آخر تحديث عن موضوع الصحة هلاك والمرض علاج

موضوع شيق :D

يعطيك العافية على المواضيع القيمة ،،، وجعلها الله في ميزان حسناتك ،،، ولاتخبل علينا بالاخبار والمواضيع الشيقة ...

وشكرا

عبدالمانع

anwarica كتب:

العقل السليم فى الجسم السليم ------>>> المثل يحتاج إلى تعديل

الحياة الطويلة في الجسم المريض :lol: :lol: :lol:

والله أنا خايف من المشاركات دى نسبة التدخين تزيد :)

أكرر لو كان التبغ مفيد فى نقطه فهو مضر فى 1000 نقطة ، وعلينا الحذر :D

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لاتنسوا موضوع الأخ فيصل عن أخطار السيجارة للتذكير:

/index.php?showtopic=56289

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الحياة الطويلة في الجسم المريض

:lol: :lol:

والله بتحصل الأعمار بيد الله ..

طيب نخليه أحسن: العقل زينه فى الفترينه B)

فعلا المعلومة جديدة جداً أول مرة اعرف ان قله الرياضة لها فوايد :D

ومتشكرين يا دكتور

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أول مرة اعرف ان قله الرياضة لها فوايد

يظهر أن كل حاجة لها فائدة ثانوية مع الضرر...

موضوع مشهور أوى ونسيته ... اللى بيتعاطوا المخدرات .... تيجى تعطيهم بنج ولا يأثر لأن المخ متكيف جاهز :)

يعنى لازم تزود له الجرعة .. وهم أقل تأثرا بالسموم عامة لأنهم أخذوها بالبطئ :D

:lol: محمد

:lol: :lol: أقترح حذف هذا الموضوع فوراً :lol: :lol:

أنت كده هاتخللي الي بيفكر ينحرف و يدخن و يتعاطى مخدرات مايترددش لحظة واحدة ;)

اقتباس

أقترح حذف هذا الموضوع فوراً 

أنت كده هاتخللي الي بيفكر ينحرف و يدخن و يتعاطى مخدرات مايترددش لحظة واحدة

هو ده اللى أنا خايف منه :)

بس الموضوع صحيح 100% للأسف ... عموما لا قلق ما هو الكل عارف أن سم العقرب والثعبان بهم ضرر ،صح؟ وهو إحنا بناخذ منه جرعات للأدوية ... كعلاج فقط .. حتى المخدرات لما تستخدم منها كعلاج وبنسب محدودة :D

=-=-=-=-=

يا خوفى

شركات الشيكولاته السويسرية والتبغ الأمريكية تروج أحيانا دعاية طبية كاذبة بأن منتجات الشيكولاته والتبغ مفيدة فى حالات كذا وكذا ... وكل دى رشاوى للعلماء وللتعتيم الإعلامى ..

لكن يبقى الخطر خطرا .. والتدخين قاتل ..

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للتدخين 3 فوائد افتكر منهم

أن المدخن لا يسرقه لص ==>> لأنه يكح طوال الليل :lol:

والاثنين الباقيين مزاح أيضا

==

من الحقائق العلمية المؤلمة أن الحياه فى مكان نظيف "زيادة عن اللزوم" يصيب الانسان بالأمراض لأنه يضعف المناعة!!!

اقتباس

شركات الشيكولاته السويسرية والتبغ الأمريكية تروج أحيانا دعاية طبية كاذبة بأن منتجات الشيكولاته والتبغ مفيدة فى حالات كذا وكذا

لقد حدث من الناحية الفعلية، وقد قامت شركة "فليب مورس" الأمريكية بإفتتاح مركز بحثي يقوم العلماء فيه بالعمل على مسارين:

1) البحث عن فوائد للسيجارة... وقد أجروا دراسة نشرت من قبل الشركة في إعلانات مدفوعة الأجر بأن مادة النيكوتين قادرة على قتل نوع من جراثيم الدم (لا أذكر بالضبط إسم الجرثومة).

2) تفنيد الإدعاءات بأن السيجارة هي المسبب الرئيس للأمراض التي إرتبطت بها، وهذا الأمر بالتحديد يفيد تلك الشركات للتغلب على قضايا التعويضات التي تستهلك نسبة عالية من دخلها.

وقد قامت سلسلة مطاعم "ماكدونالدز" في السنة الماضية بنسخ تجربة "موريس" عن طريق التعاقد مع مركز بحثي يقوم بعمل دراسات لها تبين بأن السمنة التي يعاني منها الإنسان الأمريكي ليس سببها العادات الغذائية فقط بل أن هذه العادات هي جزء من مشكلة اكثر تتعلق بالعادات اليومية (عدم الحركة، مشاهدة التلفاز لفترات طويلة...الخ)... وهذه الخطوة أيضاً للتغلب على القضايا المرفوعة ضدها مطالبة بالتعويضات (من السمناء).

في المحصلة، هذه هي حضارة الشيطان.

السلام عليكم

منذ فتره قرات دراسه عن فوائد التمباك, والتمباك هى ماده تبغيه توضع تحت الشفه وتستخدم بكثره فى السودان والسويد.

من فائد هذه الماده حسب الدرساه التى قرتها, هى ان المتعاطى لا يصيبه تسوس الاسنان, ولكن هناك مشكله وهى ان اللثه تتاثر بشكل سلبى مما يجعل المتعاطى تسقط اسنانه بسبب ضعف اللثه. يعنى باختصار الواحد يفقد اسنان سليمه وبسرعه بدل ما يفقدها مسوسه وبعد فتره طويله.

والسلام

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ماده تبغيه توضع تحت الشفه وتستخدم بكثره فى السودان والسويد

سبحان من جمع السويد والسودان في صعيد واحد :lol:

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يعنى باختصار الواحد يفقد اسنان سليمه وبسرعه بدل ما يفقدها مسوسه وبعد فتره طويله

:lol: :lol: :lol:

وتلك فائدة كبيرة، فحقيقة وجع الأسنان بسبب التسوس لا يطاق، لذلك من المفضل التخلص من الأسنان في سن مبكر جداً وبسرعة مثل ما تفضلت. :lol:

anwarica كتب:

من الحقائق العلمية المؤلمة أن الحياه فى مكان نظيف "زيادة عن اللزوم" يصيب الانسان بالأمراض لأنه يضعف المناعة!!!

