topics

3/26/24

ة بنسبة

مئوية % وتحسب حسب المعادلة 👇

PCT is the volume occupied by platelets in the blood as a percentage and calculated according to the formula

PCT = platelet count × MPV / 10,000

انتهينا من PLT واخواتها 😪😪

ونكمل موضوعنا وندخل للWBC واوختها 😅 نبدأ على بركة الله 😃

💢 العدد الكلي لكريات الدم البيضاء (الافضل نسميها خلايا لان تمتلك نواة 😉) WBCs .. White Blood Cells

الوظيفة الرئيسية لهذه الخلايا هي الدفاع عن الجسم ضد الأمراض المعدية والمواد المثيرة والدخيلة للجهاز المناعي وهي جزء من الجهاز المناعي...

قبل كل شيء وقبل لا نتعمق بتفاصيل الWBC لازم نعرف مصطلحين ونفرق بينهم حتى نفهم رموز الWBC.. هنا اريدكم تركزون وتنتبهون

المعروف ان كريات الدم البيضاء هي 5 انواع ✋ هذا الشيء منتهين منه 😉

الي لازم نعرفه هو الفرق بين Absolute (القيمة المطلقة) و Relative (القيمة النسبية)...

⭕ القيمة المطلقة Absolute هي ارتفاع او انخفاض في احد انواع الWBC الخمسة واحد من الانواع الخمسة مع ارتفاع WBC الكلي الTotal WBC يعني كيف ؟! 😕

اعطيكم مثال ...

الجهاز فحص او احنا فحصنا بطريقة الدفرينشيال differential leucocyte ووجدنا ارتفاع بالنتروفيل وباقي مكونات الWBC الاخرى طبيعية مع ارتفاع الWBC الكلي .. ولتكن النتروفيل 89 مثلاً والWBC الكلي 12 الف .. هنا نسمي هذه الحالة Leucocytosis with absolute neutrophilia

يعني زيادة حقيقية بالنتروفيل مع ارتفاع WBC الكلي ..

وهكذا لباقي الانواع ال4 الاخرى من الWBC

واضح لو لا 😕 ؟!! نكمل 😐

⭕ نأتي للمصطلح الثاني وهو القيمة النسبية Relative .. هو ارتفاع او انخفاض في احد انواع الWBC الخمسة مع بقاء قيمة الWBC الكلية طبيعية (اقل من 11.000) يعني كيف ؟! 😕

نأتي للمثال حتى توضح ...

ظهرت النتائج لنا بالجهاز او بطريقة differential leucocyte ارتفاع بالنتروفيل مثلا ولتكن 89 وبقاء الWBC طبيعي ولتكن 6.6 (ضمن النورمل) نسمي هذه الحالة Relative neutrophilia اي ارتفاع نسبي بالنتروفيل ...

وهكذا الحال لباقي الانواع ال4 من الWBC

طبعاً الAbsolute هو عبارة عن عدد النتروفيل لكل واحد microliter من الدم بينما القيمة النسبية Relative للنتروفيل هو عدد النتروفيل لكل 100 خلية و لذلك القيمة المطلقة اهم و افضل من القيمة النسبية بالتشخيص ...

اعتقد الدنيا لخبطت هلخصها لكم بسطرين والي ما يفهمها بعد هذه مشكلته 😁😁👊

الAbsolute هو ارتفاع نوع من انواع الwbc مع ارتفاع WBC الكلي.

الRelative هو ارتفاع نوع من انواع الwbc مع بقاء نسبة WBC الكلية طبيعية.

تمام لو لا ؟! 😉😉 طبعاً بعد بيه تفاصيل كثيرة بس مش عاوز اتشعب بالموضوع 😪😪

بكل هذا الشرح للWBC 👆👆 اردت اوصل لنقطة مهمة بموضوعي الي هي رموز الAbsolute والRelative 😪😪

يرمز للAbsolute بالرمز (#) يعني يكتب الجهاز مثلاً ليمفوسايت وبعدها رمز # (#LYM) ويرمز للRelative بالرمز (%) يعني يكتب الجهاز مثلا ليمفوسايت وبعدها رمز % (%LYM) هذا حسب جهاز Sysmex وجهاز Mindray بينما جهاز Ruby وغيره من الاجهزة يكتب القيمة المطلقة والنسبية بنفس الحقل يعني مثلا .. NEU👉 18.3 90.3%

نأتي الأن لتكملة رموز الWBC 😃 كلنا نعرف ان الWBC تنقسم الى قسمين الي هي

✨1- خلايا محببة Granulocytic Cells

✨2- خلايا غير محببة Agranulocytes cells

🔥 اولاً : الخلايا المحببة Granulocytic cells :

🔸1- الخلايا المتعادلة Neutrophils مختصرها بالتحليل هو

(NUT# , NUT%)

* الزيادة في عدد الخلايا المتعادلة تسمى بـ Neutrophilia ⬆ اسبابها :

1- أسباب أو حالات غير مرضية (الاطفال حديثي الولادة / المجهود العضلي الشديد / أثناء الشهور الأخيرة من الحمل / التوتر العصبي).

2- أسباب أو حالات مرضية مثل:

- حالات التسمم (تسمم داخلي مثل البولينا/تسمم خارجي بالرصاص او الكورتيزون او اول اكسيد الكربون).

- العدوى العامة مثل الدفتيريا والالتهاب الرئوي.

- الاورام السرطانية , وسرطان الدم الابيض غير الليمفاوي.

- التهاب اللوز والتهاب الزائدة الدودية.

- النزيف الشديد.

* الانخفاض في عدد الخلايا المتعادلة يسمى بـ Neutropenia ⬇ اسبابها :

- العدوى بالامراض الفيروسية مثل الحصبة والانفلونزا.

- الحمى التيفودية Typhoid fever / الحمى المالطية Brucellosis.

- مرض الدرن المتسبب عن البكتريا.

- فقر الدم الناتج عن نقص فيتامين B12 ونقص حامض الفوليك.

- هبوط في نشاط النخاع العظمي بسبب التعرض للإشعاع أو الاصابة بالأورام المتعددة.

- السموم التي تؤدي إلى هبوط في النخاع العظمي مثل الزرنيخ وأدوية السلفا , البنزين.

- الأدوية وهي السبب في معظم الحالات ومن أشهر هذه الأدوية مايلي :

مضاد الغدة الدرقية / مضاد الصرع / مضاد السكري / مضاد التخثر / مضادة الهستامين / مضادة الملاريا / مضادة الدرن / وبعض من المضادات الحيوية.

🔸2-الخلايا الحامضية Eosinophil مختصرها بالتحليل هو

(EOS# , EOS

بحر

18:04

* ال

زيادة في عدد الخلايا الحامضية يعرف بـ Eosinophila ⬆ واسبابها :

- الأصابة بالطفيليات مثل البلهارسيا, والانكلستوما, والملاريا.

- الأمراض الجلدية مثل الاكزيما والصدفية والجرب وغيره.

- أمراض الحساسية مثل الربو الشعبي.

- سرطان الدم غير الليمفاوي المزمن.

- تعاطي بعض الادوية مثل البنسلين.

- الأورام الخبيثة.

* الانخفاض في عدد الخلايا الحامضية يعرف بـ Eosinopenia ⬇ اسبابها :

- حالات الضغوط Stress / الصدمة Shock / والحروق Burns.

- تناول علاج الكورتيزون.

- بعد العمليات الجراحية.

🔸3- الخلايا القاعدية Basophil مختصرها بالتحليل هو

(BASO# , BASO%)

* الزيادة في عدد الخلايا القاعدية يعرف بـ Basophilia ⬆ اسبابها:

- سرطان الدم الأبيض المزمن.

- هبوط نشاط الغدة الدرقية.

- بعد عملية استئصال الطحال.

* الانخفاض في عدد الخلايا القاعدية يعرف بـ Basopenia ⬇ اسبابها:

- زيادة نشاط الغدة الدرقية.

- الالتهابات الحادة.

- العلاج بالكورتيزون.

🔥ثانياً: الخلايا الغير محببة Agranulocytes cells :

♦1- الخلايا الليمفاوية Lymphocytes ومختصرها بالتحليل هو:

(LYM# , LYM%)

* الزيادة في عدد خلايا الدم البيضاء الليمفاوية تعرف بـ Lymphocytosis ⬆ اسبابها :

- بعض حالات العدوى عند الأطفال مثل الحصبة والانفلونزا والسعال الديكي.

- الحمى التيفودية والحمى والمالطية.

- التهاب الكبد الفيروسي Viral hepatitis.

- التهاب الغدد الليمفاوية.

- سرطان الدم الليمفاوي.

