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Source of funding: no external funding. For correspondence: Quality Standards Subcommittee, American Academy of Neurology, 1080 Montreal Avenue, St. Paul, MN 55116, USA. Fax + 1 713 798 Abstract and commentary also appear in Evidence-Based Mental Health. A modified version of this abstract appears in Evidence-Based Nursing.
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567 a result he suffered bodily injuries, sufficient to at least limit his ability to escape from the drainage ditch. Left in that condition by his assailants, Cole stumbled into the ditch. Unable to escape the high water, he drowned. Therefore, we find that the death can be attributed to a measurable degree to the assault because of the injuries. Also, we find that Claimant is entitled to compensation as a dependent of the victim. The evidence is that the victim's funeral expense was $3, 002.18 and his burial expenses were $100. Of this, $255 was paid by Social Security and $645 by the Illinois Department of Public Aid. The balance was paid by Lyle Cole, the victim's brother. There were no medical and hospital expenses. The victim was 48 years old at the time of his death. He had been a construction worker but had suffered several heart attacks. As a result, he had been disabled for about one year. His only source of income was $455 monthly from Social Security disability benefits. The record does not contain evidence as to whether Claimant was receiving any widow's portion of the victim's Social Security benefits or any other public assistance income, nor is there adequate evidence as to other potential deductions under section 10.1 e ; and 10.1 g ; of the Act. Having reviewed the evidence as to the cause of death, however, we were able to make findings under section 10.1 d ; of the Act. Based upon the testimony and record evidence, we find that the victim's conduct of voluntary intoxication contributed to his death to the extent of 50%. Therefore, it is hereby ordered that any award should be reduced by 50% under section 10.1 d ; . It further ordered that this claim be returned to the Attorney General for investigation as to the amount of, for instance, brand name.
References: 4. Data on tilt1. Squibb Institute for Medical Research. 8. Bravo EL, Tarazi RC: Converting enzyme inhibition with an orally active compound in hypertensive man Hypertension 1 39--46, 1979.
Aspirin was a remarkable drug in the 19th and 20th centuries, valued for its pain relieving actions without the Aspirin Resistance stuporous effects of alcohol or opium. Yet the full value of Despite aspirin's remarkable benefits, approximately 10aspirin Figure 1 ; was not realized until the latter part of the 20th century when aspirin claimed its place in the 20% of aspirin-treated patients will have a cardiovascular pharmaceutical hall of fame as the event within 5 years of initiating single most important drug for the therapy. This led to the concept that The structure of aspirin there is a subset of "aspirin resistant" prevention of heart attack and stroke. patients who do not respond to antiplatelet clumping therapy and Today, although aspirin is a mainstay in the prevention of atherosclerotic therefore are at persistent risk of events, physicians have other drugs future cardiovascular events. Of available to replace or supplement course, true biochemical aspirin resistance must be differentiated from aspirin, principal of these being non-compliance, not taking the drug clopidogrel Plavix ; . It is fortunate that as prescribed, a more common there are aspirin alternatives because recent research indicates that there reason for therapy failure. are patients who are resistant to aspirin, and even to clopidogrel. It is difficult to assess the clinical importance of aspirin resistance since there is currently no consensus on How Anti-Platelet Therapy how to define, measure, and treat Works aspirin and clopidogrel resistance. Figure 1. Laboratory tests are just becoming Both aspirin and clopidogrel inhibit the available, and test results can vary depending on the ability of blood platelets to aggregate, or clump. Clumping is one of the early steps in producing a blood clot, which is, laboratory performing the test and which test system is used. As a result, the incidence of `resistance' has been under ordinary circumstances, a beneficial effect. For estimated to be as low as 5% in some studies, and as high example, clots prevent blood from leaking from vessels, as 60% in others. This variation probably also reflects and in their absence, in diseases such as hemophilia, differences in treatment dosage and duration, as well as survival is difficult. Nevertheless, inappropriate clot the existence of other conditions and or medications that formation, for example, in the arteries supplying blood to the heart or brain, impairs blood flow, leading to damage or might influence drug action. death of tissue. Aspirin resistance might be brought on by lifestyle, genetics, or other illnesses. Diabetes and hypertension, for Aspirin's anti-clotting action occurs because it binds to example, increase the risk of aspirin resistance. Cigarette enzymes present in platelets, cyclooxygenases, or COX-1 smoking and elevated cholesterol increase the tendency of and COX-2. These enzymes control the synthesis of platelets to aggregate and blood to clot by increasing the thromboxane A2, which increases the tendency of platelets synthesis of other compounds that offset aspirin's to clump and of blood vessels to constrict. By irreversibly reduction of thromboxane A2, thereby restoring coaguability blocking COX, aspirin reduces blood's clotting ability, to the blood. The use of non-steroidal anti-inflammatory making harmful clot formation in the coronary or cerebral drugs NSAIDs ; is also associated with aspirin resistance. arteries less likely, hence reducing the probability of heart NSAIDs include drugs such as indomethacin and common attack or stroke. over-the-counter drugs such as ibuprofen Motrin ; . NSAIDs bind to the COX enzymes, briefly impairing their Clopidogrel acts by a different mechanism, blocking the biological activity 8-50 hours however, they also prevent ability of platelets to respond to molecules that initiate aspirin from binding and impede its longer-term beneficial platelet aggregation. The end result is indistinguishable and lopressor.