←

طيب بما انك تطرقت الى موضوع المناعة هذا، ما هي الأشياء التي ينصح بها لتقوية المناعة؟؟؟ ;)

و أرجو أن لا يكون الجواب هو السيجارة أو أي شيء مثل هذا القبيل :D

اقتباس

طيب بما انك تطرقت الى موضوع المناعة هذا، ما هي الأشياء التي ينصح بها لتقوية المناعة؟؟؟ 

و أرجو أن لا يكون الجواب هو السيجارة أو أي شيء مثل هذا القبيل

:) لا إن شاء الله خيراً،

موضوع التدخين دخل به تعديل حاليا لأنه هناك نتائج جديدة قد تقلب الحال مرة أخرى (حاليا بناقش الموضوع لحين الوصول لأدق النتائج) يعنى ممكن كمان المدخنين يفقدوا ميزة التغلب على الجلطة بعد تحديد عوامل معينه..

بالنسبة للمناعة فالمقويات كثيرة، على الأقل الطعام الصحى المتكامل (لا ينقص حتى الدهون والزيوت)... والرياضة بشكل عام

ولا أعرف أهم من الطعام والرياضه لتقوية المناعة بصراحة! (رأى شخصى) لأن بقية الارشادات ستكون الابتعاد عن مسببات الأمراض على الأقل مثل البرد :)

يعطيك العافية على المواضيع القيمة ،،، وجعلها الله في ميزان حسناتك

أديني عمر وارميني في البحر

" محدش يقول مين عمر ده :) "

وبالنسبة لزيادة المناعة فالرسول عليه الصلاة والسلام أوصى بالحبة السوداء وهي اي حبة سوداء مثل الفلفل وحبة البركة

وكذلك أوصى بالسنت والسنوت (الشبت والشمر ) فهما يزيدان المناعة وفيهما شفاء لكل داء الا مرض الموت

وكذلك عسل النحل وزيت الزيتون والخل ففيهم فوائد كبيرة جدا والله أعلم

ولا تنس الأمراض، فالإصابة بها هو أفضل طريقة للمناعة... سبحان من جعل الدواء بالداء.

اقتباس

ولا تنس الأمراض، فالإصابة بها هو أفضل طريقة للمناعة... سبحان من جعل الدواء بالداء.

بالضبط مثل تطعيم شلل الأطفال عند حقن فيروس ضعيف للأطفال كى يكون مناعة ضده :)

وأيضا النظافة لأن النظافة من الايمان .. المكان النظيف جدا هو الذى يضعف المناعة ولكن النظافة جدا هذه هى نظافة زيادة عن اللزوم يعنى مثلا واحد بيمسح البيت مرتين فى اليوم ولاحاجة (ما اعتقدش حد عادى يقدر) .. أحيانا الناس اللى عندهم فوبيا من عدم النظافة (وسواس قهرى تقريبا) هم اللى يصعبوا على الواحد .. تلاقيه كل نص ساعة يغسل يده وربما أكثر!

ذكر أحد الإخوة أن شخصاً أصيب بفشل كلوي لأنه لم يكن يشرب إلا من المياة المعبئة مصنعيا ،، فتعطلت كليته عن العمل ..

الحمد لله على نعمه العافية و الصحة ..

الحمد لله ظهر الحق

بعد مباحثات (مش أنا اللى عملت المباحثات)

ثبت أن الموضوع فكرته قديمه وليست صحيحه

وهذا مقال (الشاطر يخلصه) :lol:

Preventive cardiology: Cardiovascular risk of smoking and benefits of smoking cessation 

James A Schoenberger, MD 




INTRODUCTION — The facts regarding the risk of cigarette smoking and cardiovascular disease are well known to both the medical profession and the public [1]. Nevertheless, many smokers do not believe that smoking is harmful for them. In one study, for example, over 60 percent of 737 current smokers, even those who smoked more than 40 cigarettes per day, did not believe that they were at an increased risk for a myocardial infarction [2]. 

The relationship between smoking and coronary heart disease, the effects of smoking on the atherosclerosis process, and the beneficial effects of smoking cessation will be reviewed here [3]. These issues also apply to diabetics and are discussed separately. (See "Smoking and cardiovascular risk in diabetes mellitus"). 

SMOKING AND CARDIOVASCULAR DISEASE — With respect to coronary heart disease (CHD), the following observations have been made regarding a major role for smoking: 

Smoking is an independent major risk factor for CHD, cerebrovascular disease, and total atherosclerotic cardiovascular disease [4]. 

The incidence of a myocardial infarction is increased sixfold in women and threefold in men who smoke at least 20 cigarettes per day compared to subjects who never smoked [5,6]. In the worldwide INTERHEART study of patients from 52 countries, smoking accounted for 36 percent of the population attributable risk of a first MI [7]. 

Cigarette smoking increases all-cause and cardiovascular mortality [8,9]. 

Patients who continue to smoke in the presence of established CHD have an increased risk of reinfarction and an increased risk of death, including sudden cardiac death [10,11]. 

Smoking status before coronary artery bypass graft (CABG) surgery does not affect survival after surgery, but persistent smokers after CABG have a greater relative risk of all-cause mortality (relative risk 1.6, cardiac death (relative risk 1.75), and need for repeat revascularization (relative risk 1.41) compared to those who stopped smoking for at least one year [12]. (See "Long-term outcome after coronary artery bypass graft surgery"). 

After angioplasty, persistent smokers have a greater relative risk of death (1.76) and Q wave myocardial infarction (2.0 compared to nonsmokers, and a higher relative risk of total and cardiac mortality (relative risk 1.44 and 1.49 respectively) when compared to those who quit smoking [13]. 

Among patients with left ventricular dysfunction (left ventricular ejection fraction 35 percent) in the SOLVD trial, smoking significantly increased all-cause mortality (relative risk 1.41 compared to ex-smokers or never smokers) and the incidence of death, recurrent heart failure requiring hospitalization, or myocardial infarction (relative risk 1.39) [14]. 


Passive smoking — It is estimated that exposure to second-hand smoke (ie, passive smoking) causes almost 40,000 deaths from heart disease each year in the United States [15], increasing the risk in nonsmokers of coronary disease and coronary death by approximately 20 percent in large epidemiologic studies [16,17]. The relative risk for heart disease from passive smoking at work and from home-based exposure are equivalent (relative risk 1.35 to 1.50 versus 1.49) [18]. 

A prospective study from the American Cancer Society CPS-II cohort of 309,599 married pairs and 135,237 individuals found that exposure to smoking from a wife among men who never smoked led to a 20 percent higher coronary death rate [16]. There was no significant increase in risk in nonsmoking wives of smoking husbands or in living with former smokers. 

Data from the Nurses' Health Study involving 32,046 subjects found a relationship between the amount of passive smoke exposure and the risk of CHD [19]. Compared to women not exposed to passive smoking, the relative risk of coronary heart disease, after adjustment for other cardiovascular risk factors, was 1.58 among women who reported occasional exposure and 1.91 among those reporting regular exposure. 