* الانخفاض في عدد خلايا الدم البيضاء الليمفاوية يعرف بـ Lymphocytopenia ⬇ اسبابها :

- تناول بعض الأدوية مثل مضادات السرطان.

- حالات التسمم بالبولينا الحاد أو المزمن.

- تناول علاج الكورتيزون.

- التعرض للإشعاع.

♦2- الخلايا وحيدة النواة Monocytes ومختصرها بالتحليل هو:

(MONO# , MONO%)

* الزيادة في عدد الخلايا وحيدة النوة يعرف بـ Monocytosis ⬆ اسبابها :

- العدوى بالبكتريا مثل بكتريا الدرن T.B أو التيفويد او الحمى المالطية.

- الإصابة بالطفيليات وحيدة النواة مثل الملاريا Malaria.

- الالتهابات وتقرح القولون المزمن.

- بعض الأورام.

* الانخفاض في عدد الخلايا وحيدة النواة يعرف بـ Monocytopenia ⬇ اسبابها :

- نقص فيتامين B12 وحمض الفوليك.

- سرطان الدم Leukemia.

- تليف النخاع العظمي Aplastic anaemia.

🚩ملاحظة1/ مهمة جداً 😒👊

بعض الاجهزة مثل جهاز Sysmex وجهاز Mindray وغيرها من الاجهزة ما تذكر 3 خلايا .. الي هي

Monocytes , Basophils , Eosinophils

وبدلاً من ذلك تكتب كمجموع خليط لهذه الخلايا mixture

وايضا تكتب بالتحليل بالمختصر 👈 %MXD# , MXD ( 😎

هذه ترجع حسب نوعية الجهاز

3-part WBC Differential.

5-part WBC Differential.

🚩ملاحظة2/ القيمة الطبيعية للMXD غير مذكورة بالرابط الموجود بالاسفل 👇🔗 لذلك اذكره لكم للفائدة 😄

MXD% - relative (%) (the normal is 5 - 10%)

MXD# - absolute (#) (normal 0.2 - 0.8 x 10^9 / l)

🚩ملاحظة3/ بعض الاجهزة تكتب القيم الطبيعية اسفل التحليل للتسهيل على الطبيب او الفاحص

🚩ملاحظة4/ بعض الاجهزة تضع علامة ناقص (ـــ) للدلالة على انخفاض او نقص القيمة عن القيمة الطبيعية وتضع علامة (+) للدلالة على ارتفاع او زيادة القيمة عن القيمة الطبيعية .. لتنبيه الطبيب او قارئ التحليل (صورة رقم 10) وبعض الاجهزة تضع خط اسفل القيمة المنخفضة او المرتفعة او تعطيها لون مغاير لباقي القيم الطبيعية (ص

🚩ملاحظة5/ بعض الاجهزة تعطي استنتاج او تشخيص للتحليل اسفل الورقة مثل اذا كانت زيادة بالWBC الكلي يكتب Leukocytosis او مثلاً نقص بالصفائح الدموية PLT يكتب Thrombocytopenia واذا نقص بنسبة الدم يكتب Anemia وهكذا باقي الحالات ... ).🎯🎯🎯

بحر

19:09

علم التحاليل المخبرية

تحليل CBC وعلى ماذا يدل والقيم الطبيعية لكل مكوناته ؟

الموضوع صحيح طويل ومتعب بس ما حبيت اقسمه لاجزاء حتى ما يضيع عليكم 😁😁✋

🔴 اولاً: قبل كل شيء .. ما هو تحليل CBC ؟!

هو العد الشامل لكل مكونات الدم Complete Blood Count

احد اهم تحاليل قسم امراض الدم Hematology واشهرها والذي يعتمد عليه اغلب الاطباء وبجميع الاختصاصات ولا ابالغ اذا اطلقت عليه تسمية (العمود الفقري) للتشخيص الطبي الحديث 😍😁

يعطي تفاصيل دقيقة لاهم مكونات الدم RBC , WBC, PLT

🔴ثانياً : كيف يتم عمل هذا التحليل ؟

يتم عن طريق سحب عينة دم وريديا ً 💉 ويوضع في تيوب EDTA ثم يفحص بجهاز الCBC وخلال اقل من دقيقة تحصل على النتيجة ... ومن اشهر الاجهزة بهذا المجال هي 👇😃

,,,Sysmex ,,, Mindray ,,, Horiba ,,, Ruby ,,,

وغيرهن الكثير من الاجهزة ...

🔴ثالثاً : Blood parameters مكونات التحليل او رموز التحليل ..

نبدأ اولاً بسم الله بRBC واخواتها 😃😃

🔷 كريات الدم الحمراء RBC (Red Blood Cell)

وظيفتها هي نقل الاوكسجين وثاني اوكسيد الكاربون.

blood cells contain hemoglobin, transporting oxygen and carbon dioxide.

🔷 الهيموغلوبين HGB (Hb, hemoglobin)

هو تركيز الهيموغلوبين بالدم ..

the concentration of hemoglobin in whole blood.

🔷 نسبة الدم (الهيماتوكريت) HCT (hematocrit)

هو نسبة كريات الدم الحمراء الى نسبة حجم بلازما الدم

the hematocrit reflects the ratio of red blood cells to the volume of blood plasma.

هو نفسه PCV .. Packed Cell Volume حجم خلايا الدم الحمراء المضغوطة لكن الفرق هو طريقة استخراج النتيجة ..

الPCV تكون عن طريق السنترفيوج للكابيلري centrifugation method بينما الHTC يتم استخراجها بمعادلة بجهاز الCBC الا وهي :

HCT = MCV x RBCs count/10

🔷 متوسط حجم الكرية Mean Cell Volume .. MCV:

- نقصان متوسط حجم الكرية MCV يعني أن حجم الكرية الحمراء أصغر من الحجم الطبيعي ...في هذه الحالة تعرف الكرية بMicrocyte ونجد هذا النوع من الحجم في:

✨1- فقر الدم بنقص الحديد Iron deficiency anaemia.

✨2- أنيميا البحر الأبيض المتوسط (الثلاسيميا) Thalassemia.

بينما زيادة متوسط حجم الكرية MCV يعني أن حجم الكرية الحمراء أكبر من الحجم الطبيعي... في هذه الحالة تعرف الكرية بـ Macrocyte أو انيميا الكريات الحمراء المتضخمة Megaloblastic anaemia ونجد هذا النوع في فقر الدم الناتج عن الامراض التالية:

✨1- نقص حامض الفوليك .. Folate deficiency.

✨2- نقص فيتامين deficiency B12 .

🔷 متوسط وزن هيموغلوبين كرية الدم الحمراء Mean Corpuscular Haemoglobin .. MCH:

- يعبر الMCH عن معدل وزن (كمية) الهيموجلوبين في كرية الدم الحمراء وهو مهم في تشخيص بعض انواع فقر الدم.

ان نقصان قيمة الMCH يعني نقصان كمية الهيموجلوبين في الكرية.

🔷 متوسط تركيز الهيموغلوبين في كريات الدم الحمراء .. Mean Corpuscular Haemoglobin concentration MCHC:

- يعبر الMCHC عن معدل نسبة تركيز الهيموغلوبين في كريات الدم الحمراء.

يساعد الMCHC في تشخيص انواع فقر الدم المختلفة.

نقص تركيز الMCHC يعرف بـ Hypochromia ونجده في فقر الدم الناتج عن نقص في الحديد Iron deficiency anaemia.

🔷 قياس توزيع كريات الدم بالوريد او عينة الدم Red Cell Distribution Width .. RDW :

توجد قيمتين لRDW هي:

1- RDW- SD : يعني الانحراف المعياري Standard Devieiton.

2- RDW-CV : يعني معامل الاختلاف Coefficient of Variation

الاختلاف بين القيمتين هو طريقة استخراج القيمة والوحدات فالRDW-CV يعتمد بحسابه على قيمة الCurve الناتج من توزيع الRBC مقسوم على قيمة الMCV من خلال معادلة

(Histogram width/MCV) × 100% = RDW-CV %

يمكن ما فهمتوا شيء ؟! 😳😂 نكمل

بينما قيمة RDW-SD ما يعتمد بقيمتها على قيمة الMCV وتكون وحدته هي الفيمتوليتر FL femtoliters (

اغلب الاجهزة تعطي قيمتين للRDW مثل جهاز Mindray وجهاز Sysmex (. )

بينما جهاز Cell-DYN Ruby يعطي قيمة واحدة هي RDW-SD لوحدها ( )

اكيد تسألو ايه وجه الاستفاده من قيمة RDW ؟! 😕

الفائدة هي حتى اعرف نوع الانيميا الموجودة عند المريض من خلال مقارنتها مع قيم الMCV والMCH )

حالياً انتهينا من الRBC 😁

الان نوضح PLT واخواتها بصورة سريعة لان موضوعنا الاهم هو الWBC الي هاركز عليه بهذا البوست ...

