Exercise and maintaining good physical fitness are essential for the well-being of the pregnant woman and for proper blood flow through the placenta. Therefore, those women who have no contraindications to physical activity should exercise regularly throughout their pregnancy.  

Why is it worth getting vaccinated? What is the controversy about vaccination, and is it justified?

What is the vaccine? 

The vaccine is a human-made biological preparation. The concept of the vaccine is based on the assumption that it mimics a natural infection, which leads to the body acquiring immunity, analogous to that obtained when it is first exposed to a real microorganism (virus or bacteria). The main purpose of the vaccine is to protect the body against severe disease and complications that cannot be clinically predicted, in the presence of, for example, comorbidities of different nature. Thus, obtaining acquired immunity as a result of vaccination is much safer than in the case of "natural" disease.

In the era of a pandemic, scientists took a dramatic race to find an effective and safe vaccine against the coronavirus. Research is intensive and currently over 170 different potential vaccine candidates are undergoing clinical trials, including 4 vaccine prototypes developed by Polish scientists. Both the humanitarian and economic effects of the pandemic are a strong motivator in research. The first vaccinations in some countries will be introduced as the final phase of clinical trials later this year. An article about it soon.

Fall is the time when an overlap between various seasonal pathogens such as influenza is expected, with a second attack of SARS-CoV-2. Unfortunately, the autumn season is a time of a decrease in the body's immunity, which results in a greater incidence of various types of respiratory or digestive system diseases, which potentially increases the risk of contracting coronavirus. So, in addition to increasing your immunity, it is worth getting vaccinated against influenza, pneumococci and meningococci.

Construction of the vaccine - that is, the 4 main ingredients

The vaccine consists of 4 main components that ensure its correct biological action:

- An antigen or a whole microorganism that stimulates the immune response of our body,
- Adjuvants - These are added to vaccines that cannot guarantee a strong enough immune response to achieve permanent immunity. Adjuvants are specific substances that modulate the immune response or delay the release of the applied antigen from the site of its administration. These can be aluminum compounds or diphtheria, tetanus or pertussis toxoid.
- Stabilizing substances - they are added to protect the vaccine against the influence of low or too high temperatures, or excessive deposition of the preparation on the walls of the vial. Proteins (albumin, gelatin) as well as amino acids or sugars are popularly used.
- Preservatives - they prevent the multiplication of other bacteria or fungi in the vial with the preparation. For this purpose, phenolic compounds are used.

What are the types of vaccines?

There are many variants of vaccines. However, they can be distinguished and cataloged according to their function, type of antigen used (a substance characteristic for a given microorganism) or even the ability to reproduce a living microorganism, and also according to the scope of their activity - specific and non-specific vaccines. Specific vaccines are designed to immunize against specific diseases, such as diphtheria, whooping cough, mumps. On the other hand, non-specific vaccines are non-specific products that stimulate our immune system, containing bacteria or their lysates destroyed at high temperatures.

Taking into account their most common use in the clinic, vaccines can be divided in terms of the amount of antigen they contain:

- Live - where the strains of live microorganisms used are of negligible virulence. Thus, the given microorganism has the ability to multiply in the body, but does not cause disease symptoms, which are suppressed in a special process (attenuation), where it is deprived of virulence factors. In order to achieve this, the pathogen is cultivated in conditions unusual for its development, which, as a result of mutations, allows the selection of strains with the desired properties. Among the live vaccines, the vaccines against tuberculosis, smallpox, polio, mumps, measles, rubella, varicella, rotavirus and yellow fever are constantly used.

- Inactivated - they contain dead microorganisms destroyed under the influence of chemical or physical factors, e.g. alcohols, formalin, filtration, high pressure, temperature, centrifugation. These vaccines retain their ability to trigger an immune response, but do not cause disease. Inactivated vaccines do not carry the risk of developing a full-blown disease, however, due to the lack of the possibility of microbial proliferation, they induce the immune response less well than live vaccines. Hence, they require multiple doses in order to induce effective immunity. Examples of such vaccines include the hepatitis A vaccine (hepatitis A), cholera, typhoid, plague, anthrax and rabies.
- Antigen-based - subunit - vaccines contain selected, single and purified pathogen antigens, rather than whole cells. The antigens used most often are proteins or polysaccharides. The immune response against the selected antigens is weak, which reduces the effectiveness of a single vaccination, which necessitates the use of several booster doses, as well as the addition of special carriers to the preparation. Some of these vaccines are attached to the carrier protein, diphtheria or tetanus toxoid. Such preparations are vaccines against gram-negative bacteria that cause mainly respiratory infections and meningitis (Haemophilus influenzae type b), pneumococcal pneumoniae (Streptococcus pneumoniae) and meningococcal meningococcus (Neisseria meningitidis).

Methods of vaccine administration and their effectiveness

The most common form of vaccine administration is injection (injection). There are also vaccines that are administered orally, such as, for example, against Heine-Medina disease, or by the inhalation route, such as some variants of influenza vaccines. Until 1980, smallpox was vaccinated by scarification, i.e. deliberate scratching of the epidermis with a special instrument (scarifier) ​​or a thin needle repeatedly puncturing the skin surface.

Vaccination effectiveness depends on the type of preparation used, its dose, and also on the clinical condition of the vaccinated person. According to many years of research, the vast majority of vaccines have an effectiveness of 89-98.5%. In the case of vaccination against rubella or measles, the effectiveness after 20 years is 99%, and for mumps 90-95%.

Vaccination doses and schedules are experimentally determined during clinical trials. These parameters are selected in such a way as to induce a sufficiently intense immune reaction, which will guarantee the highest vaccination effectiveness, with the lowest possible side effects.

Preventive vaccinations in Poland

In our country, compulsory vaccinations are carried out until the age of 19 and in people who are particularly exposed to contact with various pathogens, such as medical workers or emergency services. Vaccination is preceded by a qualifying medical examination. Act of 5 December 2008 on preventing and combating infections and infectious diseases in humans (Journal of Laws of 2019, item 1239); Regulation of the Minister of Health of 18 August 2011 on compulsory vaccinations (Journal of Laws of 2018, item 753).

It is worth remembering that failure to comply with the obligation to undergo compulsory vaccination is subject to administrative enforcement, i.e. the court imposes a fine or a reprimand and prevents the practice of a given profession.

Contraindications to vaccinations

Like any medical preparation, the vaccine cannot be administered under certain conditions, and these include:

- Anaphylactic shock documented from previous vaccinations
- Allergy to any ingredient (applies to all vaccines)
- Immunity disorders
- Acute illness with or without fever
- The incubation period of an infectious disease
- Some vaccinations should not be given during pregnancy, for example, for measles, yellow fever and shingles.

Anti-vaccinators - another conspiracy theory or failure of the education system?

