Al-Najaf Medical BULLETIN - University of Kufa

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Aspirin Therapy Should Be First-Line Treatment in Secondary Prevention of Stroke Hayder k. Hassoun FICM, FEN Department of neurology/Kufa college of medicine In this issue we try to give idea about different opinions and controversies regarding the use of Antiplatelet (AP) separately or in combination in secondary prevention of ischemic events (stroke, MI and peripheral ischemia), unfortunately we have no data available in our practice to judge whether use of AP as single agent regime whether more effective versus combined therapy of more than one AP .Ischemic stroke is a cecrebrovascular event that often leads to substantial disability. Although most patients survive, many are moderately to severely impaired. Additionally, each year, many people experience transient ischemic attacks (TIAs), an important stroke warning event. Both stroke and TIA are associated with increased risk for subsequent stroke and disability. The1-year risk of recurrent stroke after an initial stroke is 12%, and the 6month ischemic stroke rate after TIA has been found to be as high as 17%. Prolonged survival after stroke and TIA combined with a high risk for recurrence affords an excellent opportunity for secondary prevention. Antiplatelet therapy has been found to reduce relative risk for stroke by 15% to 37% in patients who have had a TIA or stroke. Aspirin is considered first-line therapy in secondary prevention, However, 2 OTHER Antiplatelet agents, clopidogrel and dipyridamole, either aloneor in combination with aspirin, have demonstrated efficacy in secondary prevention as well. Data from the European Stroke Prevention Study 2 (ESPS2) trials suggest that the combinationof 2 Antiplatelet agents (ie, aspirin and extended-release dipyridamole) with differing mechanisms of action may considerably reduce stroke risk. Although the choice of which of these agents to use in a particular patient is, of course, based on the person's medical history and risk profile, secondary stroke preventiontrial data are an important resource for clinicians. Such data allow neurologists to use evidencebased information in making treatment decisions for their patients with stroke and TIA.With the recent publication of the results of the Managementof Atherothrombosis With Clopidogrel in High-Risk Patients (MATCH) trial, which evaluated the safety and efficacy of Clopidogrel in combination with aspirin in the secondary prevention of stroke, neurologists now have new relevant data on which to base important treatment decisions when they are considering this combination of Antiplatelet agents. Ticlopidine is more effective than aspirin? A large multicenteric trial compared a daily dose of 500 mg ticlopidine and 1300 mg/d aspirin in 3069 patients with TIA or minor stroke. This study was associated with a statistically significant 21% reduction (P=0.024) in fatal or nonfatal stroke risk at 3 years in patients who received ticlopidine versus aspirin. The relative risk reduction of the combined outcome of stroke, MI, or vascular death was reduced by 9% in favor of ticlopidine, which was not statistically significant. Ticlopidine, however, can lead to neutropenia inup to 0.8% of patients and therefore is no longer the drug of choice. Clopidogrel is an antiplatelet agent that is chemically related to ticlopidine. A pivotal randomized, blinded, international trial, Clopidogrel versus Aspirin in Patients at Risk of Ischemic Events (CAPRIE), examined the relative safety and efficacy of daily doses of 75 mg clopidogrel versus 325 mg aspirin in nearly 20 000 patients with stroke, MI, or peripheral arterial disease. The results of the trial showed that Clopidogrel was more effective than aspirin in preventing a combined end point of ischemic stroke, MI, or vascular death. The trialists found a significant 8.7% reduction in relative risk (P=0.043) for clopidogrel versus aspirin. Although the CAPRIE trial was not powered to detect treatment differences within patient subgroups, a subgroup analysis, which was not part of the original design, was performed. Overall, when the results for these subgroups were examined, there was no significant difference between clopidogrel and aspirin inpatients with stroke or MI. There was, however, a significant benefit favoring clopidogrel in patients with peripheral arterial disease. The combination of aspirin plus slowrelease dipyridamole was investigated in the Second European Stroke Prevention Study (ESPS-2). ESPS-2 analyzed 6602 stroke or TIA patients who were randomly assigned to 4 treatment arms: placebo; aspirin alone (25 mg twice daily); extended-release dipyridamole alone (200 mg twice daily); or aspirin (25 mg twice daily) plus extended-releasedipyridamole (200 mg twice daily). The trial showed additive effects of aspirin and dipyridamole. The aspirin-plus-dipyridamole regimen of ESPS-2 produced a statistically significant 37% reduction (P=0.00l) in risk of fatal or nonfatal stroke over 2 years compared with placebo, similar to the risk reduction of the earlier ESPS- 1 trial (38%). Neither aspirin nor dipyridamole or the