Hutchinson gilford childhood progeria. What does the Progeria Foundation do? Progeria – a rare disease of rapid aging

Progeria

In children

Although childhood progeria can be congenital, most patients with Clinical signs usually appear in the 2-3rd year of life. The child's growth slows down sharply, atrophic changes dermis, subcutaneous tissue, especially on the face and limbs. The skin becomes thinner, becomes dry, wrinkled, and there may be scleroderma-like lesions and areas of hyperpigmentation on the body. Veins are visible through thin skin. Appearance patient: large head, frontal tubercles protrude above a small, pointed (“bird-like”) face with a beak-shaped nose, the lower jaw is underdeveloped. Muscle atrophy and degenerative processes in teeth, hair and nails are also observed; changes in the osteoarticular apparatus, myocardium, hypoplasia of the genital organs, disturbance fat metabolism, lens opacification, atherosclerosis.

Average duration life with childhood progeria - 13 years. Most sources give ages of death between 7 and 27 years, with cases of adulthood being very rare. There is only one known case of a patient who survived the 27-year mark - a Japanese man described by Ogihara and others in 1986 who lived for 45 years.

In adults

Adult progeria is autosomal recessive type inheritance. The defective gene is WRN (ATP-dependent helicase gene). It is assumed that the process is related to a violation of DNA repair, metabolism connective tissue.

Histological picture: flattening of the epidermis, homogenization and sclerosis of connective tissue, atrophy of subcutaneous tissue with its replacement by connective tissue fibers. Clinically, the disease manifests itself during puberty. Slow growth and symptoms of hypogonadism are noted. Usually in the third decade of life, the patient’s hair turns gray and falls out, cataracts develop, the skin gradually becomes thinner and the subcutaneous tissue on the face and limbs atrophies, as a result of which the arms and especially the legs become thin. Foci of scleroderma-like compaction and dyschromia appear, most pronounced in the distal parts of the limbs and on the face, which, along with a thin beak-shaped nose and narrowed oral opening, gives it a mask-like appearance. In areas exposed to pressure, hyperkeratosis develops, chronic poor healing trophic ulcers. Osteoporosis, metastatic calcification of soft tissues, and, less commonly, osteomyelitis are detected. Diabetes mellitus is often observed, the signs of which, like the symptoms of early generalized atherosclerosis, are usually detected in patients aged 30-40 years; malignant neoplasms are possible (for example, skin cancer, sarcoma, adenocarcinoma).

The diagnosis is made based on clinical picture. Differential diagnosis is carried out with congenital poikiloderma, scleroderma. Treatment is symptomatic, mainly aimed at preventing atherosclerotic complications, eliminating diabetes mellitus, trophic ulcers. It is carried out by a therapist, endocrinologist or other specialist, depending on the prevailing clinical symptoms. The prognosis for recovery is poor; Most patients die from atherosclerotic complications and malignant neoplasms. Prevention has not been developed.

Aging

A severe form of human progeria, Hutchinson-Gilford syndrome, has been found to be associated with molecular changes that are characteristic of normal aging, such as genomic instability, decreased telomere length, and disruption of stem cell homeostasis. These data, together with genetic studies of lifespan, have led to the hypothesis that progeria syndromes accelerate the progression of lifespans. pathological changes which usually control the normal aging process.

In art

• In the "Metal Gear Solid" series of games main character Solid Snake was born under circumstances artificial insemination and interventions genetic engineering into human genetics - for the purpose of correcting DNA and cloning human genes from father to son. As a result, due to genetic interference and a violation of the genetic program (genetic defect), Solid Snake began to develop progeria by the age of 40. Quote: "Otacon: Loose skin, hardened arteries...Symptoms of your early aging very reminiscent of Werner's syndrome..."
• In A. Reutov’s novel “Hackers of Dreams,” a team of Hackers introduces the idea of ​​progeria to the main villain of the novel, Lord Dags.
• In Chuck Palahniuk's novel Ghosts, one of the characters, Mr. Witter, is not actually an old man, as the other characters think he is, but a 13-year-old boy with progeria.
• The Blade Runner character J.F. Sebastian suffers from progeria.
• In the third episode of the first season of The Invisible Man, a woman named Gloria was infected with a special form of Werner's syndrome and could infect others. She infected the main character.
• In the book by the Strugatsky brothers “The Beetle in the Anthill” Lev Abalkin was a progressor on a planet whose entire population was infected with a certain virus that caused rapid aging. At the time of writing the work, the authors did not even suspect the existence of progeria.
• In Ruggero Deodato's film The Phantom of Death, the main character learns that he has progeria, which causes mental disorder and leads to a series of murders.
• Progeria is also mentioned in the film The Curious Case of Benjamin Button. Which tells about a man who was born old, and with age he became younger.
• In the episode "Candle in the Wind" of Stargate SG-1, one of the main characters was infected with microscopic robots that accelerated his aging
• In episode 21 of season 2 of Bones, the victim, Chelsea Cole, suffered from progeria.
• In the series X-Files Season 1 episode 16 "Young at Heart" this disease is mentioned.
• In the series Smallville, in episode 6 of season 2, this disease is mentioned.
• In the feature film Jack, Robin Williams plays a teenager with progeria (premature aging).
• Leon Botha, who gained popularity after the band's videos Die Antwoord