Two meta-analyses of published studies involving smokers or nonsmokers living with smokers reported that the relative risk of CHD associated with environmental tobacco smoke was 1.25 to 1.3 [20,21]; this risk increased by 25 percent after adjusting for diet and was the same in men and women and in those exposed at home or in the workplace. Moreover there was a dose-response relationship with a relative risk of 1.23 and 1.31 for nonsmokers exposed to 1 to 19 and 20 cigarettes per day, respectively, as compared to nonsmokers not exposed to smoke [21]. 

One report evaluating the effect of passive smoking included measurement of serum cotinine concentrations to assess environmental exposure objectively [22]. A group of 2105 nonsmoking British men were divided into quartile based upon serum cotinine. During 20 years of follow-up, there were 8.29 CHD events and strokes per 1000 patients per year. Compared to those in the lowest quartile of serum cotinine, those in the second, third, and fourth quartiles had an increased risk of CHD events and strokes (adjusted hazard ratios 1.45, 1.49, and 1.57, respectively). In comparison, the hazard ratio for a comparable group of active smokers was 1.66. 


Cigar smoking — Although there is an established association between cigar smoking and cancer of the upper respiratory, lungs, and gastrointestinal tract and the risk of chronic obstructive lung disease, cigars are generally perceived as being safer than cigarettes. Moreover, data about the role of cigar smoking and the risk of cardiovascular disease are limited. Cigar smoke contains the same toxic and carcinogenic compounds that are found in cigarette smoke, and subjects who smoke four or more cigars per day are exposed to an amount of smoke equivalent to 10 cigarettes; even those who do not inhale are exposed to their own environmental smoke. Cigar smoking may result in endothelial dysfunction [23]. One cohort study of 17,774 men followed for 14 years found that, compared to nonsmokers, those who smoked cigars were at a greater risk for developing coronary heart disease (relative risk 1.27); there was a dose-response relationship and the relative risk for those who smoke less than or greater than 5 cigars per day were 1.2 and 1.56, respectively [24]. 

An American Cancer Society study of 121,278 men 30 years of age found that current cigar smokers 75 years of age had an increased risk of death from coronary heart disease (adjusted rate ratio 1.3); there was no increased risk in those >75 years of age or former cigar smokers of any age [25]. 

Smokeless tobacco — The use of snuff and other types of smokeless tobacco is increasing, particularly among adolescents and young adults; however, the cardiovascular health hazards of smokeless tobacco are not well established [26]. One population based study of 687 men, aged 24 to 64, with a first-time myocardial infarction and 687 matched controls found no difference in the incidence of myocardial infarction between nonsmoking regular snuff users compared to those who never used any tobacco products (adjusted odds ratio 0.96) [27]. 

In contrast, a much larger study of over 135,000 male construction industry employees from Sweden, including over 6000 smokeless tobacco users, found that the age-adjusted relative risk of cardiovascular mortality was 1.4 for smokeless tobacco users [28]. For men aged 35 through 54 at the start of follow-up, the relative risk was 2.1. 

SMOKING AND ATHEROSCLEROSIS — The direct effect of smoking on the development of atherosclerosis was assessed in the ARIC (Atherosclerosis Risk in Communities) study [29]. This study consisted of 10,914 patients in whom intimal-medial thickness of the carotid artery was measured by ultrasound over a three-year period. Current smoking was associated with a 50 percent increase in the progression of atherosclerosis versus nonsmokers during the study period, and patients with environmental tobacco smoke exposure had a 20 percent greater rate of atherosclerosis progression compared to patients without environmental tobacco smoke exposure (show figure 1). 

Although more pack-years of exposure was independently associated with faster progression, the progression rates of current and previous smokers did not differ, suggesting that some of the adverse effects of cigarette smoking may be cumulative and irreversible. Another study of patients with preexisting coronary disease found that smoking accelerates the progression of lesion size and new lesion formation as assessed by serial coronary angiography [30]. 

Smoking has also been correlated with increases in atherosclerotic disease of the thoracic aorta [31] and the carotid arteries [32]. 

Pathogenesis — Although the relationship between CHD and smoking, even when passive, appears clear, the mechanism by which it occurs is incompletely understood. Multiple factors may be involved since smoking has a variety of effects that may contribute to atherogenesis [3]. (See "Pathogenesis of atherosclerosis"). 

Smoking is associated with an adverse effect on serum lipids (elevated low density lipoproteins and triglycerides and reduced high density lipoproteins) [33] and with insulin resistance [34,35]. 


In addition, free radicals in cigarette smoke damage lipids, resulting in the formation of proatherogenic oxidized particles, specifically oxidized low density lipoprotein cholesterol [36-38]. A similar effect is seen with acute passive smoking [39]. (See "Lipoprotein classification; metabolism; and role in atherosclerosis", section on Lipoproteins and atherosclerosis). 

Cigarette smoking activates the sympathetic nervous system, producing an increase in heart rate and blood pressure, and cutaneous and perhaps coronary vasoconstriction [40-42]. 

Smoking enhances the prothrombotic state via inhibition of tissue plasminogen activator release from the endothelium [43], elevation in the blood fibrinogen concentration [44], increased platelet activity (possibly due to enhanced sympathetic activity) [45], increased expression of tissue factor [46], and, in patients with advanced lung disease, elevated whole blood viscosity due to secondary polycythemia. 

Smoking can damage the vascular wall, possibly leading to impaired prostacyclin production and enhanced platelet-vessel wall interactions [47]. This can reduce the elastic properties of the aorta, resulting in stiffening of and trauma to the wall [48]. 

Smoking, even when passive, impairs endothelium-dependent vasodilation of normal coronary arteries and reduces coronary flow reserve [49-53]. Smoking can also potentiate the endothelial dysfunction induced by hypercholesterolemia [51,54]. The effect on endothelial function results from oxidative stress with enhanced oxidation of LDL and from reduced generation of nitric oxide [50,53,55-57]. 

Smoking has been correlated with elevated levels of C-reactive protein and fibrinogen [58,59]. In addition, concentrations of soluble adhesion molecules are higher in smokers than nonsmokers [57,59]. These findings suggest that smoking contributes to the inflammatory response that is a factor in the pathogenesis of atherosclerosis. (See "C-reactive protein in cardiovascular disease"). 

Smoking has been correlated with elevations in serum homocysteine, which is thought to induce vascular injury by multiple mechanisms [58]. (See "Overview of homocysteine"). 


Role of carbon monoxide — Carbon monoxide is inhaled in cigarette smoke. It binds more avidly than oxygen to hemoglobin, reducing the amount of hemoglobin available to carry oxygen and impeding oxygen release by hemoglobin that is not directly bound to carbon monoxide. (See "Smoke inhalation"). This effect can be detected clinically by measuring carboxyhemoglobin levels which average 5 to 10 percent higher in smokers than nonsmokers, in whom levels are less than 1 percent. 