💥 الصفائح الدموية PLT Platelate

المعروف ان وظيفتها هي تكوين الخثرات (الجلطات) لايقاف النزيف والسيطرة عليه...

💥 قياس متوسط حجم الصفائح الدموية Mean Platelet Volume .. MPV

💥 قياس توزيع الصفائح الدموية Platelet Distribution Width .. PWD

💥 قياس نسبة خلايا صفائح الدم الكبيرة P- LCR

Platelet Larger Cell Ratio %

💥 قياس الحجم الذي تشغله الصفائح الدموية في الدم

PCT .. Platelate crite

الحجم الذي تشغله الصفائح الدموية بالدم ممثل

بحر

18:04

💢فحص الكومبز

Coomb test

لا يعتبر فحص الكومبز من ضمن الفحوصات الروتينيه في بنك الدم

🕸الفكره العامه للفحص:

إكتشاف الخلايا المتحسسه بأجسام مضاده غير كامله

( غالبا من نوع IgG )

وقد تكون تلك الخلايا تحسست داخلياً في جسم المصاب او تم تحسيسها خارجياً في المختبر كما سيتم التوضيح

(الخلايا المتحسسه هي تلك التى تحتوي على سطحها أجسام مضاده غير كامله )

ونظرا لان مصل الكومبز هو عباره عن أجسام مضاده تكون ضد الأجسام المضاده الخاصه بالإنسان وبعض بروتينات المكمله فبالتالي نستطيع إكتشاف الخلايا المتحسسه

ولهذا الفحص نوعان:

أولاً

🔹 فحص الكومبز المباشر

والغرض منه هو إكتشاف الأجسام المضاده #المرتبطه_على سطح_الخلايا_الحمراء داخليا في جسم المريض

🔎متى يستخدم فحص الكومبز المباشر؟؟

1-في حالة إنحلال الدم الجنيني HDN

2-تحلل الدم بسبب المناعة الذاتيه

3-تحلل الدم بسبب عدم التطابق عند نقل الدم

(التحري في حال نقل الدم الخاطئ )

💉عينه المريض / دم كامل

⚓طريقة العمل

1⃣-تأخذ #عينة_دم المريض

2⃣-تغسلها ثلاث مرات

3⃣-تحضر منها محلول معلق

4⃣-تأخذ قطره منها الى أنبوبه آخرى

5⃣-مع قطره من مصل الكومبز

6⃣-أمزج ثم رسب وشاهد التخثر 💢

بحر

18:04

علم التحاليل المخبرية

🎯🎯🎯

💥 للذين يستفسرون ! لماذا في اغلب حالات الصفار ←البيلروبين ،، تكون الانزيمات في اطار الطبيعي ؟؟

-------------------------------

🔰 في البداية دعونا نفهم المفردات التالية فهما دقيقا : ↓↓

🔹 عشان نكون اكثر دقة ونحن نسمي البيلروبين لازم نحدد ونقول : بيلروبين مرتبط ، اوغير مرتبط

conjecated or unconjected bilirubin.

🔹 الكبد هو المسؤول الاول عن استقلاب ومعالجة البيلروبين وجعله يؤدي وظيفته لخدمة الجسم .

🔹يعتبر فحص البيلروبين مؤشر لوظيفة الكبد الاخراجية ( waste ) .

🔹 انزيم ALT ( GPT) يوجد بشكل رئيسي ويحتل cytosol في سيتوبلازم الخلايا الكبدية . ← فعند اختراق جدار الخلية الكبدية والوصول الى السيتوبلازم ك عدوى او injury مثل :

viral or chemically induced hepatitis.

❗️اذا في حالات تلف او عطب في عصارة السيتوبلازم للخلية الكبدية ! بسبب عدوى فيروسية او مواد كيميائية سامة سيطرح انزيم ALT في بلازما الدم وسنراه مرتفعا حسب شدة دمار الخلايا .

🔹 انزيم AST ( GOT ) يوجد جزء منه في ال cytosol للخلية الكبدية ويسمى ( ASTc ) ← وسيرتفع في الحالات المذكورة اعلاه 🔝 ،

❗️وفي جزء منه موجود داخل Mitochالخلية ويسمى ( ASTm) ويكون مؤشر جيد لانه بيفرز بكثرة وخصوصا عندما يكون السبب :

ethanol as in alcoholic hepatitis,

الاشخاص الذين يعانون من التهاب الكبد بسبب تعاطي الكحول !

❗️ايضا في معانا AST بنسب قليلة يفرز من اعضاء اخرى مثل ←القلب ، الكلى ، العضلات .

💥وعشان كذا لم نعتمد AST كمؤشر رقم 1 للامراض الكبد ! ولكننا اعتمدنا ALT لان الكمية التي تفرز من اعضاء غير الكبد ( قليلة جدا جدا ولاتشكل فارق) بعكس زميلة AST ← كما وضحنا 🔝

🔹يفرز AST بما يعادل 7000 times ←وعمره في الدم (يظل متواجد):

half-life →17 hrs only.

🔹يفرز ALT بما بعادل 3000 times

وعمره في الدم

half-lifes →47 hrs .

❗️عند اصابة الكبد بمختلف المسببات سنلاحظ ← ALT اكثر دائما من AST ؟!

بالرغم من انه يفرز بكمية اقل كمااشرنا🔝? والسبب يعود لل ←half-lifes .

🔹 عند تكسر RBCs hemolysis ← امراض التكسرات وغيرها ←ينتج لنا بيلروبين غير مرتبط unconjected.

وعادة يكون بنسب قليلة في الدم ❗️

وفي هذه الحالة لادخل للكبد بالموضوع وبالتالي ← تكون الانزيمات طبيعية 💥

واحيانا يكون AST في

high normal or normal

🔹 عند اصابة الكبد ايا كان السبب ←ادى الى تحطيم والعبث بخلاياه ←ينتج لنا بيلروبين مرتبط وغير مرتبط بشكل دراماتيكي .

←ونلاحظ ارتفاع مطرد لل AST , ALT

وكلما كان معدل دمار وخلايا الكبد كبير ←سنلاحظ ارتفاع ↑↑ كبير لهما قد يصل الى 15 ضعف او 20 ضعف او اكثر !

💥 في حالة البيلروبين الكبدي hepatitis jaundice تكون نسبة الانزيمات كبيرة جدا في السيرم وجزئياتها متزاحمة بشكل كبير ←فلايستطيع المحلول المستخدم لشغل الانزيم ( substrat ) قرائة تلك الالاف من الجزئيات ←لماذا ❓↓↓

🔰 لنفرض ان10جزء من محلول التفاعل يتفاعل مع 10 جزء مقابله من انزيم AST مثلا ،،، ←في الدقيقة الواحدة

في الحالة الطبيعية عندما يكون تركيز الانزيم normal يمشي الامر بسلام ويتم التفاعل حيث يحطم جزء من substrat

جزء من الانزيم بكل تناغم في 3 دقائق ( reaction time ) ونحصل على امتصاصية قرائة صحيحة موزعة توزيع صحيح عل وقت التفاعل ←وتكون نتيجة القرائات صح .

❗️الا اذا 🚫 وهنا لازم نركز على الكلام الجاي ↓↓

🔹 وجود العدد الهائل من جزئيات الانزيم ولنفرض انها 2000 جزء ستقابل 10 اجزاء فقط من محلول substrat !

←تخيلوا معركة غير متكافئة بالعدد وتفاعل من طرف واحد فقط ←فسوف ينقض 500 جزء من الانزيم مثلا ←عل جزء 1 من substrat وسيحطمة ← وهكذا وبسرعة تحطم وتفاعل كبيرة ومتسارعة جدا جدا ستنهي جزئيات الانزيم جزئيات المحلول في الثواني الاولى←ينتهي التفاعل قبل انتهاء الدقيقة الاولى ❗️❗←وينتج لنا خطأ في مسار التفاعل والقانون المحتسب المعروف لدينا ⤵️⤵️

💥 ايش الحل لهذه 🔝 المشكلة ( التقنية ) نقول : ↓↓

🔰 اذا كنت تشتغل على جهاز

full automatic spectrometer,

هنا لاخوف لان تلك الاجهزة تعمل تخفيف للعينة تلقائي .

