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)

The in vivo effect of yeast-derived recombinant human granulocyte-macrophage colony-stimulating factor (rh GM-CSF) was investigated in 30 patients with advanced malignancy in a phase Ib trial. Patients were treated at four different dose levels (120 to 1,000 micrograms/m2/d) by either daily intravenous (IV) bolus injection or 24-hour continuous infusion. Administration of rh GM-CSF resulted in a broad spectrum of dose- and schedule-dependent hematopoietic effects. Sustained infusion of rh GM-CSF elicited a maximum 17-fold average peak increase of the total WBC count with mainly neutrophils, eosinophils, and monocytes accounting for this rise, and increases in bone marrow cellularity with a shift to immature myeloid elements. Elevation of lymphocytes, platelets, and reticulocytes was not induced. Within five days after discontinuation of treatment the leukocytosis had disappeared. Adverse reactions encountered with rh GM-CSF seen in 65% of the patients studied were never life-threatening and always rapidly reversible. They included mild myalgias, facial flushing, low-grade fever, headache, bone discomfort, nausea, dyspnea, and transient decline of platelet counts. These results suggest that rh GM-CSF can be safely administered at the doses and schedules used and that it can induce in vivo some of the biological effects reported in in vitro studies. Although no objective antitumour responses have been seen, the ability of rh GM-CSF to increase number and function of leukocytes in vivo may prevent neutropenia and infections when GM-CSF is added to cytotoxic cancer therapy.
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PMID:Hematopoietic responses in patients with advanced malignancy treated with recombinant human granulocyte-macrophage colony-stimulating factor. 264 95

A double-blind, placebo-controlled trial was carried out in 40 patients affected by multi-infarct dementia to see if a daily intravenous infusion of 3 mg co-dergocrine mesylate ('Hydergine') over 14 days would improve severely deteriorated elderly patients and shorten the latent period (3 months) which is observed when the drug is given orally. All the patients had severe mental impairment, psychological deficit or altered consciousness. A Hachinski score of 7 or more, and a cumulative score of at least 12 points on SCAG scale Items 1, 2 and 4 (anxiety/depression) and/or Items 5, 6 and 8 (alertness/confusion) were required for admission. After 1 week of intravenous infusion of placebo, patients were randomly allocated to treatment with co-dergocrine mesylate or placebo, from Day 1 to Day 14. The solutions were infused over a period of 2 hours. During the follow-up period from Day 15 to Day 21, the patients did not receive any treatment. Thirty-six patients (17 on co-dergocrine mesylate, 19 on placebo) completed the study. The results, as rated on the SCAG scale, indicated significant improvements, in favour of co-dergocrine mesylate, in cognitive dysfunction, mood depression, withdrawal and overall impression. Furthermore, the factor fatigue on the Nowlis scale and clinical global assessments by physicians also showed significant advantages of the co-dergocrine mesylate group over placebo. Nine out of 17 co-dergocrine mesylate patients complained of side-effects, usually experienced during infusion; they consisted mainly of nausea (6 patients), gastric discomfort (2 patients), and tremor, nasal congestion, flushing, hypotension and hypertension (1 patient each). Despite the appearance of side-effects, general tolerability was rated as 'good' by both physicians and patients. It is concluded, therefore, that intravenous high dose co-dergocrine mesylate treatment has a fast and clinically relevant effect on the key clinical symptoms of multi-infarct dementia.
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PMID:Effects of intravenous high dose co-dergocrine mesylate ('Hydergine') in elderly patients with severe multi-infarct dementia: a double-blind, placebo-controlled trial. 268 Feb 86

The existence of racial differences in alcohol sensitivity between Oriental and Caucasian populations has been well documented. The primary manifestation is a highly visible facial flushing (47-85% in Orientals vs 3-29% in Caucasians) accompanied by other objective and subjective symptoms of discomfort. Even among different Oriental groups, subtle differences in the flushing response and alcohol consumption can exist. North and South American Indian populations differ in phenotypes for alcohol dehydrogenase and aldehyde dehydrogenase, but systematic studies comparing degree of flushing, alcohol elimination rates and blood acetaldehyde levels in these populations are lacking. Although flushing does not automatically 'immunize' an individual against alcohol use, those susceptible tend to consume less alcohol, at least in Orientals. However, the flushing phenomenon cannot be the sole explanation for differences in incidences of alcoholism among different racial groups. Socio-cultural, environmental and genetic factors also have to be considered. An increased incidence of flushing has been found to associate with a familial risk of development of future alcoholism in a Caucasian population. It remains to be determined whether the same is true in Orientals. Most biochemical investigations of the flushing phenomenon have focused on aspects of alcohol metabolism. Based on recent findings, a convincing mechanism is the higher accumulation of acetaldehyde in flushing subjects because they have an unusual, less-active liver aldehyde dehydrogenase isozyme (ALDHI). The possibility that an 'atypical' alcohol dehydrogenase, which is present in 85-90% of Oriental subjects, can contribute to increased blood acetaldehyde levels in flushing subjects cannot be ruled out. Based on results of a small number of pedigree studies which demonstrated familial resemblances in flushing, a pharmacogenetic defect in ALDHI has been proposed to be responsible for flushing. Other possible biochemical mechanisms (e.g. prostaglandins) and genetic defects need to be investigated.
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PMID:Racial differences in alcohol sensitivity. 293 17