In healthy subjects, carbon monoxide administration, under conditions similar to cigarette smoking, does not affect blood pressure, plasma catecholamines, platelet aggregation, or serum C-reactive protein [60]. Since these parameters are changed with smoking, the observations suggest that some factor other than carbon monoxide is responsible. 

In comparison, carbon monoxide exposure in patients with CHD results in severe adverse effects. These include exercise-induced ischemia at a lower level of work, ventricular dysfunction, and increased number and complexity of ventricular arrhythmias [61,62]. 

Role of nicotine — Nicotine in cigarette smoke plays a major role in the transient smoking-related increases in cardiac output, heart rate, and blood pressure. (See "Cardiovascular effects of nicotine"). 

It is not clear if nicotine plays a direct role in the development of atherosclerosis. Nicotine has been reported to have variable effects on nitric oxide [63,64], but does not appear to increase lipid deposition in the vascular wall [65]. Nicotine may contribute to acute endothelial dysfunction in smokers [66]. 

Role of oxidative stress — Free radical-mediated oxidative stress may play a pivotal role in the development of atherosclerosis. (See "Antioxidants in coronary heart disease", section on Pathophysiology). 

Free radicals are present in both the gas and "tar" phases of cigarette smoke [67] and may also be generated from endogenous sources in response to smoking [68]. A study in human coronary artery endothelial cells found significantly lower nitric oxide production with exposure to smokers' serum than nonsmokers' serum, an effect that was mitigated by the addition of antioxidants [69]. In humans, antioxidant therapy improves endothelial dysfunction in smokers [70]. However, chronic administration of antioxidants such as vitamin C, vitamin E, and beta carotene do not appear to improve long-term outcomes with the possible exception of specific patient subsets. (See "Antioxidants in coronary heart disease"). 

SMOKING AND OUTCOME AFTER MI TREATED WITH THROMBOLYSIS — Despite the important role of cigarette smoking in the development of atherosclerosis, several studies have reported that smokers who receive a thrombolytic agent for an acute myocardial infarction have a better outcome than nonsmokers [71-78]. This phenomenon is called the "smoker's paradox." (See "Thrombolytic agents in acute ST elevation (Q wave) myocardial infarction: Clinical use"). 

As an example, the International Tissue Plasminogen Activator/Streptokinase Mortality trial, which involved 2366 nonsmokers, 2244 exsmokers, and 3649 active smokers, found that nonsmokers, compared to the other two groups, had a higher incidence of in-hospital complications including shock, stroke, and bleeding [71]. Nonsmokers also had a higher in-hospital and six month mortality than exsmokers or active smokers. 

Similar findings were noted in TIMI II and GUSTO I [72,73]. GUSTO I was largest trial to evaluate the impact of cigarette smoking on outcome as it included 11,975 nonsmokers, 11,117 exsmokers, and 17,507 current smokers [73]. Nonsmokers had a significantly higher rate of in-hospital complications and a higher in-hospital (9.9 versus 3.7) and 30 day mortality (10.3 versus 4.0 percent). 

The reason for the surprisingly better outcomes after thrombolysis in smokers may be related to the following factors: 

Smokers have a higher hematocrit and baseline level of fibrinogen, suggesting a hypercoagulable state [74,75]. This could explain the angiographic finding that the mechanism of infarction in smokers is more often thrombosis of a less critical atherosclerotic lesion than in nonsmokers [74]. More active thrombogenic mechanisms may lead to a larger thrombus component that is more susceptible to thrombolytic therapy, resulting in smokers having a higher patency rate and being more likely to have TIMI-3 flow in the infarct artery after thrombolysis [74,75,79]. 

Smokers have an otherwise better risk profile than nonsmokers; they tend to be significantly younger (mean 11 years in GUSTO I) and have a lower incidence of diabetes, hypertension, previous infarction, and severe coronary disease than nonsmokers [71-78]. Also, for unclear reasons, smokers are more likely to have an inferior rather than anterior wall infarction [74,75,78]. After adjustment for these clinical factors, some [73,74,76] but not all [78] studies reported that smoking history was of not an independent prognostic factor (show figure 2). 


The smoker's paradox appears not to apply to patients presenting with unstable angina. In a multicenter registry that included almost 8000 patients with unstable angina, intensive care unit mortality was lower for smokers than for exsmokers or nonsmokers (0.7 versus 1.0 and 1.5 percent, respectively) [78]. However, when corrected for age and other cardiovascular risk factors, smoking history was not an independent predictor. 

CARDIOVASCULAR BENEFITS OF SMOKING CESSATION — The benefits of quitting cigarette smoking are also firmly established but perhaps less well known and accepted. Among subjects without known CHD, the reduction in cardiac event rate associated with smoking cessation ranges from 7 to 47 percent [80-82]. The cardiac risks associated with cigarette smoking diminish relatively soon after smoking cessation and continue to fall with increasing length of time since quitting [83]. Similar benefits have been noted in patients with cardiovascular disease. 

Myocardial infarction — Smoking cessation improves outcomes in patients who have had a myocardial infarction [11,84-88]. The range of benefits can be illustrated by the following findings: 

The mortality benefit of smoking cessation was assessed in a meta-analysis of 20 studies including 12,603 smokers, of whom 5659 ceased smoking and 6944 continued to smoke [87]. All patients had had an MI, CABG, angioplasty, or known CHD. The relative risk of mortality for smokers who quit compared with those who continued to smoke was 0.64 (95% CI 0.58-0.71). The benefit was not affected by age, sex, index cardiac event, country, or the year in which the study began. 

The effect of smoking cessation on recurrent coronary events was evaluated in a retrospective, population-based cohort study of 2619 patients who survived to hospital discharge after a first myocardial infarction [88]. At the time of the infarction, roughly equal percentages were nonsmokers, former smokers, and current smokers (56 percent of whom quit smoking). 


Using the nonsmokers as the reference group, the multivariable risk ratio (RR) for recurrent coronary events was nonsignificantly increased in former smokers (RR 1.17) and significantly increased for active smokers (RR 1.51). Among those who quit smoking (patients who quit and restarted were considered active smokers), the risk ratio progressively and significantly decreased with longer duration of cessation (RR 1.62 at 0 to <6 months, 1.60 from 6 to <18 months, 1.48 for 18 to <36 months, and 1.02 for 36 months). A possible contribution from confounding factors, such as quitters being more likely to be compliant with other aspects of therapy, could not be excluded. 

Stroke — The risk of ischemic stroke also decreases over time after smoking cessation. In one series of middle-aged women, for example, the excess risk among former smokers largely disappeared two to four years after cessation [89]. The continued decline in risk over time after smoking cessation suggests that more than one mechanism may be involved. The early benefit may result from improved coagulation parameters or reversal of endothelial dysfunction, while the late benefit may reflect slowing or even reversal of the atherosclerosis process. 