Notes

Literature

• Fedorova E. V. About congenital progeria. - 1980. - T. 4. - P. 66. - (Pediatrics).

Wikimedia Foundation. 2010.

Progeria is a rare genetic disease, first described by Guilford, which manifests itself as premature aging of the body associated with its underdevelopment. Progeria is classified into childhood, called Hutchinson (Hutchinson)-Gilford syndrome, and adult progeria, called Werner syndrome.

With this disease, there is severe growth retardation since childhood, changes in skin structure, cachexia, absence of secondary sexual characteristics and hair, underdevelopment internal organs and the look of an old man. Wherein mental condition The patient is age appropriate, the epiphyseal cartilaginous plate closes early, and the body has childlike proportions.

Progeria is an incurable disease and is the cause of serious atherosclerosis, which as a result develops strokes and various types. And in the end this genetic pathology leads to death, i.e. it is fatal. As a rule, a child can live on average thirteen years, although there are cases with a life expectancy of more than twenty years.

Hutchinson-Gilford infantile progeria

This disease is extremely rare in the ratio of 1:4000000 newborns in the Netherlands and 1:8000000 in the USA. Moreover, the disease affects more boys than girls (1.2:1).

Two forms of Hutchinson-Gilford progeria are considered: classical and non-classical.

Currently, more than one hundred cases of childhood progeria have been described. Moreover, this disease mainly affects children of the white race. Hutchinson-Gilford progeria is characterized by polymorphic lesions. Children with this syndrome appear quite normal at birth. But by a year or two there is a serious lag in growth. Typically, such children are characterized by too short stature and even lower body weight in accordance with their length.

Children with progeria are characterized by complete baldness of not only the scalp, but also the absence of eyelashes and eyebrows. early age. The skin appears weak and wrinkled as a result of the absolute loss of subcutaneous fat present in the skin. The head is characterized by disproportion of the craniofacial bones, which resemble the face of a bird with a hooked nose, abnormally small lower jaw, bulging eyeballs and protruding ears. It is these features, a large bald spot and a small jaw, that give the child the appearance of an old person.

Other clinical manifestations progeria include: irregular and late eruption teeth, thin and high voice, pear-shaped rib cage and reduced in size collarbones. The limbs are usually thin, and the changed elbows and knee joints Give the sick child a “rider pose.”

In children under one year of age, scleral-like compactions, congenital or acquired, are observed on the buttocks, thighs and lower abdomen. Children with progeria are characterized by hyperpigmentation of the skin, which only intensifies over the years, and hypoplasia of the nails, in which they become yellow, thin and convex, reminiscent of watch glasses. However, starting from the age of five, a widespread form of atherosclerosis develops with extensive damage to the aorta and arteries, especially the mesenteric and coronary ones. And much later, heart murmurs and cardiac hypertrophy appear in the left ventricle. The early onset of atherosclerosis in children causes their short life span. But it is considered the main cause of death.

There are known cases of progeria ischemic stroke. Such children in mental development are absolutely no different from healthy children, sometimes even ahead of them. Children with this diagnosis live on average about fourteen years.

With childhood progeria of non-classical form, body length lags slightly behind weight, hair is preserved for a long time, and lipodystrophy progresses much more slowly; a recessive type of inheritance is possible.

baby progeria photo

Progeria causes

Until now, the exact causes of progeria have not been clarified. The presumptive etiology of the development of this disease is a metabolic disorder in the connective tissue, as a result of the proliferation of fibroblasts through cell division and increased collagen formation with reduced synthesis of glycosaminoglycans. The slow formation of fibroblasts is explained by disturbances in the intercellular substance.