G Some cases of TB may not be detected during the first year. Screening of new entrants has consistently failed to pick up many new cases and the emphasis has now shifted to identifying people who are symptomatic. Locality and Deprivation Susceptibility to TB infection is strongly influenced by nutritional status, level of immunity and the presence of other infections such as HIV. Overcrowded living conditions increase the chance of TB infection being passed on. Exposure to TB does not necessarily result in disease. A person in good physical health has a much lower chance of succumbing to TB even if they come into contact with someone with smear positive pulmonary TB. However, a person with latent infection can develop disease symptoms years later if their general health and immunity deteriorates. The highest numbers of TB cases are concentrated in the south of the Borough, Figure 9.8. There is a correlation between the number of TB cases and area deprivation correlation coefficient 0.57 ; , Figure 9.9; and between the number of TB cases and the proportion of houses that were overcrowded correlation coefficient 0.74 ; , Figure 9.10.
Onmedica poll sanofi-aventis and bristol-myers squibb bms ; have announced that the european commission has granted a new indication for the antiplatelet agent plavix ® clopidogrel bisulfate ; to include patients with st-segment elevation acute myocardial infarction stemi ; who are eligible for thrombolytic therapy and lotrimin.
About halozyme therapeutics, inc halozyme is a biopharmaceutical company developing and commercializing products based on the extracellular matrix for the drug delivery, oncology, and dermatology markets.
Jones PW, Quirk FH, Baveystock CM, Littlejohns P. A selfcomplete measure of health status for chronic airflow limitation. The St. George's Respiratory Questionnaire. Rev Respir Dis 1992; 145: 13211327. McSweeny AJ, Grant I, Heaton RK, Adams KM, Timms RM. Life quality of patients with chronic obstructive pulmonary disease. Arch Intern Med 1982; 142: 473478. Ketelaars CA, Schlosser MA, Mostert R, et al. Determinants of health-related quality of life in patients with chronic obstructive pulmonary disease. Thorax 1996; 51: 3943. Hajiro T, Nishimura K, Tsukino M, Ikeda A, Koyama H, Izumi T. Comparison of discriminative properties among disease-specific questionnaires for measuring health-related quality of life in patients with chronic obstructive pulmonary disease. J Respir Crit Care Med 1998; 157: 785790. Murdoch I, Sthl E, Ahlstrm L, Lfdahl CG. Understanding patients' needs: the impact of COPD. Eur Respir J 2003; 22: Suppl. 45, 69S. Mahler DA, Faryniarz K, Tomlinson D, et al. Impact of dyspnea and physiologic function on general health status in patients with chronic obstructive pulmonary disease. Chest 1992; 102: 395401. Elias Hernandez MT, Ortega Ruiz F, Sanchez Riera H, Otero Candelera R, Sanchez Gil R, Montemayor Rubio T. Role of dyspnea in quality of life of the patient with chronic obstructive pulmonary disease. Arch Bronconeumol 1999; 35: 261266. Rennard S, Decramer M, Calverley PM, et al. Impact of COPD in North America and Europe in 2000: subjects' perspective of Confronting COPD International Survey. Eur Respir