Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The activity of a therapeutic drug against Paget's disease is judged by a reduction in the level of hydroxyprolinuria and of alkaline phosphatasaemia, these being the metabolic signs of the bone changes, and by a decrease in bone pain which may accompany the bone changes in Paget's disease. The effect of aspirin is only moderate and is produced only with large doses that are often not well tolerated. The cortisone drugs are also active only at high doses that should be avoided. The action of sodium fluoride is uncertain. Mithramycin is always effective; it leads to a decrease in the levels of hydroxyprolinuria and of alkaline phosphatosaemia and to disappearance of the pain. At the dose levels used by the authors, mithramycin induces only certain metabolic anomalies (rise in transaminases, decrease in the prothrombin level...) which return to normal at the end of treatment. However, the long-term tolerance of mithramycin is unknown and the authors think that its use in cases of Paget's disease should be severely restricted. Sodium etidronate, a diphosphonate that inhibits both bone resorption and osteoformation also decreases regularly the levels of hydroxyprolinuria and of alkaline phosphatasemia and often decreases the pain. It is usually well tolerated. However at the dose rate of 20 mg/kg/day it may lead to the development of osteomalacia.
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PMID:[Non-hormonal drug treatment in Paget's disease]. 13 65

A group of patients with athero-arteriosclerotic vascular disease (coronary heart disease and atherosclerosis of the extremities) have been subjected to platelet antiaggregating-antidyslipidaemic treatment with a chlofibrate-dipyridamol association; a control series was treated with chlofibrate alone. Frequency of angina pectoris, pain intensity and trinitrine consumption ware evaluated in patients with coronary heart disease, claudicometry, oscillometry and thermometry in patients with atherosclerosis of the extremities. The following laboratory parameters were also analysed: cholesterolaemia, triglyceridaemia, prothrombin activity, fibrinogenaemia, uricaemia and tolerance of oral glucose loading. Analysis of the results has shown that the association improved the parameters considered in statistically significant fashion; chlofibrate alone led to significant modifications of coronaropathic group parameters (with the exception of pain intensity) whereas it did not lead to significant changes in parameters evaluated for atherosclerosis of the extremities. All laboratory parameters were modified favourably by the association to a statistically greater extent than by chlofibrate alone. Both the association and chlofibrate were well tolerated.
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PMID:[The clofibrate-dipyridamole combination in the treatment of athero-arteriosclerotic vasculopathy]. 43 77

Evidence of severe liver damage was found in a young women who ingested an overdose of acetaminophen in a suicide attempt. Clinical features included prolonged nausea and vomiting and pain and tenderness over the liver. Biochemical findings included an SGOT value of over 3,000 and a prolonged prothrombin time, with normal alkaline phosphatase and near normal serum bilirubin. Spontaneous recovery was complete.
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PMID:Hepatotoxicity in acetaminophen poisoning. 84 23

In this presentation we have contrasted the normal blood-clotting mechanism with the failure to form blood clots in hemophiliacs due to the absence of protein factors necessary for conversion of prothrombin to thrombin. The statistics, hereditary basis, and long-term disabling consequences of hemophilia to the severely ffected patient are described. The systemic means of minimizing severe joint disabilities and serious internal bleeding hazards by employing concentrates of antihemophilic factors to reverse the bleeding defects are discussed. Availability and advantages of the types of concentrates are explained. The fatalistic attitude of hemophiliacs toward hepatitis is discussed, along with admonitions to avoid the use of aspirin, alcohol, and buttock injections. Alternative medications for pain are recommended; and injection sites for pediatric patients are suggested. The details of simplified oral surgical management of hemophilic patients without hospitalization are described, including local anesthetic injection technique, method of performing extractions, general anesthesia techniques when indicated, materials for packing of extraction sockets, regimen and precautions in use of Amicar administration for clot maintenance, postoperative diet, and postsurgical activity guidelines. Also noted is the self-administration of intravenous concentrate infusions at home in the event of hemorrhagin, so that bleeding is on the way to bein controlled even before the patient reaches the hospital. We avoided orthodontic treatment of hemophilic patients in the past; however, recently developed bracket-fixation techniques and auxiliary aids; along with an enlightened understanding that gingival bleeding is ot to be feared, have changed our attitude, and we now treat hemophilic patients in much the same manner as otherwise normal orthodontic patients...
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PMID:Orthodontics and dentistry for the hemophilic patient. 110 95