In reasons childhood syndrome Progeria is considered to be a mutation in the LMNA gene, which is responsible for encoding lamin A. This is a protein that makes up one of the layers of the nucleus of the cell membrane.

In many cases, progeria appears sporadically, and in some families it occurs in siblings, especially in consanguineous marriages, and this indicates a possible autosomal recessive type of inheritance. When studying the skin of patients, cells were found that had an impaired ability to repair breaks and damage in DNA, as well as reproduce genetically homogeneous fibroblasts, change the atrophic dermis and epidermis, contributing to the disappearance of subcutaneous tissue.

Adult progeria is characterized by autosomal recessive inheritance with defective gene ATP-dependent helicase or WRN. There is a suggestion of a linking chain of disturbances between DNA repair and connective tissue turnover.

It has also been established that Hutchinson-Gilford progeria has disorders in carrier cells that cannot fully get rid of DNA cross-links caused by chemical agents. When diagnosing these cells with this syndrome, it was found that they are not able to fully undergo the division process.

In 1971, Olovnikov suggested that telomeres shorten in the process of cell formation. And in 1992, this was already proven in patients with adult progeria syndrome. An analysis that links the Hayflick limit, telomere length and the activity of the enzyme telomerase allows us to combine the natural process of aging with the formation of clinical symptoms Hutchinson-Gilford progeria infantile. Since this form of progeria is extremely rare, one can only hypothesize about the type of inheritance, which is similar to Cockayne syndrome and is manifested by certain features of premature aging.

There are also statements about Hutchinson-Gilford progeria being an autosomal dominant mutation that arose de novo, i.e. without inheritance. It became an indirect confirmation of the syndrome, which was based on measurements of telomeres in carriers of the disease, their parents and donors.

Progeria symptoms

The clinical picture of childhood progeria is characterized by characteristic premature atherosclerosis, myocardial fibrosis, and cerebral circulation, increased lipoproteins and cholesterol levels, prothrombin time in tests, early heart attacks, skeletal abnormalities. IN in this case there are pronounced disproportions of the face and skull, underdevelopment of the jaw and teeth, and displacement of the hips. Long Bones at normal cortical structure and progression of peripheral demineralization are subject to recurrent pathological fractures.

The joints are characterized by tight mobility, especially the knees with possible contractures of the hip, ankle, elbow and wrist joints. At X-ray studies demineralization is detected near joints with osteoporosis, varus and hallux valgus deformities lower extremities. Tumors and thickening of collagen fibers are also very common.

Werner's syndrome or adult progeria manifests itself from 14 to 18 years and is characterized by stunting, universal graying with parallel progression.

As a rule, progeria syndrome develops after twenty years and differs early baldness, thinning of the skin on the face and limbs, characteristic pallor. Under too-tight skin, superficial blood vessels, and subcutaneous fatty tissue and the muscles located underneath completely atrophy, so the limbs look disproportionately thin.

Then the skin over the bone protrusions gradually becomes thicker and ulcerates. After thirty years, patients with progeria develop cataracts in both eyes, the voice becomes weak, high-pitched and hoarse, and the skin is noticeably affected. This manifests itself in the form of sclerocerma-like changes in the limbs and face, ulcers on the legs, calluses on the feet and telangiectasia. Such patients are usually short in stature, with a moon-shaped face, a beak-like nose, like a bird’s, a narrowed mouth opening and a sharply protruding chin, a full body and thin limbs.

In patients with progeria, the functions of the sweat and sebaceous glands are impaired. On the protrusions of the bones, general hyperpigmentation appears, and the shape of the nail plates changes. And then various injuries Trophic ulcers appear on the legs and feet. In addition to thinning, patients experience significant changes in muscles and bones, calcification, generalized, osteoarthritis with erosions. Such patients have limited finger movements and flexion contracture. Patients with progeria are characterized by bone deformation, as in rheumatoid e, pain in the limbs, flat feet and osteomyelitis.

During X-ray examinations, osteoporosis of bones, heterotopic calcifications of the skin and subcutaneous tissue, ligaments and tendons are revealed. Also, cataracts slowly progress, developing, interfering with the activity of cardio-vascular system. In most patients, intelligence decreases.

After forty years of progeria against the background of diabetes mellitus, dysfunction of the parathyroid glands and other diseases, almost 10% of patients develop tumor pathologies in the form osteosarcoma, astrocytoma, thyroid adenocarcinoma, and skin.