J 2002; 20: 799805. Bellia V, Catalano F, Scichilone N, et al. Sleep disorders in the elderly with and without chronic airflow obstruction: the SARA study. Sleep 2003; 26: 318323. Breathing fear: the COPD effect. Report commissioned by Allen & Hanburys and the British Lung Foundation, September 2003. Oga T, Nishimura K, Tsukino M, Hajiro T, Ikeda A, Mishima A. Relationship between different indices of exercise capacity and clinical measures in patients with chronic obstructive pulmonary disease. Heart Lung 2002; 31: 374381. Berry MJ, Rejeski WJ, Adair NE, Zaccaro D. Exercise rehabilitation and chronic obstructive pulmonary disease stage. J Respir Crit Care Med 1999; 160: 12481253. Stavem K, Boe J, Erikssen J. Health status, dyspnea, lung function and exercise capacity in patients with chronic obstructive pulmonary disease. Int J Tuberc Lung Dis 1999; 3: 920926. Hajiro T, Nishimura K, Tsukino M, Ikeda A, Oga T. Stages of disease severity and factors that affect the health status of patients with chronic obstructive pulmonary disease. Respir Med 2000; 94: 841846. Carter R, Holiday DB, Nwasuruba C, Stocks J, Grothues C, Tiep B. 6-minute walk work for assessment of functional capacity in patients with COPD. Chest 2003; 123: 14081415. Aliverti A, Stevenson N, Dellac RL, Lo Mauro A, Pedotti A, Calverley PMA. Regional chest wall volumes during exercise in chronic obstructive pulmonary disease. Thorax 2004 In press ; . Sthl E, Jansson S-A, Jonsson A-C, Svensson K, Lundbck B, Andersson F. Health-related quality of life, utility, and productivity outcomes instruments: ease of completion by subjects with COPD. Health Qual Life Outcomes 2003; 1: 18. Murray CJL, Lopez AD, Mathers CD, Stein C. The Global Burden of Disease 2000 Project: global programme on evidence for health policy discussion, paper number 36. Geneva: WHO, 2001. Sin DD, Tu JV. Inhaled corticosteroids and the risk of mortality and readmission in elderly patients with chronic obstructive pulmonary disease. J Respir Crit Care Med 2001; 164: 580584 and metrogel.
Stanley SLJ. Amoebiasis. Lancet 2003; 361: 1025-34. Mineno T, Avery MA. Giardiasis: recent progress in chemotherapy and drug development. Curr Pharm Design 2003; 9: 841-55.
For mortality, the drug-eluting stent with clopidogrel vs drug-eluting stent without clopidogrel comparison was P .10; and for composite of death or myocardial infarction, the drug-eluting stent with clopidogrel vs drug-eluting stent without clopidogrel comparison was P .02 and mobic.
Ped zahjenm podvn gemfibrozilu je teba co nejlpe zvldnout jin zdravotn problmy jako nap. hypotyrezu nebo diabetes mellitus a pacienty pevst na bznou nzkotucnou dietu, kterou je teba dodrzovat i bhem podvn ppravku. L9pid se podv perorln. Dospl Dvkovac rozmez je 900 mg az 1 200 mg denn. Pouze dvka se zaznamenanm vlivem na morbiditu, byla denn dvka 1 200 mg. Denn dvka 1 200 mg se podv rozdlen ve dvou dvkch po 600 mg denn, pl hodiny ped sndan a pl hodiny ped vece. Dvka 900 mg se podv v jedn dvce pl hodiny ped vece.
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FIGURE 1. Sites of action of aspirin and clopidogrel. ADP adenosine diphosphate; COX-1 cyclooxygenase 1; GP glycoprotein; TXA2 thromboxane A2 and moduretic.