The case is reported of a 44-year-old European who was bitten on the foot in Djibouti, probably by an African viper. Unusually, there wasn't any pain, nor any cardiovascular collapse nor any local swelling. An oedema of the lower limb started the day afterwards. Two days after the bite, the patient presented a generalized haemorrhagic syndrome, which led to his admission. There was a consumption of fibrinogen and prothrombin, without any decrease in the platelet count. Heparin was started (100 IU.kg-1.day-1), as well as fluid replacement (albumin, fresh frozen plasma, packed red cells). This allowed him to be transferred to France, where he arrived in anuria, with hyperpyrexia, and severe lower limb oedema and a haemorrhagic syndrome. There was a major extensive retroperitoneal haematoma spreading to the perineum. The four limbs were ischaemic. The patient's condition continued to worsen, developing hypoxic pulmonary oedema. He died on the seventh day after the bite, during a session of haemodialysis, from cardiovascular failure resistant to all the usual drugs. The principles of anti-venom therapy are recalled. Indeed, this should be started early enough and relies on large amounts of serum (greater than 50 ml).
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PMID:[Fatal poisoning caused by African viper's bite (Echis carinatus)]. 144 1

Hypercoagulable states are disorders of blood coagulation, which include deficiencies of natural anticoagulants, disorders of the fibrinolytic system, presence of antiphospholipid antibody and abnormalities of platelet function. These disorders are well known causes of venous thromboembolic disease and are being recognized in association with arterial thromboembolic occurrences with increasing frequency. The performance of standard prosthetic vascular reconstructions may result in disastrous outcomes in patients with unrecognized and untreated hypercoagulable states. From 1986 to 1990, we identified 12 patients with hypercoagulable states, six of whom presented with evidence of arterial thromboembolism. All of the patients were men who smoked and were somewhat younger than the usual patient with atherosclerosis. Their ages ranged from 41 to 62 years. Four patients presented with ischemic rest pain, one patient with blue toe syndrome and one with rapidly progressive claudication. Four patients had undergone prior vascular reconstruction and two had previous pulmonary emboli. Evaluation of these patients to identify hypercoagulability included determinations of prothrombin time (PT) and partial thromboplastin time (PTT), platelet count, antithrombin III, protein C, free protein S and total protein S levels, along with platelet aggregometry. Two patients had protein S deficiency, one had protein C deficiency, one patient had protein C and S deficiency and two patients had hyperaggregable platelets. Four patients had prosthetic reconstructions and two had autogenous reconstructions. Three of the four patients undergoing prosthetic reconstructions had subsequent loss of limb and one patient died. Only one patient with prosthetic reconstruction had a patent graft on long term anticoagulation. Both patients undergoing autogenous procedures had successful revascularization with limb salvage.
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PMID:Hypercoagulable states in arterial thromboembolism. 154 37

Haemostasis was studied in patients receiving diclofenac for postoperative pain relief. Intravenous diclofenac 75 mg over 60 min, followed first by an infusion of 5 mg/h for 15 h and then by 50 mg every 8 h orally was administered to 20 patients undergoing total hip replacement. Eighteen patients receiving a placebo infusion and dextropropoxyfen per os served as controls. The results showed no statistically significant differences between the groups in blood loss, bleeding time (IVY), partial activated thromboplastin time and prothrombin complex assay or in platelet count. The measurements were performed preoperatively, 3 h postoperatively and on the fourth and tenth postoperative days. Plasma concentrations were also determined in ten patients undergoing knee arthroscopy. An i.v. diclofenac infusion of 75 mg over a period of 15 min was administered either once (to half of the patients) or twice. The mean diclofenac concentrations were 28 +/- 5 nmol/ml (+/- s.d.) after 15 min and 36 +/- 12 nmol/ml after the second infusion. The bleeding time in the arthroscopy patients receiving one or two bolus infusions of 75 mg diclofenac remained at the control level. It is concluded that diclofenac given as an intravenous infusion of 75 mg in 60 min, then 5 mg/h for 15 h, followed by 50 mg every 8 h orally, is a safe as dextropropoxyfen for pain relief in patients undergoing major orthopaedic surgery as far as coagulation data are concerned.
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PMID:Effect of a non-steroidal anti-inflammatory drug, diclofenac, on haemostasis in patients undergoing total hip replacement. 163 74