Death usually a consequence cardiovascular pathologies and malignant tumors.

At histological analysis Progeria syndrome establishes atrophy of the skin appendages where the eccrine glands are preserved; the dermis is thickened, collagen fibers are hyalinized, and nerve fibers are destroyed.

In patients, the muscles completely atrophy and there is no subcutaneous fat.

The disease is diagnosed based on the clinical symptoms of progeria. If the diagnosis is in doubt, the ability of fibroblasts to multiply in culture is determined (reduced indicator for Werner syndrome). For differential diagnosis Progeria takes into account Hutchinson-Gilford, Rothmund-Thomson syndromes and systemic scleroderma.

Progeria treatment

To date, there is no specific treatment for progeria; it has not yet been developed. Basically, therapy is symptomatic in nature with the prevention of complications after atherosclerosis and the treatment of trophic ulcers.

For an anabolic effect, growth hormone is prescribed, which in some patients increases body weight and length. The entire therapeutic process is carried out by a number of specialists, such as an endocrinologist, therapist, cardiologist, oncologist and others, depending on the prevailing symptoms.

But in 2006, US researchers noted progression in the treatment of progeria as an incurable disease. They introduced a farnesyltransferase inhibitor into the culture of damaged fibroblasts, which had previously been tested on cancer patients. And this process returned the aging cells to their normal shape. This drug was well tolerated, so there is now hope that in the future it will be possible to use it to prevent progeria in childhood.

The effectiveness of Lonafarnib (farnesyl transferase inhibitor) is to increase the amount of fat under the skin, body weight, bone mineralization, which will ultimately reduce fractures.

But, nevertheless, this disease is still characterized by unfavorable prognosis. On average, patients with progeria live to the age of thirteen, dying from hemorrhages and heart attacks.

People first started talking about premature aging syndrome 100 years ago. And it’s not surprising: such cases occur once in 4-8 million babies. Progeria (from the Greek pro - earlier, gerontos - old man) - or Hudchinson Guilford syndrome. This disease is also called childhood old age. This is an extremely rare genetic disease that accelerates the aging process by approximately 8-10 times. Simply put, a child ages 10-15 years in one year.

Children with progeria appear normal for 6 to 12 months after birth. After this, they develop symptoms characteristic of old age: wrinkled skin, baldness, brittle bones and atherosclerosis. An eight-year-old child looks 80 years old - with dry, wrinkled skin and a bald head. These children usually die at the age of 13-14 after several heart attacks and strokes against the background of progressive atherosclerosis, cataracts, glaucoma, total loss teeth, etc. And only a few live to 20 years or longer. People call this disease “canine old age.”

There are now about 60 known cases of progeria in people around the world. Of these, 14 people live in the United States, 5 in Russia, and the rest in Europe. Features of such patients include dwarf stature, low weight (usually not exceeding 15-20 kg), excessively thin skin, poor joint mobility, underdeveloped chin, small face in comparison with the size of the head, which gives a person bird-like features. Due to the loss of subcutaneous fat, all blood vessels are visible. The voice is usually high. Mental development appropriate for age. And all these sick children are strikingly similar to each other.

Until recently, doctors were unable to determine the cause of the disease. And only recently, American researchers discovered that the cause of “childhood old age” is a single mutation. Progeria is caused by a mutated form of the LMNA gene. According to the director National Institute genome research by Francis Collins, who led the study, this disease is not hereditary. A point mutation - when only one nucleotide is changed in a DNA molecule - occurs anew in each patient. Genetic mutation in the protein Lamin A causes accelerated aging of the body. And the young man - with his large protruding ears, bulging eyes and swollen veins on his bald skull - turns into a one hundred and sixteen year old man.

Hussein Khan and his family are unique in their own way: they are the only known to science a case where more than one family member suffers from progeria. And thanks to this family, scientists were able to make real breakthrough in understanding the nature of the disease. Hana's husband and wife are cousins. Neither of them has progeria, nor do their two children, 14-year-old Sangeeta and two-year-old Gulavsa. Their 19-year-old daughter Rehena and two sons: 7-year-old Ali Hussein and 17-year-old Ikramul suffer from this disease. None of them have practically any chance of living even to 25, and this is probably the saddest thing.