In Poland, the favorable epidemiological situation of diseases such as diphtheria, polio, measles, whooping cough or tetanus was achieved mainly thanks to the compulsory vaccination of children against these diseases as early as 1950. Over the last decade, despite the consistently highly evaluated performance of vaccinations, there has been a decline. To maintain population (collective) immunity, which prevents the epidemic spread of disease, it is necessary to achieve vaccination status at a level above 90%. So it is very important to vaccinate yourself and your offspring in order to maintain herd immunity as long as possible.

The anti-vaccine demonstrations that have intensified in recent years have resulted in an increase in the number of people refusing to vaccinate their children, which raises well-founded concerns about the health of the population. It is assumed that if this trend continues to increase in strength in the coming years, population immunity against some diseases will be lost (shocking data indicate that the number of avoiding compulsory vaccination in 2009 was around 3,000, while in 2011 it was already over 4.5 thousand. In 2016 it was already 23.1 thousand).

Contrary to appearances, the anti-vaccine movement is not a new social trend. The beginnings of anti-vaccination attitudes date back to the beginnings of the introduction of vaccinations in the nineteenth century by Edward Jenner, who proved that the passage of the disease called vaccinia protects against infection with smallpox. Critics' skepticism was mainly related to the high mortality rate of 30%, which at that time was not a frightening result, considering the fact that it was the first vaccine in the world. The remaining number of vaccinated subjects experienced various complications, which led to the introduction of approval criteria for the vaccine for use. One of the notable critics of vaccination was Alfred Russel Wallace, who at the time preached the theory of natural selection, of which he was a co-discoverer. Such an outstanding, yet controversial figure among the anti-vaccine activists confirmed its members in the conviction of their infallibility. However, they did not take into account that Wallace's scientific views oscillated around the evolutionary reduction of the population by eliminating weaker, sickly organisms.

Already then, in 1840, some countries tried to fight the anti-vaccine movement by introducing legal acts obliging citizens to vaccinate smallpox and penalties for evading. Some critics of vaccination called it a violation of their freedom.

Anti-vaccine views flourished again in modern times, in the 1970s, during the controversy over the DTP vaccine against diphtheria, tetanus and pertussis. Said vaccine was said to cause neurological problems in 36 children which has not been scientifically tested. In 1974, the Association of Parents of Vaccine Damaged Children was established in Great Britain, whose main goal was to attract media attention and spread controversy over the DTP vaccine. Unfortunately, as a result of these actions, in 1977 the number of children immunized fell from 77% to 33%. Three outbreaks of whooping cough followed shortly after, and over 100,000 children became ill.

In 1982, in the US, anti-vaccine sentiment was heightened after the publication of the DTP video Vaccination Roulette, which linked the vaunted DTP vaccine to brain damage and retardation. It was another painful shot at population immunity as there was again a big decline in vaccinations, not only for DTP but also for other compulsory vaccinations.

The 1996 fight against Polio in Africa undertaken by Nelson Mendela was finally considered a win. 50 million children were vaccinated, and polio cases fell from 350,000 worldwide to less than 500 in 2001. In 2003, Nigerian political and religious leaders began preaching anti-vaccine views and boycotting the campaign. The consequence of the boycott was the re-spread of polio to 15 other countries, which had not yet been announced to completely eradicate the disease.

Finally, the 1998 article that laid the foundations for the anti-vaccine crowd today, published by Andrew Wakefield. In an article that is almost legendary, the author points to the alleged relationship of the MMR ternary vaccine against rubella, measles and mumps with autism. For many years, the research community has struggled to fend off vaccine critics from this article. In addition to making a wrong research hypothesis and completely falsifying the results, the author has exposed the scientific community to a loss of credibility, giving many people an excuse to undermine the credibility of all researchers. Wakefield himself lost his license to practice and eventually renounced this publication.

Vaccination is still a controversial topic these days, which is surprising. It would seem that with such advanced science, access to knowledge and education, doubts about vaccines will be dispelled once and for all. Unfortunately, this is not the case. Conspiracy theories of anti-vaccine movement supporters are based on views of general political hypocrisy by governments that deliberately conceal vaccination data while carrying out their plans. One of the common conspiracy theories is also the theory that pharmaceutical companies paid scientists to falsify research results, improve performance statistics and low risk of vaccine complications. Conspiracy theories are an expression of reluctance and distrust towards scientific research on the safety of medical preparations. Many people do not understand the concept of clinical trials, let alone the need for them.

According to the latest psychological and sociological research, conspiracy theorists usually believe not only in one theory on one topic, but also in other conspiratorial ideologies such as global warming, the existence of extraterrestrial life or the shape of the Earth (flat earths). Moreover, according to research from 2019, the reasons why parents do not vaccinate their children are multidimensional. The anti-vaccine movement is very old and, according to researchers, unfortunately it will not leave society soon. The amazing career of conspiracy theories is closely related to the development of the Internet. This was due to the phenomena of information bubbles, the disappearance of the categories of truth and falsehood, and difficulties in distinguishing opinions from facts. This phenomenon demonstrates how a growing group of conspiracy theorists, including anti-vaccines, sow disinformation, undermining public confidence in science and medicine. This phenomenon should be watched closely as its consequences will be felt by entire populations.

Source:

• Andrews N., et al.. Thimerosal Exposure in Infants and Developmental Disorders: A Retrospective Cohort Study in the United Kingdom Does Not Support a Causal Association. „Pediatrics”. 114 (3), s. 584–591, 2004. DOI: 10.1542/peds.2003-1177-L. PMID: 15342825.
• CDC: Immunization Safety and Autism – Thimerosal and Autism Research chart. Centers for Disease Control and Prevention, 27 sierpnia 2010. [dostęp 2 lipca 2017].
• dr med. Ernest Kuchar: Które szczepionki zawierają tiomersal?. mp.pl – Pediatria, 31 maja 2012. [dostęp 2 lipca 2017].
• Folegatti PM i wsp. Safety and immunogenicity of the ChAd0x1 nCoV-19 vaccine against SARS-CoV-2: a preliminary report of a phase 1/2, single blind, randomised controlled trial. The Lancet, July 20, 2020
• Heron, et al.. Thimerosal Exposure in Infants and Developmental Disorders: A Prospective Cohort Study in the United Kingdom Does Not Support a Causal Association. „Pediatrics”. 114 (3), s. 577–583, 2004. DOI: 10.1542/peds.2003-1177-L. PMID: 15342825.
• Hviid, et al.. Association Between Thimerosal Containing Vaccine and Autism. „Journal of the American Medical Association”. 290 (13), s. 1763–1766, 2003. DOI: 10.1001/jama.290.13.1763.PMID: 14519711.
• Institute of Medicine: Immunization Safety Review: Vaccines and Autism. The National Academies Press, 2004. ISBN 978-0-309-09237-1.
• Jackso LA i wsp. An mRNA Vaccine against SARS-CoV-2 — Preliminary Report. New England Journal of Medicine, July 14, 2020
• Le T.T. i wsp. The COVID-19 vaccine development landscape. Nature reviews. 09 April 2020
• Madsen, et al.. Thimerosal and the Occurrence of Autism: Negative Ecological Evidence From Danish Population-Based Data. „Pediatrics”. 112 (3), s. 604–606, 2003. PMID: 12949291.
• Stehr-Green P., et al.. Autism and thimerosal-containing vaccines: Lack of consistent evidence for an association. „American Journal of Preventive Medicine”. 25 (2), s. 101–106, 2003.
• Thompson, et al.. Early Thimerosal Exposure and Neuropsychological Outcomes at 7 to 10 Years. „New England Journal of Medicine”. 357, s. 1281–1292, 2007.