Effect of age — The relative benefits of smoking cessation are equivalent in young and old patients. In one study of 1893 patients with CHD who were older than 55 years, the mortality after six year follow-up was significantly higher among patients who continued to smoke compared to those who stopped (relative risk 1.7) [90]. The benefits were equivalent in those aged 55 to 64 and over age 65 and were the same as observed among comparable patients aged 34 to 54. 

Despite these facts, approximately 25 percent of the adult United States population continues to smoke and there has been little change in the prevalence of smoking since 1990 (show figure 3) [91]. Nearly equal numbers of men and women smoke; in both sexes smoking rates are higher in less educated and poorer segments of the population. Approximately 70 percent of cigarette smokers state that they would like to quit smoking. 

Possible deleterious effects — There are no convincing reasons not to quit smoking although several issues have been raised: 

Nicotine withdrawal and depression can occur as a result of quitting. While the depression associated with cessation is usually mild, it may be sufficiently severe to require counseling, antidepressant therapy, or a return to smoking. 

Many smokers, especially women, cite gain in weight as a reason not to quit smoking. This issue was studied in the third National Health and Nutrition Survey conducted from 1988 through 1991 [92]. The long term gain in weight for smokers who quit compared to smokers who continued to smoke was 4.4 kg for men and 5.0 kg for women. Smokers who quit were significantly more likely to gain weight than those who never had smoked. 

Cessation has been associated with exacerbations of ulcerative colitis [93], and nicotine is now being evaluated as a therapeutic agent in this condition. 


An analysis of the health care costs of smoking cessation revealed short-term savings, but increased health care costs in the long run since former smokers lived longer and used greater amounts of terminal health care [94]. This observation has no relevance to the individual who, by quitting smoking, can markedly improve his or her health. From a public health standpoint it can be argued that any other effective measure for prevention of cigarette use may also increase health care costs in the long run, but the promotion of healthy, long lives should be the goal of modern society. 

Methods of smoking cessation — Physicians often fail to intervene against smoking [95]. The lack of economic incentives for physicians to promote smoking cessation and pessimism among physicians regarding the effects of these interventions may explain these findings [91]. 

There are a number of ways that physicians can and should actively intervene against smoking in virtually all smokers (show table 1). Behavioral therapy, nicotine replacement, and the use of antidepressant medications may each improve the quit rate. (See "Overview of smoking cessation"). 



