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OVERVIEW OF PROGERIA: a rare disease CHILD

OVERVIEW OF PROGERIA: a rare disease CHILD

Kamal Singh Rathore, Sunita P., Khushboo Sharma, RKNema

Progeria is a rare, genetic fatal condition produces rapid aging starting in childhood also known as "syndrome Hutchinson-Gilford progeria" or "HGPS" and "syndrome Hutchinson-Gilford "in which symptoms similar to those aspects of aging are manifested at an early age. Progeria was first described in an academic journal by Dr. Jonathan Hutchinson in 1886 and Dr. Hastings Gilford in 1897 – both in England.

Its name is derived from Greek and means "prematurely old." Approximately 1 in 4,000,000 people are diagnosed with this condition. Those born with progeria usually live close to 13-20 years, is a genetic condition that presented as a new mutation and is usually not hereditary, although there is a unique heritable. This is in contrast to other rare premature aging syndrome, but similar, dyskeratosis congenita (DKC), which is inherited and is often expressed several times in a family line.

Although born looking healthy, children with Progeria begin to display many characteristics of accelerated aging at around 18-24 months of age. Progeria signs include growth retardation, loss body fat and hair, aged-looking skin, stiffness of joints, hip dislocation, generalized atherosclerosis, cardiovascular disease (the heart) and stroke. The children look very similar, despite different ethnic backgrounds. Children with Progeria die of atherosclerosis (disease the heart), to an average age of thirteen years (with a range of about 8-21 years). According to Hayley's page "Currently there are 53 cases Progeria known throughout the world and only two in the United Kingdom. "Progeria There is an incidence of approximately 1 in every 4 to 8 million newborns. Children and girls are at equal risk of having Progeria.

Symptoms

Progeria is a genetic disorder that causes progressive children to age rapidly, from their first two years of life. The condition is rare, since 1886, only about 130 cases of progeria have been documented in scientific literature. Usually within the first year of life, growth slows a child with progeria as height and weight to fall below average their age and weight for height falls under. Motor development and mental development remain normal.

Signs and symptoms of this progressive disorder include:

• Limited growth or poor growth during the first year of life
• Narrow, shrunken or wrinkled face
• failure to thrive
• Baldness (alopecia)
• Insulin-resistant diabetes (diabetes that does not respond readily to insulin injections)
• Skin changes similar to that seen in scleroderma (the connective tissue becomes tough and hardened)
• The loss of eyebrows and eyelashes
• a characteristic (Small face and jaw, pinched nose)
• Short stature and small, fragile bodies like those of older people
• Large head for size of face (macrocephaly)
• Open soft spot (fontanelle)
• Small jaw (micrognathia)
• Dry, scaly, thin
• Limited range of motion
• Teeth – delayed or absent formation
• Later the condition causes of wrinkled skin, atherosclerosis and cardiovascular problems.
• Slow growth, with below-average height and weight
• A narrow face and aquiline nose, that makes the child must be old
• Head too big for the face
• Prominent scalp veins
• Prominent eyes
• Small lower jaw (micrognathia)
• High-pitched voice
• Delayed and abnormal tooth formation
• Fat Loss body and muscle
• Stiff joints
• Hip dislocation

Causes

Progeria usually occurs without cause – not seen in siblings of affected children. In extremely rare cases more than one child from the same family may have the condition.

It is only very rarely seen in more than one child in a family. Progeria is a childhood disorder caused by a mutation at position 1824 of LMNA gene (Lamin A), in place of cytosine with thymine, creating a useless form of the protein Lamin A. Lamin A is part of the building blocks the nuclear envelope. 90% of children with progeria have a mutation in the gene that encodes the protein lamin A. a protein that contains the cell nucleus together. It is believed that the defective Lamin A protein makes the nucleus unstable. This instability seems to lead to premature aging in Progeria patients.

Diagnosis

Diagnosis is suspected according to the signs and symptoms such as skin changes, abnormal proliferation and loss of hair. It can be confirmed through genetic testing. The health professional may suspect Progeria if signs and symptoms are there – aging skin, hair loss, joint stiffness, etc. This can be confirmed through genetic testing. The Foundation for Progeria Research has created a Diagnostics Testing Program.