Autor: dr n.med. Kamila Rawojć

Hashimoto's disease is a chronic inflammation of the thyroid gland caused by autoimmune diseases. As a result of the dysfunction of the immune system, antibodies against the thyroid gland are produced. The thyroid gland secretes less and less thyroxine and triiodothyronine - hormones responsible for e.g. for regulating metabolism. Hashimoto's disease is one of the most common causes of hypothyroidism.
You can also come across the term "lymphocytic thyroiditis" - it is associated with the presence of diffuse lymphocytic inflammatory infiltrates within the thyroid parenchyma. As the disease progresses, more and more extensive foci of fibrosis appear with the simultaneous atrophy of the thyroid parenchyma. This process is chronically progressive and takes years. It is worth noting that the thyroid gland in the course of Hashimoto's inflammation does not hurt. Hashimoto's disease, on the other hand, can cause symptoms related to a disturbed thyroid function. In the event of their occurrence, an endocrinologist should be consulted, who will carry out diagnostics, diagnose and propose appropriate treatment.

Make an appointment now - to see the Hashimoto's disease physician at our hospital

Hashimoto's disease - symptoms

In the initial stage, Hashimoto's disease may not present the symptoms typical of hypothyroidism. Many patients first develop mild, transient hyperthyroidism, such as symptoms such as hyperactivity, excessive sweating, hot flushes, and palpitations. Short-term hyperthyroidism may result from the initial destruction of the parenchyma and an increased release of hormones from the damaged tissue.
This is followed by an asymptomatic period during which thyroid hormone levels remain normal.
In the following months, Hashimoto's syndrome progresses to typical hypothyroidism. The thyroid gland is gradually degraded - the follicular cells of the thyroid gland are atrophied. Deficiency of thyroxine and triiodothyronine results in the appearance of symptoms: constant fatigue, drowsiness, frequent depressive states, dry skin, feeling cold and weight gain. Due to slower bowel movements, a person with Hashimoto's syndrome may suffer from chronic constipation. Some patients develop the so-called mucoid swelling, most evident around the face. Women with Hashimoto's disease are more likely to report menstrual disorders.
The severity of the symptoms listed above depends on the degree of thyroid hormone deficiency and the duration of Hashimoto's disease. Long-term untreated hypothyroidism may result in infertility, the development of cardiovascular diseases, and in extreme cases may even lead to a life-threatening hypometabolic crisis.
In addition to global symptoms resulting from disturbances in thyroid hormone release, local symptoms related to changes in the volume of the thyroid gland may also be noticeable. The classic Hashimoto syndrome leads to an enlargement of the thyroid gland and the formation of the so-called will. The circumference of the neck increases. If a large goiter is pressed against adjacent structures, difficulty swallowing and a feeling of distension around the neck may appear. Hashimoto's thyroiditis can also take the form of atrophy - then no typical thyroid goiter is observed.

Hashimoto's thyroiditis - causes

Hashimoto's autoimmune disease can develop at any age, even in children. The highest percentage of cases is observed at the age of 45-65. Women get sick even 10-20 times more often than men, which may be related to the participation of estrogens in the pathogenesis of immune system disorders.
Hashimoto's thyroiditis may be genetic. If Hashimoto's disease is present in your family, anti-thyroid antibodies are found in the blood of family members.
The risk of developing Hashimoto's syndrome is higher in people with other autoimmune diseases (type I diabetes, Addison's disease adrenal cortex, systemic lupus erythematosus, Sjörgen's syndrome, rheumatoid arthritis).
Environmental factors also play a role. The risk of developing Hashimoto's thyroid disease is greater in people who have frequent viral infections and are treated with highly active antiviral drugs. The thyroid gland is also adversely affected by exposure to X-rays and therapy with radioactive iodine. Toxic compounds in cigarette smoke weaken the body's overall immune processes, increasing the risk of autoimmunity.

Hashimoto's disease in women after childbirth

Postpartum thyroiditis occurs in about 5-10% of women. The disease can take two forms:
1. Monophasic - when there is only temporary hyperthyroidism,
2. Classic - covering two phases:
◦ I - hyperthyroidism and euthyroidism (lasting about 1-2 months)
◦ II - hypothyroidism (lasting about 6 months).
Hypothyroidism associated with postpartum Hashimoto's disease lasts longer in one third of women and requires further treatment.
Postpartum Hashimoto's disease is caused by specific changes in the way the immune system works during pregnancy and after birth. In a pregnant woman, the immune system is controlled to protect the fetus from rejection (the baby is a source of "foreign" antigens from the father to the mother's body). The phenomenon of microchimerism, i.e. the penetration of fetal cells into the maternal circulation, may play a significant role in the development of postpartum Hashimoto's disease. Childbirth is a turning point in which the protective profile of the immune system is withdrawn. Then, the immune reaction against the cells of the fetus remaining in the mother's body is disinhibited, resulting in the initiation of autogression against thyroid antigens.
Having Hashimoto's disease after the first birth significantly increases the risk of developing Hashimoto's disease after having another baby. Women with diagnosed disturbances in the level of thyroid hormones should be under close supervision of an endocrinologist.
Hashimoto's syndrome diagnosis - necessary tests

Laboratory tests

1) The level of anti-thyroid antibodies:
• anti-TPO - antibodies directed against thyroid peroxidase (TPO). TPO is an enzyme that is involved in the synthesis of thyroid hormones.
• anti-TG - antibodies directed against thyroglobulin (TG). TG is a protein produced by thyroid follicular cells. On the way of further changes, thyroid hormones (triiodothyronine T3 and thyroxine T4) are formed from TG.
In the course of Hashimoto's disease, the level of anti-thyroid antibodies (anti-TPO and anti-TG) is increased.
2) Hormone levels:
◦ Thyroid stimulating hormone (TSH), produced by the pituitary gland and stimulating the secretion of thyroid hormones,
◦ Thyroxine T4,
◦ Triiodothyronine T3.
Typical for Hashimoto's syndrome is an increase in TSH levels and a decrease in the level of free thyroxine. In the advanced stage of the disease, the concentration of free triiodothyronine in the blood also decreases.

Ultrasound examination of the thyroid gland

The ultrasound image of the thyroid gland may vary depending on the severity of Hashimoto's inflammation. In the early stages of the disease, only the size of the gland is enlarged. In the next stages, the heterogeneity of the structure of the thyroid parenchyma with a decrease in its echogenicity can be noticed. There is also a fibrosis, the extent of which increases with the progression of the disease.

