Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016382 (flushing)
6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper reviews a wide range of somatization-related symptoms that are encountered in dermatology. These include the unexplained cutaneous sensory syndromes especially the cutaneous dysesthesias associated with pain, numbness and pruritus; traumatic memories in post-traumatic stress disorder (PTSD) which are experienced on a sensory level as 'body memories' and may present as local or generalized pruritic states, urticaria and angioedema; and unexplained flushing reactions and profuse perspiration, in addition to unexplained exacerbations of stress-reactive dermatoses such as psoriasis and atopic eczema secondary to the autonomic hyperarousal in PTSD; classic 'pseudoneurologic' symptoms associated with dissociation including unexplained loss of touch or pain, in addition to the self-induced dermatoses such as dermatitis artefacta and trichotillomania that are encountered with dissociative states; and body dysmorphic disorder where the patient often presents with a somatic preoccupation involving the skin or hair.
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PMID:Somatization disorders in dermatology. 1645 79

Endometriosis is an estrogen-dependent gynaecological disease associated with pain and infertility, which occurs in humans and menstruating primates. In this study, the marmoset monkey (Callithrix jacchus), which is a non-menstruating primate with high circulating estrogen levels, was used to test firstly the hypothesis that endometriosis is based on uterine shedding into the peritoneal cavity, secondly to study the pathogenesis of endometriosis due to its estrogenic situation. Female marmoset monkeys (n = 29) were exposed to two different experimental procedures (non-invasive versus invasive) for intrapelvic placement of endometrial cells by uterine flushing over an experimental period of 2-3 years. First endometriotic foci were detected by colour Doppler ultrasound at the bladder, the uterus and the ovaries at the earliest after 4 months of either treatments. However, invasive induction was more effective in terms of the time-course of induction and the number of resulting endometriotic foci. The analysis of the endometriotic foci by histology, immunohistochemistry and molecular techniques allowed a division into two distinct groups: an initial developing stage occurred, which under further treatment led to the second stage of established endometriosis. Both procedures showed a treatment-dependent increase of vascular supply to the endometriotic foci over the experimental period. The invasive method induced the final established stage of endometriosis more rapidly, with the expression of steroid receptors, aromatase, 17betaHSD1 and CD10. Altogether, 72% of the treated marmoset monkeys developed endometriosis under our endometrial reflux protocols. Our data support the theory that endometriosis can be induced artificially in a non-menstruating primate (C. jacchus) by endometrial shedding into the peritoneal cavity. Because the marmoset is a primate with very high peripheral estrogen levels, this offers an interesting model for studying the pathogenesis of this estrogen-dependent disease, as well as for therapeutic impacts on enzymes involved in steroid metabolism.
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PMID:Induction of endometriosis in the marmoset monkey (Callithrix jacchus). 1660 6

Lacrimation and nasal secretion during attacks of cluster headache appear to be due to massive trigeminal-parasympathetic discharge. In addition, the presence of oculo-sympathetic deficit and loss of thermoregulatory sweating and flushing on the symptomatic side of the forehead indicate that the cervical sympathetic pathway to the face is injured in a subgroup of cluster headache patients. In this review, it is argued that a peripheral rather than a central lesion produces signs of cervical sympathetic deficit, probably resulting from compression of the sympathetic plexus around the internal carotid artery. Although trigeminal-parasympathetic discharge appears to be the main trigger for vasodilation during attacks, supersensitivity to neurotransmitters such as vasoactive intestinal polypeptide, together with release of sympathetic vasoconstrictor tone, may boost facial blood flow in patients with cervical sympathetic deficit. In addition, parasympathetic neural discharge may provoke aberrant facial sweating during attacks in patients with cervical sympathetic deficit. Although neither trigeminal-parasympathetic discharge nor cervical sympathetic deficit appears to be the primary trigger for attacks of cluster headache, these autonomic disturbances could contribute to the rapid escalation of pain once the attack begins. For example, a pericarotid inflammatory process that excites trigeminal nociceptors might initiate neurogenic inflammation and trigeminal-parasympathetic vasodilation. To complete the loop, neurogenic inflammation and trigeminal-parasympathetic vasodilation could provoke the release of mast cell products, which aggravate inflammation and intensify trigeminal discharge.
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PMID:Mechanisms of autonomic disturbance in the face during and between attacks of cluster headache. 1668 2