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REFERENCES 
1. Ockene, IS, Miller, NH. Cigarette smoking, cardiovascular disease, and stroke. A statement for healthcare professionals from the American Heart Association. Circulation 1997; 96:3243. 
2. Ayanian, JZ, Cleary, PD. Perceived risks of heart disease and cancer among cigarette smokers. JAMA 1999; 281:1019. 
3. Ambrose, JA, Barua, RS. The pathophysiology of cigarette smoking and cardiovascular disease: an update. J Am Coll Cardiol 2004; 43:1731. 
4. Jee, SH, Suh, I, Kim, IS, Appel, LJ. Smoking and atherosclerotic cardiovascular disease in men with low levels of serum cholesterol: the Korea Medical Insurance Corporation Study. JAMA 1999; 282:2149. 
5. Njolstad, I, Arnesen, E, Lund-Larsen, PG. Smoking, serum lipids, blood pressure, and sex differences in myocardial infarction. A 12-year follow-up of the Finnmark Study. Circulation 1996; 93:450. 
6. Prescott, E, Hippe, M, Schnohr, P, et al. Smoking and the risk of myocardial infarction in women and men: Longitudinal population study. BMJ 1998; 316:1043. 
7. Yusuf, S, Hawken, S, Ounpuu, S, et al. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Lancet 2004; 364:937. 
8. Qiao, Q, Tervahauta, M, Nissinen, A, Tuomilehto, J. Mortality from all causes and from coronary heart disease related to smoking and changes in smoking during a 35-year follow-up of middle-aged Finnish men. Eur Heart J 2000; 21:1621. 
9. Foody, JM, Cole, CR, Blackstone, EH, Lauer, MS. A propensity analysis of cigarette smoking and mortality with consideration of the effects of alcohol. Am J Cardiol 2001; 87:706. 
10. Tofler, GH, Muller, JE, Stone, PH, et al. Comparison of long-term outcome after acute myocardial infarction in patients never graduated from high school with that in more educated patients. Multicenter Investigation of the Limitation of Infarct Size (MILIS). Am J Cardiol 1993; 71:1031. 
11. Goldenberg, I, Jonas, M, Tenenbaum, A, et al. Current smoking, smoking cessation, and the risk of sudden cardiac death in patients with coronary artery disease. Arch Intern Med 2003; 163:2301. 
12. van Domburg, RT, Meeter, K, van Berkel, DF, et al. Smoking cessation reduces mortality after coronary artery bypass surgery: a 20-year follow-up study. J Am Coll Cardiol 2000; 36:878. 
13. Hasdai, D, Garratt, KN, Grill, DE, et al. Effect of smoking status on the long-term outcome after successful percutaneous coronary revascularization. N Engl J Med 1997; 336:755. 
14. Suskin, N, Sheth, T, Negassa, A, Yusuf, S. Relationship of current and past smoking to mortality and morbidity in patients with left ventricular dysfunction. J Am Coll Cardiol 2001; 37:1677. 
15. Glantz, SA, Parmley, WW. Passive smoking and heart disease. Mechanisms and risk. JAMA 1995; 273:1047. 
16. Steenland, K, Thun, M, Lally, C, et al. Environmental tobacco smoke and coronary heart disease in the American Cancer Society CPS-II cohort. Circulation 1996; 94:622. 
17. Wells, AJ. Passive smoking as a cause of heart disease. J Am Coll Cardiol 1994; 24:546. 
18. Wells, AJ. Heart disease from passive smoking in the workplace. J Am Coll Cardiol 1998; 31:1. 
19. Kawachi, I, Colditz, GA, Speizer, FE, et al. A prospective study of passive smoking and coronary heart disease. Circulation 1997; 95:2374. 
20. Law, MR, Morris, JK, Wlad, NJ. Environmental tobacco smoke exposure and ischaemic heart disease: An evaluation of the evidence. BMJ 1997; 315:973. 
21. He, J, Vupputuri, S, Allen, K, et al. Passive smoking and the risk of coronary heart disease--a meta-analysis of epidemiologic studies [see comments]. N Engl J Med 1999; 340:920. 
22. Whincup, PH, Gilg, JA, Emberson, JR, et al. Passive smoking and risk of coronary heart disease and stroke: prospective study with cotinine measurement. BMJ 2004; 329:200. 
23. Santo-Tomas, M, Lopez-Jimenez, F, Machado, H, et al. Effect of cigar smoking on endothelium-dependent brachial artery dilation in healthy young adults. Am Heart J 2002; 143:83. 
24. Iribarren, C, Tekawa, IS, Sidney, S, et al. Effect of cigar smoking on the risk of cardiovascular disease, chronic obstructive pulmonary disease, and cancer in men. N Engl J Med 1999; 340:1773. 
25. Jacobs, EJ, Thun, MJ, Apicella, LF. Cigar smoking and death from coronary heart disease in a prospective study of US men. Arch Intern Med 1999; 159:2413. 
26. Gupta, R, Gurm, H, Bartholomew, JR. Smokeless tobacco and cardiovascular risk. Arch Intern Med 2004; 164:1845. 
27. Huhtasaari, F, Lundberg, V, Eliasson, M, et al. Smokeless tobacco as a possible risk factor for myocardial infarction: a population-based study in middle-aged men. J Am Coll Cardiol 1999; 34:1784. 
28. Bolinder, G, Alfredsson, L, Englund, A, de Faire, U. Smokeless tobacco use and increased cardiovascular mortality among Swedish construction workers. Am J Public Health 1994; 84:399. 
29. Howard, G, Wagenknecht, LE, Burke, GL, et al. Cigarette smoking and progression of atherosclerosis. The Atherosclerosis Risk in Communities (ARIC) Study. JAMA 1998; 279:119. 
30. Waters, D, Lesperance, J, Gladstone, P, et al for the CCAIT Study Group. Effects of cigarette smoking on the angiographic evolution of coronary atherosclerosis. A Canadian Coronary Atherosclerosis Intervention Trial (CCAIT) Substudy. Circulation 1996; 94:614. 
31. Inoue, T, Oku, K, Kimoto, K, et al. Relationship of cigarette smoking to the severity of coronary and thoracic aortic atherosclerosis. Cardiology 1995; 86:374. 
32. Howard, G, Burke, GL, Szklo, M, et al. Active and passive smoking are associated with increased carotid wall thickness. The Atherosclerosis Risk in Communities Study. Arch Intern Med 1994; 154:1277. 
33. Craig, WY, Palomaki, GE, Haddow, JE. Cigarette smoking and serum lipid and lipoprotein concentrations: an analysis of published data. BMJ 1989; 298:784. 
34. Facchini, FS, Hollenbeck, CB, Jeppesen, J, et al. Insulin resistance and cigarette smoking. Lancet 1992; 339:1128. 
35. Reaven, G, Tsao, PS. Insulin resistance and compensatory hyperinsulinemia: the key player between cigarette smoking and cardiovascular disease?. J Am Coll Cardiol 2003; 41:1044. 
36. Miller, ER, Appel, LJ, Jiang, L, et al. Association between cigarette smoking and lipid peroxidation in a controlled feeding study. Circulation 1997; 96:1097. 
37. Heitzer, T, Yla-Herttuala, S, Luoma, J, et al. Cigarette smoking potentiates endothelial dysfunction of forearm resistance vessels in patients with hypercholesterolemia. Role of oxidized LDL. Circulation 1996; 93:1346. 
38. Pech-Amsellem, MA, Myara, I, Storogenko, M, et al. Enhanced modifications of low-density lipoproteins (LDL) by endothelial cells from smokers: a possible mechanism of smoking-related atherosclerosis. Cardiovasc Res 1996; 31:975. 
39. Valkonen, M, Kuusi, T. Passive smoking induces atherogenic changes in low-density lipoprotein. Circulation 1998; 97:2012. 
40. Cryer, PE, Haymond, MW, Santiago, JV, Shah, SD. Norepinephrine and epinephrine release and adrenergic mediation of smoking-associated hemodynamic and metabolic events. N Engl J Med 1976; 295:573. 
41. Winniford, MD, Wheelan, KR, Kremers, MS, et al. Smoking induced coronary vasoconstriction in patients with atherosclerotic coronary artery disease. Evidence for adrenergically mediated alterations in coronary artery tone. Circulation 1986; 73:662. 
42. Narkiewicz, K, van de Borne, PHJ, Hausberg, M, et al. Cigarette smoking increases sympathetic outflow in humans. Circulation 1998; 98:528. 
43. Newby, DE, Wright, RA, Labinjoh, C, et al. Endothelial dysfunction, impaired endogenous fibrinolysis, and cigarette smoking. A mechanism for arterial thrombosis and myocardial infarction. Circulation 1999; 99:1411. 
44. Kannel, WB, D'Agostino, RB, Belanger, AJ. Fibrinogen, cigarette smoking, and risk of cardiovascular disease: insights from the Framingham Study. Am Heart J 1987; 113:1006. 
45. Fusegawa, Y, Goto, S, Handa, S, et al. Platelet spontaneous aggregation in platelet-rich plasma is increased in habitual smokers. Thromb Res 1999; 93:271. 
46. Matetzky, S, Tani, S, Kangavari, S, et al. Smoking increases tissue factor expression in atherosclerotic plaques: implications for plaque thrombogenicity. Circulation 2000; 102:602. 
47. Nowak, J, Murray, JJ, Oates, JA, et al. Biochemical evidence of a chronic abnormality in platelet and vascular function in healthy individuals who smoke cigarettes. Circulation 1987; 76:6. 
48. Stefanadis, C, Tsiamis, E, Vlachopoulos, C, et al. Unfavorable effect of smoking on the elastic properties of the human aorta. Circulation 1997; 95:31. 
49. Celermajer, DS, Sorensen, KE, Georgakopoulos, D, et al. Cigarette smoking is associated with dose-related and potentially reversible impairment of endothelium-dependent dilation in healthy young adults. Circulation 1993; 88:2149. 