DDAVP was administered at 0.4 microgram kg-1 intravenous (i.v.) and subcutaneous (s.c.) routes to 6 healthy subjects in a double blind crossover study. Both study treatments were well tolerated. Flushing occurred after both treatments but was more prominent after i.v. than after s.c. DDAVP. Mild transient local discomfort at the s.c. injection site occurred in 5 of 6 subjects. The mean peak factor VIII (FVIII) response was 369% and 247% of baseline after i.v. and s.c. DDAVP respectively and the maximum increase in FVIII occurred earlier with the i.v. route. Changes in FVIII antigen (FVIII:Ag) and von Willebrand factor antigen (vWF:Ag) were also monitored. Tissue-type plasminogen activator (t-PA) activity measured by a chromogenic assay employing soluble fibrin had a median peak value of 2.9 IU ml-1 at 20 min after i.v. and of 1.9 IU ml-1 at 60 min after s.c. DDAVP. t-PA antigen was also measured so that the specific activity of circulating t-PA could be determined. Preinjection median values of 14,650 and 13,700 IU mg-1 increased to peak median values of 236,200 IU mg-1 at 20 min after i.v. and 202,400 IU mg-1 at 60 min after s.c. DDAVP. Plasminogen activator inhibitor (PAI) activity fell following DDAVP and became undetectable in some subjects during the sampling period. The ratio of maximum fibrinolytic response was similar to the ratio of maximum haemostatic responses obtained by two routes of injection. Our results indicate that s.c. DDAVP might successfully replace i.v. DDAVP in several applications such as confirmation of haemostatic or fibrinolytic responsiveness in patient groups; for obtaining FVIII enriched plasma; as well as its obvious potential usefulness in home treatment of haemophilia A and von Willebrand's disease.
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PMID:Fibrinolytic and haemostatic responses to desamino-D-arginine vasopressin (DDAVP) administered by intravenous and subcutaneous routes in healthy subjects. 312 7

An autopsy case of systemic mastocytosis without cutaneous involvement in a 76-year-old woman was described. The patient presented with general malaise, chest and epigastric discomfort, flushing of the face and progressive hepatosplenomegaly, and she terminated in hemorrhagic complications of DIC within 2 months. There was neither rash nor urticaria pigmentosa recognizable in the entire course. The diagnosis was made by the histologic identification of abnormal aggregates of mast cells in a bone marrow aspirate. These mast cell granules were chloroacetate esterase-positive, peroxidase-negative, and electronmicroscopically they were composed of fine granular materials containing variable numbers of lamellar structures. At autopsy, diffuse infiltration of the mast cells was found in the liver, spleen, bone marrow, lymph nodes, lungs, kidneys, stomach, and adrenal glands.
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PMID:Systemic mastocytosis without cutaneous involvement. 355 89

Treatment for 2 days with disulfiram (3.5 mg/kg once daily) and calcium carbimide (0.7 mg/kg twice daily) in social drinkers produced, as compared to controls, similar blood ethanol values, 2- to 3-fold increases in blood acetaldehyde, respectively, and increased heart rate, pulse pressure, skin temperature, and flushing following 0.15 g/kg of ethanol taken 12 hr after the last drug administration. Peak blood acetaldehyde concentration was greater for calcium carbimide compared to disulfiram (p less than 0.05) and subjects treated with calcium carbimide experienced greater discomfort compared to disulfiram due to palpitations and shortness of breath, and they reported less intention to drink during the reaction. However, neither drug produced sufficient aversion to curtail further drinking totally. With repeated drinks, there was an overall reduction of blood acetaldehyde concentration for calcium carbimide of 85% and for disulfiram of 35%. These data may provide a biochemical basis for the claims of certain alcoholics that they can drink to "burn off" the effects of these drugs.
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PMID:A placebo-controlled double-blind comparative clinical study of the disulfiram- and calcium carbimide-acetaldehyde mediated ethanol reactions in social drinkers. 634 21