There is no diagnostic test confirms progeria. Generally, doctors make a diagnosis based on signs and symptoms such as lack of growth and hair loss, which usually are not fully apparent until the child is nearly 2. However, with the discovery of genetic mutation that causes progeria, it is possible to perform a genetic test for mutations in LMNA first suspicion of progeria. The sooner you know your child has progeria, As soon as your doctor may recommend treatments that can help relieve the signs and symptoms of the disease.

A blood test may reveal that your child has a low level of high density lipoprotein (HDL), the so-called good cholesterol that helps keep arteries open. This laboratory finding is not diagnostic by itself, but may support a diagnosis of progeria.

Treatment

There are no effective treatments have been tested.

• Most treatment focuses on reducing complications (such as cardiovascular disease), with a bypass operation or low-dose aspirin. A daily dose can help prevent heart attacks and strokes.
• treatment of growth hormone has been tried.
• Drugs known as farnesyltransferase inhibitors (FTI), which were developed to treat cancer, have shown promise in laboratory studies on the correction of the cellular defects that cause progeria. FTIs are being studied in human clinical trials for the treatment of progeria. has been proposed, but their use has been limited especially animal models. A Phase II clinical trials with FTI lonafarnib began in May 2007.
• Physical therapy and occupational. These can help with stiffness and hip problems, and may allow your child to stay active.
• high-calorie nutritional supplements. For example extra calories in your child's daily diet can help prevent weight loss and ensure adequate nutrition.
• The feeding tube. Children who eat little benefit from a feeding tube and syringe. You can use the syringe to push pumped breast milk or formula through the tube to make it easier for your child to feed.
• Extraction of teeth. your child's permanent teeth may begin to come before their teeth fall milk. The extraction can help prevent problems associated with the late loss of baby teeth, such as overcrowding and the development of a second row of the permanent teeth when teeth are in.

Prognosis

There is no known cure. Few people with progeria exceed 13 years of age. At least 90% of patients die from complications of atherosclerosis such as heart attack or stroke.

Mental development is not affected. The development of symptoms is comparable to aging at a rate six to eight times faster than normal, although certain age-related conditions do not occur. Specifically, patients show no neurodegeneration or cancer predisposition. They do not develop physically mediated "wear" conditions commonly associated with aging, such as cataracts (caused by UV exposure) and osteoarthritis (caused by mechanical wear).

Epidemiology

Classical Hutchinson-Gilford Progeria almost never transmitted from father to son. It is usually caused by a new (sporadic) mutation during cell division early in the child. Usually genetically dominant, therefore, parents who are healthy do not usually pass it to their children. Affected children rarely live long enough for the children themselves.

Research indicates that a chemical (hyaluronic acid) can be found greatly elevated levels in the urine of Hutchinson-Gilford Progeria Syndrome. The same anomaly was found in Werner syndrome, which sometimes called 'progeria of the adult. "

Lamin A

Nuclear lamin A protein is a scaffolding on the inner edge of the nucleus that helps organize nuclear processes such as RNA and DNA synthesis.

Pre-laminated A contains a CAAX box at the C-terminus of the protein (where C is a cysteine and A is any aliphatic amino acid). This ensures that the cysteine is farnesylated and allows pre-laminated A to bind membranes, specifically the nuclear membrane. After of pre-laminated A has been localized to the nuclear membrane of cells, C-terminal amino acids, including the farnesylated cysteine, are broken off by a specific protease. The resulting protein is now the lamin A is no longer bound to the membrane, and carries out functions within the nucleus.

In 2003, researchers at NHGRI, together with colleagues at the Progeria Research Foundation, the New York State Institute for Basic Research in Developmental Disabilities, and the University of Michigan, found the Hutchinson-Gilford progeria is caused by a small mutation, point in a single gene known as lamin A (LMNA). Parents and siblings of children with progeria are almost never affected by the disease. According to this clinical observation, the mutation appears in almost all cases that occur in sperm before conception. It is remarkable that almost all cases is derived from the substitution of a single base pair among the approximately 25,000 DNA base pairs that make up the LMNA gene. The LMNA gene encodes two proteins, lamin A and lamin C, which is known to play a key role in stabilizing the inner membrane of the cell nucleus. In laboratory tests with cells taken from progeria patients, researchers have found that the mutation responsible for Hutchinson-Gilford progeria gene causes LMNA to produce an abnormal form of the protein lamin A. That abnormal protein appears to destabilize the nuclear membrane of the cell in a way that can be particularly harmful to tissues routinely subjected to intense physical force, such as the cardiovascular and musculoskeletal systems. Interestingly, mutations in different the same LMNA gene have been shown to be responsible for at least a half dozen other genetic disorders, including two rare forms of muscular dystrophy. In addition to its implications for diagnosis and possible treatment for progeria, the discovery of underlying genetics of this model of premature aging may help shed new light on things human normal aging process.

