Systemic support in hair formation and growth in cases of alopecia and hair shaft diseases

When approaching the problem of hair diseases, one cannot help but start with an assessment of the physiology of hair growth and its chemical composition. The physiological change in hair manifests itself in daily diffuse hair loss.

The constant growth and change of hair consists of three phases: anagen (active growth), catagen (separation from the hair papilla) and telogen (rest). The rate of hair growth has its own rhythm. In old age, this rhythm is disrupted and differs significantly from the hair change of a young person. In addition, it should be taken into account that the thickness, composition and density of hair in an elderly person changes with age, which can already begin at the age of 55–65 years. During the anagen phase, the formation of the hair shaft occurs. Normally, on the scalp, where long hair is predominantly located, the anagen period lasts from 3 to 7 years. In a child, the relatively short anagen period contributes to the formation of vellus blond hair. The next phase (catagen) lasts 2–3 weeks, and the resting phase (telogen) lasts approximately 100 days. Metabolically, the telogen follicle is inactive. There are approximately 100 thousand hairs on the scalp.

During a given period of time, 5-20% of hair is in the telogen phase, which leads to 50-100 hairs falling out daily, that is, 80-95% of hair is in the anagen phase, and 1% of hair is in the catagen phase. Thus, when assessing the condition of hair in pathology, the doctor must rely on an understanding of the norm. Number of hairs per 1 cm2 of skin: on the scalp – 346–400, on the stomach – 52–99. Long hair grows at a rate of 0.1–0.5 mm per day. Thus, within a month it can lengthen by 3–15 mm. The growth rate of long hair and the area it occupies reaches a maximum until 30–35 years of age. The lifespan of each hair ranges from 50 days to several years. Mostly scalp hair grows for 2–4 years, and eyelashes – 3–4 weeks.

According to the classification, hair diseases are divided into congenital and acquired, into cicatricial and non-scarring alopecia, into focal and diffuse alopecia. Separately, it should be noted such an important group of pathologies as hair shaft disease. If we dwell on a separate topic - focal and diffuse (anagen, telogen and androgenetic) alopecia, it should be emphasized that even with these pathologies, it is imperative to take into account that an important component of treatment is to support the structural development of hair. To a greater extent, this also applies to diseases of the hair shaft.

For hair formation in hair follicles, an appropriate concentration of amino acids is required. It is this factor that presupposes their supply from the outside, which in the case of pathology must be provided with appropriate medications.

Diffuse hair loss is a symptom included in some nosological forms of alopecia.

It is known that diffuse hair production is characteristic of such clinical diagnoses as acute or chronic telogen effluvium, anagen effluvium, androgenetic alopecia, and a number of genetic diseases.

Anagen alopecia can be a sign of various intoxications (poisoning with heavy metal salts, taking medications such as anticoagulants, cytostatics, borates, thyreostatic and cholesterol-lowering drugs, hypervitaminosis). These substances inhibit mitosis of hair follicle papilla cells. A classic example of the cause of anagen alopecia is the systematic use of medications and radiation therapy in the treatment of cancer. When the metabolic and mitotic activity of the follicular epithelium suddenly declines, the hair shaft becomes thinner and narrower at the end. In this case, the distal part of the thinned shaft breaks, and the hair itself falls out of the follicle. Unlike telogen effluvium, anagen effluvium does not have a 3-month period before the onset of hair loss. A characteristic feature of the clinical course of anagen alopecia is that hair loss occurs very quickly.

In the absence of these factors, we can talk about idiopathic cases, which involve generalized forms of diffuse hair growth in middle-aged women related to chronic baldness. If a significant amount of hair enters the catagen phase prematurely, then alopecia appears after 2–3 months. This alopecia is called telogen effluvium and quite often develops after childbirth or a serious illness, which is prolonged up to several months, and, as a rule, ends with complete recovery after the cause is eliminated. The term “telogen effluvium” refers to the loss of unaltered hair due to the premature transition of the hair follicle from the anagen stage to the telogen stage. The etiological components of telogen effluvium are as follows: firstly, metabolic disorders, and secondly, physiological factors. In the first option, many hairs suddenly go into the catagen phase, and then into the telogen phase.

Chronic telogen effluvium in women is often confused with androgenetic alopecia, in which frontoparietal alopecia is usually observed. In patients with telogen effluvium, the telogen count rarely exceeds 50%. During treatment for telogen effluvium, first of all, you should stop medications that could be causing hair loss, plan detoxification therapy, prescribe hepatoprotectors and a complex drug responsible for restoring hair structure.

