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)

In a single-dose, a double-blind crossover study in 40 patients with chronic pain due to advanced cancer, zomepirac sodium (Zomax), a new, single-entity, non-narcotic analgesic, was compared to oxycodone with APC (Percodan) and placebo. Both a verbal and a curvilinear visual analog scale were used in the study, and the results obtained were comparable. Zomepirac sodium, 100 mg, provided analgesia equal to oxycodone with APC in all assessments of pain intensity and pain relief. The analgesic activity of zomepirac sodium was apparent by 1 hour, reached a peak between 3 and 4 hours after administration, and lasted at least 6 hours. Zomepirac sodium, 100 mg, appears to be an acceptable alternative to narcotic combinations such as oxycodone with APC in the management of moderate to severe cancer pain. The visual analog scale presented appears to be useful in the evaluation of analgesic efficacy and appears to be acceptable as an alternative to the more conventional verbal scale.
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PMID:Analgesic efficacy of zomepirac sodium in patients with pain due to cancer. 703 68

Fibrinolysis of 19 patients who developed CVI after deep vein thrombosis was examined. Mean age of patients at the first thrombosis was 31.8 years. For testing fibrinolysis fibrinogen, plasminogen, AP, ECLT, with venous occlusion were determined. In 10 patients t-PA and PAI-1 activities were also measured and plethysmography was carried out. For screening blood coagulation abnormalities of TCT count, PT, APTT, TT, AT III, protein C were tested. The common abnormality was the decreased fibrinolysis. Patients had been on coumarin for 6.14 years before entering the study. Under coumarin treatment 6 patients had relapsed DVT, 4 had crural ulcer and CVI deteriorated in 8 patients. Therefore we added fibrinolysis increasing PPS to coumarin. PPS dose was individually determined by PPS loading test (150-500 mg). Mean observation time with the combined treatment was 2.92 years. Clinical check up and fibrinolysis test were carried out every 6 months. Clinical improvement occurred in 13 patients, (decrease of swelling, pain etc). Two out of 4 patients with stasis ulcer experienced complete healing; in 1 the ulcer territory diminished in size. Maximum venous outflow improved in 7 patients, 3 patients were non-responders. We observed an increase of fibrinolysis in 10 patients. Venous occlusion enhanced the fibrinolysis increasing effect of PPS. The activity reached its maximum by the first control. The fibrinolysis increase and the clinical improvement do not always run parallel, therefore other effects of PPS as the reason for being beneficial in CVI must be considered (antiinflammatory, ect.). Combination of coumarin and PPS seems to be an effective therapy in CVI with decreased fibrinolysis.
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PMID:[Management of chronic venous insufficiency with the combination of coumarin (Syncoumar) and oral pentosan polysulfate (PPS, SP 54) (preliminary report)]. 767 12

We investigated the role of human protein C in an animal model of inflammatory hyperalgesia. Pain was induced by intraplantar injection of carrageenan (3 mg) into the hind paw of rats. The pain threshold was measured by exerting increasing amounts of pressure (in mmHg) on the paw until a struggle reaction was observed. Protein C (8-800 IU/kg) was administered intravenously immediately after carrageenan. Controls received either intraplantar injections of saline (100 microliters) instead of carrageenan or carrageenan alone. Effects on pain threshold were expressed in percent of the pretreatment value. Carrageenan alone lowered the mean pain threshold after 3 h to 33.2 +/- 2.2% of the pretreatment level. Addition of protein C resulted in a dose-dependent rise in pain threshold towards the level observed in control animals treated with saline instead of carrageenan (pain threshold after 800 IU/kg protein C = 62.9 +/- 2.3% of pretreatment level), demonstrating an antinociceptive effect. Protein C had no effect in animals not preconditioned with intraplantar carrageenan. Thus protein C clearly antagonized the inflammatory pain induced by carrageenan. The antinociceptive action of protein C was antagonized by injection of a monoclonal antibody against protein C, providing additional evidence that the effect was protein C-mediated.
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PMID:Antinociceptive properties of protein C in a model of inflammatory hyperalgesia in rats. 779 39