Carbetimer (carboxyimamidate) was administered at a dose of 6,500 mg/m2/day intravenously for 5 consecutive days to 14 patients with measurable metastatic or recurrent colorectal cancer in a single institution phase II study of the Northern California Oncology Group. A total of 38 cycles of therapy were administered; nine patients completed at least three cycles of treatment. No partial or complete responses were observed. One patient did have a greater than 50% response in the liver while developing new retroperitoneal lymphadenopathy and is considered a nonresponder. Carbetimer was well tolerated with elevations of calcium from 10.2 to 12.5 mg/dl in nine patients, prolongation of prothrombin time and partial thromboplastin time in 14 patients, proteinuria in 10 patients, dizziness in six patients, nausea in two patients, and venous pain during infusion in three patients. Myelosuppression was not observed. Carbetimer at this dose and schedule is inactive in the treatment of colorectal cancer.
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PMID:A phase II trial of carbetimer for the treatment of colorectal cancer. A trial of the Northern California Oncology Group. 219 95

Cigarette smoking-induced alterations in drug absorption, distribution, metabolism, excretion, and effectiveness are reviewed. Drug therapy can be affected pharmacokinetically by polyaromatic hydrocarbons and pharmacodynamically by nicotine. Pentazocine and phenylbutazone show increased metabolism in smokers and may have to be given in higher dosages. Smokers experience less pain relief with propoxyphene than do nonsmokers. Codeine, meperidine, and morphine are unaffected pharmacokinetically, and the effect on acetaminophen is probably not clinically important. Carbamazepine, phenytoin, and phenobarbital are not influenced. Heparin metabolism is elevated in smokers; this effect may necessitate modest increases in dosage. Warfarin clearance is increased, but this is not associated with a change in prothrombin time. Pindolol and propranolol are unaffected pharmacokinetically, but direct effects of nicotine may interfere with blood pressure control. Smoking transiently diminishes the diuretic effect of furosemide, inconsistently affects protein binding of lidocaine, and has no effect on prednisone, prednisolone, or dexamethasone. The metabolism of estrogens to less active metabolites is increased. Smoking is associated with decreased subcutaneous absorption of insulin and increased dosage requirements. Healing of GI ulcers with histamine H2-receptor antagonists may be compromised in smokers; sucralfate is probably more useful. Imipramine, benzodiazepines, chlorpromazine, and glutethimide may be influenced, and theophylline metabolism is accelerated. Cigarette smoking can affect the pharmacokinetic and pharmacodynamic properties of many drugs.
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PMID:Cigarettes and drug therapy: pharmacokinetic and pharmacodynamic considerations. 240 22

The authors report a case of acute spinal epidural hematoma occurring in a patient receiving antiplatelet drugs. A 76-year-old man with a history of cerebral infarction had been taking antiplatelet agents for one year. He suddenly developed severe back pain which woke him from sleep, and numbness of his lower extremities was then noted. He was hospitalized 15 hours later. Neurological examination revealed flaccid paralysis of both lower extremities with negative Babinski's reflex, and sensory disturbance below the level of L1. The bleeding time and prothrombin time were prolonged. Computed tomographic (CT) scan revealed a biconvex, relatively hyperdense mass in the posterior spinal canal at the level of T12. Metrizamide myelography disclosed an incomplete blockage caused by an epidural mass at the level of T11. Post-myelographic CT scan demonstrated a sharply demarcated extradural filling defect at the level of T11. Seventeen hours after the onset of symptoms, an emergency laminectomy was performed extending from T12 to L3, and the epidural clot was totally evacuated. Histological examination of the capsule of the hematoma revealed no vascular anomalies. The patient made a good postoperative recovery. To the authors' knowledge, this is the first reported case of spontaneous intraspinal hemorrhage in a patient taking antiplatelet drugs. Acute onset of persistent pain anywhere along the spinal axis and the development of spinal neurological deficits in a patient on antiplatelet therapy should raise the suspicion of a spinal epidural hematoma. It should be stressed that prompt neuroradiological diagnosis and rapid surgical decompression are essential to allow good recovery. The present case illustrates that neurological emergencies can occur in patients receiving antiplatelet therapy.
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PMID:[A case of acute spinal epidural hematoma in a patient with antiplatelet therapy]. 279 70


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