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At least 595 records · Page 33Linked to original sources
PubMed1985

Measurement of skin blood-flow and water evaporation as a means of objectively assessing hot flushes after orchidectomy in patients with prostatic cancer.

Hot flushes can occur after orchidectomy for carcinoma of the prostate and are sometimes greatly distressing for patients. Attacks are difficult to register because of their transient and unpredictable nature and have been the object of very little scientific investigation. In 13 postorchidectomy patients who reported hot flushes we recorded cutaneous blood-flow and sweating by use of a laser-Doppler flowmeter and an evaporimeter. A total of 23 attacks were recorded. The rate of evaporation increased by more than 60 g/m2/h in ten attacks, from 10 to 60 g/m2/h in five attacks, and by less than 10 g/m2/h in seven attacks. The cutaneous blood-flow increased synchronously with the increase in evaporation. The intensity of the attacks as experienced by the patients corresponded closely to recorded measurements.

Aged↗
PubMed1993

Unilateral loss of facial flushing and sweating with contralateral anhidrosis: harlequin syndrome or Adie's syndrome?

A 45-year-old woman presented with a 10 year history of asymmetrical facial flushing and sweating after exertion or in hot weather. During these episodes the right side of her face remained dry and white, while the left side normally flushed. Sweating was impaired on the left side in the limbs and trunk. She also had areflexia in the lower limbs and slow pupillary reactions to light and darkness, as seen in Adie's syndrome. The topography of the sweating disorder suggested that the lesion involved the sympathetic pathways at the level of spinal cord. The relationship with the harlequin syndrome and related disorders is discussed.

Adie Syndrome↗
PubMed1986

Flushing of the face as a result of chewing food.

This case depicts a clinical situation in which the patient's face became flushed after chewing food for approximately 30 seconds. The distribution of the flushing accurately defines the distribution of the zygomaticofacial branch of the trigeminal nerve. A theory involving the parasympathetic supply to this area is presented to explain this clinical pattern.

Child↗
PubMed1995

Mechanisms of physiological gustatory sweating and flushing in the face.

Mechanisms of physiological gustatory sweating and flushing were investigated in 21 patients with a facial nerve lesion compromising parasympathetic outflow to the lacrimal gland, and in 13 patients undergoing diagnostic blockade of the stellate ganglion. Vascular responses and electrodermal activity (which reflects sweating) were monitored on each side of the forehead before and during gustatory stimulation with chillies or Tabasco sauce (derived from chillies). Vascular responses in the cheeks were also monitored in 14 patients with a facial nerve lesion. Sympathetic blockade increased gustatory vasodilatation but prevented gustatory sweating on the blocked side of the forehead. A facial nerve lesion did not affect gustatory sweating in the forehead or vasodilatation in the cheeks. However, a facial nerve lesion impaired vasodilatation in the forehead in all six patients who ate chillies, and also in four of five patients whose blood vessels dilated extensively on the normally-innervated side of the forehead when the patients tasted Tabasco sauce. These findings suggest that sympathetic sudomotor activity mediates physiological gustatory sweating in the forehead, whereas sympathetic vasoconstrictor tone inhibits gustatory vasodilatation in the forehead. A parasympathetic vasodilator reflex in the facial nerve contributes actively to gustatory flushing in the forehead, but some other unidentified mechanism influences vascular responses in the cheeks.

Adrenergic Fibers↗
PubMed1985

The effects of naloxone infusion and stellate ganglion blockade on hot flushes in the human male.

A 77-yr-old man presented with severe episodes of hypotension, flushing and sweating starting immediately after infarcting his only remaining functioning testis. The attacks were shown to be mediated by the cervical sympathetic chain, the reaction on the face and neck being abolished by a stellate ganglion block. The severity and frequency of sweating was also considerably reduced with naloxone as may be seen in female climacteric flushing. Injection of testosterone significantly reduced the frequency and severity of the attacks, which were unaltered by oestrogen treatment.

Aged↗
PubMed2006

Nicotinic acid induces secretion of prostaglandin D2 in human macrophages: an in vitro model of the niacin flush.

Nicotinic acid is a safe, broad-spectrum lipid agent shown to prevent cardiovascular disease, yet its widespread use is limited by the prostaglandin D2 (PGD2) mediated niacin flush. Previous research suggests that nicotinic acid-induced PGD2 secretion is mediated by the skin, but the exact cell type remains unclear. We hypothesized that macrophages are a source of nicotinic acid-induced PGD2 secretion and performed a series of experiments to confirm this. Nicotinic acid (0.1-3 mM) induced PGD2 secretion in cultured human macrophages, but not monocytes or endothelial cells. The PGD2 secretion was dependent on the concentration of nicotinic acid and the time of exposure. Nicotinuric acid, but not nicotinamide, also induced PGD2 secretion. Pre-incubation of the cells with aspirin (100 microM) entirely prevented the nicotinic acid effects on PGD2 secretion. The PGD2 secreting effects of nicotinic acid were additive to the effects of the calcium ionophore A23187 (6 microM), but were independent of extra cellular calcium. These findings, combined with recent in vivo work, provide evidence that macrophages play a significant role in mediating the niacin flush and may lead to better strategies to eliminate this limiting side effect.

