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 bioavailability of two different s.c. doses of Desmin (a new low molecular weight dermatan sulfate) was evaluated in 12 healthy volunteers (6 men, 6 women aged 22-45 years) who were injected, on 3 separate days and with a wash-out period of at least 21 days between each administration, with 200 and 300 mg of Desmin by the s.c. route and 200 mg by the i.v. route. Immediately before injection and at various times thereafter (after 15 min and 30 min for i.v. only and after 1, 2, 3, 4, 6, 8, 12, and 24 h for both s.c. and i.v. dosing), blood samples were drawn to investigate bioavailability by measuring several coagulation parameters: activated partial thromboplastin time, thrombin time, inhibition of factor Xa, Heptest, and heparin cofactor II. Furthermore the local tolerance of the s.c. and i.v. injections were investigated. The s.c. administration of the two Desmin doses had a negligible effect on the activated partial thromboplastin time and a very small effect on the thrombin time, measured with human thrombin; in contrast, Heptest, heparin cofactor II, and anti-Xa activities increased, with a good drug bioavailability (more than 100%). The plasma effects of Desmin were dose dependent only when measured by Heptest, which also gave a greater response after the s.c. administrations. There were no symptoms of intolerance or pain at the injection site after single i.v. and s.c. Desmin administration.
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PMID:Bioavailability of Desmin, a low molecular weight dermatan sulfate, after subcutaneous administration to healthy volunteers. 935 83

Nine patients, mean age 55 years, with testicular hydroceles, were treated by aspiration and two-component fibrin glue injection. One patient was treated twice. The glue contains 70-110 mg fibrinogen and 500 IU human thrombin in 0.5- and 2-ml injections, respectively (Tisseel duo quick, Immune AB). The smaller glue volume was used in 4 cases and the larger volume in 6 cases. The average volume of hydrocele fluid was 77 (range 60-120) ml. Treatment caused no pain or discomfort other than puncture of the skin and no pain-relieving medication was required afterwards. In this series there were no infections but one conservatively treated hematoma. The hydrocele of that patient disappeared. Although the hydroceles recurred in 9 cases during the mean follow-up of 3.5 months, in 2 patients the hydroceles were clinically smaller than the original one and symptoms were milder subjectively. Our findings suggest that fibrin-adhesive glue is not sufficiently effective in treatment of testicular hydroceles.
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PMID:Results of fibrin glue application therapy in testicular hydrocele. 964 70

In order to evaluate whether different clinical presentations of unstable angina are associated with a different degree or pattern of activation of the hemostatic, fibrinolytic and inflammatory systems, we measured plasma levels of thrombin-antithrombin III, plasmin-alpha2- antiplasmin complexes and C-reactive protein, as markers of activation of coagulation, fibrinolysis and inflammation respectively, in two groups of patients: 7 patients with de novo unstable angina (Group 1) and 7 patients with destabilizing unstable angina (Group 2). Blood samples were taken on admission for measuring levels of C-reactive protein and during ischemic episodes at the onset of ECG changes and pain (0 min) and after 5, 15 and 60 min in order to assess the peak values of thrombin-antithrombin III and plasmin-alpha2-antiplasmin during the episode. Thrombin-antithrombin III levels in Group 1 were 1.8 microgram/l (0.3-4.15) at 0 min and increased to 17 micrograms/l (2.8-60) after 5 to 15 min (p = 0.013); conversely thrombin-antithrombin III levels in Group 2 were 2.15 microgram/l (1.4-3.8) at 0 min and raised to 4 micrograms/l (2-43) after 5 to 15 min (NS). No significant differences in both groups were observed in plasmin-alpha2-antiplasmin levels (Group 1:650 micrograms/l, ranged 492-956, at 0 min vs 670 microgram/l, range 415-977, at peak; Group 2: 480 micrograms/l, range 274-955, at 0 min vs 502 micrograms/l, range 304-1027, at peak; NS). Inversely, C-reactive protein levels on admission were 4 mg/dl (range 2-27) in Group 1, and 1 mg/dl (range 0.6-4) in Group 2 (p = 0.006). In conclusion, patients with de novo unstable angina have significantly enhanced thrombin (but not plasmin) production during spontaneous ischemic episodes than patients with destabilizing unstable angina. Furthermore, patients with de novo unstable angina have enhanced acute phase responses than patients with destabilizing unstable angina. Our data suggest that different pathogenetic mechanisms may be responsible for acute ischemic episodes in unstable angina and may explain different response to antithrombotic therapy in unstable angina patients.
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PMID:[Clinical presentation of unstable angina may influence the formation of thrombin during spontaneous episodes of ischemia]. 970 80