Thyroid scintigraphy

Scintigraphy is a complementary examination to the ultrasound of the thyroid gland. Iodine tracer uptake is heterogeneous in Hashimoto's disease. This fact is used in the differential diagnosis in the early stage of the disease, when hyperthyroidism is present - it allows to distinguish Hashimoto's syndrome from Graves-Basedow's disease.
Thyroid biopsy
If the ultrasound also shows the presence of nodules on the thyroid gland, your doctor may order a thyroid biopsy. The biopsy is performed under ultrasound guidance and involves taking a material for histopathological examination with a thin needle. In the course of Hashimoto's disease, there is a visible image of damaged epithelium, inflammatory lymphocytic infiltrates and fibroblast clusters. Hashimoto's disease increases the risk of thyroid cancer, so the appearance of a palpable lump in a person with Hashimoto's thyroiditis is an indication for extended diagnosis.

Hashimoto's disease - treatment

Pharmacotherapy is indicated in the case of symptomatic hypothyroidism and in the presence of elevated TSH levels with a reduced level of thyroxine. Compression symptoms resulting from excessive thyroid enlargement (goiter formation) may also be an indication for taking medications.
Drug treatment is based on the oral intake of levothyroxine tablets. Levothyroxine works in a similar way to thyroxine naturally synthesized in the body. Taking the drug prevents the secondary effects of thyroxine deficiency in the body. In young people, it is possible to reduce goiter after several months of treatment with levothyroxine. In the elderly, especially when the thyroid gland has numerous fibrosis, it is no longer possible to reduce the volume of the goiter.
Levothyroxine tablets should be taken on an empty stomach, at least half an hour before breakfast. The dose is always determined individually. In most cases, drug treatment must be carried out for life.
The use of immunosuppressants, e.g. glucocorticosteroids, is not recommended, mainly due to the low benefit-to-side-effects ratio. An exceptional situation is a hypometabolic crisis, which is life-threatening, when it is necessary to quickly stabilize the patient's clinical condition.

Hashimoto's disease - diet

People with autoimmune thyroid disease should pay close attention to their diet. The goal of the diet is to provide the necessary nutrients and compounds needed for the efficient synthesis of thyroid hormones. Due to the overweight often accompanying Hashimoto's disease, the caloric content of food should be monitored.
Hashimoto - substances desirable in the diet
People with Hashimoto's disease should ensure an adequate supply of:
1) Wholesome protein, because it is a building block of hormones (eggs, meat, sea fish),
2) Omega 3 fatty acids - stimulate the conversion of triiodothyronine into thyroxine (T3-> T4), omega 3 fatty acids also have anti-inflammatory effects (linseed oil, olives),
3) Vitamin D with anti-inflammatory properties (fish, oils, dietary supplements with vitamin D),
4) Iodine - iodine is a component of thyroid hormones (seafood, fish, iodized salt), it should also be emphasized that an excess of iodine can be as harmful to the thyroid as its deficiency,
5) Selenium - selenium is part of the enzymes influencing the thyroid hormone balance (shrimps, sardines, eggs, mushrooms).

Find out more - Hashimoto's diet.

Hashimoto's - what products should be limited?

Avoid excessive consumption of products containing goitrogenic substances. These substances bind to iodine and prevent it from attaching to particles of thyroid hormones. The products containing the goitreating substances include: green and black tea, soybeans, peanuts, red pepper, mustard.
Vegetables such as Brussels sprouts, cabbage, broccoli or spinach should be eaten cooked - this allows you to reduce the content of goitrogenic substances. You should not completely give up eating these vegetables as they are a valuable source of vitamins and minerals.
In the case of diagnosed intolerance to gluten or lactose, it is advisable to avoid products containing these substances.

FAQs:
1. How is Hashimoto's disease diagnosed?
Hashimoto's disease diagnosis includes:
• analysis of clinical symptoms (fatigue, dry skin, depression, slow heart rate, tendency to be overweight),
• imaging tests (ultrasound of the thyroid gland, possibly scintigraphy),
• laboratory tests (levels of TSH, thyroid hormones and anti-thyroid antibodies).
• in some cases, the doctor may decide to perform a thyroid biopsy followed by a histopathological analysis of the sample.
2. What is the treatment of Hashimoto's disease?
Treatment is undertaken in people with a deficiency of thyroid hormones shown in laboratory tests and in people with goiter causing oppressive symptoms. Treatment is symptomatic by taking drugs containing levothyroxine orally, which replaces the function of natural thyroxine.
3. What are the dietary recommendations for Hashimoto's disease?
The basis is a properly balanced diet, i.e. rich in substances that are the building blocks of hormones and compounds involved in the metabolism of thyroid hormones. Desirable ingredients in the diet of a person with Hashimoto's disease are: complete protein, omega-3 fatty acids, vitamin D, iodine, selenium. Avoid consuming highly processed products (cookies, sweets), which are high in calories and at the same time of poor nutritional value. It is also advisable to limit products rich in iodine-binding compounds, i.e. soybeans, tea (black and green), peanuts, mustard.

Thyroid diseases - check for symptoms

The thyroid gland is an endocrine gland at the front of the neck that releases hormones that regulate many important processes in the body. Hormones secreted by the thyroid gland (thyroxine T4 and triiodothyronine T3) affect, among others, on metabolism, water balance, and regulate the functioning of the nervous and reproductive systems. Symptoms associated with abnormal thyroid gland function are often ignored by patients. Sometimes thyroid symptoms are so nonspecific or masked by other conditions that patients are not at all aware that they may have thyroid problems. Meanwhile, thyroid disease can lead to many serious health complications. They are especially dangerous for pregnant women and for the baby developing in the mother's body. In addition, nodules may form within the thyroid parenchyma - some of them may be a sign of a malignant neoplastic process. How to recognize thyroid disease? What symptoms might suggest thyroid problems? We invite you to read the article below.

Make an appointment now - to a doctor who treats thyroid diseases at our hospital

Hypothyroidism

Hypothyroidism is a condition in which the thyroid gland produces too little thyroxine and / or triiodothyronine.

The causes of hypothyroidism

The most common cause of hypothyroidism is Hashimoto's disease, in which the immune system attacks its own thyroid gland, gradually destroying the thyroid parenchyma. Hashimoto's thyroiditis is a condition that mainly affects women. This is related to the role of the female hormones, estrogen, which are involved in modulating the inflammatory response at the level of the thyroid gland.
Another cause of damage to the thyroid parenchyma may be radioiodine therapy or radiation therapy to the neck area used in the treatment of cancer. Sometimes it is necessary to have a thyroidectomy (surgical excision of the gland), which completely deprives the body of thyroid hormones.
Iodine is a component of thyroid hormones, therefore iodine deficiency in the diet may result in their decreased synthesis. The production of thyroid hormones is also suppressed in the event of an overdose of iodine compounds.
Hormonal disturbances related to the hypothalamic-pituitary-thyroid axis (e.g. hypopituitarism, hypothalamic tumors) may also result in insufficient thyroxine production by the thyroid gland.