🔰واذا كنت تشتغل على اجهزة

manual spectrometer

هنا لازم تعمل تخفيف لكل عينة ( بيلروبين - صفار ) ومطلوب لها انزيمات AST , ALT عشان انت بالتخفيف ترتب صفوف ومسار التفاعل الذي سوف يحصل ،

ويكون التخفيف حسب قوة الصفار ←فنبدا بتخفيف 1:5 اي :

جزء 1من السيرم و4 اجزاء من محلول التخفيف ←ونضرب الناتج × 5 .

وهكذا وهكذا ..الخ

🔰 اخيرا :

اذا لم نخفف العينة ←واشتغلناه مباشرة سوف يكون هناك عشوائية وانحرافات لمسار التفاعل ←الامر الذي يجعل الجهاز يعطينا قرائة عشوائية مخلوطة ( وعادة يكون normal ←مثلا : كأن يعطينا تركيز AST 20 بينما هو اصلا تركيزة 1500 ❗️

---------------------

بحر

15:11

علم التحاليل المخبرية

👌اولآ: ال bilirubin نستدل به على الوظيفه الاخراجيه له.

يعني اي disorder في الوظيفه الاخراجيه بيحصل معنى increase in bilirubin

😊امثله على ذالك:

كما في حالة

📌Hemolytic juandice

ونعرفها باختصار كالاتي👇👇

The production of bilirubin increases when large quantities of red blood cells are broken down.

📌 Crigler-Najjar syndrome

ونعرفهاباختصاركالاتي👇👇

is a severe condition characterized by high levels of a toxic substance called bilirubin in the blood (hyperbilirubinemia). Bilirubin is produced when red blood cells are broken down. This substance is removed from the body only after it undergoes a chemical reaction in the liver, which converts the toxic form of bilirubin (called unconjugated bilirubin) to a nontoxic form called conjugated bilirubin. People with Crigler-Najjar syndrome have a buildup of unconjugated bilirubin in their blood (unconjugated hyperbilirubinemia).

📌 Gilbert Syndrome

ونعرفها باختصار كالاتي 👇👇

is a mild genetic disorder in which the liver does not properly process a substance called bilirubin. Bilirubin is made by the break down of red blood cells.

في هاذي الحالات طبعا يحدث increase of bilirubin وتكون الانزيمات الكبديه طبيعيه

لماذا😕؟؟

👌طبعا ماترتفع هنا لان الخلايا الكبديه هنا ماحصلها دمار والانزيمات الكبديه ترتفع في حاله دمار الخلايا الكبديه.

😉طيب ممكن مثال على ارتفاع انزيمات الكبد والبيلوروبين معآ؟؟

نعم احد هاذه الحالات هيا

📌Acute and chronic hepatitis.

👌يرتفع البيلوروبين هنا مع ارتفاع الانزيمات والسبب نتيجه لل

يع disorder في الوظيفه الاخراجيه بيحصل معنىincrease in bilirubin

وايضا ارتفاع الانزيمات الكبديه بيحصل نتيجه ال destruction يالي حاصل في خلايا الكبد والذي تعتبر مسؤوله عن افراز هاذي الانزيمات لذالك بيحصل لها ارتفاع.

😎طيب متى ممكن اننا نشوف البيلوروبين طبيعي وفي ارتفاع للانزيمات ؟؟

👌طبعا في حاله ال Cirrhosis لانه هنا نجد انه في خلايا سليمه وخلايا مدمره ولذالك ترتفع الانزيمات ويكون البيلوروبين طبيعي والسبب ان الخلايا السليمه تؤدي الوظيفه الاخراجيه بدلا عن الخلاياء المدمره.

😊طيب نجي الان لتلخيص عن اسباب زياده الصفراء:

أسباب زيادة الصفراء :

🔴- Pre-hepatic:

بسبب زيادة تكسير RBCs

إما مشاكل بسبب

📌تضخم الطحال (Splenomegaly)

📌وانيميا تكسيريه مثل

➖thalassemia.

➖sickle cell anemia.

➖G6PD deficiency.

➖incorrect blood transfusion.

➖hemolytic anemia by

chemicals or toxins.

👌في هاذا الحالات المذكوره بيحصل increase of

Unconjugated bilirubin

🔴- post-hepatic :

بسبب مشاكل القنوات المرارية والمرارة

"Inflammation or stones or tumor....etc"

وفي هاذي الحالات دي بيزيد أولا conjugated bilirubine

وانزيم ALP

ومع الوقت بيحصل effects on liver ويزيد ال Unconjugated bilirubine

مباشرة slightly increase في AST و ALT

🔴-hepatic:

Liver disease divide into tow type:

1-امراض الكبد يالي بتسبب تلف في خلايا الكبد(viruses,parasite,lipids,drugs....etc)

وهنا بيزداد البيلوروبين المباشر وغير المباشر

conjugated bilirubine and Unconjugated bilirubine

ايضا بيحصل زياده في انزيمات الكبد (ALT,AST,ALP)

وال ALT بيزداد اولا

2-مرض كبدي وراثي:

وهنا بيؤثر على unconjugated bilirubine

وبحوله الى conjugated bilirubine

مثل

Crigler-Najjar syndrome and Gilbert Syndrome.

وفي هاذي الحالات بيزيد ال

unconjugated bilirubin

ومثل هاذي الحالات تضهر بكثره مثل اثناء الصيام والحمل وانزيمات الكبد تكون طبيعيه جدا.

👏الخلاصه

نقدر نقول ان هناك 3 حالات.

الحاله الاولى يرتفع البليوروبين مع عدم ارتفاع الانزيمات الكبديه في الغالب كما في حالة الprehepatic وكرجلر وجلبرت وهنا يكون الغير المباشر80%

الحاله الثانيه يرتفع البليوروبين مرتفع ويكون الغير مباش من 50-70% وترتفع got.gpt.ggt كما في حالة الامراض الكبديه الا انه في ال cirrhosis قد لا يرتفع البليوروبين

الحاله الثالثهpost hepa وفيها يرتفع البليوروبين ويكون المباشر70%ويرتفع الalpاما الgpt.gotفقد ترتفع قليلا

وان شاء الله تصل المعلومه بالشكل المطلوب لجميع الاعضاء😊

والصلاه والسلام على رسول الله محمد ابن عبد الله

بحر

14:53

group. Cardiac and aortic damage caused by CP was attenuated by IRB treatment owing to the anti-inflammatory and antiapoptotic effects of IRB.

ABSTRACT

OBJECTIVES: Cisplatin (CP) is frequently used in various types of cancers. The cardiotoxic effects of this agent limit its usage. Our study seeks to investigate the protective effects of Irbesartan (IRB) on CP-induced cardiotoxicity.

MATERIALS AND METHODS: The following four groups comprised thirty-two rats: control, CP, CP+IRB, and IRB. On the fourth day of the experiment, 5 mg/kg of CP was given to CP and CP+IRB groups intraperitoneally, and for seven days, water or IRB 50 mg/kg (orally) was administered. Vascular endothelial growth factor (VEGF), caspase-3 (Cas-3), vascular cell adhesion molecule-1 (VCAM-1), NADPH oxidase-1 (NOX-1), creatine kinase MB (CK-MB), and lactate dehydrogenase (LDH) were measured.

RESULTS: The levels of VCAM-1, NOX-1, VEGF, Cas-3, and LDH were increased in the CP group. The treatment with IRB decreased VCAM-1, NOX-1, VEGF, Cas-3, and LDH levels significantly (P0.05). Histopathological examination revealed normal heart architecture in Control and IRB groups. While marked hyperemia and myocardial cell degeneration were noticed in the CP group, significant amelioration was observed in the CP+IRB group. Aortas in the CP group showed endothelial damage and desquamation. IRB treatment markedly ameliorated histopathological findings in the CP+IRB group. Cardiac and aortic damage caused by CP was attenuated by IRB treatment owing to the anti-inflammatory and antiapoptotic effects of IRB.

CONCLUSION: IRB may help reduce the severity of CP-induced cardiac injury by limiting leukocyte migration and reducing inflammation and apoptosis.

PMID:37885998 | PMC:PMC10598814 | DOI:10.22038/IJBMS.2023.70997.15422

23:06

PubMed articles on: Cardio-Oncology

The (pro)renin Receptor - A Regulatory Nodal Point in Disease Networks

Curr Drug Targets. 2023 Oct 25. doi: 10.2174/0113894501250617231016052930. Online ahead of print.

ABSTRACT

[This retracts the article DOI: 10.3389/fsurg.2022.862617.].