Aspirin↗
PubMed1983

Cyproterone acetate in treatment of post-orchidectomy hot flushes. Double-blind cross-over trial.

12 patients with troublesome hot flushes after orchidectomy (as a primary treatment for prostatic carcinoma) were treated with cyproterone acetate or placebo in a double-blind cross-over trial. The frequency of hot flushes was significantly reduced during the three weeks that cyproterone acetate (100 mg three times a day) was given. 5 patients complained of lassitude while on cyproterone acetate, but in none was it necessary to discontinue treatment.

Aged↗
PubMed2003

Aldehyde dehydrogenase 2 genotypes, alcohol flushing symptoms and drinking patterns in Thai men.

The drinking behavior, alcohol-induced facial flushing and ALDH2 genotypes were determined in 283 Thai men comprising 85 who were alcohol-dependent, 62 hazardous/harmful drinkers and 136 non-drinkers or infrequent drinkers. A structured interview questionnaire, containing the 'tri-level' method and the Alcohol-Use Disorders and Associated Disabilities Schedule, was used to determine the quantity of drinking and the number of alcohol-related adverse experiences. The study revealed the mutant ALDH2*2 allele in 44 (15.5%) subjects. The risks of being alcohol-dependent and of having hazardous/harmful drinking were lower in individuals with heterozygous ALDH2*1/*2, compared with homozygous ALDH2*1/*1 [relative probability ratios (95% CI) 0.14 (0.05-0.41) and 0.23 (0.08-0.61), respectively]. Eighty percent of those who were heterozygous and 28% of those who were homozygous ALDH2*1 reported flush symptoms after drinking alcohol. Twenty-nine percent of homozygous ALDH2*1 individuals, but only 9% of heterozygous subjects, drank almost everyday (24-30 days/month). Similarly, higher percentages of people drinking beyond the safety limit (>60 g/day) and having alcohol-related problems were observed in homozygous ALDH2*1 compared with heterozygous individuals: 32% vs. 5% and 27% vs. 12%, respectively. Overall, the study supports the role of the mutant ALDH2*2 allele in preventing high alcohol consumption and the development of alcohol dependence in a Thai population.

Adult↗
PubMed1999

Co-distribution of sensory gating and impaired niacin flush response in the parents of schizophrenics.

Complex illnesses may result from the interaction or addition of multiple factors. We examined the familial co-distribution of two abnormalities common in schizophrenia: impaired auditory sensory gating and impaired flush response to niacin. In ten families, the obligate carrier parent had sensory-gating deficits, while eight of the ten parents without a family history of schizophrenia had impaired flush response. No parents had both deficits. The data are consistent with a theory suggesting the interaction of these two factors in some cases of schizophrenia.

Evoked Potentials, Auditory↗
PubMed1999

Facial flushing during provocation in women.

Facial flushing was studied in 38 young women who scored high or low on trait anger. To induce anger in the subjects, their task was to solve a difficult puzzle, with or without harassment from a female research assistant. Facial blood flow increased in response to provocation, together with increases in cardiovascular and electrodermal activity. Flushing was associated with large increases in electrodermal activity and small increases in diastolic blood pressure. Subjects high in trait anger reported most anger and embarrassment, but physiological activity did not differ from subjects with low trait anger. The findings suggest that sympathetically mediated vasodilatation in facial blood vessels competes with cutaneous vasoconstriction during anger. Unpleasant sensations of facial warmth might heighten aversive emotional experiences, but dilatation of facial blood vessels could also act as a type of "safety valve" by opposing increases in blood pressure. An angry predisposition may influence the subjective experience of anger in women, but does not seem to have a major influence on physiological reactivity to mild provocation.

Adult↗
PubMedDate not supplied

Drug-alcohol flush reaction and breath acetaldehyde concentration: no interference with an infrared breath alcohol analyzer.

Human volunteers were given a small dose of ethanol (0.25 g/kg body weight) after pretreatment with either calcium carbimide (50 mg) or a placebo according to a crossover design. Calcium carbimide, an inhibitor of aldehyde dehydrogenase, caused intense facial flushing and a pronounced rise in the concentration of acetaldehyde in breath. At 15-min intervals throughout the experiment, breath-ethanol concentrations were determined both by gas chromatography (GC) (specific method) and by infrared (IR) spectrometry with an Intoxilyzer model 4011 breath-alcohol analyzer. The results with these two independent methods of analysis were compared in experiments with and without calcium carbimide pretreatment. The regression equations relating breath-ethanol determinations by GC and IR methods in the two test situations were not significantly different. The elevated breath concentrations of acetaldehyde associated with a drug-alcohol flush reaction do not invalidate the use of infrared breath-alcohol devices for evidential purposes.

Acetaldehyde↗
PubMed1990

Effects of aspirin upon the flushing reaction induced by niceritrol.

