subtype of panic disorders. Neither the distribution of the A2aAR 1976T > C genotypes (P = 0.296) or alleles (P = 0.864), nor the age of onset (P = 0.719) were significantly different among genotype groups. Furthermore, no association was demonstrated between this A2aAR polymorphism and either mitral-valve prolapse or agoraphobia in panic-disorder patients. These findings suggested that it is unlikely that the A2aAR 1976T > C polymorphism plays a major role in panic disorder pathogenesis in the Chinese population. The positive association between this polymorphism and panic disorder found in western population but not in Asian population suggests that this association could be ethnicity-dependent. The 1976C > T polymorphism may be in linkage disequilibrium with a functional variant that affects panic disorder, and the extent of this linkage disequilibrium is not similar for all ethnic populations.
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PMID:Association study of A2a adenosine receptor genetic polymorphism in panic disorder. 1577 65

BACKGROUND Myasthenia gravis (MG) is an autoimmune disease characterized by antibodies binding skeletal muscle acetylcholine receptors (AChR). Rarely does the disease manifest with orolaryngeal symptoms before ocular ones. We present a case of MG that on initial presentation had symptoms of cranial nerves (CN) IX and X weakness, including dysphagia and dysphonia. CASE REPORT A 51-year-old woman with panic attacks presented to the Emergency Department (ED) with complaints of her throat closing, swallowing difficulty, and hoarse voice. Multiple ED visits revealed no etiology. However, she developed stridor, which prompted further evaluation. Laryngoscopy and imaging studies revealed no gross abnormalities; therefore, her symptoms of dysphonia and difficulty breathing were attributed to anxiety. Her hospital course was complicated by a cardiac arrest requiring intubation. ECHO, CTA chest, and MRI brain were unremarkable. Her cardiac arrest was hypothesized as being secondary to laryngeal spasm. During her ICU course, she failed extubation multiple times due to acute respiratory failure. An autoimmune etiology was suspected, prompting a paraneoplastic screen, which revealed elevated levels of AChR antibodies at 124 mmol/L. MG was diagnosed and treatment with plasmapheresis and steroids was initiated. However, complications of thrombocytopenia, anemia, and ARDS ensued, so MG treatment was discontinued. The patient was eventually transferred to a LTACH. Thereafter, at outpatient followup, her MG was treated with mycophenolate and prednisone, which led to significant symptom improvement. CONCLUSIONS MG commonly presents in the third decade with clinical features of ptosis, diplopia, and facial weakness. However, initial and isolated symptoms of dysphagia and dysphonia are rare, leading to missed diagnoses. Our case of a middle-aged woman posed a diagnostic challenge because of her uncommon presentation and comorbidities of panic attacks and obesity. This case highlights the crucial need for a high index of clinical suspicion for MG in any patient presenting with symptoms of CN IX and X weakness.
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PMID:Cranial Nerve IX and X Weakness: An Unusual Initial Presentation of Myasthenia Gravis. 3277 33