Symptoms of hypothyroidism

Hypothyroidism slows down the metabolic processes and reduces the excitation of the nervous system. In children, this can lead to mental retardation (called cretinism). In adults, the deficiency of thyroid hormones may be responsible for malaise, decreased concentration and psychomotor slowing down. Symptoms of a diseased thyroid are often explained by work, stress and general exhaustion - we rarely think that it may be a sign of a hormonal imbalance. Dry skin and brittle hair are often perceived only as a cosmetic problem, resulting from the wrong choice of cosmetics or insufficient care.
It often happens that the potential symptoms of thyroid disease in adults are analyzed only after the couple has been unsuccessfully trying to conceive for a long time (hypothyroidism negatively affects fertility). Before serious complications related to thyroid disorders occur, it is worth taking an interest in your own health and checking whether our ailments may be the result of thyroid disorders.

What symptoms might indicate an underactive thyroid?

Thyroid symptoms caused by hypothyroidism include:
- chronic fatigue,
- feeling cold in an environment with a neutral temperature,
- fatigue, drowsiness regardless of the number of hours slept,
- lack of concentration, dullness,
- bradycardia (low heart rate),
- swelling,
constipation
- dry skin
- excessive hair loss,
- difficulty in maintaining a healthy body weight, tendency to gain weight,
- irregular menstruation in women.
In some types of hypothyroidism (most often Hashimoto's thyroiditis), goiter is formed. An increase in the circumference of the neck is observed. An enlarged thyroid gland can compress adjacent structures and cause discomfort when swallowing.

How do you finally recognize hypothyroidism?

The symptoms of a diseased thyroid gland may coexist or be very similar to those resulting from other neurological or cardiological conditions.
In the case of hypothyroidism, a blood test of the thyroid gland shows an increased level of the thyroid stimulating hormone TSH secreted by the pituitary gland, as well as a decreased level of thyroxine T4. In advanced and untreated hypothyroidism, there is also a reduction in triiodothyronine levels. Your doctor may also perform an ultrasound to assess the structure and size of the thyroid gland.

Treatment of hypothyroidism

Treatment depends on the type of hypothyroidism. When hypothyroidism is due to damage to the thyroid gland, treatment is by taking orally medications that contain thyroid hormones. When the cause of the insufficient production of thyroid hormones is iodine deficiency, iodine supplementation is recommended.

Overactive thyroid gland

Hyperthyroidism is a condition in which thyroxine and triiodothyronine are produced by the thyroid gland in too large amounts.

The causes of an overactive thyroid gland

The most common causes of hyperthyroidism include:
excessive production of thyroid hormones by autonomic toxic nodules (secretion beyond the control of the pituitary gland),
Graves' disease (an autoimmune disease),
disorders of the hypothalamic-pituitary-thyroid axis,
hormone production by the placenta in pregnant women,
overdosing of orally taken drugs containing thyroid hormones
taking certain medications, e.g. lithium carbonates used in the treatment of mental disorders (relatively rarely).

Symptoms of an overactive thyroid gland

The effect of an overactive thyroid gland is called thyrotoxicosis (poisoning with excess thyroid hormones). The symptoms of thyrotoxicosis include:
nervous hyperactivity,
losing weight for no apparent reason,
excessive sweating
tachycardia (increased heart rate)
chronic diarrhea
more frequent urination, increased thirst,
possible muscle weakness,
menstrual disorders in women,
decreased libido in men.
In the case of Graves' disease, there may also be so-called thyroid ophthalmopathy - a feeling of distraction of the eyeballs, burning eyes, exophthalmia, visual disturbances (e.g. double vision).
Jak potwierdzić stan nadczynności tarczycy?
W badaniach laboratoryjnych (badaniach krwi) poziom TSH jest obniżony przy podwyższonym poziomie hormonów tarczycy (tyroksynie T4 i trójjodotyroninie T3). Następnie wykonywane jest badanie USG pod kątem obecności guzków i/lub stanu zapalnego w obrębie tarczycy. Badanie uzupełniające stanowi scyntygrafia, które polega na ocenie wychwytu jodu przez tarczycę. Guzki najbardziej wychwytujące jod to tzw. guzki gorące – są one odpowiedzialne za nadmierne wydzielanie hormonów tarczycy, niezależnie od stymulacji z poziomu przysadki mózgowej.

Treatment of an overactive thyroid gland

Treatment consists of:
taking medications that inhibit the secretion of thyroid hormones (so-called thyreostatic drugs),
taking beta-blockers,
destroying the nodules with radioactive iodine,
excision of a part of the thyroid gland along with nodules producing excess hormones.

Thyroid cancer

Lumps on the thyroid gland can be benign or malignant (cancer of the thyroid gland). The vast majority of detected nodules (approx. 95%) are benign changes. Some of the lumps can be easily palpated. Smaller nodules are only detectable on ultrasound. An indication for an ultrasound of the thyroid gland, in addition to palpable nodules, should also be an increase in the circumference of the neck. People with autoimmune thyroiditis should undergo regular ultrasound examinations, as chronic inflammation increases the risk of developing a malignant neoplasm.
Ultrasound examination of the thyroid gland allows us to initially distinguish benign lesions from potentially malignant nodules. Thyroid cancer is usually characterized by:
- clear borders of the nodule with an irregular "jagged" shape,
- the presence of calcifications within the nodule,
- heterogeneous structure of the inside of the nodule with no fluid content,
- a nodule with no increased flow, surrounded by an inflamed thyroid parenchyma, with a markedly increased flow.

Treatment of thyroid cancer

Treatment of a malignant thyroid gland may include:
- surgical excision of the nodule with part of the thyroid gland,
- total thyroidectomy,
- radioiodine therapy,
- taking medicines containing thyroid hormones (to prevent the effects of an underactive thyroid gland).

FAQs:
1.What causes thyroid disease?
In most cases, thyroid disorders develop due to autoimmune disorders, e.g. Hashimoto's disease causing hypothyroidism or Graves' disease causing hyperthyroidism. Environmental factors, diet and genetic predisposition play a role in the pathogenesis of thyroid diseases.
2. How to recognize thyroid disease?
Symptoms related to the abnormal secretory function of the thyroid hormones (hypothyroidism or hyperthyroidism) may be related to:
- acceleration or slowing down of the metabolic rate (losing weight or a tendency to gain weight),
- psychomotor disorders (slowness and depressive states or excessive psychomotor agitation),
disturbances in intestinal motility (chronic constipation or diarrhea),
fast or slow heart rate (bradycardia or tachycardia),
- menstrual disorders, infertility,
- cosmetic problems - excessive skin dryness, hair loss.
You should also be concerned about the swelling of the face or pain and bulging eyes. An enlarged neck circumference may indicate a pathological enlargement of the thyroid gland (goiter development). Palpable nodules on the thyroid gland are an indication for an ultrasound examination.
3. What doctor deals with the diagnosis and therapy of thyroid diseases?
The doctor to go to in case of suspected thyroid disease is an endocrinologist. If additional tests or procedures are required, the endocrinologist will refer the patient to a radiologist or general surgeon.