combination reduced mortality. Taken together, these study results show that the combination of aspirin plus dipyridamole is superior to aspirin alone in the prevention of stroke after TIA or stroke. The bleeding risk is not higher than with aspirin alone. Therefore, aspirin plus dipyridamole is the first-line treatment for secondary prevention of stroke. Clopidogrel is superior to aspirin for a combined end point of stroke, MI, and vascular death and is first-line treatment for high-risk patients with multiple vascular risk factors (eg, peripheral arterial disease). Whether the combination of clopidogrel plus aspirin is superior to aspirin alone is under investigation Secondary end point analysis showed a nonsignificant RRR of 7.1% for ischemic stroke (fatal or not) for clopidogrel plus aspirin vs. clopidogrel alone (95% CI, 8.5 to 20.4; P = .35), and an RRR of 2.0% for the combination vs monotherapy for any stroke (95% CI, 13.8 to 15.6; P = .79). However, the combination of clopidogrel plus aspirin resulted in a significantly greater incidence of s e r i o u s , l i f e - t h r e a t e n i n g b l e e d i n g complications than was observed with clopidogrel alone (P
Updated Bronchoscopy in early detection of subclinical lung cancer Fadhil Ghaly Yousif MRCS . FIBMS Department of cardiothoracic surgery, Alseder teaching hospital Lbronchoscope history reflectance imaging and fluorescent imaging. Since the introduction of rigid bronchoscope by Gustav Killian in 1897, pulmonary endoscopy This simple solution is made possible as the “dichroic filter- colour filter-combination” used in the standard 3 CCD color reflectance has become one of the cornerstones of respiratory imaging for the red and green signals happens to medicine. A revolutionary step took place when be very close to the optimal red and green channels for auto fluorescence imaging. Professor Shigeto Ikeda introduced the flexible The upper pair of images in Fig. 1 shows a bronchoscope to Europe in 1967. The updated situation Two major changes are now on the verge of arriving on this scene: 1. Screening of early stage cancers with very high sensitivity and specificity, by identification of proteomic mass spectrometric patterns in blood serum (1). Quite convincing demonstrations of this technology have been made for breast, colon, prostate and ovarian cancers, so that in all likelihood a similar procedure will soon be developed for early stage lung cancers. The applied methods seem to be adaptable to high throughput screening and thus should be relatively low cost. 2. The development of more optimal as well as s i g n i f i c a n t l y s i m p l i f i e d f l u o re s c e n c e bronchoscopes (2). This latter was made possible by the careful in situ clinical spectroscopic study of light induced tissue fluorescence in normal and diseased bronchial mucosa (3). This field, which has recently been reviewed (2), was launched mainly by the efforts of Profio and colleagues in the seventies (4) and was further developed by several groups (1), some of which are cited here. Todays autofluorescence bronchoscopes are based on the strongly reduced green autofluorescence intensity that is observed in some precancerous bronchial lesions upon violet light excitation. This reduction in green autofluorescence is not observed in the normal mucosa surrounding the lesions, so that the diseased mucosa can be identified by the change in the autofluorescence intensity. This phenomenon was first reported by Hung et al. (5). Furthermore, the addition of backscattered red light, which is presented for the first time in an image in this paper, also helps in the photon statistics by adding intensity to the rather weak red reference signal. Fluorescence bronchoscopes were originally quite complex and needed one or more image intensifiers, especially when video- moderate dysplasia situated on a spur in the intermediate bronchus. The lesion is clearly visible as a bright red zone on the greenish healthy background in the fluorescence image shown on the left. In the white light image the same lesion appears as a slightly reddish zone and is much more difficult to distinguish. The second lower set of images shows a severe dysplasia on a spur in the left upper lobe bronchus. In this case the lesion was hardly visible in conventional white light bronchoscopy while fluorescence endoscopy revealed a bright reddish zone on the healthy green background. The lesions were identified as moderate and severe dysplasia , respectively, after endoscopy. Careful comparison of autofluorescence bronchoscopy with the “golden standard”, i.e. white light bronchoscopy, showed significant increases in sensitivity (from 48 fi 72%) for the detection of moderate and severe dysplasia as well as CIS, with a specificity of 94% in both techniques the detection of pre-malignant mucosa, from 39% in white light bronchoscopy to 79% in autofluorescence bronchoscopy. Here, however, the specificity decreased from 91% to 87% (6). Following these studies with prototypes, a multicentre trial with the commercial version of the autofluorescence bronchoscope was undertaken in which the detection of both preinvasive and