The association between cancer and hypercoagulability states is well known. It usually presents as a complication of gastrointestinal tract adenocarcinomas. We present the case of patient diagnosed of prostatic adenocarcinoma who was admitted because of pain and inflammation in the left side of the neck. The ultrasound study showed a jugular vein thrombosis. In the bibliographic review (MEDLINE 1990-1995), we have not found any similar reports Jugular vein thrombosis is a rare complication and usually is secondary to central vein catheter insertion, although it has been also described with ovarian hyperstimulation syndrome, infections, head and neck tumors and rarely in other neoplastic diseases. The physiopathologic process is not well known, although it is known that neoplastic cells interact with the thrombin and plasmin generating systems and that there is also a decrease in coagulation inhibitors, all of which leads to prothrombin activation in the absence of the corresponding increases in thrombin inhibitor complexes.
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PMID:[Jugular thrombosis and adenocarcinoma of the prostate: a state of hypercoagulability?]. 1068 25

The treatment of acute myocardial infarction consists of pain and anxiety relief, anti-ischaemic treatment and antithrombotic therapy. Due to its bleeding complications and, in some cases, procoagulant effects, antithrombotic therapy has consequences for coronary procedures in the setting of acute myocardial infarction. Antiplatelet therapy has no procoagulant effects, and its bleeding complications can easily be managed. Antithrombin therapy has rebound effects, for which no clear solution is available. Thrombolytic therapy has also procoagulant effects, which may interfere with coronary procedures in the early hours of acute myocardial infarction. Heparin may counteract the thrombolysis-induced thrombin generation, but has an unpredictable effect. Postprocedural therapy after angioplasty in the setting of acute myocardial infarction should consist of antiplatelet therapy.
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PMID:What an interventional cardiologist should know about the pharmacological treatment of acute myocardial infarction. 1040 64

Background: Enhanced thrombin generation has been found in patients with peripheral arterial obstructive disease (PAOD). The objective of this study is to investigate the effect of thrombin inhibition in PAOD patients. Methods: Argatroban (20 mg/day) was infused intravenously over 2 hours for 14-68 days in 27 patients with chronic PAOD of the lower extremities. Plasma thrombin-antithrombin III complex (TAT) levels and clinical signs were assessed. Results: TAT levels before argatroban therapy were significantly higher in the PAOD patients than in age- and gender-matched controls. In the PAOD patients, TAT levels increased stepwise in the presence of rest pain classified as Fontain III and IV. To assess the effect of thrombin inhibition, we divided the patients into a high-TAT group (pretreatment TAT level >/=5 ng/ml, n = 12) and a low-TAT group (pretreatment TAT level <5 ng/ml, n = 15). In the high-TAT group, TAT levels were suppressed in 8 of 12 patients after the administration of argatroban, along with improvement of their clinical symptoms and a decrease in the size of ischemic skin ulcers, indicating that argatroban clearly inhibited thrombin generation in vivo. Even in the low-TAT group, argatroban improved the clinical signs and symptoms, and also reduced the size of ischemic skin ulcers although TAT levels remained within the low range (<5 ng/ml) in 13 of the 15 patients, indicating that PAOD signs and/or symptoms may be related to small amounts of thrombin generated locally at the sites of atherothrombotic stenotic lesion. Conclusions: These results suggest that thrombin generation was enhanced in PAOD and that the amount was related to disease severity. Thrombin inhibition by argatroban may break this vicious cycle and lead to clinical improvement in PAOD.
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PMID:Effect of Thrombin Inhibition on Patients with Peripheral Arterial Obstructive Disease: A Multicenter Clinical Trial of Argatroban. 1060 16

Detailed knowledge of the pathophysiology as well as the dynamic nature of coronary thrombus formation provides a valuable tool for correct management and proper adjunctive therapy in patients with acute coronary syndromes. Coronary thrombosis is in the majority of cases caused by disruption or fissuring of an atherosclerotic plaque. At the lesion thrombogenic material will be exposed to the flowing blood leading to activation of platelets and the formation of a platelet clot. Simultaneously, the coagulation system is activated resulting in increased thrombin formation. Thrombin is a key mediator in arterial thrombosis, due to its effect on both platelets and fibrin generation. Thrombin contributes to the stabilization of an initially loose platelet clot by generating cross-bound fibrin within the thrombus. During the course of an acute coronary syndrome, the patient presents changing chest pain and dynamic ischaemic ECG findings. This is likely to be related to the dynamic nature of the pathophysiology. The presence of a non-occlusive coronary thrombus may deprive the myocardium its normal blood flow and oxygen supply, leading to ischaemic pain. During lysis or embolization, blood supply may be restored, but the presence of thrombus fragments in the microcirculation holds the potential to sustained interference with myocardial metabolism. The emboli contain activated platelets which release vasoconstrictors that may compromise the microcirculation. Recurrent thrombus formation at the lesion site may result in occlusion of the artery adding to the dynamic nature of the clinical presentation. In conclusion, platelets, the coagulation system, and the endothelium cause a dynamic process of intermittent occlusion, vasospasm and embolization of thrombus material.
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PMID:Pathophysiology of coronary thrombosis. 1105 8