A 27-year-old woman suffered from a sudden onset of slight paralysis of the right side of her body and the inability to express herself by speech, writing, or signs. She was admitted to the National Rehabilitation Hospital in Washington, D.C., in the US. 6 months prior to these events, she had been in a motor vehicle accident and had since experienced headaches and generalized musculoskeletal pain. The only drug she took was an oral contraceptive (OC), which she took irregularly. Health workers could not arouse her upon admission. Clinical examination revealed symptoms consistent with a left hemispheric stroke. Cerebral computed tomography and magnetic resonance imaging revealed a left temporoparietal infarct. Her free protein S was only 27% on admission and 14% 11 days after admission (normal range, 55-125%). Over the next 72 hours, her physical condition deteriorated, entailing focal motor seizures, right Babinski's sign, loss of pain reflex response on her right side, and complete paralysis of the right side of her body. The left middle cerebral artery appeared to be constricted, which physicians first believed was caused by vasculitis but later found was the result of emboli. The patient developed right femoral vein deep thrombosis. The physicians treated her initially with heparin and followed with warfarin therapy. Nevertheless, embolus. Health workers placed a filter in her inferior vena cava and continued warfarin therapy. She did not experience any more thrombotic or embolic episodes during the rest of her hospital stay. OCs reduce circulating levels of free protein S which, along with activated protein C, inhibits clotting. OCs likely reduced her already existing low levels of free protein S. Deficiency of free protein S was likely responsible for the cerebral infarction and her thrombotic and embolic episodes.
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PMID:A case of cerebral infarction in association with free protein S deficiency and oral contraceptive use. 823 70

In 103 patients with peripheral arterial disease (PAD) of the lower limbs, coagulation and fibrinolytic parameters were evaluated to identify hemostatic abnormalities characteristic of this patient population. PAD was defined as clinically stable Leriche stage 2 (based on clinical history, peripheral pulses, ankle-arm index, and treadmill test) for at least 3 months, walking distance > 100 m, and no other major illnesses, rest pain, or trophic lesions. Defibrotide, a polydeoxyribonucleotide derivative with vascular effects, was administered to the patients as part of a multicenter trial. The PAD patients exhibited a prothrombotic state as evidenced by high D-dimer in all but 24% of the patients (average 797 +/- 802 vs. 163 +/- 54 ng/mL normal population; p < 0.001) and high thrombin-antithrombin III complex (TAT) levels (10.2 +/- 8.9 vs. 2.5 + 1.5 ng/mL; p < 0.001) with low to normal levels of protein C (86 +/- 25 vs. 102 +/- 18%; p < 0.01) and plasminogen activator inhibitor-1 (PAI-1) antigen (5.9 +/- 4.5 vs. 1.3 + 0.7 ng/mL; p < 0.001) were elevated in 79% of the patients. These results suggest that there is ongoing thrombosis in the majority of PAD patients. Differences from normal controls were observed for t-PA, PAI-1, protein C, and protein S; however, it is not certain that the thrombosis in patients with PAD is due to these factors.
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PMID:Plasma levels of the molecular markers of coagulation and fibrinolysis in patients with peripheral arterial disease. 880 27

