مريضه تحتاج لمساعدتكم
 

اخواني و اصدقائي
السلام عليكم و رحمه الله و بركاته
لدي مريضه في حاله حرجه فهي مريضه بالحساسيه ام لاطفلين يتيمين
حالتها نادره جدا واحد في المليون اتولي علاجها املها الوحيدعلاج موجود في اوربا و خاصه هولند و انجلترا من منكم له صديق يستطيع احضار الدواء بجزاه الله خيرا ان شاء الله و سوف اقوم بارسال ثمن العلاج قبل ان يرسله من مالي الخاص ابتغاء الله و رسوله و كما تعود منكم المشاركه فشاركوني في هذه المشكله
اسم الدواء التجاري Cetor
الاسم العلمي C1-Inhibitor Concentrate
قال رسول الله صلي الله عليه و سلم
يكون يوم القيامه قوما يمرون علي الصراط كبرق الخاطف تشخص منه الابصار لا هم بأنبياء و لاهم بصديقين و هم بشهداء
انهم قوما تقضي علي ايديهم حوائج الناس
صدق رسول الله صلي الله عليه وسلم
اللهم اجعلنا منهم ان شاء الله
اخوكم
دكتور شريف الباجوري
مدرس الباطنه و المناعه بكليه الطب

السلام عليكم ورحمة الله ...
 

أولا أهنئكم على افتتاح هذه الخيمة التي ستكون بفضل من الله العلي القدير ثم بفضلكم ملاذا للباحثين عن أنجح الوسائل الطبية في العلاج !

ثانيا : أستاذي الفاضل د. شريف .... هل يوجد هذا الدواء الذي ذكرته في دولة الأمارات .... أو هل للشركة المصنعة وكيل في الدولة قد يساعدنا في حل هذه المشكلة ؟ هل هناك طريقة معينة يمكنني بها البحث عن هذا الدواء أو طلبه من الخارج ثم ارساله لكم ؟؟؟

هذا والله من وراء القصد ... أخوك الصغير أحمد ..

ردا علي رسالتك ارقيقه
 

الاخ العزيز احمد
السلام عليكم ورحمه الله و بركاته
نشكركم علي سرعة تجاوبكم علي هذه الحاله ارجو منكم ان تبحث عنه في دوله الامرات الشقيقه التي طالما وقفت بجوار اشقائها المصرين
حيث استيراد هذا الدواء في مصر امر صعب و يحتاج الي وقت و اسف ان اقول ان الوقت ليس في صالحنا و اريد ان اذكر انني سأقوم بدفع قيمه الدواء حتي لا يفهم اننا نتلقي تبرعات من اي شخص انما قصد من اشراك الاخوه في احضار الدواء و ليس دفع ثمنه
اخوكم الفقير الي الله
دكتور / شريف الباجوري

سأحاول أن أبحث عن هذا الدواء هنا في أمريكا بإذن الله.

ودعاؤنا للمريضة أن يشفيها الله من عنده.

سؤال
 

إن لم يصل الدواء بعد بوسعي إرساله من أوربا عبر الـــ DHL مجانا ولست بحاجة لأن يرسل لي ثمنه000
المسألة إنسانية000 وقيمة الإنسان عندي أيا كان فوق كل اعتبار 000

الاخ العزيز
السلام عليكم و رحمه الله و بركاته
لن استلم الدواء ان حضر ان شاء الله حتي تقوم بأستلام ثمنه و سوف ارسل العنوان مع المبلغ اي كان ثمنه و لان اقبل بغير هذا
حتي وان لم يرسله احد
اخوك
دكتور شريف الباجوري

وفقكم الله وجعله في ميزان حسناتكم


اختكم
دلوعه

الاخت العزيزه الدلوعه
السلام عليكي و رحمه الله و بركاته
انتي لم تكوني ابدا دلوعه بل كنتي قدر المسئوليه دائما
شكرا لدعواتك فأنا احوج ما اكون اليها
اخوكي
شريف الباجوري

عاجل لا يحتمل التاخير .....
 

السلام عليكم.........

يا دكتور الله يرحم والديك ...

