0
Ehlers-Danlos type 3 is the hypermobility form of the Ehlers-Danlos Syndrome. Affects 1 in 10,000 to 15,000 and is caused by an autosomal dominant or autosomal recessive mechanism. Extreme flexibility is the hallmark of this type. It is one of the most surviable types of EDS.
What else can I help you with?
Who discovered ehlers-danlos syndrome?
Ehlers-Danlos Syndrome was discovered by Edvard L. Ehlers, a Danish dermatologist who first discovered the disease in 1901. Henri-Alexandre Danlos, a French dermatologist published his own description of the disease in 1908.
What is the life span of a person with Ehlers-Donlos Syndrom?
The life span of individuals with Ehlers-Danlos Syndrome can vary depending on the type and severity of the condition. While certain types may have a normal life expectancy, others that affect major organs like the heart can potentially lead to complications that may affect longevity. It is important for individuals with Ehlers-Danlos Syndrome to receive appropriate medical care and management to address potential health issues.
Is there any treatment for ehlers-danlos syndrome?
Treatment for Ehlers-Danlos syndrome focuses on managing symptoms and preventing complications. This can include physical therapy to strengthen muscles, joint protection strategies, pain management, and monitoring for cardiovascular and other complications associated with the condition. In some cases, surgery may be needed to address specific issues such as joint dislocations.
Who is a carrier of Ehlers-Danlos Syndrome?
In my case, it was my father, who was "double jointed" like me. He was never diagnosed, but died at age 75 of Parkinson's with dementia. I am female and have fibromyalgia in addition to the EDS. I think my 26 year old son has at least the FM, if not the EDS also.The three most prevalent types of Ehlers-Danlos Syndrome (Hypermobility, Classic, and Vascular) are autosomal dominant defects. This means that they are dominant traits, which are not passed on via the X or Y chromosomes. Being a carrier is only applicable to recessive traits, so for these types of EDS, there really aren't "carriers." You either have an inherited defect that causes EDS, or you don't.If one parent has one of these three types of EDS, then each child has a 50% chance of inheriting the dominant gene. If both parents have one of these types of EDS, then each child has a 75% overall chance of inheriting a type of EDS (a 50% chance of inheriting one or the other, and a 25% chance of inheriting both defects).Some of the more rare forms of EDS are inherited recessively, so one can be a carrier of these. However, with about 100 total cases identified of these rare forms, it's very unlikely that any one person will be a carrier of these.
What is Ehliers-Danlos Syndrome Dermatosparaxis Type?
To get horny for a long period of time. Um, no. And if that lasts more than four hours, dude, call your doctor. ;-) The Dermatosparaxis Type of EDS (formerly Type 7C) is extremely rare, with about 10 cases identified ever. It is characterized by extremely fragile, sagging skin and is caused by a defect in the ADAMTS2 gene. Mutations in this gene cause a dramatic reduction in the enzyme produced by this gene; the reduction in the enzyme means that procollagen is not processed correctly, so that collagen fibrils aren't formed correctly, so that the connective tissue within the body is very weak. My understanding is that the common symptoms of the three more prevalent types (hypermobility, classic, and vascular) can be present in any of the more rare forms of EDS.
Who are Ehlers-Danlos syndromes named for?
Dr. Ehlers and Dr. Danlos
Who discovered ehlers-danlos syndrome?
Ehlers-Danlos Syndrome was discovered by Edvard L. Ehlers, a Danish dermatologist who first discovered the disease in 1901. Henri-Alexandre Danlos, a French dermatologist published his own description of the disease in 1908.
What are the Ehlers-Danlos syndromes?
The Ehlers-Danlos syndromes (EDS) refer to a group of inherited disorders that affect collagen structure and function
How common are Ehlers-Danlos syndromes?
Today, according to the Ehlers-Danlos National Foundation, one in 5,000 to one in 10,000 people are affected by some form of EDS
Where is the Ehlers-Danlos Support Group-UK?
Farnham, Surrey
When was Ehlers-Danlos Syndrome identified?
Hello, I see you are asking "What is ehlers danlos syndrome?" Ehlers-Danlos syndrome is a group of inherited disorders that affect your connective tissues — primarily your skin, joints and blood vessel walls. Connective tissue is a complex mixture of proteins and other substances that provide strength and elasticity to the underlying structures in your body. For more information, you can visit this URL - skincarehealthcenter. com/condition/ehlers-danlos-syndrome/c/12004
What are the symptoms of Ehlers Danlos Syndrome?
According to the Mayo Clinic there are a number of things that can be considered symptoms of Ehlers Danlos Syndrome. Some of these symptoms are stretchy and fragile skin, overly flexible joints, and fatty lumps at pressure points.
How is Ehlers-Danlos Syndrome divided?
classical, hypermobility, vascular, kyphoscoliosis, arthrochalasia, and dermatosparaxis
What is Ehlers-Danlos syndrome?
Ehlers=Danlos syndrome is a defect in collagen. The most obvious manifestations i hyperextensible joints ("double jointedness"). It can also cause joint pain and affect other systems, especially the vascular system (blood vessels).
What is Ehliers-danlos syndrome dermatosaraxis?
Ehlers-Danlos syndrome is an inherited connective tissue disorder. It is caused by a defect in the structure, production, and processing of collagen or proteins.
The India rubber man at the carnival may be suspected of having what disease?
ehlers-danlos syndrome
What is the pathology of ehlers-danlos syndrome?
Ehlers-Danlos syndrome is a group of connective tissue disorders characterized by defects in collagen synthesis and structure. This results in hypermobility of joints, skin elasticity, and tissue fragility. It is typically caused by mutations in genes involved in collagen production.