invasive bronchial lesions was evaluated. In this trial the sensitivity was found to increase from white light endoscopy (25%) to autofluorescence bronchoscopy (67%), i.e. an increase of nearly a factor of three. Specificity however decreased from 90% to 66% (6). This device has now been officially approved in the US, Canada, Europe and Japan and is to be used together with white light bronchoscopy for the detection of pre-invasive lung cancer. Both Storz and Wolf are expected to report on more extensive clinical trials in the near future. Fig. 1. Autofluorescence images (left) of moderate rate imaging was first attempted (5). The flip-flop filter between the source and the endoscope, together with the filtering of the light returned from the bronchi, enables sequential white light (upper) and severe (lower) dysplasia together with the corresponding white light reflectance (right) bronchial images. References 1. ANDERSSON-ENGELS S, JOHANSSON J, SVANBERG S: Medical Diagnostic System Based on Simultaneous Multispectral Fluorescence Imaging. Applied Optics 33: 80228029 (1994) 2. BELINSKY SA, NIKULA KJ, PALMISANO WA, MICHELS R, SACCOMANNO G, GABRIELSON E, BAYLIN SB, HERMAN JG: Aberrant methylation of p16(INK4a) is an early event in lung cancer and a potential biomarker for early diagnosis. PNAS of the USA 95: 1189111896 (1998) 3. CAVALIERE S, FOCCOLI P, TONINELLI C, FEIJO S: Nd:YAG laser therapy in lung cancer: an 11 year experience with 2,253 applications in 1'585 patients. J Bronchology 1: 105111 (1994) 4. CHEN JT, HO WL, CHENGYW, LEE H: Detection of p53 mutations in sputum smears precedes diagnosis of non-small cell lung carcinoma. Anticancer Res 20: 26872690 (2000) 5. DOIRON DR, PROFIO E, VINCENT RG, DOUGHERTY TJ: Fluorescence bronchoscopy for detection of lung cancer. Chest 76: 2732 (1979) 6. FRANKLIN WA: Pathology of lung cancer. J Thorac Imaging 15: 312 (2000) Erythropoietin (Epo.) in chronic renal disease Sabah Al-Helu Al Sadre Teaching Hospital Head of Nephrology department Epo. Is a glycoprotein hormone encoded by a gene on the Long arm of chromosome 7 (7q) and 90% is produced in the kidney (the remainder in the Liver and other sites.) in response to hypoxia. In the anaemia of chronic renal failure, the diseased kidneys try to make enough erythropoietin. The principal action of the hormone is to stimulate the proliferation, survival & differentiation of erythrocyte precursors. The manufacture of Epo. for clinical use became possible when the human gene as successfully inserted into cultured hamster ovary cells . The recombinant derived human Epo. (Epoetin ) must be given Subcutaneously (which may be more effective ) or i.v, the t 1/2 is 4 hours & appears not to be affected by dialysis . Maximum reticulocyte response occurs in 4 days. Self Administration at home 3times a week is practical. The does is adjusted by response. Iron reserves must be adjust for optimal Erythopiesis i.e. serum ferritin should exceed 100 mic/1 . Epo. is available as 2 preparations, Epoetin alpha &Epoetin beta Which are interchangeable. Significantly enhances the patient quality of life, patient become independent of Blood transfusion. Recombinant Epo.has also been used in anaemia's of Rheumatoid arthritis, following cancer therapy, mylodysplastic s y n d r o m e & Z i d o v u d i n e t r e a t e d AIDS.Athlete's intake events & cycling seeking advantage through increased Haemoglobin concentration has miss-used it. In CRF plasma Epo is used within the normal range and thus it is in-appropriately low for the degree of anaemia (relative deficiency of Epo.) In patient with poly cystic kidneys anaemia is often less severe or absent, while in some interstitial disorders it appears disproportionately severe for the degree of renal failure this is probably because of these disorder on the interstitial fibroblast that secret EPO. Recombinant human EPO is effective in correcting the anaemia of CRF the target Hb is between 10-12g/d Adverse effect A dose dependent increase in atrial blood pressure follows the rise in red cell mass & encephalopathy may occur in some previously hypertension patients, arteriovenous shunt of dialysis patients, especially those that are compromised, may thrombosis as a result of increased blood viscosity. Iron v inject‹‹‹ions‹‹‹.Trans‹‹‹ien‹‹‹t influenz‹‹‹a slike symptom‹‹‹s may ‹‹‹acco‹‹‹mpa‹‹‹ny the f‹‹‹ir et i. par‹‹‹‹enteral i‹‹‹‹ron‹‹‹‹ the‹‹‹‹‹rapy may‹‹‹‹‹ b eneeded, ‹‹this ‹‹can be a‹‹ cau‹‹se ‹‹‹inadequ‹‹‹at respons‹e to the h‹ormone‹&deficien‹‹cy m‹‹ay . occur as increased haematopoiesis for store)?000 + w .x B(. Hb pat-Hb target‹)x e3 as…‹‹‹ ( not rec‹‹‹omm‹‹‹‹ended for‹‹‹‹ chil‹‹‹‹dr tn)or iron‹ suc‹rose inje‹ctio‹n or infu‹sion , ‹In ) ravenous iron likes iron dextran in correcting anemia in CRF deficie‹ncy‹. : Failure of Epo 1.In pressure of iron deficiency. 2.active inflammation 3.malignancy 4.Patie‹nt wi‹th alumin‹‹um overlo‹‹ad whi‹‹ch . may occur in dialysis The‹‹‹se facto‹‹‹rs ne‹‹‹‹ed correcti‹‹‹‹on befo‹‹‹‹re . starting therapy 8 9
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Al-Najaf Medical BULLETIN - University of Kufa

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