PMID:37886634 | PMC:PMC10599136 | DOI:10.3389/fsurg.2023.1307330

23:06

PubMed articles on: Cardio-Oncology

ubMed articles on: Cardio-Oncology

Irbesartan ameliorates inflammation via transendothelial leukocyte migration due to VCAM-1/NOX-1 signaling in cisplatin-induced cardiotoxicity

Iran J Basic Med Sci. 2023;26(11):1298-1304. doi: 10.22038/IJBMS.2023.70997.15422.

crucial in determining the relationship between potential treatment benefits and cardiotoxicity, and whether the continuation of treatment is appropriate on a case-by-case basis. Early risk stratification,

ABSTRACT

Despite current advancements in chemotherapy, immunotherapy and targeted treatments, the potential for major adverse cardiovascular events, regardless of previous cardiac history, persists. Scoring systems, such as the Heart Failure Association-International Cardio-Oncology Society (HFA-ICOS) risk assessment tool, can be utilized to evaluate several factors including prior cardiac history, risk factors and cardiac biomarkers to categorize patients into low, moderate, high, and very high-risk groups. Common cardiotoxicity complications include new or worsening left ventricular ejection fraction (LVEF), QT interval prolongation, myocardial ischaemia, hypertension, thromboembolic disease, cardiac device malfunction and valve disease. Baseline electrocardiogram (ECG) and transthoracic echocardiogram (TTE) are routinely performed for all patients commenced on cardiotoxic treatment, while other imaging modalities and biochemical markers have proven useful for monitoring. Management mainly includes early risk stratification and prompt identification of cardiovascular complications, with patient-specific surveillance throughout treatment. A multidisciplinary approach is crucial in determining the relationship between potential treatment benefits and cardiotoxicity, and whether the continuation of treatment is appropriate on a case-by-case basis. Early risk stratification, optimizing the patient's cardiovascular status prior to treatment, and prompt identification of suspected cardiotoxicity are key in significantly reducing risk. This article provides a comprehensive review of the various types of treatment-related cardiotoxicity, offering guidance on identifying high-risk patients, recognizing early signs of cardiotoxicity, and outlining appropriate treatment approaches and follow-up care for such cases.

PMID:37886969 | PMC:PMC10605822 | DOI:10.3390/cimb45100526

23:06

PubMed articles on: Cardio-Oncology

Retraction: Longitude variation of the microRNA-497/FGF-23 axis during treatment and its linkage with neoadjuvant/adjuvant trastuzumab-induced cardiotoxicity in HER2-positive breast cancer patients

Front Surg. 2023 Oct 11;10:1307330. doi: 10.3389/fsurg.2023.1307330. eCollection 2023.

volumes receiving 2 Gy (p = 0.03), 4 Gy (p = 0.02) and 5 Gy (p = 0.02). The increase in hscTnI observed in patients receiving anti-HER2 therapy after adjuvant RT was positively associated with radiation doses on the heart, LV and LAD.

ABSTRACT

Anti HER2 therapy and left breast adjuvant radiation therapy (RT) can both result in cardiotoxicity. The aim of this study was to evaluate the influence of radiation dose on cardiac structures on the values of the early cardiotoxicity marker high-sensitivity cardiac troponin I (hscTnI) in patients with HER2-positive left breast cancer undergoing adjuvant concomitant antiHER2 therapy and radiotherapy, and to establish a correlation between the hscTnI values and cardiac radiation doses. Sixty-one patients underwent left breast hypofractionated radiotherapy in parallel with anti-HER2 therapy: trastuzumab, combined trastuzumab-pertuzumab or trastuzumab emtansine (T-DM1). The hscTnI values were measured prior to and upon completion of radiotherapy. A significant increase in hscTnI was defined as >30% from baseline, with the second value being 4 ng/L or higher. Dose volume histograms (DVH) were generated for the heart, left ventricle (LV) and left anterior descending artery (LAD). The hscTnI levels were corelated with radiation doses on cardiac structures. An increase in hscTnI values was observed in 17 patients (Group 1). These patients had significantly higher mean radiation doses for the heart (p = 0.02), LV (p = 0.03) and LAD (p = 0.04), and AUC for heart and LV (p = 0.01), than patients without hscTnI increase (Group 2). The patients in Group 1 also had larger volumes of heart and LV receiving 2 Gy (p = 0.01 for both) and 4 Gy (p = 0.02 for both). LAD differences were observed in volumes receiving 2 Gy (p = 0.03), 4 Gy (p = 0.02) and 5 Gy (p = 0.02). The increase in hscTnI observed in patients receiving anti-HER2 therapy after adjuvant RT was positively associated with radiation doses on the heart, LV and LAD.

PMID:37887554 | PMC:PMC10605836 | DOI:10.3390/curroncol30100654

23:06

PubMed articles on: Cardio-Oncology

Cardiac Toxicities in Oncology: Elucidating the Dark Box in the Era of Precision Medicine

Curr Issues Mol Biol. 2023 Oct 15;45(10):8337-8358. doi: 10.3390/cimb45100526.

follow-up, suggesting early myocardial relaxation abnormalities. PBT shows promise as a cardiac-sparing RT technology.

ABSTRACT

1. Background: We sought to determine acute and subacute changes in cardiac function after proton beam (PBT) and photon beam (PhT) radiotherapy (RT) using conventional and two-dimensional speckle tracking echocardiography (2D-STE) in patients with malignant breast and thoracic tumors. 2. Methods: Between March 2016 and March 2017, 70 patients with breast or thoracic cancer were prospectively enrolled and underwent transthoracic echocardiography with comprehensive strain analysis at pretreatment, mid-treatment, end of treatment, and 3 months after RT. 3. Results: PBT was used to treat 44 patients; PhT 26 patients. Mean ± SD age was 55 ± 12 years; most patients (93%) were women. The median (interquartile range) of the mean heart dose was lower in the PBT than the PhT group (47 [27-79] vs. 217 [120-596] cGy, respectively; p < 0.001). Ejection fraction did not change in either group. Only the PhT group had reduced systolic tissue Doppler velocities at 3 months. 2D-STE showed changes in endocardial and epicardial longitudinal, radial, and circumferential early diastolic strain rate (SRe) in patients undergoing PhT (global longitudinal SRe, pretreatment vs. end of treatment (p = 0.04); global circumferential SRe, pretreatment vs. at 3-month follow-up (p = 0.003); global radial SRe, pretreatment vs. at 3-month follow-up (p = 0.02) for endocardial values). Epicardial strain values decreased significantly only in patients treated with PhT. Patients in the PhT group had a significant decrease in epicardial global longitudinal systolic strain rate (GLSRs) (epicardial GLSRs, at baseline vs. at end of treatment [p = 0.009]) and in GCSRe and GRSRe (epicardial GCSRe, at baseline vs. at 3-month follow-up (p = 0.02); epicardial GRSRe, at baseline vs. at 3-month follow-up (p = 0.03)) during treatment and follow-up. No changes on 2D-STE were detected in the PBT group. 4. Conclusions: Patients who underwent PhT but not PBT had reduced tissue Doppler velocities and SRe values during follow-up, suggesting early myocardial relaxation abnormalities. PBT shows promise as a cardiac-sparing RT technology.

PMID:37887865 | PMC:PMC10607871 | DOI:10.3390/jcdd10100418

23:06

PubMed articles on: Cardio-Oncology

Correlation of High-Sensitivity Cardiac Troponin I Values and Cardiac Radiation Doses in Patients with Left-Sided Breast Cancer Undergoing Hypofractionated Adjuvant Radiotherapy with Concurrent Anti-HER2 Therapy

Curr Oncol. 2023 Oct 6;30(10):9049-9062. doi: 10.3390/curroncol30100654.

and indirect relationships between cardiovascular disease and cancer, allowing biomarkers a greater role in the development and success of novel anticancer therapies.

ABSTRACT

Cardiotoxicity is a growing concern in the oncology population. Transthoracic echocardiography and multigated acquisition scans have been used for surveillance but are relatively insensitive and resource intensive. Innovative imaging techniques are constrained by cost and availability. More sensitive, cost-effective cardiotoxicity surveillance strategies are needed. Circulating cardiovascular biomarkers could provide a sensitive, low-cost solution. Biomarkers such as troponins, natriuretic peptides (NPs), novel upstream signals of oxidative stress, inflammation, and fibrosis as well as panomic technologies have shown substantial promise, and guidelines recommend baseline measurement of troponins and NPs in all patients receiving potential cardiotoxins. Nonetheless, supporting evidence has been hampered by several limitations. Previous reviews have provided valuable perspectives on biomarkers in cancer populations, but important analytic aspects remain to be examined in depth. This review provides comprehensive assessment of critical challenges and solutions in this field, with focus on analytical issues relating to biomarker measurement and interpretation. Examination of evidence pertaining to common and serious forms of cardiotoxicity reveals that improved study designs incorporating larger, more diverse populations, registry-based approaches, and refinement of current definitions are key. Further efforts to harmonize biomarker methodologies including centralized biobanking and analyses, novel decision limits, and head-to-head comparisons are needed. Multimarker algorithms incorporating machine learning may allow rapid, personalized risk assessment. These improvements will not only augment the predictive value of circulating biomarkers in cardiotoxicity but may elucidate both direct and indirect relationships between cardiovascular disease and cancer, allowing biomarkers a greater role in the development and success of novel anticancer therapies.