Short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT) and short-lasting unilateral neuralgiform headache attacks with cranial autonomic features (SUNA) are described, although SUNA is rarely reported. The phenotype of SUNCT and SUNA was characterized from a large series of patients (43 SUNCT, 9 SUNA). Three attack types were identified: stabs, groups of stabs and saw-tooth attacks. The mean duration of stabs was 58 s (1-600 s); stab groups, 396 s (10-1200 s); and saw-tooth, 1160 s (5-12 000s). The attack frequency was a mean of 59 attacks/day (2-600), and this depended largely on the type of attack. The pain was orbital, supraorbital or temporal in 38 (88%) SUNCT and 7 (78%) SUNA, and also occurred in the retro-orbital region, side, top, back of head, second and third trigeminal divisions, teeth, neck and ear. All SUNCT patients had conjunctival injection and tearing. Two SUNA patients had conjunctival injection, four had tearing, but none had both. Other cranial autonomic symptoms included nasal blockage, rhinorrhoea, eyelid oedema, facial sweating/flushing and ear flushing. Cutaneous stimuli triggered attacks in 74% of SUNCT but only in 22% of SUNA patients. The majority (95% SUNCT and 89% SUNA) had no refractory period between attacks. For SUNCT 58% and for SUNA 56% of patients were agitated with the attacks. We propose a new set of diagnostic criteria for these syndromes to better encompass the clinical presentations and which include a wider range of attack length, wider trigeminal pain distribution, cutaneous triggering and lack of refractory period.
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PMID:Short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT) or cranial autonomic features (SUNA)--a prospective clinical study of SUNCT and SUNA. 1690 53

Tramadol is a synthetic, centrally acting opioid analgesic. An extended-release tablet formulation of tramadol (tramadol ER) allows gradual release of the active drug, permitting once-daily administration. Tramadol ER administered once daily is equivalent in bioavailability to immediate-release tramadol administered four times daily, with prolonged absorption and lower peak plasma concentrations. Tramadol ER was significantly more effective than placebo in the treatment of moderate to moderately severe chronic pain in patients with osteoarthritis of the knee and/or hip in randomised, double-blind, placebo-controlled trials. In a flexible-dose trial in patients with osteoarthritis of the knee, the mean reduction from baseline in pain intensity scores over 12 weeks was significantly greater in recipients of tramadol ER than in placebo recipients. In a fixed-dose trial in patients with osteoarthritis of the knee and/or hip, the mean improvements from baseline in the pain and physical function subscale scores of the Western Ontario and McMaster Universities Osteoarthritis Index over 12 weeks were significantly greater in tramadol ER than placebo recipients. Common adverse events reported in patients with moderate to moderately severe chronic pain treated with tramadol ER 100-300 mg once daily were dizziness (excluding vertigo), nausea, constipation, somnolence and flushing.
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PMID:Tramadol extended-release tablets. 1710 Apr 15

Paroxysmal extreme pain disorder (PEPD), previously known as familial rectal pain (FRP, OMIM 167400), is an inherited disease causing intense burning rectal, ocular, and submandibular pain and flushing. Fertleman et al. (this issue of Neuron) show that mutations in SCN9A, the gene encoding the sodium channel Na(V)1.7 channels, are responsible for this syndrome. Together with earlier work implicating a distinct class of functional mutations in SCN9A in a distinct inherited pain syndrome, these results point to Na(V)1.7 channels as key players in signaling nociceptive information and as a potential target for drug therapy of chronic pain.
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PMID:Painful channels. 1714 99

