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 use of 1 deamino-8-D-arginine vasopressin (DDVAP), is reported in seven patients with von Willebrand's disease and mild haemophilia undergoing elective surgery. There were no haemorrhagic complications, and both the quality of the clot formed and the rate of healing appeared entirely normal in all patients. No patient received blood products. Local burning pain due to paravenous leakage at the infusion site in a single patient, and transient facial flushing in another were the only side effects encountered. In addition to the anticipated rise in F.VIII:C and F.VIIIR:Ag, shortening of the bleeding time was observed in all five patients with von Willebrand's disease receiving DDAVP. Three additional patients who received intranasal DDAVP showed an inconsistent response in the laboratory parameters measured.
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PMID:Clinical experience with arginine vasopressin (DDAVP) in von Willebrand's disease and mild haemophilia. 697 Sep 7

Prostacyclin (PGI2) was given intravenously in doses of 1 to 5 ng/kg/min to eight consecutive patients with end stage peripheral arteriosclerosis and ischaemic ulcers. Seven patients had intense ischaemic pains. Complete or partial healing of ulcers were seen in six cases (complete in three). In those whose ulcers healed (complete or partially) relief of ulcer pain was remarkable. Acute studies of the effect of prostacyclin on skin temperature of ischaemic areas showed no correlation with clinical effects. Seven patients had more or less pronounced subjective side effects, most often flushing, nausea, headache and uneasiness. As we previously have seen equally good healing and pain relieving effects by the administration of prostaglandin E1 without these side effects the latter compound is so far preferred in the treatment of severe peripheral artery disease. Controlled studies of the effect are needed.
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PMID:The effect of intravenous prostacyclin on resting pains and healing of ischaemic ulcers in peripheral artery disease. 702 66

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

The efficacy and safety of 0.3 mg buprenorphine on single and repeated intramuscular administration (every 4 to 8 hours as needed) were compared to those of 10 mg intramuscular morphine. Fifty adult patients experiencing moderate to severe postoperative pain were evaluated up to three days following surgery. Results showed that 0.3 mg buprenorphine was as effective as 10 mg morphine, whether given as a single dose or on a repeat-dose schedule. The patterns of analgesia were similar and without indication of increasing dosage requirements with time. Minor side effects encountered were brief and minimal, including such conditions as drowsiness, dizziness, diaphoresis, flushing, and nausea.
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PMID:The study of analgesics following single and repeated doses. 722 17

Haemolytic transfusion reactions can be defined as the occurrence after transfusion of measurably increased destruction of red cells, of donor or recipient, by alloantibodies. They may be acute (occurring within 24 hours of transfusion) or delayed (when signs of red cell destruction do not occur until 4 to 10 days after transfusion). The severest signs and symptoms of acute reactions follow intravascular red cell lysis and progress to anaemia, fever, haemoglobinuria and jaundice. The subjective responses of pain, restlessness, nausea, skin flushing, dyspnoea and shock are mediated by cleavage products of complement (C3a, C5a) activated by red cell antigen-antibody reaction. The bleeding and renal failure complications that follow are multi-factoral in aetiology but also stem from the activation of intravascular clotting and from the vasomotor disturbances following histamine and kinin release.
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PMID:Clinical presentation of haemolytic transfusion reactions. 739 74

Iloprost is a synthetic stable analogue of prostacyclin (PGI2), which shares its antiaggregating and vasodilating properties. Iloprost has been administered by i.v. route to patients with critical limb ischaemia (CLI) of different origin (maximal dosage: 2 ng/kg/min 6 hours/day infusion for 14-28 days). In patients with claudicatio intermittens (Fontaine stage II) iloprost improved the time to claudication and the maximal walking distance on treadmill, with an effect still lasting 60 days after suspension. This benefit was not related to a significant improvement in blood flow. Five multicentric, perspective, randomized versus placebo studies in patients with more severe CLI (Fontaine stage III-IV) susceptible to surgical treatment, showed that iloprost was able to reduce pain and ulcer dimensions. Furthermore, tha amputation rate of the ischemic limb was significantly lower in patients treated with iloprost during a 6 month follow-up (p < 0.01). Iloprost was also more effective than aspirin in causing pain relief and ulcer healing in patients with thromboangiitis obliterans and more effective than nifedipine in reducing frequency, intensity and duration of ischemic episodes in patients with Raynaud's phenomenon. Minor side effects of iloprost administration are represented by facial flushing, tachycardia, headache, nausea, vomiting, abdominal cramping, diarrhoea, whose frequency ranges from 16% to 70%; major collateral effects, occurring in less than 5% of patients, are above all represented by severe hypotension and angina pectoris. Clinical data indicate therefore that iloprost treatment can allow to improve the clinical conditions and the prognosis in patients with critical ischemia of the limbs, not candidate to surgical revascularization, by causing a relief of pain, a reduction in ulcer dimensions and deferring amputation.
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PMID:[The role of iloprost in the treatment of critical ischemia of the limbs]. 750 14