PMID:37889193 | DOI:10.1161/JAHA.123.029574

23:06

PubMed articles on: Cardio-Oncology

Detection of Early Myocardial Dysfunction by Imaging Biomarkers in Cancer Patients Undergoing Photon Beam vs. Proton Beam Radiotherapy: A Prospective Study

J Cardiovasc Dev Dis. 2023 Oct 4;10(10):418. doi: 10.3390/jcdd10100418.

derived cardiac organoids and heart-on-chip are promising in vitro platforms for predicting and minimizing anti-cancer drug-induced cardiotoxicity.

ABSTRACT

Cardiovascular disease (CVD) caused by anti-cancer drug-induced cardiotoxicity is now the second leading cause of mortality among cancer survivors. It is necessary to establish efficient in vitro models for early predicting the potential cardiotoxicity of anti-cancer drugs, as well as for screening drugs that would alleviate cardiotoxicity during and post treatment. Human induced pluripotent stem cells (hiPSCs) have opened up new avenues in cardio-oncology. With the breakthrough of tissue engineering technology, a variety of hiPSC-derived cardiac microtissues or organoids have been recently reported, which have shown enormous potential in studying cardiotoxicity. Moreover, using hiPSC-derived heart-on-chip for studying cardiotoxicity has provided novel insights into the underlying mechanisms. Herein, we summarize different types of anti-cancer drug-induced cardiotoxicities and present an extensive overview on the applications of hiPSC-derived cardiac microtissues, cardiac organoids, and heart-on-chips in cardiotoxicity. Finally, we highlight clinical and translational challenges around hiPSC-derived cardiac microtissues/organoids/heart-on chips and their applications in anti-cancer drug-induced cardiotoxicity. • Anti-cancer drug-induced cardiotoxicities represent pressing challenges for cancer treatments, and cardiovascular disease is the second leading cause of mortality among cancer survivors. • Newly reported in vitro models such as hiPSC-derived cardiac microtissues/organoids/chips show enormous potential for studying cardio-oncology. • Emerging evidence supports that hiPSC-derived cardiac organoids and heart-on-chip are promising in vitro platforms for predicting and minimizing anti-cancer drug-induced cardiotoxicity.

PMID:37889357 | DOI:10.1007/s10565-023-09835-4

23:06

PubMed articles on: Cardio-Oncology

Circulating Cardiovascular Biomarkers in Cancer Therapeutics-Related Cardiotoxicity: Review of Critical Challenges, Solutions, and Future Directions

J Am Heart Assoc. 2023 Oct 27:e029574. doi: 10.1161/JAHA.123.029574. Online ahead of print.

utilized to study cardiovascular risk across a range of cancer types and cancer therapies with the ultimate goals of both developing generalizable risk stratification tools as well as validating interventions which prevent overt cardiovascular compromise.

ABSTRACT

Survival with operable breast cancer has improved markedly in recent decades, however, treatment-related cardiovascular toxicities threaten to offset these gains. Ovarian function suppression paired with aromatase inhibition, for premenopausal women with hormone receptor (HR)-positive breast cancer, is a newer widely adopted therapy with the potential for significant long-term cardiovascular toxicity. Abrupt estrogen deprivation for non-cancer reasons is associated with accelerated coronary artery disease. Women with breast cancer treated with aromatase inhibition in addition to ovarian function suppression experience a dual hit with regards to estrogen exposure. The CaRdiac Outcomes With Near-complete estrogen deprivation (CROWN) study seeks to understand the early, subclinical natural history of cardiovascular compromise in young women undergoing near-complete estrogen deprivation (NCED) therapy. It is critical to understand the early subclinical development of cardiovascular disease to identify a window for therapeutic intervention before overt cardiovascular events occur. This three-site regional study (Atrium Health Wake Forest, Duke, and Virginia Commonwealth University) uses serial stress cardiac magnetic resonance (CMR) imaging and cardiac computed tomography angiography (CCTA) obtained during the initial two years of NCED therapy to study myocardial prefusion reserve (MPR), large cardiovascular vessel changes, left ventricular function, and other cardiovascular parameters. The CROWN cohort will consist of 90 premenopausal women with breast cancer, 67 with HR-positive disease receiving NCED and 23 comparators with HR-negative disease. Participants will undergo three annual CMR scans and two CCTA scans during the two-year study period. After initial activation hurdles, accrual has been brisk, and the study is expected to complete accrual in December 2024. Efforts are in place to encourage participant retention with the study primary outcome, change in MPR between the two groups, to be reported in 2026-2027. The results of this study will enable premenopausal women with breast cancer to balance the health burdens of cancer at a young age and treatment-related cardiovascular morbidity. Finally, the tools developed here can be utilized to study cardiovascular risk across a range of cancer types and cancer therapies with the ultimate goals of both developing generalizable risk stratification tools as well as validating interventions which prevent overt cardiovascular compromise.

PMID:37890547 | DOI:10.1016/j.ahj.2023.10.007

23:06

PubMed articles on: Cardio-Oncology

Recent advances in pluripotent stem cell-derived cardiac organoids and heart-on-chip applications for studying anti-cancer drug-induced cardiotoxicity

Cell Biol Toxicol. 2023 Oct 27. doi: 10.1007/s10565-023-09835-4. Online ahead of print.

then provide example protocols for murine tissue harvesting and processing that can support use in downstream applications of the reader's choosing.

ABSTRACT

Cancer survivors who have received thoracic radiation as part of their primary treatment are at risk for developing radiation-induced cardiotoxicity (RICT) due to incidental radiation delivered to the heart. In recent decades, advancements in radiation delivery have dramatically improved the therapeutic ratio of radiation therapy (RT)-efficiently targeting malignancies while sparing the heart; yet, in many patients, incidental radiation to the heart cannot be fully avoided. Cardiac radiation exposure can cause long-term morbidity and contribute to poorer survival in cancer patients. Severe cardiac effects can occur within 2years of treatment. Currently, there is no way to predict who is at higher or lower risk of developing cardiotoxicity from radiation, and the critical factors that alter RICT have not yet been clearly identified. Thus, pre-clinical investigations are an important step towards better prevention, detection, and management of RICT in cancer survivors. The overarching aim of this chapter is to provide researchers with foundational and technical knowledge in the use of mice and rats for RICT investigations. After a brief overview of RICT pathophysiology and clinical manifestations, we discuss important considerations of RICT study design, including animal selection and radiation planning. We then provide example protocols for murine tissue harvesting and processing that can support use in downstream applications of the reader's choosing.

PMID:37890926 | DOI:10.1016/bs.mcb.2023.02.014

23:06

PubMed articles on: Cardio-Oncology

Cardiovascular Impact of Near Complete Estrogen Deprivation in Premenopausal Women with Breast Cancer: The CROWN Study

Am Heart J. 2023 Oct 25:S0002-8703(23)00300-9. doi: 10.1016/j.ahj.2023.10.007. Online ahead of print.

recommendations of 7 selected guidelines into rules and proposed action measures. Patient suitability and care suggestions were assessed for several use case examples.

ABSTRACT

BACKGROUND: Millions of cancer survivors are at risk of cardiovascular diseases, a leading cause of morbidity and mortality. Tools to potentially facilitate implementation of cardiology guidelines, consensus recommendations, and scientific statements to prevent atherosclerotic cardiovascular disease (ASCVD) and other cardiovascular diseases are limited. Thus, inadequate utilization of cardiovascular medications and imaging is widespread, including significantly lower rates of statin use among cancer survivors for whom statin therapy is indicated.

METHODS: In this methodological study, we leveraged published guidelines documents to create a rules-based tool to include guidelines, expert consensus, and medical society scientific statements relevant to point of care cardiovascular disease prevention in the cardiovascular care of cancer survivors. Any overlap, redundancy, or ambiguous recommendations were identified and eliminated across all converted sources of knowledge. The integrity of the tool was assessed with use case examples and review of subsequent care suggestions.

RESULTS: An initial selection of 10 guidelines, expert consensus, and medical society scientific statements was made for this study. Then 7 were kept owing to overlap and revisions in society recommendations over recent years. Extensive formulae were employed to translate the recommendations of 7 selected guidelines into rules and proposed action measures. Patient suitability and care suggestions were assessed for several use case examples.