Adult progeria (Werner syndrome) is a hereditary or family disease. It manifests itself as premature aging, starting at the age of 20-30, accompanied by early graying, baldness and arteriosclerosis. Adult progeria manifests itself in the following symptoms. Slowly developing juvenile cataract. The skin of the feet, legs, to a lesser extent, hands and forearms, as well as the face, gradually becomes thinner, the subcutaneous tissue and muscles in these areas atrophy. On lower limbs 90% of patients develop trophic ulcers, hyperkeratosis and nail dystrophy.

Atrophy of the facial skin ends with the formation of a beak-shaped nose (“bird nose”), narrowing of the mouth and a sharpening of the chin, reminiscent of a “scleroderma mask.” From endocrine disorders hypogenitalism is noted, late appearance or absence of secondary sexual characteristics, dysfunction of the upper and lower parathyroid glands(violation calcium metabolism), thyroid gland(exophthalmos) and pituitary gland (moon-shaped face, high-pitched voice). Osteoporosis is often observed. Changes in the fingers resemble those seen in sclerodactyly. Most patients with Werner syndrome die before age 40. Trials are currently underway to treat the disease with stem cells.

Progeria translated from ancient Greek means old man. Is rare genetic disease, in which irreversible changes occur in the body, leading to premature aging. There is childhood progeria, called Hutchinson-Gilford syndrome, and adult progeria, known as Werner syndrome.

Mutations in the LMNA gene lead to childhood progeria syndrome. It is this gene that produces the protein lamin, which helps retain the cell nucleus. Scientists believe that a defective lamin protein leads to instability of cell nuclei, which contributes to early aging.

At birth, children with this syndrome appear healthy in appearance and physical appearance. The disease begins to manifest itself at the age of 1.5-2 years. This is expressed by loss of hair and weight, protruding veins are observed, and wrinkled skin is formed. In addition, negative processes are accompanied by complications more common to older people: stroke, cardiovascular diseases, osteoporosis, joint stiffness, generalized atherosclerosis.

One interesting point is observed with this disease. Despite their different ethnic backgrounds, children with this syndrome are externally similar to each other. The most common cause of progeria from which children die is atherosclerosis, and the age to which they live is 13 years. True, the age range ranges from 8 to 21 years.

Adult progeria, according to many years of observations, begins in adolescence, the range is from 15 to 20 years. Naturally, the disease also affects the life expectancy of patients, which is shortened to 40-50 years. Death occurs due to stroke, myocardial infarction, and malignant tumors. The cause of the disease is still unknown and to this day occupies the minds of scientists around the world.

You should know that progeria is a genetic disease, not hereditary. It turns out that the parents are not carriers of this disease. Scientists suggest that a sporadic mutation occurs either in the sperm or in the egg even before the moment of conception. It is also worth noting that if parents have a child with CSGP, then the probability of having a second child of the same kind is small and amounts to 1 in 4-8 million. There are some progeria syndromes that are passed down through generations, but this is not the case with classic CSGP.

Before illness, both sexes (female and male) and all races exclusively are equal. The disease is quite rare and occurs in only one in 8 million children worldwide. Known on this moment 42 cases of this disease.

Progeria is a serious disease that has no cure. This genetic disease develops in children of any gender, turning them into old people in a short period of time. Progeria is dangerous not only for children, but also for adults. After all, the disease can begin to progress at different ages.

General information about the disease

This pathology is dangerous because it triggers in the body premature aging. The disease goes by two different names. If it is found in children, they are diagnosed with Hutchinson-Gilford syndrome. If the disease manifests itself in an adult, he is diagnosed with Werner syndrome.

Statistics show that progeria is more common in boys than in girls. The average life expectancy of a child diagnosed with this condition ranges from 10 to 13 years. There have been very rare cases where patients with this pathology lived to be 20 years old. Unfortunately, the disease cannot be treated and is fatal.

The symptoms of progeria are very scary. Sick children are very far behind their peers in physical development. In addition, the patient’s body wears out very much: the structure of the skin is disrupted, there are no signs of secondary sexual development, and the internal organs remain underdeveloped. In addition to the symptoms described above, there is another one - external aging of the body. That is, little children look like old people, which greatly affects their emotional state.

The mental development of patients with progeria is absolutely normal. The body retains childlike proportions, but despite this, the epiphyseal cartilage quickly overgrows, and in its place an epiphyseal line is formed, as in adults. Children, whose bodies grow up very quickly, face various serious adult diseases: diabetes mellitus, cardiovascular diseases, atherosclerosis, stroke and others.

