Complement component 8 deficiency
آخر تحديث 18 Aug 2020
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Complement component 8 deficiency is a disorder that causes the immune system to malfunction, resulting in a form of immunodeficiency. Immunodeficiencies are conditions in which the immune system is not able to protect the body effectively from foreign invaders such as bacteria. People with complement component 8 deficiency have a significantly increased risk of recurrent bacterial infections, particularly by a bacterium called Neisseria meningitidis. Infection by this bacterium causes inflammation of the membranes surrounding the brain and spinal cord (meningitis). Although meningitis can be life-threatening, individuals with complement component 8 deficiency are less likely to die from the infection than people in the general population who contract it.
الوصف
Complement component 8 deficiency is a disorder that causes the immune system to malfunction, resulting in a form of immunodeficiency. Immunodeficiencies are conditions in which the immune system is not able to protect the body effectively from foreign invaders such as bacteria. People with complement component 8 deficiency have a significantly increased risk of recurrent bacterial infections, particularly by a bacterium called Neisseria meningitidis. Infection by this bacterium causes inflammation of the membranes surrounding the brain and spinal cord (meningitis). Although meningitis can be life-threatening, individuals with complement component 8 deficiency are less likely to die from the infection than people in the general population who contract it.
The severity of complement component 8 deficiency varies widely. While some people with this condition experience one or more infections, others do not have any health problems related to the disorder.
There are two types of complement component 8 deficiency, types I and II, classified by their genetic cause. The two types have the same signs and symptoms.
Inheritance patterns
The source lists the following possible inheritance patterns: Autosomal recessive. More than one pattern can apply in different cases.
Related genes
Other names
C8 deficiency
Related patient information and medicines
Patient information leaflet
الأطعمة الغنية بالكالسيوم
Calcium is an important nutrient with many functions. نقص الكالسيوم You need to make sure you are consuming enough calcium-rich food if you have low calcium levels in the blood (hypocalcaemia) or are taking steroids. Why is فيتامين د important for calcium. فيتامين د is needed so that the body can absorb calcium effectively. Some people are at.
Patient information leaflet
نقص فيتامين سي
فيتامين C cannot be made by the human body and so is an essential component of the diet. It is needed for the health and repair of various tissues in the body, including skin, bone, teeth and cartilage. Persistent lack of dietary vitamin C in can lead to a condition called scurvy. Symptoms of scurvy include easy bruising, easy bleeding and joint.
Patient information leaflet
هل يمكنني تناول فيتامين ب12 وفيتامين ج معًا؟
Why this happens ... نقص G6PD Very high doses of فيتامين C can cause oxidative stress and lead to the breakdown of red blood cells (haemolysis) in individuals with نقص إنزيم G6PD. Our Medicines Interaction Checker helps you check whether your prescriptions, over-the-counter medicines, and supplements are safe to take together. Disclaimer.
Patient information leaflet
هل يمكنني تناول حمض الفوليك وفيتامين B2 معًا؟
يوجد no known harmful interaction between folic acid (Vitamin B9) and Vitamin B2 (riboflavin). لماذا يحدث هذا Folic acid and Vitamin B2 are both water-soluble B vitamins. ...onvert folic acid into its active form (methylfolate)Important precautions نقص فيتامين B12 (Pernicious Anaemia) Folic acid can mask the symptoms of vitamin B12.
Patient information leaflet
الشمس وحروق الشمس
Benefits of sunshine Vitamin D Vitamin D is vital for good health. فيتامين د is made in the skin with the help of sunlight. ...of vitamin DPeople need vitamin D for bone health as well as our body functions. Children with severe نقص فيتامين د may develop a condition known as rickets. Adults with severe نقص فيتامين د may develop a.
Patient information leaflet
هل يمكنني تناول هيدروكسوكوبالامين وليبيتور معًا؟
There are no known interactions between hydroxocobalamin (Vitamin B12) and Lipitor (atorvastatin). It is safe to take these two medications together. Why this happens These medications are processed by different pathways in the body. Hydroxocobalamin is a synthetic form of Vitamin B12 used to treat deficiencies, while Lipitor is a statin used to.
قراءة إضافية ومراجع
- Complement component 8 deficiency; MedlinePlus, National Library of Medicine.
- Bubeck D. The making of a macromolecular machine: assembly of the membrane attack complex. Biochemistry. 2014 Apr 1;53(12):1908-15. doi: 10.1021/bi500157z. Epub 2014 Mar 18.
- Kaufmann T, Hansch G, Rittner C, Spath P, Tedesco F, Schneider PM. Genetic basis of human complement C8 beta deficiency. J Immunol. 1993 Jun 1;150(11):4943-7.
- Kojima T, Horiuchi T, Nishizaka H, Fukumori Y, Amano T, Nagasawa K, Niho Y, Hayashi K. Genetic basis of human complement C8 alpha-gamma deficiency. J Immunol. 1998 Oct 1;161(7):3762-6.
- Merle NS, Noe R, Halbwachs-Mecarelli L, Fremeaux-Bacchi V, Roumenina LT. Complement System Part II: Role in Immunity. Front Immunol. 2015 May 26;6:257. doi: 10.3389/fimmu.2015.00257. eCollection 2015.
- Rosa DD, Pasqualotto AC, de Quadros M, Prezzi SH. Deficiency of the eighth component of complement associated with recurrent meningococcal meningitis--case report and literature review. Braz J Infect Dis. 2004 Aug;8(4):328-30. doi: 10.1590/s1413-86702004000400010. Epub 2004 Nov 19.
- Saucedo L, Ackermann L, Platonov AE, Gewurz A, Rakita RM, Densen P. Delineation of additional genetic bases for C8 beta deficiency. Prevalence of null alleles and predominance of C-->T transition in their genesis. J Immunol. 1995 Nov 15;155(10):5022-8.
تاريخ المقال
المقال متاح أيضًا باللغة الإنجليزية, الألمانية, إسبانية, الفرنسية, إيطالي, البرتغالية, الهندية, العبرية, العربية ,، و السويدية.
18 Aug 2020 | أحدث إصدار
1 Dec 2015 | نُشر في الأصل
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