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

In a randomized open controlled study the clinical effects and tolerability of prostaglandin E1 (PGE1) and the stable prostacyclin (PGI2) analogue, iloprost in the management of diabetic and non-diabetic patients with advanced peripheral arterial occlusive disease (PAOD Fontaine stage IV) were compared. 267 patients were enrolled in this multicentre study and treated for 21-28 days, either by daily infusions of 6 h with iloprost or 2 x 2 h with PGE1. At the end of treatment patients were assessed for evidence of improvement of trophic lesions, relief of rest pain and change of global clinical status. 228 patients were considered as evaluable for efficacy analysis, which revealed 52.7% responders in the iloprost group and 43.1% for PGE1 (p = 0.148). Whereas iloprost showed similar effects in diabetics and non-diabetics (53.3% and 51.4% response rates, respectively), the diabetics treated with PGE1 had a considerably poorer outcome (36.6% versus 53.3%). At 6 months follow-up 62.2% of patients in both groups were alive with a viable limb. Slightly more iloprost patients underwent major amputation (32.1% versus 27.2%), but the number of deaths was reduced by 50% in the iloprost group compared to the PGE1 group (7.5% versus 14.6%, p = 0.10). Side-effects such as headache, flushing and gastrointestinal symptoms were significantly more common in the iloprost group (73.9%) than in the PGE1 group (31.0%), particularly during the first 3 days of dose titration. No specific toxic or unexpected reactions were reported in either group.
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PMID:Treatment of patients with peripheral arterial occlusive disease Fontaine stage IV with intravenous iloprost and PGE1: a randomized open controlled study. 769 55

To study the efficacy of extracorporeal shock-wave lithotripsy (ESWL) of pancreatic duct stones, seventeen patients (mean age: 42 years) with recurrent attacks of abdominal pain as a result of chronic calcifying pancreatitis were treated with this method. In all cases, endoscopic removal of the stones proved impossible. When there was fragmentation, the remaining calculi and fragments either evacuated spontaneously, or attempts were made to extract them endoscopically, followed by flushing. In 13 patients (76%), fragmentation of stones was achieved, and 11 of these patients had dramatic pain relief directly after ESWL (65%). However, complete ductal clearance of stones was achieved in only seven patients (41%); at the last follow-up (12-59 months after ESWL, mean: 30 months), all seven were free of symptoms. Of the six patients with stone fragmentation without ductal clearance, three were operated on because of recurrent complaints. The only complication due to the procedure was an exacerbation of pancreatitis in one patient, which was treated conservatively. If pancreatic stones cannot be removed endoscopically, ESWL seems to be preferable to surgery, which may still be performed in case of failure. It seems important to achieve ductal clearance and not merely stone disintegration in order to obtain the desired long-term clinical effects.
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PMID:Extracorporeal shock-wave lithotripsy of pancreatic duct stones: immediate and long-term results. 800 83

Sixteen patients with intracerebral tumors received intraarterial cisplatin, teniposide, and BCNU combined with intravenous cisplatin, teniposide, and cytosine arabinoside. Oral glycerol and intravenous mannitol were given along with the intravenous chemotherapy in an attempt to increase drug delivery to tumor by augmenting tumor blood flow. Thirteen additional patients were treated with the same regimen, but received all the chemotherapy intravenously. Of the 16 patients receiving intraarterial chemotherapy (median survival, 14 weeks), none responded, 5 (31%) were stable for > 8 weeks, 8 (50%) failed, and 3 (19%) were unevaluable due to early death. Of the 13 patients receiving all their treatment intravenously (median survival, 13 weeks), 3 (23%) responded, 1 (8%) was stable, 7 (54%) failed, and 2 (15%) were unevaluable due to early death. In the patients receiving intraarterial chemotherapy, toxicity included ipsilateral retinal toxicity (2 patients), ocular pain or headache (10), periorbital swelling and flushing (6), increased brain edema with focal neurological deficits and drowsiness (5), and catheter-related carotid artery thrombosis followed by fatal herniation (1). Myelosuppression was worse in patients who received all their treatment intravenously than in those receiving intraarterial chemotherapy (p < 0.05). Neutropenic sepsis developed in 4 patients on the intraarterial arm (1 fatal) and in 5 patients on the intravenous arm (2 fatal). Other toxic effects were similar whether or not patients received intraarterial treatment or only intravenous treatment. Overall, toxicity of this regimen was excessive, and response rates were lower than would have been expected with single agent therapy.
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PMID:Feasibility study of intraarterial vs intravenous cisplatin, BCNU, and teniposide combined with systemic cisplatin, teniposide, cytosine arabinoside, glycerol and mannitol in the treatment of primary and metastatic brain tumors. 812 May 74


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