50. Barua, RS, Ambrose, JA, Eales-Reynold, LJ, et al. Dysfunctional endothelial nitric oxide biosynthesis in healthy smokers with impaired endothelium-dependent vasodilatation. Circulation 2001; 104:1905. 
51. Sumida, H, Watanabe, H, Kugiyama, K, et al. Does passive smoking impair endothelium-dependent coronary artery dilation in women? J Am Coll Cardiol 1998; 31:811. 
52. Celermajer, DS, Adams, MR, Clarkson, P, et al. Passive smoking and impaired endothelium-dependent arterial dilatation in healthy young adults. N Engl J Med 1996; 334:150. 
53. Kaufmann, PA, Gnecchi-Ruscone, T, di Terlizzi, M, et al. Coronary heart disease in smokers: vitamin C restores coronary microcirculatory function. Circulation 2000; 102:1233. 
54. Heitzer, T, Yla-Herttuala, S, Luoma, J, et al. Cigarette smoking potentiates endothelial dysfunction of forearm resistance vessels in patients with hypercholesterolemia. Role of oxidized LDL. Circulation 1996; 93:1346. 
55. Kugiyama, K, Yasue, H, Ohgushi, M, et al. Deficiency in nitric oxide bioactivity in epicardial coronary arteries of cigarette smokers. J Am Coll Cardiol 1996; 28:1161. 
56. Ichiki, K, Ikeda, H, Haramaki, N, et al. Long-term smoking impairs platelet-derived nitric oxide release. Circulation 1996; 94:3109. 
57. Mazzone, A, Cusa, C, Mazzucchelli, I, et al. Cigarette smoking and hypertension influence nitric oxide release and plasma levels of adhesion molecules. Clin Chem Lab Med 2001; 39:822. 
58. Bazzano, LA, He, J, Muntner, P, et al. Relationship between cigarette smoking and novel risk factors for cardiovascular disease in the United States. Ann Intern Med 2003; 138:891. 
59. Bermudez, EA, Rifai, N, Buring, JE, et al. Relation between markers of systemic vascular inflammation and smoking in women. Am J Cardiol 2002; 89:1117. 
60. Zevin, S, Saunders, S, Gourlay, SG, et al. Cardiovascular effects of carbon monoxide and cigarette smoking. J Am Coll Cardiol 2001; 38:1633. 
61. Allred, EN, Bleecker, ER, Chaitman, BR, et al. Short-term effects of carbon monoxide exposure on the exercise performance of subjects with coronary artery disease. N Engl J Med 1989; 321:1426. 
62. Aronow, WS, Casssidy, J, Bangrow, JS, et al. Effect of cigarette smoking and breathing carbon monoxide on cardiovascular hemodynamics in anginal patients. Circulation 1974; 50:340. 
63. Mayhan, WG, Sharpe, GM. Chronic exposure to nicotine alters endothelium-dependent arteriolar dilatation: effect of superoxide dismutase. J Appl Physiol 1999; 86:1126. 
64. Li, Z, Barrios, V, Buchholz, JN, et al. Chronic nicotine administration does not affect peripheral vascular reactivity in the rat. J Pharmacol Exp Ther 1994; 271:1135. 
65. Sun, YP. Circulation 2001; 104:810. 
66. Neunteufl, T, Heher, S, Kostner, K, et al. Contribution of nicotine to acute endothelial dysfunction in long-term smokers. J Am Coll Cardiol 2002; 39:251. 
67. Pryor, WA, Stone, K. Oxidants in cigarette smoke. Radicals, hydrogen peroxide, peroxynitrate, and peroxynitrite. Ann N Y Acad Sci 1993; 686:12. 
68. Svrivastava, SK, Barua, RS, Saha, DC, et al. Endogenous free radical generating sources are involved in smoking-mediated dysfunction of nitric oxide biosynthesis in human coronary artery endothelial cells: an in vitro demonstration. J Am Coll Cardiol 2003; 41 Suppl A:306A. 
69. Barua, RS, Ambrose, JA, Srivastava, S, et al. Reactive oxygen species are involved in smoking-induced dysfunction of nitric oxide biosynthesis and upregulation of endothelial nitric oxide synthase: an in vitro demonstration in human coronary artery endothelial cells. Circulation 2003; 107:2342. 
70. Heitzer, T, Just, H, Munzel, T. Antioxidant vitamin C improves endothelial dysfunction in chronic smokers. Circulation 1996; 94:6. 
71. Barbash, GI, White, HD, Modan, M, et al. Significance of cigarette smoking in patients receiving thrombolytic therapy for acute myocardial infarction. Experience gleaned from the International Tissue Plasminogen Activator/Streptokinase Mortality Trial. Circulation 1993; 87:53. 
72. Mueller, HS, Cohen, LS, Braunwald, E, et al. Predictors of early morbidity and mortality after thrombolytic therapy of acute myocardial infarction. Analyses of patient subgroups in the Thrombolysis in Myocardial Infarction (TIMI) trial, phase II. Circulation 1992; 85:1254. 
73. Barbash, GI, Reiner, J, White, HD, et al. Evaluation of paradoxic beneficial effects of smoking in patients receiving thrombolytic therapy for acute myocardial infarction: mechanism of the "smoker's paradox" from the GUSTO-I trial, with angiographic insights. Global Utilization of Streptokinase and Tissue-Plasminogen Activator for Occluded Coronary Arteries. J Am Coll Cardiol 1995; 26:1222. 
74. Grines, CL, Topol, EJ, O'Neill, WW, et al. Effect of cigarette smoking on outcome after thrombolytic therapy for myocardial infarction. Circulation 1995; 91:298. 
75. Gomez, MA, Karagounis, LA, Allen, A, et al. Effect of cigarette smoking on coronary patency after thrombolytic therapy for myocardial infarction. TEAM-2 Investigators. Second Multicenter Thrombolytic Trials of Eminase in Acute Myocardial Infarction. Am J Cardiol 1993; 72:373. 
76. Gottlieb, S, Boyko, V, Zahger, D, et al. Smoking and prognosis after acute myocardial infarction in the thrombolytic era (Israeli Thrombolytic National Survey). J Am Coll Cardiol 1996; 28:1506. 
77. Ishihara, M, Sata, H, Tateishi, H, et al. Clinical implications of cigarette smoking in acute myocardial infarction: Acute angiographic findings and long-term prognosis. Am Heart J 1997; 134:955. 
78. Ruiz-Bailen, M, de Hoyos, EA, Reina-Toral, A, et al. Paradoxical effect of smoking in the Spanish population with acute myocardial infarction or unstable angina: results of the ARIAM Register. Chest 2004; 125:831. 
79. de Chillou, C, Riff, P, Sadoul, N, et al. Influence of cigarette smoking on rate of reopening of the infarct-related coronary artery after myocardial infarction: a multivariate analysis. J Am Coll Cardiol 1996; 27:1662. 
80. Rose, GA, Hamilton, PJS, Colwell, L, et al. A randomized controlled trial of antismoking advice: 10 year results. J Epidemiol Community Health 1982; 36:102. 
81. Multiple Risk Factor Intervention Trial Research Group. Multiple risk factor intervention trial; Risk factor changes and mortality results. JAMA 1982; 248:1465. 
82. Hjermann, I, Velve Byre, K, Holme, I, et al. Effect of diet and smoking intervention on the incidence of coronary heart disease. Report from the Oslo Study Group of a randomised trial in healthy men. Lancet 1981; 2:1303. 
83. The health benefits of smoking cessation. A report of the Surgeon General, Washington, DC: U.S. Department of Health and Human Services. 1990 DHHS Publication (CDC) 90-8416. 
84. Wilhelmsson, C, Vedin, JA, Elmfeldt, D, et al. Smoking and myocardial infarction. Lancet 1975; 1:415. 
85. Hermanson, B, Omenn, GS, Kronmal, RA, Gersh, BJ. Beneficial six-year outcome of smoking cessation in older men and women with coronary artery disease. Results from the CASS registry. N Engl J Med 1988; 319:1365. 
86. Wilson, K, Gibson, N, Willan, A, Cook, D. Effect of smoking cessation on mortality after myocardial infarction: meta-analysis of cohort studies. Arch Intern Med 2000; 160:939. 
87. Critchley, JA, Capewell, S. Mortality risk reduction associated with smoking cessation in patients with coronary heart disease: a systematic review. JAMA 2003; 290:86. 
88. Rea, TD, Heckbert, SR, Kaplan, RC, et al. Smoking status and risk for recurrent coronary events after myocardial infarction. Ann Intern Med 2002; 137:494. 
89. Kawachi, I, Colditz, GA, Stampfer, MJ, et al. Smoking cessation and the decreased risk of stroke in women. JAMA 1993; 269:232. 
90. Hermanson, B, Omenn, GS, Kronmal, RA, Gersh, BJ. Beneficial six-year outcome of smoking cessation in older men and women with coronary artery disease. Results from the CASS registry. N Engl J Med 1988; 319:1365. 
91. Behaviorial Risk Factor Surveillance System. Survey data, 2000. Centers for Disease Control and Prevention. Access at: http://www.cdc.gov/nccdphp/brfss/index.htm. 
92. Flegal, KM, Troiano, RP, Pamuk, ER, et al. The influence of smoking cessation on the prevalence of overweight in the United States. N Engl J Med 1995; 333:1165. 
93. Motley, RJ, Rhodes, J, Ford, GA, et al. Time relationships between cessation of smoking and onset of ulcerative colitis. Digestion 1987; 37:125. 
94. Barendregt, JJ, Bonneux, L, van der Maas, PJ. The health care costs of smoking. N Engl J Med 1997; 337:1052. 
95. Frank, E, Winkleby, MA, Altman, DG, et al. Predictors of physicians smoking cessation advice. JAMA 1991; 266:3139