Venous thrombosis represents a manifestation of disordered hemostatic balance. The classical presentation is of pain and swelling of the lower limb, although clinical history and examination are notoriously misleading in reaching a diagnosis. A number of acquired predispositions have been associated with a tendency to thrombosis, such as immobilisation, surgery, malignancy and certain types of oral contraception, but in at least half of the instances no predisposition can be identified. A variety of genetic risk factors have also been identified. Mutations within the genes for antithrombin, protein C and protein S are associated with a venous thromboembolic phenotype. The commonest thrombophilic predisposition however is a variant of coagulation factor V, factor V Leiden, which results from a single amino acid substitution rendering the factor V molecule resistant to activated protein C. Factor V Leiden is present in approximately 5% of individuals of European origin, and is found in up to 40% of those with confirmed venous thrombosis. Increasingly it is recognised that venous thrombosis should be considered a polygenic disorder, with interactions between the various single gene defects which predispose to thrombosis, as well as normal genetic variation between individuals in the levels of both procoagulant and anticoagulant proteins, all determining which individuals will express the phenotype of venous thrombosis.
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PMID:The inherited basis of venous thrombosis. 942 12

Thrombophilia is characterised by elevated thrombotic and embolic risk and may be caused by congenital or acquired coagulating inhibitor deficit. A young man was repeatedly admitted to Emergency Medicine Units because of pain, oedema and slight functional impairment of the left leg, and recurrent thrombophlebitis was diagnosed. During the most recent hospitalization, vena cava thrombosis was diagnosed and therapeutic management consisted of application of a caval filter and administration of dicoumarin anticoagulants. This case can be classified as a hereditary protein S deficiency with APC-resistance. However, non-strenuous, protracted and repeated physical trauma may have acted synergically with the congenital coagulation inhibitor deficiency, determining the thrombotic episodes, which are probably provoked by transient and functional alterations of the non-thrombogenic properties of the endothelium.
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PMID:[Deficit of anticoagulant factors, endothelial stress and thrombophilia]. 948 20

A 32 year old white female, in apparently good health, failed to respond to conservative wound care for alveolar osteitis after a routine mandibular first molar extraction. Curettage and biopsy of necrotic alveolar bone from the #30 socket escalated her pain such that hospitalization was necessary for pain management with intravenous morphine. Twelve months prior to admission she had been placed on exogenous estrogen (Premarin, 0.625 mg/day) after a partial oophorectomy. While hospitalized, she was found to have resistance to activated protein C (APCR). Premarin was discontinued. After discharge, weekly changes of an antibiotic impregnated dressing allowed for progressive regeneration of bone and epithelium with gradual reduction in her pain. She was found to be heterozygous for the mutant Factor V Leiden, a heritable factor for increased tendency to form thrombi, so-called thrombophilia. We speculate that the exogenous estrogen administration exacerbated the thrombophilia associated with the Factor V Leiden mutation by compounding the patient's resistance to activated protein C thereby contributing to her development of osteonecrosis and severe alveolar neuralgia.
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PMID:Exogenous estrogen may exacerbate thrombophilia, impair bone healing and contribute to development of chronic facial pain. 985 7

The 26th Congress of the Scandinavian Society of Anaesthesiology and Intensive Care Medicine took place in the state-of-the art Tromso University Hospital. There were over 500 participants, and approximately 300 oral and poster presentations highlighted the latest progress in diverse areas. Much interest focused on activated protein C (APC) and other ways forward in sepsis treatment, pain management, novel markers of neurotrauma and antioxidants in bypass surgery. The meeting continues to be the leading anaesthesiology and intensive care conference in the region.
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PMID:The 26th Congress of the Scandinavian Society of Anaesthesiology and Intensive Care Medicine, Tromso, Norway, 13-17 June 2001. 1151 33

Painful bilateral ophthalmoparesis, marked proptosis, increased intraocular pressure, and blindness developed in a 29-year-old woman with protein C deficiency and catastrophic antiphospholipid syndrome. Magnetic resonance imaging of the orbits showed bilateral proptosis, globe tenting, and tethering of the optic nerves consistent with an orbital ischemic syndrome. Despite aggressive therapy for antiphospholipid syndrome, the patient died. The autopsy showed necrosis of orbital tissues. This is the first report of orbital ischemic syndrome from protein C deficiency and antiphospholipid syndrome.
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PMID:Catastrophic antiphospholipid antibody syndrome manifesting as an orbital ischemic syndrome. 1175 55


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