Sexual maturation is a period in the life of every human being, during which individuals of both sexes, through intensive morphological and physiological changes, achieve sexual maturity and reproductive capacity. Puberty is a term commonly used as synonymous with puberty, but it often carries additional information about changes in the cognitive, psychological and social spheres. Puberty is one stage in the lifelong evolution of the hypothalamic-pituitary-gonadal system.
In the pathology of this period, we distinguish two groups of disorders - premature puberty and delayed puberty.

Make an appointment now - to the doctor dealing with the treatment of delayed puberty at our hospital

Late puberty - what is it?

Delayed puberty has a statistical definition based on epidemiological studies. The onset of development, including growth closely related to maturation, takes place at different times and is influenced by genetic and environmental factors. In our latitude, we are talking about such a situation when the somatic and hormonal features of puberty are not present in girls over the age of 13 and boys are over 14, or menarche (first menstruation) does not appear before the age of 16. Puberty is also considered delayed when the first signs of puberty are timely but have not progressed since then. Patients may develop pubic and axillary hair because its development depends on the androgens produced by the adrenal glands.
Delayed puberty occurs in 3% of the population. It affects boys more often than girls and in most cases is a temporary disorder that resolves spontaneously over time and further sexual development is normal, leading to normal growth and fertility. A transient delay is understood to be a delay not exceeding 6 months at any stage of maturation. However, early diagnosis, causal treatment and stimulation of puberty in cases of organic causes of delayed puberty are essential in order to achieve normal puberty progression and proper final growth.

Delayed puberty may be a consequence of:
- constitutional growth and development retardation (KOWR) due to chronic diseases,
- impaired hormonal function of the gonads caused by their primary damage with secondary increases in gonadotropin levels (primary hypogonadism, hypergonadoropic hypogonadism),
- primary damage to the hypothalamic-pituitary system with a low concentration of gonadotrophins (secondary hypogonadism, hypogonadotrophic hypogonadism).

Constitutional Retardation of Growth and Development (KOWR)

This problem is the most common cause of delayed puberty. Untreated children begin puberty between the ages of 14 and 17 and reach normal final height. The maturation of the endocrine system is also delayed proportionally to the delay in the development of somatic features. Moreover, the basal concentration of gonadotrophins corresponds to the values ​​corresponding to the bone age of the 1st growth age.
Hypergonadotrophic (primary) hypogonadism
It is the lack of gonadal function during puberty or puberty caused by their damage on both sides. The ability of gonadoliberin and gonadotropins is not disturbed, and the lack of negative regulation of their secretion by the gonadal hormones is the cause of the excess of gonadotropins in the blood.
Hypogonadotrophic (secondary) hypogonadism
This is a lack of gonadal function due to a lack of gonadotrophin secretion. It is characterized by a reduced level of the pituitary gland hormones - follicle stimulating hormone (FSH) and luteinizing hormone (LH). Congenital isolated hypogonadotrophic hypogonadism is difficult to differentiate from constitutional growth and puberty retardation. It should be remembered that the analysis of the growth process is important here - in congenital isolated hypogonadism it is delayed until the chronological age, but adequate to the bone age.

Delayed puberty - classification of causes

Reasons for delayed puberty in girls:
I. Idiopathic (constitutional retardation of growth and development of KOWR).
II. Primary damage to the gonads (hypergonadotrophic hypogonadism):
- Turner syndrome: is the most common cause of primary hypogonadism in women. It is caused by the lack of one X chromosome or a disturbance of its structure (or both X chromosomes). The two main problems in this syndrome are growth retardation and a lack of puberty;
- enzymatic blocks for the production of estrogens,
- premature loss of ovarian function,
- damage to the gonads in the course of radio- or chemotherapy, as a result of inflammation, cancer or mechanical injuries.
III. Injury to the hypothalamus and pituitary gland (hypogonadotrophic hypogonadism):
- developmental defects of the central nervous system,
- Kallman syndrome: the most common form of isolated gonadotropin deficiency associated with an olfactory disorder. this disease is passed on as a dominant trait linked to the X chromosome;
- Prader-Willi syndrome: birth defect syndrome caused by a chromosomal aberration. The clinical picture of the disease includes: short stature, mental retardation, underdevelopment of the genital organs and obesity caused by a lower energy requirement than in healthy people, with a simultaneous constant unrestrained feeling of hunger;
- Laurence-Monn syndrome: an autosomal recessive disorder; In this syndrome, apart from short stature, there is a delay in intellectual development, retinitis pigmentosa and a delay in sexual maturation;
- idiopathic hypopituitarism,
- organic lesions of the hypothalamus and pituitary gland of neoplastic, inflammatory, vascular or traumatic origin.
IV. Functional hypogonadotrophic hypogonadism:
- disturbances in the body's energy balance (malnutrition, anorexia, excessive physical training),
- chronic diseases of the circulatory system and kidneys,
- absorption disorders,
- Hypothyroidism,
- debilitating mental illness.

Delayed puberty - diagnosis

The aim of the diagnosis of delayed puberty are measures aimed at assessing the degree of maturity (pubertal stage, determining the age of the skeleton) and explaining the causes of delayed sexual development.
The maturation scale should be used to assess the advancement of maturation. For this purpose, the methods used in auxology (the science of development) come to the rescue, which uses the following methods of assessing the course of puberty:
1) growth rate (percentile grids),
2) bone age,
3) evaluation of the pubertal stage according to the Tanner scale:
a) for pubic hair (pubarche) - 5 stages,
b) for axillary hair - 4 stages,
c) for the assessment of the development of the mammary glands (thelarche) - 5 stages.
In addition to the assessment of the degree of maturity, an interview should also be conducted:
family, taking into account the age of puberty of parents and siblings,
concerning health condition (past diseases, injuries),
concerning neurological symptoms (changes in behavior, changes in appetite, headache, fainting).
In the next stage of explaining the causes of delayed puberty in a child, the following are also important:- Laboratory tests:
basic: blood count, blood fall, GOT (glutamine-oxaloacetate transaminase), GPT (glutamine-pyruvate transaminase), yGT (γ glutamyl-transferase), AP (alkaline phosphatase), creatinine, total protein, IgA, celiac disease laboratory parameters, test urine,
- hormonal tests, which include, among others determination of the level of thyroid hormones (TSH, FT4), gonadotropins (LH and FSH), estradiol, prolactin, progesterone;
- dynamic hormone tests: GnRH stimulation test (gonadoliberin antagonist),
determination of sex chromosomes when Turner syndrome is suspected;
- picture diagnosis:
- ultrasound of the ovaries and uterus,
-RTG of the hand and wrist to determine bone age,
- magnetic resonance imaging of the head when lumpy lesions in the brain are suspected;
- molecular and genetic research have a special place. Karyotype testing should be considered in all children with delayed puberty.