السلام عليكم

بتهرج يا :angry: anwarica . اكيد بتهرج يعني ايه بعد كل المهرجان اللي انت عملته ده تيجي وتقول ان الموضوع بعد البحث ثبت خطئه. اعتقد انه اقل وصف يمكن لهذا الامر انه تهريج واستخفاف بمن يقرءون الموضوع و ليس لديهم من العلم بما يكفي لتحديد الخطأ من الصواب في عالم الطب. اولي بك ان تأتي معتذرا ومعترفا بخطئك بدل من كل هذا سعادة التي أتيتنا بها لتقول هذا الكلام خطأ.

قل لي كم عضو قرأ هذا الموضوع وخد المعلومة المهببة دي من حضرتك ولم يعد للموضوع ليعرف انك كنت علي خطأ :angry: :angry: .

للأسف منتهي الاستخفاف :( .واعتقد انك تستأهل عقاب من الادارة ، فقط لو كانت تهتم.

والسلام عليكم

بسم الله الرحمن الرحيم

السلام عليكم ورحمة الله وبركاته

يؤسفني أن هذا الرد صدر من عضو فعال وقديم في المنتدى ( AhmedSameh )

من قواعد طرح المشاركات

اقتباس

7. يتم حذف اي مشاركة تحتوي علي الفاظ وعبارات واعمال مخالفة للشرع او الاخلاق او التي تجرح مشاعر الآخرين وربما يتم سحب العضوية ..

8. عدم طرح أي اقتراح بخصوص المنتدى أو شكوى ضد أي مشرف أو عضو علنا ، ولتقديم شكوى يجب مراسلة المشرف اذا كانت الشكوي بخصوص عضو أو إدارة المنتدى اذا كانت الشكوي بخصوص مشرف.

اقتباس

.واعتقد انك تستأهل عقاب من الادارة ، فقط لو كانت تهتم.

نعم تهتم الادارة لمشرفيها ولا ترضى بأي نوع من التهكم أو الاستهزاء بأي مشرف في الفريق العربي

أرجوا من الأخ AhmedSameh وضع مشاركة إعتذار للمشرف Anwarica هنا و إلا ستتخذ الإجراءات حيال المخالفه .

===

السلام عليكم

بالنسبة للأجراءات ، فيمكنك اتخاذ ما يناسب منها اخي فيصل ، و سيكون لك بالغ الاحترام لأني احترم من ينفذون القواعد.

اما بالنسبة ل anwarica فهو مشرف مهم في المنتدي ، ولكن ما صدر مني تجاهه ليس اساءة . بل هو رأي لكنه غاضب -واعتقد انه موضوعي - و اعتقد ان الغضب في محله حتي لو كنت تعتقد اخي فيصل انه ليس كذلك .

وانا اعتذر هنا -بعد مراجعة نفسي - لكل اعضاء المنتدي عن كلمة (مهببة) فقط ، والسبب انها تعتبر لفظة غير لائقة تماما.علما بأنها ليست موجهة الي anwarica بل هي وصف للمشاركة

اقتباس

المعلومة المهببة دي

وانا اكرر اعتذاري هنا عن هذه الكلمة لكل اعضاء المنتدي وليس ل anwarica ، لأنها ليست اساءة له ،وسوف استبدلها بكلمة (ضارة للغاية) اما باقي كلامي فأنا مصر عليه تماما وانا اري انه في محله.

وأشكرك اخي فيصل علي الاهتمام.

و بالتأكيد انا اهتم بأن ابقي هنا ولكن ليس علي حساب القواعد.

وأرجو الا ينسي ما صدر من anwarica تجاه كل الاعضاء الذين قرءوا المشاركة من خطأ.

والسلام عليكم

يا خبر كل ده حصل :)

حسنا المعلومة تحتاج لإعادة شرح مفصل... وسأعدلها فى المشاركة الأولى لكى تتضح .. على فكره الخطأ جزئى وليس كلى والحمد لله :D

هذه ليست أول معلومة طبية يتم إثبات خطأها (والحمد لله إنى مش اللى طلعت النتيجة الأولى) .. فمثلا من 20 سنه فى مناهج الطب .. كانوا يكتبون (التدخين عاده وليست إدمان) والآن اكتشفوا إنها إدمان .. :lol: :lol: :lol:

عادى جدا هو الطب طول عمره كده .. لأننا للأسف نتكلم عن شئ لم نصنعه .. بل كلنا مخلوقات من صنع الله تعالى ...

اقتباس

اولي بك ان تأتي معتذرا ومعترفا بخطئك بدل من كل هذا سعادة التي أتيتنا بها لتقول هذا الكلام خطأ.

حسنا أنا راجع أوضح الخطأ .. ولكن لست المسئول عن المعلومة بمعنى مش من إختراعى :blink: هكذا درسنا .. وأرفقت المشاركة بين الأطباء لنقاشها .. وأخيرا وجدت تحديث لها ولم أسكت ..

المفروض تعطووووونى جائزة على التفتيش :lol: :lol: