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)

Nine patients with the loin-pain/haematuria syndrome are described. The previously reported clinical features of severe recurrent loin pain and tenderness in young women, the relationship of symptoms to use of oral contraceptives, and the demonstration of intrarenal vascular abnormalities by angiography are confirmed. Histology revealed minor non-specific abnormalities, and electron microscopy showed fibrin in the afferent arteriole and in glomerular capillaries of one patient only. No diagnostic changes were found on renography. In all patients except one the heparin-thrombin clotting-time was abnormal, suggesting increased platelet activity or release and providing further evidence of a vascular disorder.
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PMID:The loin-pain/haematuria syndrome. 8 67

48 patients with acute deep venous thrombosis of the lower limbs were treated with sodium heparin. In 23 patients heparin was injected subcutaneously (s.c.) twice a day and in 25 patients heparin was given by continuous intravenous perfusion (i.v.). Pain and edema disappeared after 8.7 days (s.c.) and 11.7 days (i.v.) respectively. One non fatal pulmonary embolism occurred in each group. A second venography was performed in 24 patients after 7 days of treatment and revealed no difference between the two groups. As judged by repeated thrombin time determination, anticoagulation was ineffective on at least one day in 39% of patients treated subcutaneously and in 60% of patients treated intravenously. The two pulmonary embolisms occurred in patients with ineffective anticoagulation. It is concluded that heparin may be used either intravenously or subcutaneously in the treatment of acute deep venous thrombosis. Thromboembolic complications occurred with both methods of treatment when anticoagulation was ineffective.
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PMID:[Heparin treatment. Comparison between intravenous and subcutaneous administration]. 50 73

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

Kinins are potent mediators of rheumatoid inflammation. The components of the kinin-forming system are hyperactive in RA. Excessive release of kinins in the synovial fluid can produce oedema, pain and loss of functions due to activation of B1 and B2 receptors. These receptors could be stimulated via injury, trauma, coagulation pathways (Hageman factor and thrombin) and immune complexes. The activated B1 and B2 receptors might cause release of other powerful non-cytokines and cytokines mediators of inflammation, for example, PGE2, PGI2, LTs, histamine, PAF, IL-1 and TNF derived mainly from polymorphonuclear leukocytes, macrophages, endothelial cells and synovial tissue. These mediators are capable of inducing bone and cartilage damage, hypertrophic synovitis, vessels proliferation, inflammatory cells migration, and possibly angiogenesis in pannus formation. These pathological changes, however, are not yet defined in human model of chronic inflammation (RA). Hence, the role of kinin and its interacting inflammatory mediators would soon start to clarify the detailed questions they revealed in clinical and experimental models of chronic inflammatory joint diseases. Several B1 and B2 receptor antagonists are being synthesized in an attempt to study the molecular functions of kinins in inflammatory processes (RA, periodontitis and osteomyelitis), and they represent and important area for continued research in rheumatology. Future development of specific, potent and stable B1 and B2 receptor antagonists or combined B1 and B2 antagonists with y-IFN might serve as pharmacological basis of more effective rationally-based therapies for RA. This may lead to significant advances in our knowledge of the mechanisms and therapeutics of rheumatic diseases.
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PMID:Involvement of the kinin-forming system in the physiopathology of rheumatoid inflammation. 133 58

Changes in platelet function have been observed for sickle cell disease (SCD). Levels of the arachidonic acid metabolites, thromboxane A2 (released by stimulated platelets) and prostacyclin (released from vascular endothelium), which stimulate and inhibit platelets, respectively, have been implicated in overall regulation of platelet function. Circulating basal levels of thromboxane and prostacyclin were determined in 1) a group of SCD volunteers (n = 21; at half-yearly steady state intervals and also at 24 hr, 72 hr, and 7 days after start of pain crisis) and 2) an age-, sex-, and race-matched control group (n = 18; single determinations). Circulating levels of beta-thromboglobulin (beta-TG), as well as thrombin (clotting)-stimulated platelet release of thromboxane, were also determined. Statistically significant decreases were found for prostacyclin, basal thromboxane, and thrombin-induced (maximal) thromboxane (alone or per platelet), for steady state SCD vs. normal controls. In addition, significant increases in maximal thromboxane were identified in crises (24, 72 hr) compared with steady state. Crisis beta-TG (24 hr) was significantly elevated compared with controls or steady state SCD. The ratio of basal thromboxane to prostacyclin was increased in crisis, but not significantly. Crisis frequency may correlate in part with changes in platelet function: steady state maximal thromboxane and released thromboxane per platelet were significantly lower in SCD volunteers who had crises during the study vs. those who did not (equivalent study time). The data support altered platelet function in SCD, possibly refractoriness (desensitization), manifest as decreased thromboxane release, to thrombin and/or other stimuli: alternate explanations are discussed.
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PMID:Platelet regulatory prostanoids and platelet release products in sickle cell disease. 153 87

Six patients suffering from solitary cryofibrinogenaemia are described. In one patient idiopathic cryofibrinogenaemia was present, while the others showed secondary cryofibrinogenaemia associated with borrelia infection, chronic venous insufficiency with pulmonary embolism, primary biliary cirrhosis, diabetes mellitus or von-Willebrand syndrome. Subcutaneous injections of the thrombin-like snake poison batroxobin/ancrod were administered over a period of several weeks. Five patients experienced almost complete remission of their symptoms, especially of pain following cold exposure. In one patient partial relief was achieved. Overall we found a 75% reduction of symptoms. When blood fibrinogen levels are carefully monitored this therapy is an efficient and safe form of treatment for cryofibrinogenaemia.
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PMID:[Cryofibrinogenemia--successful therapy by decreasing fibrinogen]. 186 Jul 98