The usefulness of niceritrol as a lipid-lowering agent is limited by a prostaglandin-mediated flushing reaction after each dose occurring in the early stages of treatment. We have tested the effect of premedication with aspirin on the reaction to 250 mg niceritrol in 30 healthy male volunteers using both subjective and observed assessments of severity. Both 300 mg and 600 mg of aspirin significantly reduced the severity of flushing when compared with placebo. No significant difference was seen between the two dose levels. Prior dosing with aspirin may increase acceptability of niceritrol and hence improve compliance.

Adolescent↗
PubMed1989

Hot flushes are induced by thermogenic stimuli.

Hot flushes were caused by hot drinks, alcohol, radiant heaters and thermal blankets in men undergoing treatment for carcinoma of the prostate and in menopausal women. Avoiding or changing these commonplace stimuli appears to reduce the frequency of flushing.

Aged↗
PubMed2006

"Flush-free niacin": dietary supplement may be "benefit-free".

This report describes a patient with coronary artery disease who was instructed to take extended-release niacin to treat low high-density lipoprotein cholesterol and instead purchased "flush-free niacin" available at the pharmacy. There was no significant change in his lipids. Once the patient switched to extended-release niacin, the anticipated beneficial effects were seen. The article reviews the composition of flush-free niacin, its purported and real lipid effects, and warns against the effects of misleading marketing.

Cholesterol, HDL↗
PubMedDate not supplied

Lowering of blood acetaldehyde but not ethanol concentrations by pantethine following alcohol ingestion: different effects in flushing and nonflushing subjects.

A rise in blood acetaldehyde concentrations following alcohol ingestion was significantly inhibited when healthy nonflushing subjects were administered a clinical dose of pantethine orally. However, similar findings were not observed in flushing (alcohol-sensitive) subjects lacking hepatic low Km aldehyde dehydrogenase (ALDH). The blood ethanol concentrations were not altered by this treatment in either flushing or nonflushing subjects. Acetaldehyde (45 microM) added in vitro to whole blood and plasma obtained 1 hr after pantethine administration disappeared as the incubation continued similarly as with blood and plasma obtained prior to pantethine treatment. Pantethine-related metabolites, such as taurine, pantetheine, coenzyme A, and pantothenate, activated ALDH in vitro. Hepatic acetaldehyde levels following ethanol loading of rats treated with pantethine were much lower than in untreated rats. The pantethine action observed only in nonflushing subjects might be due to an accelerated oxidation of acetaldehyde by the activation of low Km ALDH by pantethine-related metabolites formed in the liver.

Acetaldehyde↗
PubMed1997

Recurrent near-syncope with flushing.

Episodic vasomotor instability with flushing is an uncommon presentation that is suggestive of an endocrine etiology. This report is the case of a 42-year-old woman who presented to the ED 5 times in a 2-week period for recurrent, self-limited episodes of light-headedness associated with tachycardia, hypertension, and flushing. The patient's diagnosis eluded detection in both the outpatient and the inpatient settings for several months. The clinical diagnosis was ultimately confirmed by biochemical test samples obtained in the ED during a subsequent symptomatic event. The differential diagnosis of this patient's presentation includes pheochromocytoma, carcinoid syndrome, medullary thyroid carcinoma, systemic mastocytosis, and other endocrine and toxicologic diseases. ED management of the patient with transient yet significant vasomotor changes includes a workup for syncope, initiation of focused biochemical investigations, referral to the appropriate consultant, and consideration for admission.

Adult↗
PubMed1990

Congenital Horner's syndrome with unilateral facial flushing.

Two patients with congenital Horner's syndrome had unilateral facial flushing. Both showed pupillary supersensitivity to epinephrine as well as anhidrosis on the affected side of the face and neck. Facial skin temperature after exercise increased on the intact side, but decreased on the affected side. Thermal vasodilation in the major portions of the face is regulated by sympathetic vasodilator fibres, and less predominantly by adrenergic vasoconstrictor fibres. The asymmetry of facial flushing may have been caused by impaired sympathetic vasodilation and further intensified by active vasoconstriction due to supersensitivity to circulating catecholamine on the affected side.

Adult↗
PubMed1990

Loss of facial sweating and flushing in Holmes-Adie syndrome.

We investigated pupillary responses to parasympathetic (pilocarpine) and sympathetic agents (tyramine, cocaine, and phenylephrine) in a 51-year-old woman with tonic pupils, loss of muscle stretch reflexes in the limbs, and hemifacial loss of sweating and flushing (Ross' syndrome). A smaller pupillary response to tyramine and cocaine eyedrops on the symptomatic side indicated that outflow was disrupted in the postganglionic section of the ocular sympathetic pathway. A greater response to phenylephrine eyedrops on this side was consistent with denervation supersensitivity to adrenergic agents. Loss of thermoregulatory sweating and flushing and emotional blushing in the forehead, cheek, and chin indicated that sympathetic disruption was proximal to the bifurcation of the common carotid artery, probably in the superior cervical ganglion. A similar degenerative process may be responsible for loss of muscle stretch reflexes, tonic pupils, and other autonomic disturbances in Ross' syndrome.

Adie Syndrome↗