Delayed puberty - treatment

Treatment of delayed treatment requires a precise diagnosis of the cause, assessment of bone age and psychological consequences for the patient and her family in order to select the best and most effective method of therapy and provide information on the course of the entire treatment process and its prognosis.

Treatment of constitutional growth and development retardation (KOWR)

Constitutional growth and maturation retardation do not require treatment. Untreated children achieve normal sexual development and final height according to their potential. However, in a situation where this leads to psychological conflicts related to reduced self-esteem in relation to properly maturing peers, pharmacological treatment with the use of low doses of sex steroids is recommended.
The aim of such treatment is to stimulate sexual maturation, but not to accelerate skeletal maturation. Girls can be given low, gradually increasing doses of estrogen over a period of about 6-12 months.

Treatment of primary and secondary hypogonadism

In all cases of hypogonadism, the aim should be to treat the underlying disease.
Therefore, in the treatment of primary hypogonadism, substitution of androgen preparations in the form of gels, tablet patches and intramuscular injections with prolonged action and short-acting preparations are used.
In the case of secondary hypogonadism, in some cases there is a chance of restoration of fertility as a result of the use of exogenous gonadotrophins (FSH, LH). Substitution with sex steroids is also used. Girls, after reaching the skeletal age of 12 years, are initially given low doses of estradiol which are gradually increased as prescribed by the doctor. After the development of secondary sexual characteristics (on average after 2-3 years), full cyclic estrogen-progestogen supplementation is introduced, which results in regular monthly cycles.
In girls with Turner syndrome, one of the main goals of treatment is to improve final height. Growth stimulation is achieved by administering synthetic growth hormone preparations by daily subcutaneous injections. Such treatment is carried out from around the age of 6 until skeletal maturity is 14 years old. In order to achieve optimal growth, estrogen substitution, followed by estrogen-progestogen substitution, is introduced later than in other cases of hypogonadism.

Source:
1. M. Pawlikowski, Endokrynologia, Wydawnictwo Lekarskie PZWL, Warszawa 2003
2. G. Jarząbek-Bielecka, R. Czepczyński, M. Pisarska-Krawczyk, W. Kędzia, P. Wojtyła-Buciora, Problem hypogonadyzmu ze szczególnym uwzględnieniem problemu u dziewcząt, Medycyna Rodzinna 2018; 21(1): 58-63
3. https://www.medme.pl/choroby/opoznione-dojrzewanie-plciowe,286.html
4. G. Jarząbek-Bielecka, E. Sowińska-Przepiera, A.Szafińska-Dolata, W. Kędzia, A. Kędzia, Hipogonadyzm hipogonadotropowy jako przyczyna opóźnionego pokwitania dziewcząt, Endokrynologia Pediatryczna, Vol. 13/2014 Nr 4(49)
5. https://www.mp.pl/pacjent/pediatria/choroby/endokrynologia/68501,opoznione-dojrzewanie-plciowe
6. G. Jarząbek-Bielecka, E. Sowińska-Przepiera, A.Szafińska-Dolata, W. Kędzia, A. Kędzia, Opóźnione pokwitanie dziewcząt, Endokrynologia Pediatryczna, Vol. 13/2014 Nr 3(48)
7. E. Krajewska-Siuda, E. Małecka-Tendera, Konstytucjonalne opóźnienie wzrastania i dojrzewania – trudności diagnostyczne i prognozowanie wzrostu, Endokrynologia Pediatryczna, Vol. 1/2003 Nr 3
FAQ

1. Is it possible to completely recover from delayed puberty?
Congenital or acquired damage to the pituitary or gonads is unfortunately a permanent feature and requires the constant administration of sex hormones. This procedure allows for the full development of external gender characteristics. Girls (with a preserved uterus) experience regular menstrual bleeding, but the prognosis of having children is very uncertain.

2. What is delayed puberty?
In our latitude, we refer to delayed puberty when somatic and hormonal features of puberty are not present in girls over the age of 13 and boys over 14, or menarche (first menstruation) does not appear before the age of 16. Puberty is also considered delayed when the first signs of puberty are timely but have not progressed since then. Patients may develop pubic and axillary hair because its development depends on the androgens produced by the adrenal glands.

Sexual maturation is a period in the life of every human being during which hormonal and somatic changes take place in the body, leading to sexual maturity and fertility. Sexual maturation is one stage in the lifelong evolution of the hypothalamic-pituitary-gonadal system.
The period of sexual maturation is characterized by two independent processes. The first is adrenarche, during which there is an increase in the activity of the adrenal glands in terms of secreting steroid hormones, and the second is gonadarche characterized by an increase in the activity of the gonads.
In the pathology of this period, we distinguish two groups of disorders - premature puberty and delayed puberty.

Make an appointment now - to the doctor dealing with the treatment of premature puberty in our hospital

Premature puberty - what is it?

Maturation is a very complex process influenced by a number of genetic, environmental and socio-economic factors (including nutritional status). The onset of sexual maturation in the hypothalamic-pituitary-gonadal endocrine system is considered to be the increase in the amplitude and frequency of pulsatile secretion of gonadoliberin (GnRH) after childhood rest. Activation of pulsatile GnRH secretion leads to an increase in the secretion of gonadotrophins by the pituitary gland, which stimulate the gonads to produce sex steroids and gametes. The term premature puberty in our latitude describes the appearance of puberty (secondary sexual characteristics) before the age of 8 in girls and 9 years in boys.
Premature puberty may be of central (gonadotropin-dependent) origin associated with the early activation of the hypothalamic-pituitary axis or peripheral (pseudo) without activation of this axis.
Central precocious puberty (true, GnRH-weighted) is when a child of a younger than normal age for the onset of puberty presents with the same symptoms and in the same sequence as during true puberty. Breast and pubic hair development and growth acceleration occur in a similar sequence to normal puberty, except that they occur earlier in life. It is related to the earlier activation of areas in the brain responsible for the control of the ovaries and testes (activation of the gonadal axis).
Peripheral premature puberty (pseudo-GnRH-independent) is when the body begins to produce sex hormones without stimulating the gonadal axis described above. Typically, pubic and axillary hair develops with epidermal acne symptoms, behavioral difficulties, and growth acceleration with bone maturation. Such changes may appear in connection with congenital disorders of the adrenal glands or even neoplastic processes within the adrenal glands or gonads.