Infection in Australian naval personnel. Med J Aust. 1989; 151 2 ; : 71-75. 11. Health status of Vietnam veterans. II. Physical health. The Centers for Disease Control Vietnam Experience Study. JAMA 1988; 259 18 ; : 2708-2714. 12. Roselle GA, Danko LH, Mendenhall CH. A four-year review of patients with hepatitis C antibody in Department of Veterans Affairs facilities. Mil Med. 1997; 162 11 ; : 711-714. 13. Spolarich AW, Russo B. Hepatitis C and veterans. December 1998 January 1999. The VVA Veteran. 14. United States Department of Veterans Affairs, Board of Veterans' Appeals. Board of Veterans' Appeals Decisions 1994-1996. Pub. No. 98-09166 CD-ROM ; . US Government Printing Office. Washington, DC. 1998. Chapter 18: HCV HIV COINFECTION Section 1: OVERVIEW Misha Cohen, OMD, LicAc 1. Cohen M, Gish R. The Hepatitis C Help Book. St. Martin's Press. New York, New York. 2000: 68. 2. Clark A. HIV and hepatitis coinfection oral presentation ; . XIII International Conference on AIDS. Durban, South Africa. 2000. 3. Nadler JP. HIV and hepatitis C - another perspective. Infect Med. 2001; 18 6 ; : 292-296. 4. Sherman KE, Rouster SD, Chung RT, Rajicic N. Hepatitis C virus prevalence among patients infected with human immunodeficiency virus: a cross-sectional analysis of the US adult AIDS Clinical Trials Group. Clin Infect Dis. 2002; 34 6 ; : 831-837. 5. Thomas D, Vlahov D, Solomon L, et al. Correlates of hepatitis C virus infections among injection drug users. Medicine. 1995; 74 4 ; : 212-20. 6. Ragni MV, Belle SH. Impact of human immunodeficiency virus infection on progression to end-stage liver disease in individuals with hemophilia and hepatitis C virus infection. J Infect Dis. 2001; 183 7 ; : 1112-1115. 7. Poles MA, Dieterich DT. Hepatitis C virus human immunodeficiency virus coinfection: clinical management issues. Clin Infect Dis. 2000; 31 1 ; : 154-161. 8. Thomas DL, Shih JW, Alter AJ, et al. Effect of human immunodeficiency virus on hepatitis C virus infection among injecting drug users. J Infect Dis. 1996; 174 4 ; : 690-695. 9. Merrik ST, Sepkowitz SA, Boyle BA, Jacobs JL. Seroprevalence of hepatitis C antibody and hepatitis B surface antigenemia in a large urban HIV clinic. Abstract 22263. XII International Conference on AIDS. Geneva, Switzerland. 1998. 10. Proietti F, Caiaffa W, Carneiro-Proietti AB, et al. Seroprevalence correlates of HIV and HCV infection among injection drug users IDUs ; attending an outreach syringe exchange program SEPs ; in five Brazilian cities. Abstract WeOrA530. XIII International Conference on AIDS. Durban, South Africa. 2000. 11. Greub G, Ledergerber B, Grob P, et al. Impact of HCV infection on HIV progression and survival in the Swiss HIV cohort studies. Abstract MoPeB2139. XIII International Conference on AIDS. Durban, South Africa. 2000. 12. Dieterich DT. Coinfection with hepatitis C virus HCV ; and HIV. 37th Annual Meeting of the Infectious Diseases Society of America IDSA ; . Philadelphia, Pennsylvania. 1998, for example, brand name.
Subjects in the clopidogrel ASA group who permanently discontinued their study medications due to adverse events other than bleeding, thrombocytopenia or allergy, compared to the placebo ASA group. Further interpretation of this observation is however difficult because the nature of these adverse events could not be determined, which is unfortunate as information on all adverse events associated pharmacological treatment may be considered critical to fully determine the role of a pharmaceutical agent. Although it was not the focus of our evaluation, the combined use of clopidogrel and ASA was also recently studied in ACS patients undergoing percutanous coronary intervention PCI ; . A subgroup of the CURE trial population, comprised of 2658 patients in whom PCI was performed, were enrolled in the PCI-CURE trial. In this subgroup, 1313 patients were randomly assigned to doubleblind treatment with clopidogrel and ASA while 1345 were in the placebo ASA group.19 Patients received this regimen for six days median ; before PCI. After PCI, over 80% of subjects in both groups received an open-label thienopyridine either clopidogrel or ticlopidine ; in combination with ASA for two to four weeks, after which the initial study medication was restarted for three to 12 months mean of 8 months ; .19 Most patients 82% and 81% in each group, respectively ; received an intracoronary stent. The incidence of cardiovascular death, MI or urgent revascularization was lower in the clopidogrel ASA group, compared to the placebo ASA group, both at 30 days 4.5% vs. 6.4%, RR 0.70, 95%CI, 0.50-0.97, p 0.03 ; and at the end of follow-up 18.3% vs. 21.7%, RR 0.83, 95%CI, 0.70-0.99, p 0.03 ; . As with the CURE trial, this effect was mainly driven by a reduction in non-fatal MI both at 30 days 2.1% vs. 3.8%, RR 0.56, 95%CI, 0.35-0.89 ; and at the end of follow up 4.5% vs. 6.4%, RR 0.71, 95%CI, 0.51-0.99 ; . There was no difference in cardiovascular death between the two groups. 19 From a safety perspective, there were no differences between groups in the incidence of major bleeding both at 30 days 1.6% vs. 1.4%, RR 1.13, 95%CI, 0.61-2.10, p 0.69 and nordette.