CONCLUSION: A simple rules-based application was designed to provide a potential format to deliver critical cardiovascular disease best-practice prevention recommendations at the point of care for cancer survivors. A version of this tool may potentially facilitate implementing these guidelines across clinics, payers, and health systems for preventing cardiovascular diseases in cancer survivors.

TRIAL REGISTRATION: ClinicalTrials.Gov Identifier: NCT05377320.

PMID:37891699 | DOI:10.1186/s40959-023-00179-w

23:06

PubMed articles on: Cardio-Oncology

Methods to assess radiation-induced cardiotoxicity in rodent models

Methods Cell Biol. 2023;180:127-146. doi: 10.1016/bs.mcb.2023.02.014. Epub 2023 Apr 24.

ABSTRACT

The prevalence of patients with hyperuricemia or gout is increasing worldwide. Hyperuricemia and gout are primarily attributed to genetic factors, along with lifestyle factors like consuming a purine-rich diet, alcohol and/or fructose intake, and physical activity. While numerous studies have reported various comorbidities linked to hyperuricemia or gout, the range of these associations is extensive. This review article focuses on the relationship between uric acid and thirteen specific domains: transporters, genetic factors, diet, lifestyle, gout, diabetes mellitus, metabolic syndrome, atherosclerosis, hypertension, kidney diseases, cardiovascular diseases, neurological diseases, and malignancies. The present article provides a comprehensive review of recent developments in these areas, compiled by experts from the Young Committee of the Japanese Society of Gout and Uric and Nucleic Acids. The consolidated summary serves to enhance the global comprehension of uric acid-related matters.

PMID:37892201 | PMC:PMC10604821 | DOI:10.3390/biom13101519

23:06

PubMed articles on: Cardio-Oncology

Simplified rules-based tool to facilitate the application of up-to-date management recommendations in cardio-oncology

Cardiooncology. 2023 Oct 27;9(1):37. doi: 10.1186/s40959-023-00179-w.

HHF with preserved LVEF and HfpEF will be used interchangeably, considering that the findings in most HFpEF studies are driven by HTN.

ABSTRACT

The neurohormonal model of heart failure (HF) pathogenesis states that a reduction in cardiac output caused by cardiac injury results in sympathetic nervous system (SNS) activation, that is adaptive in the short-term and maladaptive in the long-term. This model has proved extremely valid and has been applied in HF with a reduced left ventricular (LV) ejection fraction (LVEF). In contrast, it has been undermined in HF with preserved LVEF (HFpEF), which is due to hypertension (HTN) in the vast majority of the cases. Erroneously, HTN, which is the leading cause of cardiovascular disease and premature death worldwide and is present in more than 90% of HF patients, is tightly linked with SNS overactivity. In this paper we provide a contemporary overview of the contribution of SNS overactivity to the development and progression of hypertensive HF (HHF) as well as the clinical implications resulting from therapeutic interventions modifying SNS activity. Throughout the manuscript the terms HHF with preserved LVEF and HfpEF will be used interchangeably, considering that the findings in most HFpEF studies are driven by HTN.

PMID:37892623 | PMC:PMC10607346 | DOI:10.3390/jcm12206486

23:06

PubMed articles on: Cardio-Oncology

Exploring the Multifaceted Nexus of Uric Acid and Health: A Review of Recent Studies on Diverse Diseases

Biomolecules. 2023 Oct 13;13(10):1519. doi: 10.3390/biom13101519.

rats were given DOX (2.5 mg/kg) intraperitoneally over a 14-day period. Group I served as the control and received tween 80 (0.2%), group II received the vehicle and DOX,

ABSTRACT

Citronellol has been reported to have anti-inflammatory, anti-cancer, and antihypertensive activities, but its effect on myocardial ischemia is still unclear. The aim of this study was to investigate the therapeutic effects and pharmacological mechanisms of citronellol on ischemia. Therefore, a rat model of myocardial ischemia was established using the doxorubicin (DOX) model. To induce cardiotoxicity, the rats were given DOX (2.5 mg/kg) intraperitoneally over a 14-day period. Group I served as the control and received tween 80 (0.2%), group II received the vehicle and DOX, group III received the standard drug dexrazoxane and DOX, whereas groups IV, V, and VI were treated orally with citronellol (25, 50, and 100 mg/kg) and DOX, respectively. After treatment, the rats were euthanized, and blood samples were collected to assess the levels of serum cardiac markers, lipid profiles, and tissue antioxidant enzymes. The gene expressions of eNOS, PPAR-g, IL-10, VEGF, and NFkB-1 were also determined using real-time polymerase chain reactions. Simultaneous treatment with DOX and citronellol reduced cardiac antioxidant enzymes and lipid biomarkers in a dose-dependent manner. Citronellol also increased the expression of anti-inflammatory cytokines while reducing the expression of pro-inflammatory cytokines. Therefore, it can be concluded that citronellol may have potential cardioprotective effects in preventing DOX-induced cardiotoxicity.

PMID:37893193 | PMC:PMC10604204 | DOI:10.3390/biomedicines11102820

23:06

PubMed articles on: Cardio-Oncology

The Sympathetic Nervous System in Hypertensive Heart Failure with Preserved LVEF

J Clin Med. 2023 Oct 12;12(20):6486. doi: 10.3390/jcm12206486.

of doxorubicin in liposomes has been proposed. Caelyx and Myocet are different formulations of pegylated (PLD) and non-pegylated liposomal doxorubicin (NPLD),

ABSTRACT

Doxorubicin is a widely used anticancer agent as a first-line treatment for various tumor types, including sarcomas. Its use is hampered by adverse events, among which is the risk of dose dependence. The potential cardiotoxicity, which increases with higher doses, poses a significant challenge to its safe and effective application. To try to overcome these undesired effects, encapsulation of doxorubicin in liposomes has been proposed. Caelyx and Myocet are different formulations of pegylated (PLD) and non-pegylated liposomal doxorubicin (NPLD), respectively. Both PLD and NPLD have shown similar activity compared with free drugs but with reduced cardiotoxicity. While the hand-foot syndrome exhibits a high occurrence among patients treated with PLD, its frequency is notably reduced in those receiving NPLD. In this prospective, multicenter, one-stage, single-arm phase II trial, we assessed the combination of NPLD and ifosfamide as first-line treatment for advanced/metastatic soft tissue sarcoma (STS). Patients received six cycles of NPLD (50 mg/m2) on day 1 along with ifosfamide (3000 mg/m2 on days 1, 2, and 3 with equidose MESNA) administered every 3 weeks. The overall response rate, yielding 40% (95% CI: 0.29-0.51), resulted in statistical significance; the disease control rate stood at 81% (95% CI: 0.73-0.90), while only 16% (95% CI: 0.08-0.24) of patients experienced a progressive disease. These findings indicate that the combination of NPLD and ifosfamide yields a statistically significant response rate in advanced/metastatic STS with limited toxicity.

PMID:37894403 | PMC:PMC10605752 | DOI:10.3390/cancers15205036

23:06

PubMed articles on: Cardio-Oncology

The Protective Effect of Citronellol against Doxorubicin-Induced Cardiotoxicity in Rats

Biomedicines. 2023 Oct 18;11(10):2820. doi: 10.3390/biomedicines11102820.

notable accumulation in proximity to tumor sites, indicative of amplified tumor targeting precision. Intriguingly, the Car/H-dot shows remarkable efficacy in eliminating tumors across insulinoma animal

ABSTRACT

Platinum-based anticancer agents have revolutionized oncological treatments globally. However, their therapeutic efficacy is often accompanied by systemic toxicity. Carboplatin, recognized for its relatively lower toxicity profile than cisplatin, still presents off-target toxicities, including dose-dependent cardiotoxicity, neurotoxicity, and myelosuppression. In this study, we demonstrate a delivery strategy of carboplatin to mitigate its off-target toxicity by leveraging the potential of zwitterionic nanocarrier, H-dot. The designed carboplatin/H-dot complex (Car/H-dot) exhibits rapid drug release kinetics and notable accumulation in proximity to tumor sites, indicative of amplified tumor targeting precision. Intriguingly, the Car/H-dot shows remarkable efficacy in eliminating tumors across insulinoma animal models. Encouragingly, concerns linked to carboplatin-induced cardiotoxicity are effectively alleviated by adopting the Car/H-dot nanotherapeutic approach. This pioneering investigation not only underscores the viability of H-dot as an organic nanocarrier for platinum drugs but also emphasizes its pivotal role in ameliorating associated toxicities. Thus, this study heralds a promising advancement in refining the therapeutic landscape of platinum-based chemotherapy.