The femoral artery remains the most used peripheral site for radiological catheter access. With a greater number of both diagnostic and therapeutic procedures being performed by interventional radiologists and cardiologists, and with larger catheters being used for stenting and endovascular grafting, the incidence of iatrogenic pseudo-aneurysms reported has reached as high as 0.5-2%. Ideally, they should thrombus spontaneously. However, when this does not occur, management options include: observation, ultrasound-guided obliterative compression, direct thrombin injection, embolization, stent graft insertion, and very rarely-surgery. During a 7-year period (1992-1999) we treated 131 cases of femoral artery false aneurysms. Until 1998 ultrasound-guided compression-obliteration, with a 95% success rate, was our method of choice. Since 1998, direct thrombin injection, with 100% success in 24 cases, has become our preferred method. It is pain-free, fully successful even in anticoagulated patients, and is currently our treatment of choice.
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PMID:[Femoral artery pseudo-aneurysms--changes in treatment, report of 7 years]. 1106 48

Complex regional pain syndrome (CRPS) is a disabling disease characterized by the classic symptoms and signs of inflammation. In this study we investigated the innate cytokine profile in patients with CRPS to determine a possible role of the immune system in the pathophysiology of CRPS. The cytokine profile before and after lipopolysaccharide and thrombin stimulation was determined in 26 severely affected CRPS patients and 20 healthy controls. No difference in the production of pro- and anti- inflammatory cytokines between patients and controls was found. Hence, our results do not support a role of genetic factors responsible for the cytokine profile in the pathophysiology of CRPS. These findings encourage further investigations of mechanisms responsible for neurogenic-induced inflammation.
Pain 2001 Apr
PMID:Innate cytokine profile in patients with complex regional pain syndrome is normal. 1127 82

Thirty-three subjects with sickle cell disease (SCD), 11 during episodes of pain and 22 during periods without pain, were evaluated for in vivo thrombogenic activities as compared with 10 normal black control subjects. Measurements were performed for (1) platelet surface activation, assessing flow cytometric expression of activated integrin alpha(IIb)beta(3) receptor (GPIIb/IIIa, CD41a) and P-selectin (CD62p); (2) platelet and erythrocyte surface procoagulant activities, measuring flow cytometric binding of activated factor (FVa) and annexin V; (3) plasma levels of platelet-specific secreted proteins platelet factor 4 (PF4) and beta-thromboglobulin (betaTG); (4) plasma markers of thrombin generation, prothrombin activation fragment (F(1.2)), and thrombin: antithrombin complex (TAT); and (5) plasma markers of fibrinolysis, D -dimer, and plasmin:antiplasmin complex (PAP). As compared with control subjects, asymptomatic subjects with SCD demonstrated significantly increased platelet activation (P <.01 for P-selectin and annexin V binding), elevated plasma levels of PF4 and betaTG (P <.01 and P <.03, respectively), and increased plasma concentrations of F(1.2), TAT, PAP, and D -dimer (P <.05 in all cases). During episodes of SCD pain, platelet activation was increased as compared with periods without pain (P <.01 for expression of activated integrin alpha(IIb)beta(3) receptor and P-selectin and binding of FVa and annexin V), erythrocytes expressed procoagulant activities (P <.01 for FVa and annexin V binding), and platelet microparticles appeared in the circulation (3% to 30%; P <.001). SCD pain episodes were associated with elevated plasma levels of F(1.2), TAT, PAP, and D -dimer (P <.05 as compared with asymptomatic intervals). The frequency of pain episodes correlated with enhanced platelet procoagulant activity (r = 0.61, P <.05) and elevated plasma fibrinolytic activity (r = 0.74, P <.01) measured during periods without pain. Plasma fibrinolytic activity was inversely correlated with time to the next pain episode (r = -0.50, P <.05). Thus, asymptomatic subjects with SCD exhibit ongoing platelet activation, thrombin generation, and fibrinolysis that increases during episodes of pain. These changes are predictive of frequency of pain and interval to next pain episode, thereby implicating thrombogenic activity in the development of SCD pain episodes.
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PMID:Thrombogenesis in sickle cell disease. 1138 49


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