Paroxysmal extreme pain disorder (PEPD), previously known as familial rectal pain (FRP, or OMIM 167400), is an inherited condition characterized by paroxysms of rectal, ocular, or submandibular pain with flushing. A genome-wide linkage search followed by mutational analysis of the candidate gene SCN9A, which encodes hNa(v)1.7, identified eight missense mutations in 11 families and 2 sporadic cases. Functional analysis in vitro of three of these mutant Na(v)1.7 channels revealed a reduction in fast inactivation, leading to persistent sodium current. Other mutations in SCN9A associated with more negative activation thresholds are known to cause primary erythermalgia (PE). Carbamazepine, a drug that is effective in PEPD, but not PE, showed selective block of persistent current associated with PEPD mutants, but did not affect the negative activation threshold of a PE mutant. PEPD and PE are allelic variants with distinct underlying biophysical mechanisms and represent a separate class of peripheral neuronal sodium channelopathy.
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PMID:SCN9A mutations in paroxysmal extreme pain disorder: allelic variants underlie distinct channel defects and phenotypes. 1714 94

The clinical symptoms of migraine are widely accepted to be related to the involvement of the autonomic nervous system, and especially to dysfunction in the regulation of the circulatory system and autonomic balance. Disturbance of the autonomic nervous system is a primary characteristic of migraine Therefore, patients with migraine have a variety of symptoms, such as vasodilatation (flushing), pilo-erection, nausea, vomiting, diarrhea, cutaneous vasoconstriction (pallor), and diaphoresis. The electrocardiographic changes seen during a migraine attack compared with the pain-free period could be secondary to reversible disturbances of the state of autonomic innervation of the heart and coronary arteries. Dysfunction of ANS may affect atrial and ventricular repolarization. For instance, increased sympathetic activity causes sinus tachycardia, but increased parasympathetic activity causes sinus bradycardia, atrioventricular block, and ST-segment and T-wave abnormalities. Comprehensive electrocardiographic analyses have been providing more details in terms of the detection of abnormalities in atrial and ventricular repolarization which potentially may result in arrhythmias in patients with migraine. However, there is no information in literature reporting the frequency of cardiac arrhythmias in migraine patients who had cardiac repolarization abnormalities. In this review, detailed electrocardiographic findings and their relation with the autonomic nervous system, including recent observations, have been evaluated. However, further studies are needed to investigate the association between autonomic dysregulation and cardiac repolarization abnormalities in patients with migraine.
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PMID:Autonomic dysfunction and cardiac repolarization abnormalities in patients with migraine attacks. 1732 46

The characteristics of disturbing primary headache and the occurrence of headache types were studied by sending a questionnaire to 1132 Finnish families of 6-year-old children. Children with headache in the preceding 6 months and their controls were clinically examined at the ages of 6 and 13. During the follow-up, half of the headaches, classified as migraine at age 6 years, were unchanged and 32% turned into tension-type headache. In children with tension-type headache, the situation was unchanged in 35%, and in 38% of children the headache type had changed to migraine. At preschool age the most common location of headache was bilateral and supraorbital, and at puberty bilateral and temporal. During the follow-up, symptoms concurrent with headache, such as odour phobia, dizziness and balance disturbances became more typical, whereas restlessness, flushing and abdominal symptoms became less marked. The early manifestation of both migraine and tension-type headache predict equally often migraine in puberty with marked changes in concurrent symptoms and pain localization.
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PMID:Changing headache from preschool age to puberty. A controlled study. 1737 6

Adenosine, a ubiquitous metabolic intermediate in the body, is involved in nearly every aspect of cell function, including neuromodulation and neurotransmission. Adenosine A(1) and A(2) receptors are widely distributed in the brain and spinal cord, and are a novel, non-opiate target for pain management. The potential of adenosine as a non-narcotic analgesic in anesthetized patients has been explored in clinical trials, including double-blind studies versus placebo and remifentanil infusion. These studies suggest that, compared to placebo or remifentanil, an intraoperative adenosine infusion stabilizes core hemodynamics and reduces the requirement for anesthesia during surgery. Further, adenosine improves postoperative recovery, as indicated by lower pain scores and less opioid consumption. The safety profile of adenosine has been well characterized based on use of currently approved adenosine products. The most common adverse events associated with its use include flushing, chest discomfort, dyspnea, headache, gastrointestinal discomfort, and lightheadedness. These effects are generally well tolerated and transient. Further studies are warranted to investigate the full potential of adenosine as a non-opioid analgesic in the perioperative setting.
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PMID:Adenosine as a non-opioid analgesic in the perioperative setting. 1764 10


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