In addition to the above-mentioned forms of premature puberty, there are also mild variants of it. These are:
A) adrenarche praecox- is associated with the activity of the adrenal glands. It can occur in both girls and boys and is associated with slightly increased body hair, acne or a change in the smell of sweat;
B) thelarche praecox - isolated breast enlargement, that is, one that is not accompanied by other symptoms of puberty or increased hormone secretion;
C) menarche praecox - premature first menstruation that occurs as a result of the increase in the sensitivity of the endometrium to estrogen levels after activation of the hypothalamic-pituitary-ovary axis, where estrogen levels are too low to cause other pubertal symptoms.

In all cases of premature puberty, an appropriate and, above all, prompt intervention of an endocrinologist is required to establish the causes and initiate possible timely treatment.

Premature puberty - symptoms

The symptoms of premature puberty are:
- premature development of secondary sexual characteristics (in girls, the first symptom is usually enlargement of the nipples),
- acceleration of the growth rate inadequate to the chronological age,
- acceleration of skeletal growth and maturation,
- low final height,
- incorrect body proportions,
- psychosexual development in line with chronological age,
- additionally, there may be acne, oily hair and "puberty" smell of sweat.

Premature puberty - causes

There are many causes of premature puberty, and they should be divided into gonadotropin-dependent and non-gonadotropin-dependent causes.

Premature puberty GnRH-dependent (central):
- intracranial tumors,
- malformations of the central nervous system (neurofibromatosis),
- irradiation of the skull,
- increased intracranial pressure (idiopathic, post-traumatic, post-inflammatory),
- organic changes in the central nervous system as a result of compression, disruption or other damage by a tumor to the nerve pathway that inhibits GnRH secretory neurons.

Premature puberty GnRH-independent (peripheral, pseudo):
- ovarian and / or adrenal gland tumors secreting estrogens,
- exposure to exogenous estrogens (iatrogenic form),
- primary hypothyroidism,
- McCune-Albright syndrome,
- congenital adrenal hyperplasia,
- adrenal gland tumors,
- adenomatous bilateral adrenal hyperplasia,
- ovarian tumors,
- exposure to exogenous androgens (iatrogenic form).

In mild types of premature puberty (adrenarche, thelarche, menarche), medicine does not yet provide a clear answer to the question of their cause.

Premature puberty - diagnosis

In the first stage of the diagnosis of premature puberty, the methods used in auxology (the science of development) are used, which use the following methods of assessing the course of puberty:
1) growth rate (percentile grids),
2) bone age,
3) evaluation of the pubertal stage according to the Tanner scale:
a) for pubic hair (pubarche) - 5 stages,
b) for axillary hair - 4 stages,
c) for the assessment of the development of the mammary glands (thelarche) - 5 stages.

In the history differentiating premature puberty, the period when the first symptoms of premature puberty appeared and how quickly they were building should be taken into account in particular. Additionally, interviews should be conducted:
family, taking into account the age of puberty of parents, siblings,
concerning the intake of exogenous hormones,
concerning health condition (past diseases, injuries),
concerning the neurological symptoms (changes in behavior, changes in appetite, headache, visual disturbances, seizures, fainting).

In the next stage of searching for the causes of premature puberty, the following are also important:
- Laboratory tests:
- hormonal tests, which include, among others determination of the level of gonadotropins, sex steroids, adrenal androgens, thyroid hormones, prolactin, progesterone;
- dynamic hormone tests used to detect enzyme deficiencies: GnRH stimulation test, ACTH test (adrenogenital syndrome), dexamethasone test (adrenal tumors);

- and imaging diagnostics:

- pelvic ultrasound to assess internal genitalia,
- ultrasound of the adrenal glands,
- X-ray of the skull,
- magnetic resonance imaging of the skull,
- computed tomography of the above-mentioned organs,
- in some cases also EEG and other tests ordered by a doctor.

Premature puberty - treatment

There are many causes of premature puberty, which are best categorized as gonadotropin dependent and independent. Such classification helps in understanding the etiology of the disorder and in making decisions about the choice of treatment.
The general goals of treating premature puberty include:
• remission or inhibition of the progression of physical symptoms and hormonal changes,
• inhibition of the rapid progression of skeletal maturation,
• achieving normal final height and correct body proportions,
• future fertility,
• reduction of the increased risk of breast cancer (in case of early menarche),
• preventing the emotional effects of premature puberty.

In the case of central premature puberty (GnRH-dependent), treatment consists of administering drugs (GnRH analogues) aimed at suppressing the activity of the gonadal axis, which stops the maturation process until the child reaches such an age and such emotional maturity, that maturation can take place.
In alleged precocious puberty (GnRH-independent), management depends on the underlying cause. Here it becomes important:
- treatment of the underlying disease of the central nervous system (central nervous system malformations),
- treatment of primary hypothyroidism,
- surgical treatment of the ovaries, adrenal glands (adrenal tumors, ovarian tumors)
- the use of antigonadotrophins, i.e. progestogen-like drugs that inhibit the development of gonads.

In mild types of premature puberty (adrenarche, thelarche, menarche), medicine does not yet provide a clear answer to the question of their cause. Therefore, these types of disorders of the maturation process are only subject to periodic medical observation, do not require treatment and do not affect the future life and development of girls.

Source:
1) Izabela Rogozińska, Przyczyny przedwczesnego dojrzewania – co nowego?, Postępy Nauk Medycznych, t. XXVII, nr 10B, 2014
2) Barbara Garanty-Bogacka, Teresa Adamczyk, Małgorzata Syrenicz, Maria Ginalska-Malinowska, Ewa Małunowicz, Mieczysław Walczak, Adrenarche praecox u 5-letniej dziewczynki z rodzinnie występującym niedoborem dehydrogenazy 3β-hydroksysteroidowej, Endokrynologia Pediatryczna, Vol. 2/2003 Nr 3(4)
3) Jarząbek-Bielecka Grażyna, Warchoł-Biedermann Katarzyna, Sowińska Elżbieta, Wachowiak-Ochmańska Katarzyna, Przedwczesne dojrzewanie płciowe, Ginekologia Polska, 2011, 82, 281-286
4) https://www.juniorowo.pl/przedwczesne-dojrzewanie/
5) Grażyna Jarząbek, Michał Pawlaczyk, Zbigniew Friebe, Przedwczesne pokwitanie dziewcząt, Seksuologia Polska 2005, 3, 1, 29.31

FAQ

1. What features of puberty in a girl might suggest precocious puberty?

In girls, the first sign of puberty is an enlargement of the mammary glands, which may initially affect only one of them. Additionally, the hair on the pubic mound or in the armpits that appears a little later is noteworthy. It is often accompanied by growth acceleration and a change in the smell of sweat, and sometimes with the appearance of seborrheic changes on the face.
When these features appear in a girl before the age of 8, they may suggest premature puberty.

2. Is it possible to cure premature puberty completely?
Treatment of premature puberty of hypothalamic origin ends when the child reaches the physiological age of puberty. Lifetime treatment is required for premature puberty associated with adrenal disease. Nodular gonadal lesions require surgical treatment. Small nodules in the hypothalamus can only be monitored with MRI every 6–12 months.