الرسايل الخاصة تكفى ... عاجل

تحياتي :heartpump

الاخ العاشق
مساء الخير
الموقع البحث الذي يتكلم عن الدواء
http://www.hereditaryangioedema.com/phamplet.htm
البحث القادم مكان الدواء و اسمه العلمي بالون الاحمر
Cetor(R), A New C1-Inhibitor Concentrate and Its Use for Treating HAE Type I and AML.
A.H.L. Koenderman, H. Hiemstra, J. Over, H.W. Eijkhout, M.H. Tissing, C.E. Hack, A. Kleine#& W.Th. Hermens# & P.W.F. Strengers. CLB, Sanquin Blood Supply Foundation, Plesmanlaan 125, 1066 CX Amsterdam, & #Cardiovascular Research Institute Maastricht (CARIM), Maastricht, The Netherlands. [123]
At CLB a C1-inhibitor concentrate of high-purity has been developed. The manufacturing process is based on DEAE-Sepharose FF, PEG precipitation and Cm-Sepharose FF steps. Virus reduction steps consist of PEG precipitation and pasteurization for 10 hours at 60 oC. An additional 15 nm filtration step has also been developed, but will be implemented in the process in a later stage.
The product was clinically evaluated in patients with hereditary angioedema (HAE), type I. In pilot transfusions, the clinical tolerance was tested. No complications were found. To analyze the pharmacokinetic parameters, three lots of the C1-inhibitor concentrate were infused in 9 patients (total of 10 transfusions) with doses of 5 - 43 U per kg body weight. The in vivo recovery after transfusion of C1-inhibitor was 74b% (SD = 13%; n=10). Administration of one unit C1-inhibitor per kg body weight led to an in vivo response corresponding to 0.016 U per ml plasma (SD = 0.003 U per ml; n=10). The volume of distribution was 81 +/- 17 h and a clearance of 1.3 +/- 0.3 ml/h/kg (n=4) were found.
The product is licensed in Netherlands since June 1997 (brand name CetorR) for the treatment of HAE. However, there is now accumulating evidence from studies in animals and patients suggesting that the adminsitration of C1-inhibitor may have a beneficial effect in a number of other clinical conditions such as sepsis, cytokine induced vascular leak syndrome or myocardial infarction (AMI) (1). An important determinant in the development of heart failure after AMI is the amount of necrotic tissue in the jeopardized myocardium. Early reperfusion of ischemic myocardium itself may induce an inflammatory reaction, which amongst others involves activation of complement. This ischaemic-reperfusion injury may damage the cardiac tissue and limit the beneficial effects of a restored circulation. In studies at CARIM, we observed in a dog model of AMI that i.v. administration of human C1-inhibitor at a dose of 500 - 1000 U per dog (approx. 25 kg) at 2 hours and 8 hours after permanent coronary artery occlusion significantly ( up to 50%) reduces infarct size as assessed at 48 hours after the occlusion. This and other animal studies show an important cardioprotective effect of C1-inhibitor in various experimental models for AMI. Whether a similar effect may occur in humans with AMI is currently studied in a trial of limited size (n=10) of which the results will be presented.
1. Hack, C.E., C1-esterase inhibitor: an anti-inflammatory agent. Biomedical Progress, 11, 57 - 61, (1998).

البحث الذي يتكلم عن طبيعه المرض و الدواء الجديد



The Hereditary Angioedema Association
presents
Frequently Asked Questions about Hereditary Angioedema




What is Hereditary Angioedema?

Hereditary Angioedema (HAE) is a rare and serious genetic condition occurring in about 1/10,000 to 1/50,000 individuals. The disease is characterized by episodes of edema (swelling) in body parts, most notably the hands, feet, face, and airway passages. In addition, patients often have bouts of excruciating abdominal pain, nausea, and vomiting that is caused by swelling in the intestinal wall.

HAE patients have a defect in the gene that controls a blood protein called C1-inhibitor. The genetic defect results in production of either inadequate or nonfunctioning C1-inhibitor protein. Normal C1-inhibitor helps to regulate the complex biochemical interactions of blood based systems involved in disease fighting, inflammatory response, and coagulation. Because defective C1-inhibitor does not adequately perform its regulatory function, a biochemical imbalance can occur and produce unwanted peptides that induce the capillaries to release fluids into surrounding tissues, thereby causing edema.

HAE is called hereditary because the genetic defect is passed on in families. A child has a 50 percent chance of inheriting this disease if one of his or her parents has it. The absence of family history does not rule out the HAE diagnosis, however. Scientists report that as many as 20 percent of HAE cases result from patients who had a spontaneous mutation of the C1-inhibitor gene at conception. These patients can pass the defective gene to their offspring.

Because the disease is very rare, it is not uncommon for patients to remain undiagnosed for many years. Many patients report that their frequent and severe abdominal pain was inappropriately diagnosed as psychosomatic, resulting in referral for psychiatric evaluation. Unnecessary exploratory surgery has been performed on patients experiencing gastrointestinal edema because abdominal HAE attacks mimic a surgical abdomen. Before therapy became available, the mortality rate from airway obstruction was reportedly as high as 30%.

What causes Hereditary Angioedema attacks?

Most attacks occur spontaneously with no apparent reason, however anxiety, stress, minor trauma, surgery, and illnesses such as colds and flu have been cited as triggers. Dental procedures make HAE patients particularly vulnerable to airway attacks. Patients have also reported swelling in extremities following typing, prolonged writing, pushing a lawn mower, hammering, shoveling, and other physical activities.

In women, menstruation and pregnancy seem to have a major effect on disease activity. Some women patients report a definite increase in the number of attacks during their menstrual periods. During pregnancy, some patients note an increase in the frequency of attacks, while others have reported a decrease. Use of oral contraceptives is associated with an increase in the frequency and severity of attacks.

How is Hereditary Angioedema diagnosed?