Plasma antithrombin III was measured by an immunological approach (AT III:Ag) using an antiserum developed in our laboratory and by its ability to inhibit thrombin (functional assay) using a chromogenic synthetic substrate in 12 patients with myocardial infarction, 9 patients with angina pectoris and 10 healthy control subjects. In the early stage (3 to 24 hours after the onset of pain) of an acute myocardial infarction AT III:Ag (115.67% +/- 21.23) was found to be significantly (p less than 0.01) higher than functional (free) AT III (92% +/- 10.27). This difference was less obvious 10 days later (AT III:Ag 118% +/- 18.93; functional AT III 104.94 +/- 14.45). There was also no significant difference between AT III:Ag and functional AT III in patients with angina pectoris as well as in controls. Since AT III:Ag represents total plasma AT III while functional AT III represents only free AT III the difference between these two variables could provide informations about the amount of the anticoagulant forming complexes with activated clotting factors. It is therefore considered that the significant increase in the difference between AT III:Ag and functional AT III in the early stage of acute myocardial infarction is likely to suggest an intravascular activation of coagulation.
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PMID:Functional and antigenic antithrombin III in angina pectoris and acute myocardial infarction patients. 210 Aug 76

Platelet activation at sites of enmeshed sickled red cells in the microcirculation may contribute to platelet plug formation and microinfarction in sickle cell anemia. To test this hypothesis platelets from 116 sickle cell anemia patients free of crisis, 32 patients with crisis, 16 convalescents within 1 week of crisis, and 180 normal controls were studied. Platelets store 90% of their ADP in dense secretory granules. During activation ADP is secreted and permanently lost from the cell. This leads to a decrease in cellular ADP concentration and a sharp rise in the ATP/ADP ratio. ATP and ADP were ethanol-extracted from platelet-rich plasma, measured in the luciferase-luciferin assay and expressed in nmoles per 10(8) cells. No adenine nucleotide differences were found in platelets from patients free of crisis compared with normal controls. The ADP concentration of platelets from patients in crisis was significantly lowered, indicating that in vivo platelet secretion of ADP had occurred. Total and released ADP was decreased from 2.69 to 1.66, and from 1.90 to 1.21 respectively, and the total ATP/ADP ratio was increased from 1.85 to 2.84 (P less than 0.001). ADP stores in platelets from convalescents were significantly different from sickle controls (P less than 0.001) but were less abnormal than ADP stores in platelets from crisis patients (P less than 0.01), indicating recovery. Total and released ADP was decreased to 1.97 and 1.31 respectively, and the ATP/ADP ratio was increased to 2.38. Platelets from patients in crisis were able to release their remaining granular ADP in response to thrombin as effectively as normal platelets. Thus significant platelet activation with ADP release occurs during acute sickle pain crisis. This might contribute to platelet plug formation and microvascular obstruction.
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PMID:Platelet activation during pain crisis in sickle cell anemia patients. 274 22

Coagulation assays in 10 women in whom 2nd-trimester abortion was induced through intra-amniotic infusion of ethacridine (Rivanol) suggested a lack of negative side effects. The mean gestational age of the study subjects was 22 weeks. Platelet count, thrombin time, partial thromboplastin time, and prothrombin time were measured in serum samples collected before and 12, 36, and 60 hours after ethacridine instillation. Also measured were soluble fibrin monomer complexes and Factors V, VII, X, and XII. In 9 of the 10 women, labor was induced by 1 dose of ethacridine and a dead fetus was expelled; the 10th woman required a 2nd instillation. The average duration of labor was 2.5 hours (range 0.5-5.0 hours) and induction-to-abortion time averaged 38 hours (range 31-47 hours). All coagulation measures were within normal limits before abortion induction and were not significantly influenced by ethacridine administration at any of the time intervals studied. Of particular interest was the lack of evidence of disseminated intravascular coagulation--a side effect of intra-amniotic instillation of hypertonic saline. The injection of ethacridine also seems to cause less pain than hypertonic saline, hypertonic glucose, or prostaglandin in F2 alpha.
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PMID:Lack of coagulation defects after the intraamniotic instillation of ethacridine (Rivanol) for second trimester abortion. 340 72

A group of 11 female patients (mean age 33.7 +/- 8 years) with a clearly proven primary Raynaud's syndrome of up to five years' duration were subjected to a two-month oral treatment with 3 X 400 mg pentoxifylline per day. The following parameters were studied without and with exposure to cold conditions: hemodynamics (finger photoplethysmography), red cell deformability (filtration test), various clotting variables (prothrombin activity, antithrombin III, plasma fibrinogen, partial thromboplastin time, thrombin time, thrombelastogram), and clinical symptomatology. After treatment 7 of the 11 patients showed a distinct improvement of peripheral blood flow and of symptoms (decrease or removal of asphyxia attacks, pain, color change) under basal conditions, as well as after exposure to cold. Red cell filtration was significantly (p less than 0.05) improved, increasing by 35% under normal conditions and by 30% after exposure to cold. Positive changes were also found in respect to antithrombin III (increase) and plasma fibrinogen (decrease). The thrombelastogram was unchanged. Clinical and instrumental improvements were probably ascribable to better microcirculatory flow due to increased red cell deformability, reduced viscosity, and decreased fibrinogen, all capable of influencing in various degrees the blood flow at the microcirculatory level.
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PMID:Functional vascular disorders: treatment with pentoxifylline. 363 42


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