Possible complications

Heart attack (myocardial infarction)

Coup

How can we help children with Progeria?

• Make a financial contribution. Donations are needed to continue the vital work. No donation is too small or too big – every penny counts in our fight for a cure!
• Donate your time. Volunteers are also important for success. Keep a special event like a bake sale or letter writing campaign, translating documents for families, help with e mail – we'll find something for you to do that fits your schedule, location and talent!
• Donate in-kind services or items. Do you own a printing supply business or office? Do you have experience in developing non-profit? These are just some of the many types of talents and connections. The more work we can get out on a pro bono basis, the more we can spend on research!
• Spread the word and make connections. Do you know someone who can do any of the above.

Caring, Coping and support

• Your child's learning has progeria can be emotionally devastating. Suddenly you know your child is facing many difficult challenges and a shorter life. For you and your family to cope This disorder involves a great commitment to physical, emotional and financial effort.
• When dealing with a condition such as progeria, support groups may be a valuable part of a broad network of social support that includes health professionals, family and friends. In a support group you with people facing similar challenges to which you are. Speaking with members of the group can help you deal with your feelings about your child's condition. If a group is not for you, talk to a therapist or a member of the clergy can be beneficial.
• Ask your doctor about self-help groups or therapists in your community. Your local health department, public libraries, Internet phone and can also be good sources to find a support group in your area.

Help the child cope

• If your child has progeria, he or she is also likely to experience fear and pain as awareness grows that shortens progeria life. Your child will eventually need your help to deal with the concept of death, and may have a series of difficult but important questions about God and religion. Your child can also ask questions about what will happen in his family after he or she dies.
• It is critical that you are able to to talk openly and honestly with their child and offer moral support that is compatible with their belief system. Ask your doctor, therapist or clergy member to help prepare for these conversations with your child. The friends you meet through support groups may also be able to offer valuable guidance.

Conclusion and General Discussion

Progeria Syndrome Hutchinson-Gilford Progeria is a rare and deadly genetic condition of children with interesting like premature aging. Children with progeria usually have a normal appearance in early childhood. At approximately nine to 24 months of age, affected children begin to experience profound growth delays, resulting in short stature and low weight. They also develop a distinctive facial features a disproportionately small face in comparison to the head, an underdeveloped jaw (micrognathia), malformations and crowding of the teeth abnormally bulging eyes, a nose, small, prominent eyes and a subtle blueness around the mouth. Furthermore, in the second year of life, the scalp hair, eyebrows and eyelashes are lost (alopecia), and hair of the scalp may be replaced by small, soft, white or blond hair. Other characteristic features include generalized atherosclerosis, cardiovascular disease and stroke, hip dislocations, unusually prominent veins of the scalp, loss of layer fat under the skin (subcutaneous fat), defects of the nails, joint stiffness, skeletal defects, and / or other abnormalities. According to reports in the literature care, people with syndrome Hutchinson-Gilford progeria early development, widespread thickening and loss of elasticity of arterial walls (arteriosclerosis) leading to life-threatening complications during childhood, adolescence or early adulthood. Children with progeria die of heart disease (atherosclerosis) at an average age of 13 years, with a range of eight to 21 years.

Progeria is caused by a mutation in the LMNA gene and lamin A. The protein lamin A is the scaffolding that holds the nucleus of a cell together. Researchers now believe that the defective lamina A protein makes the nucleus unstable. The cellular instability seems to lead to premature aging in progeria. Because neither parent carries or expresses the mutation, each case is believed to represent a sporadic mutation, the new ones that mostly occurs in a single sperm or egg immediately prior to conception.

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Support Groups

Progeria Research Foundation, Inc. – www.progeriaresearch.org

About the Author

Reader, Bhupal Nobles’ Girls’ College of Pharmacy, Udaipur-Raj.313002 INDIA
Email: kamalsrathore@yahoo.com
kamalsrathore@gmail.com
Mobile: +919828325713

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