In order to attempt to maximise preservation of the neurovascular bundles, technical modifications to RRP have been reported; many of these involve methods which improve visualisaton of the neurovascular bundles 420, 426, 427, ; . The potential problem of impotence, when preservation of the neurovascular bundle is not considered appropriate, has been addressed by sural nerve grafting, employing techniques established in the management of facial and peripheral nerve injuries 429, 430 ; . Although this approach has met with a mixed reception by urologists, claimed success rates vary with one study having reported return of erectile activity in 75% of men with maximum return of function 14-18 months post-RRP 431 ; . However, most Urologists cite much lower success rates, for example, lopdi com.
Adhesion of platelets to proteins collagen, von Willebrand factor ; , particularly under conditions of high shear stress, and the action of platelet agonists adrenaline, thrombin, ADP, thromboxane A2 ; leads to the mobilisation of calcium ion Ca + ; , which functions as a mediator of platelet activation. Aspirin inhibits thromboxane A2 synthesis by irreversibly acetylating cyclooxygenase-1; the thienopyridines clopidogrel, ticlopidine ; irreversibly block the ADP receptor; and glycoprotein IIb IIIa inhibitors block the final common pathway of platelet activation leading to fibrinogen cross-linking of platelets and platelet aggregation. Phosphodiesterase inhibitors dipyridamole, cilostazol ; elevate intracellular cyclic AMP levels and thereby inhibit platelet function. ADP adenosine diphosphate; ASA aspirin; cAMP cyclic adenosine monophosphate; GP glycoprotein; PGG2 prostaglandin G2; PAR Protease activated receptor; PGH2 prostaglandin H2; PGI2 prostacyclin; PI phosphodiesterase inhibitor; TXA2 thromboxane A2; vWF von Willebrand factor and ocuflox.
Investments being undertaken by Sanofi-Synthlabo to expand production facilities include a 50 million euro programme to develop production facilities at Notre-Dame-de-Bondeville in preparation for the launch of the company's new thrombosis drug Arixtra fondaparinux sodique ; and a 15 million euro investment programme at the Tours site. In early 2002, Sanofi-Synthlabo announced it intended to invest 16 billion euros over two years to modernise production of liquid dosage forms at the Colomiers site, whilst transferring production of semi-solid forms to the Amilly facility. The company has also announced it is investing 21 million euros for the redevelopment of the Qutigny site, which will undertake European production of Plavix by 2003. Production capacity for Stilnox is also being expanded by 30% to 100 million boxes. In 2001, SanofiSynthlabo was reported to be considering the closure within two years of its Coutances plant, which employs 85 people and specialises in oral liquid forms. Production of some products will be transferred to the Colomiers site, where production capacity is being expanded by 20%. In February 2001, SanofiSynthlabo divested its chemicals subsidiary Sylachim to Dynamit Nobel, a subsidiary of the German MG Technologies group. Sylachim has two chemical plants at Mourenx and Chasse-sur-Rhone, which will continue to produce certain active ingredients for Sanofi-Synthlabo. The company retains two plants based at Aramon and Sisteron, which produce actives for Sanofi drugs. Major investments in production facilities have included the installation and subsequent expansion of dedicated production units for irbesartan and clopidogrel at both the Aramon and Sisteron plants.
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However, in a meta-analysis, no overall difference was found between behavioral approaches and pharmacotherapy for short-term treatment outcome, except that behavioral therapy resulted in greater reduction of sleep latency time to sleep onset ; smith et al, 2002 and oxybutynin.
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In 1975, Sanofi synthesized a thienopyridine named PCR 1033. That compound is the methyl analog of ticlopidine, which means that one of the two hydrogen atoms on the bridge carbon of a ticlopidine molecule the carbon linking the thienopyridine and phenyl substituents is substituted with a methyl CH3 ; group. Maffrand Tr. 1584 and prednisolone and lopid.
Dartmouth Medical School University of South Florida Living Beyond Breast Cancer University of Iowa Pennsylvania State University University of Central Florida University of Massachusetts Washington University Research Institute for Women's Health University of Arkansas University of North Carolina at Chapel Hill Case Western Reserve University The Salk Institute for Biological Studies University of Louisiana at Monroe The Hospital for Sick Children The Susan G. Komen Breast Cancer Foundation University of Michigan SHARE.