Reasons for the development of pathology

Unfortunately, scientists have not yet thoroughly studied this pathology. They were only able to find out that the basis of the pathology is most likely a mutation of the lamin gene. It is this gene that is responsible for the processes of cell division. A failure in the genetic system deprives cells of resistance and triggers premature aging processes in the body.

Many genetic diseases are inherited. However, progeria is not transmitted. Therefore, even if one of the parents suffered from this pathology, it will not be passed on to the child.

Symptoms of progeria

As soon as the baby is born, symptoms of the disease cannot be immediately detected. He will be no different from healthy newborn babies. However, already in the first year of life, the symptoms of progeria make themselves felt. Symptoms of the disease are:

• very short stature and severe lack of body weight;
• lack of subcutaneous fat and lack of tone in the skin;
• lack of eyebrows and eyelashes;
• hyperpigmentation and bluish tint of the skin;
• disproportionate development of the skull and facial bones, bulging eyes, small lower jaw, protruding ears, hooked nose;
• late appearance of teeth that deteriorate very quickly;
• high and shrill voice;
• the chest is pear-shaped, the collarbones are small, the elbow and knee joints are “tight”;
• convex nails yellow color;
• sclera-like formations on the skin of the buttocks, lower abdomen and thighs.

At the age of five, children who suffer from progeria begin to develop atherosclerosis, which affects the aorta, coronary arteries and mesenteric arteries. Against the background of these disorders, other pathologies appear: left ventricular hypertrophy, the appearance of heart murmurs. The complex influence of all these symptoms leads to the sudden death of a sick person. Most often, patients die from ischemic stroke and myocardial infarction.

Progeria in an adult

It has already been said above that not only a child, but also an adult can suffer from of this disease. Progeria can strike at the age of 14-18 years. The patient begins to lose weight sharply, his growth slows down, and White hair and progressive alopecia is observed. Skin a person's skin becomes sharply thinner and the skin acquires an unhealthy pale tint. Under the skin you can see blood vessels, muscles and subcutaneous fat. The arms and legs look very thin, and the muscles begin to atrophy.

Cataracts appear in patients over 30 years of age eyeballs, the voice weakens, the skin over the protrusions of the bones becomes rough and covered with ulcers. Patients with progeria look the same: thin, dry limbs, a dense body, short stature, a nose in the shape of a bird's beak, a narrow mouth, a protruding chin, and numerous pigment spots on the skin.

The disease disrupts the activity of the entire body. The functioning of internal organs is disrupted, sebaceous glands, sweat glands, the cardiovascular system is disrupted, the body suffers from a lack of vitamins and minerals, osteoporosis and erosive osteoarthritis develop. The disease has a detrimental effect on intellectual abilities.

About 10% of patients face serious diseases such as breast cancer, melanoma, sarcoma, and astrocytoma. Oncology begins to develop against the background of diabetes mellitus and impaired function of the parathyroid glands. Most often, adult patients die from cardiovascular pathologies of oncology.

Diagnosis of the disease

The symptoms of progeria are very pronounced and specific. Therefore, the doctor does not need to conduct any additional tests to make the correct diagnosis.

Treatment of progeria

Unfortunately, scientists have not yet found a cure for this disease. All treatment methods that are practiced today are very often not effective enough. Since the disease cannot be treated, doctors simply regularly monitor the condition of the sick person. A person who suffers from progeria must constantly undergo medical examinations, have an ultrasound of internal organs, and monitor the condition of the cardiovascular system.

All treatment methods are aimed at reducing the rate of progression of the disease. Doctors also try to alleviate the patient’s condition as much as possible.

Today, patients with progeria are prescribed the following treatment:

• Minimum doses of Aspirin are prescribed, which can reduce the risk of a heart attack.
• Various medications are prescribed that improve well-being and eliminate symptoms of various diseases. For example, doctors prescribe medications from the group of statins, which lower blood cholesterol levels. Anticoagulants are prescribed to block the formation of blood clots. Very often, growth hormone is prescribed, which helps to accumulate weight and height.
• Patients with progeria are prescribed various physiotherapeutic procedures that develop joints. This allows the patient to remain physically active.

Small children diagnosed with progeria have their baby teeth removed, since the disease causes permanent teeth to erupt very quickly, and baby teeth to deteriorate very quickly. And if they are not removed in a timely manner, there may be problems with the eruption of molars.

Since the disease is genetic, preventive measures there is nothing against its development.