PMID:37895146 | PMC:PMC10607179 | DOI:10.3390/ijms242015466

23:06

PubMed articles on: Cardio-Oncology

Prospective, Multicenter Phase II Trial of Non-Pegylated Liposomal Doxorubicin Combined with Ifosfamide in First-Line Treatment of Advanced/Metastatic Soft Tissue Sarcomas

Cancers (Basel). 2023 Oct 18;15(20):5036. doi: 10.3390/cancers15205036.

understanding of their dose- and time-dependent impacts. This paper delves into diverse imaging modalities such as echocardiography, cardiac magnetic resonance imaging, cardiac computed

ABSTRACT

Cancer therapies have revolutionized patient survival rates, yet they come with the risk of cardiotoxicity, necessitating effective monitoring and management. The existing guidelines offer a limited empirical basis for practical approaches in various clinical scenarios. This article explores the intricate relationship between cancer therapy and the cardiovascular system, highlighting the role of advanced multimodality imaging in monitoring patients before, during, and after cancer treatment. This review outlines the cardiovascular effects of different cancer therapy classes, offering a comprehensive understanding of their dose- and time-dependent impacts. This paper delves into diverse imaging modalities such as echocardiography, cardiac magnetic resonance imaging, cardiac computed tomography, and nuclear imaging, detailing their strengths and limitations in various conditions due to cancer treatment, such as cardiac dysfunction, myocarditis, coronary artery disease, Takotsubo cardiomyopathy, pulmonary hypertension, arterial hypertension, valvular heart diseases, and heart failure with preserved ejection fraction. Moreover, it underscores the significance of long-term follow-up for cancer survivors and discusses future directions.

PMID:37895484 | PMC:PMC10608651 | DOI:10.3390/life13102103

23:06

PubMed articles on: Cardio-Oncology

H-Dot Mediated Nanotherapeutics Mitigate Systemic Toxicity of Platinum-Based Anticancer Drugs

Int J Mol Sci. 2023 Oct 23;24(20):15466. doi: 10.3390/ijms242015466.

cardiotoxicities caused by anticancer drugs and targeted therapy used to treat colorectal cancer as well as strategies focused on early diagnosing, prevention, and treatment of cardiotoxicity associated with anticancer drugs used in CRC therapy.

ABSTRACT

Cardiotoxicity is a well-known adverse effect of cancer-related therapy that has a significant influence on patient outcomes and quality of life. The use of antineoplastic drugs to treat colorectal cancers (CRCs) is associated with a number of undesirable side effects including cardiac complications. For both sexes, CRC ranks second and accounts for four out of every ten cancer deaths. According to the reports, almost 39% of patients with colorectal cancer who underwent first-line chemotherapy suffered cardiovascular impairment. Although 5-fluorouracil is still the backbone of chemotherapy regimen for colorectal, gastric, and breast cancers, cardiotoxicity caused by 5-fluorouracil might affect anywhere from 1.5% to 18% of patients. The precise mechanisms underlying cardiotoxicity associated with CRC treatment are complex and may involve the modulation of various signaling pathways crucial for maintaining cardiac health including TKI ErbB2 or NRG-1, VEGF, PDGF, BRAF/Ras/Raf/MEK/ERK, and the PI3/ERK/AMPK/mTOR pathway, resulting in oxidative stress, mitochondrial dysfunction, inflammation, and apoptosis, ultimately damaging cardiac tissue. Thus, the identification and management of cardiotoxicity associated with CRC drug therapy while minimizing the negative impact have become increasingly important. The purpose of this review is to catalog the potential cardiotoxicities caused by anticancer drugs and targeted therapy used to treat colorectal cancer as well as strategies focused on early diagnosing, prevention, and treatment of cardiotoxicity associated with anticancer drugs used in CRC therapy.

PMID:37895912 | PMC:PMC10610064 | DOI:10.3390/ph16101441

23:06

PubMed articles on: Cardio-Oncology

Multimodality Cardiovascular Imaging of Cardiotoxicity Due to Cancer Therapy

Life (Basel). 2023 Oct 23;13(10):2103. doi: 10.3390/life13102103.

CI: 0.382-0.619]; P < 0.001), and need for renal replacement therapy (OR: 0.398 [95% CI: 0.189-0.839]; P = 0.012) were also less frequent in patients on SGLT2 inhibitors.

ABSTRACT

BACKGROUND: Certain antineoplastic therapies are associated with an increased risk of cardiomyopathy and heart failure (HF). Sodium-glucose cotransporter-2 (SGLT2) inhibitors improve outcomes in patients with HF.

OBJECTIVES: This study aims to examine the efficacy of SGLT2 inhibitors in patients with cancer therapy-related cardiac dysfunction (CTRCD) or HF.

METHODS: The authors conducted a retrospective cohort analysis of deidentified, aggregate patient data from the TriNetX research network. Patients aged ≥18 years with a history of type 2 diabetes mellitus, cancer, and exposure to potentially cardiotoxic antineoplastic therapies, with a subsequent diagnosis of cardiomyopathy or HF between January 1, 2013, and April 30, 2020, were identified. Patients with ischemic heart disease were excluded. Patients receiving guideline-directed medical therapy were divided into 2 groups based on SGLT2 inhibitor use. After propensity score matching, odds ratios (ORs) and Cox proportional HRs were used to compare outcomes over a 2-year follow-up period.

RESULTS: The study cohort included 1,280 patients with CTRCD/HF (n = 640 per group; mean age: 67.6 years; 41.6% female; 68% White). Patients on SGLT2 inhibitors in addition to conventional guideline-directed medical therapy had a lower risk of acute HF exacerbation (OR: 0.483 [95% CI: 0.36-0.65]; P < 0.001) and all-cause mortality (OR: 0.296 [95% CI: 0.22-0.40]; P = 0.001). All-cause hospitalizations or emergency department visits (OR: 0.479; 95% CI: 0.383-0.599; P < 0.001), atrial fibrillation/flutter (OR: 0.397 [95% CI: 0.213-0.737]; P = 0.003), acute kidney injury (OR: 0.486 [95% CI: 0.382-0.619]; P < 0.001), and need for renal replacement therapy (OR: 0.398 [95% CI: 0.189-0.839]; P = 0.012) were also less frequent in patients on SGLT2 inhibitors.

CONCLUSIONS: SGLT2 inhibitor use is associated with improved outcomes in patients with CTRCD/HF.

PMID:37897456 | DOI:10.1016/j.jchf.2023.08.026

23:06

PubMed articles on: Cardio-Oncology

Recent Perspectives on Cardiovascular Toxicity Associated with Colorectal Cancer Drug Therapy

Pharmaceuticals (Basel). 2023 Oct 11;16(10):1441. doi: 10.3390/ph16101441.

ABSTRACT

BACKGROUND: Despite recent improvements in the treatment of cancer, little is known about the long-term survival in patients with cancer and venous thromboembolism. We aimed to examine the five-year mortality of venous thromboembolism in cancer patients in a large population-based cohort study.

METHODS: Using Danish healthcare registries from 1995 to 2020, we obtained data on cancer patients with venous thromboembolism and comparison cohorts of cancer patients without venous thromboembolism, matched in terms of cancer type, age, sex, and year of cancer diagnosis, and adjusted for level of comorbidity and frailty using the Charlson Comorbidity Index Score and Hospital Frailty Risk Score, marital status, use of selected medications, and recent surgery (<90

FINDINGS: During the study period, 886,536 patients were diagnosed with cancer. Of 1882 cancer patients diagnosed at the time of their venous thromboembolism, 44.4% (835/1882) had distant metastases. In this cohort, the one- and five-year mortality cumulative incidences were 68% (1284/1882) and 84% (1578/1882), respectively, in contrast to 38% (2135/5549) and 67% (3653/5549) in the comparison cohort. The mortality rate ratio was 4.34 (95% confidence interval [CI], 3.95-4.78) for the first year of follow-up and 3.44 (95% CI 3.17-3.73) for the five-year follow-up period. Of the 23,366 patients diagnosed with venous thromboembolism after cancer diagnosis, 18% (4183/23,366) had distant metastases at the time of cancer diagnosis. The cumulative incidence of death at one year was 45% (10,465/23,366; mortality rate ratio 3.48, 95% CI 3.37-3.60) and at five years 69% (15,669/23,366; mortality rate ratio 2.57, 95% CI 2.50-2.63).

INTERPRETATION: Despite improved cancer treatment, venous thromboembolism in cancer patients is strongly associated with a poor prognosis.

FUNDING: The study was supported by grants from the Independent Research Fund Denmark (record no. 3101-00102B) and the Karen Elise Jensen Foundation.

PMID:37809052 | PMC:PMC10558815 | DOI:10.1016/j.lanepe.2023.100739