We have had an opportunity to ask questions and the physician has answered them to my our satisfaction. We have also received information about alternative procedures to allow me to become pregnant if they exist. We understand that adoption is also an option. We understand that we may withdraw my consent at any time. We release the Fertility Center of Chattanooga, and the employees thereof from any medical or emotional risks related to voluntary participation in this program. We have read this form and acknowledge receipt of a copy and protonix.
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REPORTING SUSPECTED SIDE EFFECTS To monitor drug safety, Health Canada collects information on serious and unexpected effects of drugs. If you suspect you have had a serious or unexpected reaction to this drug you may notify Health Canada by: toll-free telephone: 866-234-2345 toll-free fax 866-678-6789 By email: cadrmp hc-sc.gc By regular mail: National AR Centre Marketed Health Products Safety and Effectiveness Information Division Marketed Health Products Directorate Tunney's Pasture, AL 0701C Ottawa ON K1A 0K9 NOTE: Before contacting Health Canada, you should contact your physician or pharmacist. MORE INFORMATION.
The comparison between asa plus dipyridamole and clopidogrel is one to evaluate noninferiority followed by superiority.
| Lopid effectsCC-MS analysis of serum for the normal subject showed that ketone bodies, acetoacetic acid, and 3-hydroxybutyric acid were present in very low amounts; benzoic acid and hippuric acid were not detectable. The concentrations of 3hydroxybutyric acid and benzoic acid were much higher in the patient's samples. Hippuric acid was not detected in the admission sample, but was present in subsequent specimens. The concentration of acetoacetic acid was high only in the patient's sample collected 5 h after admission. Both benzoic and 3-hydroxybutyric acids tended to decrease in the patient's serum over the 12 h after admission, for example, lolid 60 mg.
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Table 21. Number of Results Flagged for Bias and Imprecision for Survey POCT-0504-GL.
Published studies have shown that administration of clopidogrel within 5 days before CABG increases bleeding. The findings were consistent across all the studies, but these studies were not RCTs. Two of the studies produced evidence of an increased mortality risk in patients treated with clopidogrel prior to surgery. Additionally, two studies showed that administration of aprotinin reduced blood loss during surgery in patients treated with clopidogrel within 5 days of the operation. Most of the studies reviewed were observational, but the weight of the evidence persuaded the STS task force to recommend stopping clopidogrel 5 days before CABG. This recommendation was part of the STS guideline on antiplatelet therapy.1 The American Heart Association and the American College of Cardiology have jointly issued a guideline that makes the same recommendation regarding clopidogrel treatment in patients undergoing CABG.2.
Serum lipids, particularly high concentrations of total cholesterol and HDL cholesterol, are a major risk factor for myocardial infarction and cardiovascular mortality [10]. Coronary heart disease can be prevented by lowering the total serum cholesterol with lipid-lowering drugs such as the 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors. In a recent study there was a 31 % relative risk reduction of nonfatal myocardial infarction or death from coronary heart disease in the treated group compared with those who received placebos [Ii]. Reductions were similar for the risks of nonfatal myocardial infarction as well as death from all cardiovascular causes. Plasma cholesterol was 20% lower in the treated group than in patients who received placebos, and LDL concentrations were reduced 26%. The goal of antilipemic therapy in patients with coronary disease is to decrease the serum cholesterol to 5.17 mmolJL 200 mg dL ; and to decrease the LDL concentration to 2.86 mmollL 100 mg dL ; [12]. Because the response of the individual patient to therapy with antilipemic agents varies, measuring serum lipids is essential to titrating these drugs.
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SUMMARY OF MEDICAL HISTORY APPLICANT IS A 78-YEAR-OLD MARRIED FEMALE, APPROXIMATELY 180LBS. APPLICANT HAS EXPERIENCED HYPERTENSION, HYPERLIPIDEMIA, CLAUCOMA, HEMORRHOIDS, RECTAL BLEEDING, DEEP VEIN, THROMBOPHLEBITIS, AND A HISTORY OF CATARACT SURGERY, AN OPEN REDUCTION AND INTERNAL FIXATION OF A FRACTURED RIGHT FEMUR, AND A TOTAL ABDOMINAL HYSTERECTOMY. APPLICANT'S CURRENT MEDICATIONS INCLUDE TIMOPTIC EYE DROPS, PILOCARPINE, ATENOL, LOPID AND DIOVAN. LPI'S REVIEWING PHYSICIAN ESTIMATES LE AT 60-84 MONTHS.
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