Prostaglandin D2 (PGD2) was infused intravenously into normal male volunteers. Seven subjects received infusions of 16, 32, 64 ng/kg/min and six of these a further dose of 128 ng/kg/min. Each individual's maximum dose was limited by discomfort caused by intense facial flushing and nasal congestion. At these doses there was no significant effect on systolic or diastolic blood pressure nor on spirometric measurements. There was a small but statistically significant tachycardia at 64 and 128 ng/kg/min. Collagen- and adenosine diphosphate (ADP)-induced platelet aggregation ex vivo was not affected at any of the infusion rates. Infused PGD2 is unlikely to be a useful antithrombotic agent.
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PMID:Effects of intravenous infusions of prostaglandin D2 in man. 659 53

Much can be learned about the brain's function in pain processing through electrical stimulation. The spinothalamic tract which is conceived to be the chief pathway for nociceptive pain and whose interruption induces dissociated sensory loss can be recognized from the anterolateral columns of the spinal cord to the posterior thalamus by the induction of feelings of chiefly contralateral, somatotopographically organized, warm, cool, or cold sensations, less often burning and rarely pain. The spinoreticulothalamic tract, whose function in normal pain processing is controversial and whose interruption produces no clinically detectable sensory loss, is normally silent to stimulation. However, in patients with deafferentation pain, it appears to become sensitive to electrical stimulation, both in the anterolateral columns and in midbrain and medial thalamus, giving rise to chiefly contralateral, non-somatotopographically organized, burning or painful sensations which often reproduce fairly accurately the patient's pain. This phenomenon, which does not appear to occur in patients with nociceptive pain, may reflect denervation neuronal hypersensitivity which is a possible pathophysiological mechanism explaining deafferentation pain. The dorsal column/lemniscal system can be recognized by electrical stimulation from the spinal cord to the somatosensory cortex by the induction of paraesthesiae. Its chronic stimulation at the level of the dorsal column, the ventrocaudal nucleus or the internal capsule appears capable of suppressing deafferentation pain. The arc of neuronal tissue extending from the septal area through hypothalamus and periventricular grey to the periaqueductal grey, which acts as a receptor area for opiates and endorphins, thereby exerting an inhibitory effect on access to the spinothalamic tract, can also be exploited through chronic stimulation for the control of pain. Stimulation of the periventricular area gives rise to feelings of warmth, comfort and relaxation, of the hypothalamus, horror and autonomic effects while that of the periaqueductal grey induces discomfort, distress, anxiety and weeping, and of the septal area flushing, paraesthesiae, nausea, nystagmus and a feeling of warmth. Thus four brain systems involved in pain signalling can be recognized by electrical stimulation, one which conveys nociceptive pain to consciousness, another that suppresses it, one that may undergo denervation neuronal hypersensitivity and bring deafferentation pain into consciousness, possibly by establishing novel connectivity and one that is presumably capable of suppressing that hyperactivity.
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PMID:Identification of pain processing systems by electrical stimulation of the brain. 718 96

In an attempt to simplify the pre-operative assessment of amputation level in patients with severe occlusive arterial disease of the legs the skin perfusion pressure (SPPp) on calf and/or thigh was determined photo-electrically in 38 patients, aged 41-85 years and compared to the pressure values (SPPi) determined by the widely used but cumbersome isotope washout technique. SPPi was determined as the minimal external counter pressure (applied by a blood cuff) sufficient to stop the washout from an intracutaneous depot of Na131I- mixed with histamine. SPPp was determined as the minimal external counter pressure required to prevent skin reddening after blanching of the skin. The systolic blood pressure, determined indirectly by strain gauge technique at the same level of the leg, was used for reading the SPPp as that counter pressure at which the photo-electric tracing moves away from a straight line placed on the tracing through the counter pressure corresponding to the systolic blood pressure. In the studied range 18-88 mmHg there was no significant difference between SPPp and SPPi. The total day-to-day variation of SPPp, determined from ten double determinations in eight patients was 6.6 mmHg (range of SPPp:23-80 mmHg). The present results indicate that assessment of amputation level from SPPp using the standardized reading should offer a reliable alternative to the isotope washout method. The photo-electric technique is simple and fast, and gives only negligible discomfort to the patient.
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PMID:A simple and reliable method for determination of skin perfusion pressure in patients with severe occlusive arterial disease. 719 94

Flushing and a sensation of tightness or pain in one ear lobe was a presenting complaint of 3 patients. In one case the symptoms were confined to the ear, another was associated with sensory impairment in the distribution of the C2 and C3 segments, while the 3rd patient experienced discomfort in the area of the 1st division of the trigeminal nerve on the same side. Two out of 3 patients had evidence of hypertrophy of the ipsilateral C2-3 facet joint and the symptoms of the 3rd patient were improved by an ipsilateral C2-3 root block. A possible mechanism could be the antidromic release of vasodilator peptides from afferent nerve terminals in response to irritation of the C3 root which supplies sensory innervation to the pinna.
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PMID:The mystery of one red ear. 758 61


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