Most cases of angioedema are not HAE because they are caused by something other than C1-inhibitor deficiency. Laboratory analysis or genetic testing must confirm the HAE diagnosis. There are two specific blood tests that confirm HAE:

1). C1-inhibitor quantitative (antigenic)
2). C1-inhibitor functional

Traditionally, the disease has been classified into two types. The most common form of the disease--Type I--is characterized by low quantitative levels of C1-inhibitor and affects about 85% of patients. Type II HAE affects the other 15% and is characterized by normal or elevated levels of C1-inhibitor that has abnormal function. A paper in the September 2000 volume of the British medical journal Lancet suggests there is another form of HAE that only affects females in families, but is not caused by C1-inhibitor deficiency. It has been proposed that this disease be labeled HAE Type III.

At what age do attacks of Hereditary Angioedema start?

The age of HAE onset varies considerably, however, in one study, one half of the patients reported onset of their symptoms by the age of seven, and over two thirds became symptomatic by the age of thirteen. There also seems to be an increased frequency of attacks during puberty or adolescence.

How long do Hereditary Angioedema attacks last?

Patients often report tingling or tightness at the site where edema will occur thirty minutes to several hours later. In some cases, this sensation can be present twelve to twenty four hours before the onset of swelling. Approximately one fourth of HAE patients experience a red blotchy rash both before and during an attack. The edema itself usually lasts for twenty four to seventy two hours, but the length of an attack can range from four hours to four days.

When are Hereditary Angioedema attacks considered serious?

Swelling of the extremities is uncomfortable and, according to some patients, can be painful depending on the location of the edema. Attacks that involve the face and throat must be taken seriously and medical treatment should be sought without delay. Swelling of the throat can close the air passage and cause death by suffocation. The symptoms of an impending airway obstruction include difficulty swallowing and a change in voice pitch.

Abdominal attacks cause severe pain, nausea, vomiting, and watery diarrhea. Some patients require hospitalization for low blood pressure, dehydration, and pain management. As noted above, abdominal attacks can mimic a surgical abdomen and many patients have been subjected to unnecessary exploratory surgery.

How is Hereditary Angioedema treated?

There are three types of therapy for HAE patients.
1). Long term preventive treatment
2). Short term preventive treatment
3). Treatment of acute attacks

Long term therapy is not required for all HAE patients. In some patients attacks are mild or infrequent and no long-term therapy is required. Clinicians generally recommend long term therapy for patients who experience more than one attack per month, or who believe that the disease significantly interferes with their life style. The present drugs of choice for long-term therapy are 17 alpha alkylated androgens such as stanozolol (winstrol), danazol, and oxandrolone (oxandrin). These agents produce an increase in C1-inhibitor levels, but the exact mechanism of how they do so has not been precisely defined. Some patients report success with a class of drugs called antifibrinolytics, but their use has largely been abandoned because androgens have proven more effective.

The medical literature and practitioner experience confirms that corticosteriods (prednisone), antihistamines, and epinephrine are not effective in treating angioedema created by C1-inhibitor deficiency. However, a recent study noted success using inhaled epinephrine to prevent complete airway closure.

Short-term therapy is necessary for patients who do not require ongoing treatment but are facing dental procedures or elective surgeries. Current practice calls for daily androgen therapy, during the week prior to surgery. For emergency procedures, fresh frozen plasma (preferably a product that has been treated to inactivate viruses) can be used to prevent attacks.

There is no currently approved treatment for acute attacks available in the United States. Fresh frozen plasma is used effectively by some clinicians, but this therapy is considered controversial because of a theoretical chance for attack exacerbation. C1-inhibitor concentrate is the treatment of choice for acute attacks of HAE and has been available to patients in Europe for over a decade. C1 inhibitor concentrate treatment resolves the angioedema in thirty minutes to two hours with complete remission in twenty-four hours. C1-inhibitor concentrate has not yet been approved for use in the United States notwithstanding a double blind randomized crossover study published in the New England Journal of Medicine (circa 1996) that concluded it was safe and effective for both prevention and acute attack therapy. A C1-inhibitor concentrate phase III clinical trial sponsored by Baxter Hyland Immuno is now underway in various centers throughout the United States.

The absence of an effective acute attack therapy limits clinicians to providing supportive care. Maintaining an open airway is the primary concern for patients with laryngeal edema. Because gastrointestinal edema usually involves excruciating pain and frequent vomiting, therapy should include aggressive pain management and fluid replacement. Clinicians report that Zofran, compazine, and phernergan are effective in reducing nausea and vomiting, while either morphine, demerol, dilaudid, darvocet, or stadol can be used to relieve attack related abdominal pain. Unfortunately, the HAE literature in the mid seventies made reference to patients who developed narcotic dependency and this observation was repeated in subsequent papers. Many HAE patients have noted that physicians are often wary of prescribing pain medicine for painful abdominal attacks, and this could be due to reports contained in the literature. Any notion that the HAE population suffers from widespread narcotics addiction has been discredited by the experience of researchers who have treated relatively large numbers of patients.

Are there any new treatments on the horizon?

As noted above, the treatment of choice, C1-inhibitor concentrate, is in final clinical trials and, hopefully, will be approved in the United States sometime in 2001. A partnership between Baxter Hyland Immuno and Pharming NV