McEntire, Serina J.;Reis, Steven E.;Suman, Oscar E.;Hostler, David
Safety and Health at Work
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v.6
no.3
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pp.256-262
/
2015
Background: Heart attack is the most common cause of line-of-duty death in the fire service. Daily aspirin therapy is a preventative measure used to reduce the morbidity of heart attacks but may decrease the ability to dissipate heat by reducing skin blood flow. Methods: In this double-blind, placebo-controlled, crossover study, firefighters were randomized to receive 14 days of therapy (81-mg aspirin or placebo) before performing treadmill exercise in thermal-protective clothing in a hot room [$38.8{\pm}2.1^{\circ}C$, $24.9{\pm}9.1%$ relative humidity (RH)]. Three weeks without therapy was provided before crossing to the other arm. Firefighters completed a baseline skin blood-flow assessment via laser Doppler flowmetry; skin was heated to $44^{\circ}C$ to achieve maximal cutaneous vasodilation. Skin blood flow was measured before and after exercise in a hot room, and at 0 minutes, 10 minutes, 20 minutes, and 30 minutes of recovery under temperature conditions ($25.3{\pm}1.2^{\circ}C$, $40.3{\pm}13.7%\;RH$). Platelet clotting time was assessed before drug administration, and before and after exercise. Results: Fifteen firefighters completed the study. Aspirin increased clotting time before and after exercise compared with placebo (p = 0.003). There were no differences in absolute skin blood flow between groups (p = 0.35). Following exercise, cutaneous vascular conductance (CVC) was $85{\pm}42%$ of maximum in the aspirin and $76{\pm}37%$ in the placebo groups. The percentage of maximal CVC did not differ by treatment before or after recovery. Neither maximal core body temperature nor heart rate responses to exercise differed between trials. Conclusion: There were no differences in skin blood flow during uncompensable heat stress following exercise after aspirin or placebo therapy.
Prevention of thrombombolism after rosthetic cardiac valve replacement is essential for the patients. About 90% of patients are free of major and minor thromboembolic complications 5 year after replacement of cardiac valves with prosthetic devices when they are under control of anticoagulant therapy. Ticlopidine is a drug that alter platelet function to have an antithrombotic effect. It is an antiaggregating agent which inhibits primary platelet function to have an antithrombotic effect. It is an antiaggregating agent which inhibits primary platelet aggregation induced by ADP and increases the production of prostaglandin $D_{2}$. Aspirin in small doses inhibits platelet synthesis of prostaglandins by irreversibly blocking the enzyme cyclo-oxygenase. Platelet secretion and aggregation are impaired with Ticlopidine and Aspirin. the thromboembolic event sof 54 patient s who were treated with Ticlopidine and Aspirin after cardiac valve replacement were evaluated and compared with that of 79 patients who were treated with Wafarin and Aspirin after the same type of operation. The follow-up period ranged from 4 to 110 months (mean of 48 months). there were 11 major thromboembolic episodes including three deaths in the warfarin goup during mean follow-up period of 56 months. two cases of CVA and one hemoarthrosis were noted due to overdose of Warfarin. Inticlopidine group, there was only one fatal thromboembolic epdisode three month after mitral valve replacement during mean follow-up period of 18 months. Two episodes of hypermenorrhea resulting anemia ere noted in the ticlopidine group. We measured the parameters of platelet function in aggreagation curve of platelet with platelet aggregometer (chrono-log Aggregometer, Model No. 430) Aggregation test was performed with three final concentrations of epinephrine in 10 uM/L, ADP in 5uM/L. 28 patients with prosthetic cardiac valves and 35 healthy volunteers were subgrouped as follows to analyze the effect of antithrombotic drugs used. Group I ; 11 patients treated with 250-500 mg of ticlopidine and 0.5gm of Aspirin as a daily single dose after cardiac valve replacement (14 St. Jude Medical and 1 Carpentier-Edwards, 9 patients with atrial fibrillation among them) Group II ; 10 patients treated with 3-5 mg of Warfarin and 0.75 gm of Aspirin daily to prolong prothrombin time around 20 seconds for more than 6 months and single Aspirin dose was maintained afterward as a life-long regimes(3 St. Jude Medical, 1 Hall-Kaster and 7 Carpentier-Edwards valve, 9 patients in atrial fibrilation). Group III ; 7 patients who quit anticoagulant treatment (Warfarin + Aspirin) 6-12 months after the regime as group II (3 St. Jude Medical. 1 bjork-Shiley, 1 Hall-Kaster, 3 Carpentier-Edwards valve, 2 of them are with atrial fibrillation). Group IV ; 35 healthy vounteers (28 males and 7 females). The following results were obtained. 1. The mean maximal platelet aggregability in Group I induced by 10uM/L epinephrine was 15.6%, and 17.5 and 18.7% in BM in proportion to the induction by 5 and 10 uM/L ADP. 2. The mean maximal platelet aggregability in Group II induced by 10uM/L epinephrine was 16.5%, and 27.4 and 44.7% in BM in proportion to the induction by 5 and 10uM/L ADP. 3. The mean maximal platelet aggregability in group III induced by 10uM/L epinephrine was 65%, and 56.5 and 51.8% in BM in proportion to the induction by 5 and 10 uM/L ADP. 4. The mean maximal platelet aggregability in the normal subjects induced by 10 uM/L epinephrine was 64%, and 65 and 69% in Bm inproportion to the induction by 5 and 10 uM/L ADP. 5. Reversible change of platelet aggregation curve induced by 5 and 10uM/L was noted all of the patients in Group I. conclusion : Ticlopidine is an antiaggregating agent which inhibits primary platelet aggregation induced by ADP, and increases the production of prostaglandin $D_{2}$. Ticlopidine and Aspirin produced a significant inhibition of platelet in the presence of ADP and epinephrine in our study. Acccording to our brief experience, 250 mg of ticlopidine and low dose of Aspirin resulted synergistic superior effect to each drug alone in prevention of thromboembolism after prosthetic cardiac valve replacement.
Alnus japonica cortex has been used as antidiarrhea, antihemorrhage and the remedy of indigestion. This study was performed to investigate the effectiveness of the methanol extracts of the Alnus japonica cortex on the gastric lesion and ulcer. The methanol extract was fractionated with hexane, chloroform and butanol, followed by bioassay on antigastritic and antiulcer activity. The methanol extract showed low acute toxicity with minimum lethal dose of more than 5000 mg/kg, p.o. in mice. The chloroform and the butanol fraction reduced gastric lesion in HCI. ethanol induced gastritic model. On gastric secretion in pylorus ligated rat, the hexane and chloroform fraction decreased the volume and acidity. The butanol fraction had significant inhibitory effects on aspirin and Shay's ulcer. The butanol fraction showed a tendency to inhibit the decrease of mucin secretion due to ingestion of absolute ethanol.
To evaluate the site-specific permeation of aspalatone (acetylsalicylic acid maltol ester, AM) through gastrointestinal tract, the enzymatic degradation and permeation studies were carried out using gastric, duodenal and jejunal mucosae of rabbits. It was found that $15.2{\pm}11.4%$, $11.6{\pm}5.2$ and $0.8{\pm}0.6%$ of the donor dose of AM, salicylmaltol (SM) and aspirin (ASA) permeated through the upper gastric mucosa after 8 hr of permeation, respectively. After 8 hr of AM permeation, SM and ASA were measured to be $15.0{\pm}1.7$ and $2.6{\pm}0.8%$ of the dose in the donor solutions, respectively, and salicylic acid (SA) was not detected even after 6 hr, suggesting a very low gastric damage. For the gastric mucosa, the increase of donor dose from 100 to $1,000\;{\mu}g/ml$ increased the permeation flux dose-dependently (r=0.9905). For the duodenal and jejunal mucosae, however, AM was fully degraded into SM and SA due to the esterase activities within 30 min. AM and ASA were not detected in the receptor solution. This result indicates that AM is not a prodrug of ASA. Addition of potassium fluoride (0.5%) into the donor solution delayed the degradation of AM, but did not allow the permeation through duodenal mucosa even by the inhibition of esterase activity. The addition of $dimethyl-{\beta}-cyclodextrin$ and $2-hydroxypropyl-{\beta}-cyclodextrin$ (5%) into the donor solutions also did not show favorable effects on the permeation of AM through various mucosae. In comparison of permeation rates of AM and ASA through the upper gastric mucosa, the flux of ASA was 4.2 times faster than AM based on the molar concentration. ASA also was fully degraded in the donor solutions faced with duodenal and jejunal mucosae within 2 hr, and was not detected in the receptor solution, suggesting a slower metabolism compared with AM.
Purpose : Recently, clinical trials of steroid add-on therapy were reported with variable results in Kawasaki disease. We analyzed the clinical outcomes of patients at high risk of with Kawasaki disease(${\geq}4$ points of Harada score) treated by three commonly used different treatment regimens, with or without corticosteroids. Methods : Medical records of 96 children with Kawasaki disease treated with one of the threee regimens were reviewed retrospectively. Regimen 1 was aspirin(100 mg/kg/day) plus intravenous gamma globulin 2 g/kg single dose; regimen 2, aspirin(100 mg/kg/day) plus intravenous gamma globulin 1 g/kg single dose; regimen 3, regimen 2 plus prednisolone(2 mg/kg/day), followed by tapering two weeks and pulse therapy of methyl prednisolone performed in cases of retreatment. Also low dose aspirin was given in all three regimens for eight weeks after the acute phase. The cardiovascular and laboratory evaluations were performed on acute phase, immediate after acute phase, and subacute phase, eight weeks after treatment. Results : The frequency of coronary artery lesions and laboratory findings in the three different regimens were similar. The more rapid control of fever after treatment was noted in regimen 3. Furthermore the frequency of retreatment was decreased in regimen 3 compared to the other two regimens. Conclusion : Steroid add-on therapy showed some beneficial outcome compared to conventional treatment regimens. The role of steroid in the treatment of Kawasaki disease should be reassessed in systemic manner.
Moon, Su Jung;Lee, Su Ya;Na, Kyong Hee;Park, Sun Young;Kim, Eun Young;Kim, Kyoung Sim;Kim, Yong Wook
Clinical and Experimental Pediatrics
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v.46
no.3
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pp.302-307
/
2003
The long-term clinical issues in Kawasaki disease are concerned with the coronary artery lesions that result in aneurysmal formation, thrombotic occlusion, progression to ischemic heart disease, and premature atherosclerosis. We here report a 3 month old infant with Kawasaki disease complicated by giant coronary aneurysm with thrombosis. After urokinase(10,000 IU/kg) and heparin(400 IU/kg) were injected for two days as thrombolytic agents, thrombi were successfully dissolved. Even though long-term oral anticoagulation with low-dose aspirin, dipyridamole and coumadin were administered, thrombosis of the left main coronary artery was slowly increased. five years later, coronary angiography showed nearly total occlusion of the left anterior descending artery and collaterals from the right posterior branch and radionuclide scan demonstrated complete reversible perfusion defect of several portions of the left ventricle.
Background: Elderly patients with gastrointestinal (GI) and cardiovascular (CV) risk factors may be more easily exposed to NSAID-related side effects (SEs). Based on the ACG guideline of year 2009, the aim of the study is to evaluate proper use of NSAIDs and gastroprotective drugs according to the degree of GI and CV risk strengths in the patients. Methods: Retrospectively surveyed 410 elderly patients with NSAIDs for more than 30 days at a general hospital in Korea. GI risk factor includes age, ulcer history, high-dose NSIADs, concurrent aspirin use, steroids or anticoagulants. CV risk factor includes angina, myocardial infarction, cerebral infarction, atrial fibrillation or coronary intervention requiring low-dose aspirin. These factors were classified as high/low cardiovascular groups and high/moderate/low GI groups. Results: There were 14 patients in high CV risk group and high GI risk group. The group was recommended not to use NSAIDs as it is not adequate. There were 101 patients in high CV risk group and moderate GI risk group. This group was recommended to use naproxen and PPI/misoprostol. But all patients except one were not adequate. There were 9 patients in low CV risk group and high GI risk group. This group was recommended to use selective COX-2 inhibitor and PPI/misoprostol. 5 cases were proper while 4 cases did not. There were 285 patients in low CV risk and moderate GI risk group who were recommended to use non selective NSAIDs and PPI/misoprostol or selective COX-2 inhibitor only. 103 patients were proper while 182 patients not adequate. Overall, the SEs were higher in those cases for inadequate use of drugs comparing to the adequate. CV SEs were statistically significant. However, SEs for each risk groups were different. For the case of low CV risk group and high/moderate GI risk group, the inadequate use of drugs makes the SE high and the other groups are not. Also, it was not statistically significant. Conclusions: In elderly patients, the inappropriate use of NSAIDs can increase the risk of the disease. Therefore, GI and CV risk must be considered simultaneously, and the proper use of NSAIDs and gastroprotective drugs for each risk groups should be reconsidered.
We have observed retroperitoneal hematoma after trigger point injections of quadratus lumborum in a patient with chronic low back pain. Severe flank pain and dyspnea was observed three hours after injection of local anesthetic and steroid to the trigger point of quadratus lumborum muscle. There was fuge hematoma in abdominal CT image around the right kidney, which displaced and compressed the kidney anteriorly. Following infusion of contrast media, extravasation through renal vein and IVC was notified. Patient had a past history of having been treated with platelet aggregation inhibitor and lower dose aspirin treatment after cerebral ischemia for a year, but coagulative function was within normal range. Patient was admitted 12 days for bed rest, pain control and transfusion. We need to take greater care with a frequent aspiration and exact direction of needle, during trigger point injection of quadratus lumborum, particu right side, to avoid vascular injury.
Nonsteroidal antiinflammatory drugs (NSAIDs) are used in the treatment of extensive diseases related to various symptoms; inflammation, pain and fever. NSAIDs work by blocking prostaglandin synthesis, but adverse drug events (ADEs) have been increasing dramatically such as gastrointestinal bleeding, perforation and stenosis, a kind of serious ADEs. Therefore, NSAID-related ulcer complication guidelines have been announced containing various risk factors and symptoms. Thus, this study aims to evaluate of NSAID usage and appropriateness for prevention of NSAID-related ulcer complication based on American journal of gastroenterology (AJG) guideline 2009. Further, the study suggests Korean guideline for prevention of NSAID-related ulcer compared to AJG guideline. For this study, data was collected through electronic medical record (EMR) at Seoul national university of Bundang hospital. The primary end point was a composite of NSAID-related ulcer risk factor, types of NSAIDs, co-prescribed NSAID ulcer prevention drugs and NSAID-related ulcer after taking NSAID. The risk factors include over 65 years, high dose NSAID, previous ulcer history and taking drugs (e.g. aspirin, anticoagulant and steroid) causing ulcer. If a patient has 3 or 4 factors, that patient was classified high risk group. And if 1 or 2 factors that patient was classified moderate risk group. The patient who has no risk factor was in low risk group. I studied 8,120 patients who received NSAID from 1 January 2009 to 31 December 2009. High risk group was 16(0.2%), moderate risk group was 4,364(53.7%), and low risk group was 3,740(46.1%). The results show that high risk group should be prescribed COX-2 inhibitors with ulcer prevention drugs, and moderate or low risk group need traditional NSAIDs with ulcer prevention drugs. This may be different with 2009 AJG guideline because AJG guideline suggested taking COX-2 inhibitor alone in moderate group or taking traditional NSAID alone in low risk group could get higher ulcer complication. The results indicated that choosing preventive drug is important in case that how many risk factors the patients have. The proper drugs would be helpful for safe and effective NSAID usage in each patient group.
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