Androgenetic alopecia is characterized by baldness in the frontal and parietal areas in men, a decrease in the amount of hair in these areas in women, which is associated with a genetically determined disorder of androgen metabolism in the scalp. Androgenetic alopecia is an autosomal dominant disorder with variable penetrance in men and women equally. Progressive hair loss leads to gradual miniaturization of the hair follicle and a shortening of the anagen phase. Dihydrotestosterone, formed in the keratinocytes of the hair follicle from testosterone under the influence of the enzyme 5-alpha reductase, activates the sebaceous glands in target tissues, but at the same time inhibits metabolism in the hair follicles. Dihydrotestosterone affects the growth phase of the hair follicle (anagen) so that the hair prematurely enters the resting phase (telogen). In recent years, among women there has been an increase in the number of cases of androgenetic alopecia, which has a male pattern and clinical manifestations. The share of this type of alopecia is 90% of all baldness in women. A significant number of modern studies have shown a connection between androgenetic alopecia and metabolic syndrome. A comparison was made of lipid markers (cholesterol, triglycerides, low-density lipoprotein) in patients with androgenetic alopecia compared with healthy people. Information was obtained on the pathophysiological mechanism, which involved the association of alopecia with dyslipidemia.

The most common form of non-scarring alopecia is alopecia areata , a disease of unknown etiology. This disease occurs in all age groups, in 46% it has a tendency to spontaneous regression, but in other cases it progresses, turning into a total and even universal form. The disease quite often occurs suddenly against a background of stress; in some patients, it has a persistent course in the presence of chronic infections, hormonal abnormalities, and neurohumoral diseases. Today they are inclined to recognize the autoimmune nature of alopecia areata and the disruption of the hypothalamic effect. In addition to hair loss, in some cases one can note a significant change in the structure of the hair, characterized by thinning and fragility. In assessing hair pathology, knowledge of the normal structure of hair and its chemical composition plays a significant role. The hair follicle is represented by undifferentiated epithelial cells, where mitosis is constantly realized and cells are formed, due to which hair growth occurs and the cells of the internal epithelial container are renewed. It is known that all restored tissues contain stem cells. These cells have several characteristics - they are relatively undifferentiated, have sufficient capacity, and they are usually located in well-protected and well-vascularized areas. The location of stem cells within the hair follicle is a matter of debate, but a partial presence in the outer root receptacle is indicated below the levator pili muscle region.

A bulge appears embryonically, from which hair develops, and above this bulge a sebaceous gland is formed. Embryonic basal cells of this zone have been shown to express keratin 19. The concept that stem cells are located in the area of the protrusion explains some aspects of follicular pathology. Thus, with focal alopecia in the area of protrusion, the inflammatory infiltrate forms around the hair follicle, and with cicatricial alopecia, the infiltrate is concentrated in the upper part of the follicle, at the site of muscle attachment, in particular the zone of conditional location of stem cells.

Keratins are a group of insoluble cystine-containing helicoid protein complexes that produce epithelial vertebral tissues. The main permanent component of hair is keratin, which is a protein substance rich in sulfur (4–5%) and nitrogen (20%). Hair keratin contains cystine in amounts ranging from 11.5 to 17%. With age, the amount of cystine increases, and the breakdown products contain leucine (14%), glutamic acid (12%), and tyrosine (2%). Like the stratum corneum of the epidermis, hair keratin is highly resistant to enzymes, alkalis, acids, etc. Chemically, hair contains about 5% sulfur and pure ash, 20% silicon and 10% iron. 1 gram of dry hair contains in milligrams: nitrogen - 150, sulfur - 50, phosphorus - 0.15, sodium - 0.37, calcium - 0.13, magnesium - 0.12, iron - 0.08, manganese - 0.005, copper – 0.01.

Thus, it is necessary to draw a general conclusion that the main structural protein of horny hair cells and horny cells of the epidermis is keratin, the chemical structure of which is made up of amino acids.

Hard hair keratin has a higher level of sulfur-containing amino acids and disulfide bonds. Hard keratin hair is divided into low sulfur keratins, high sulfur keratins and high glycine keratin keratins.

The protein of trichohyalin granules is rich in citrulline, but unlike keratohyalin, it has an increased content of glutamic acid and a decreased content of cysteine.

Having focused on the chemical component of hair, it should be noted that today extremely interesting information has accumulated about the structure of hair itself. The hair shaft primarily consists of an amorphous matrix (with a high content of sulfur and ultra-high content of sulfur proteins), penetrated by keratin fibers. The stability of these protein complexes is ensured by dense keratins in hair, in contrast to the soft, flaky keratins of such tissues.

In the cells of the medula (brain part of the hair) in the suprabulbar part there are microfields outside the cytoplasm. Medulla cells contain glycogen and may contain melanosomes. Above the epidermal level, the cells dehydrate and the vacuoles become filled with air. Protein compositions in the medulla contain trichohyalin. The role of the medula is not fully understood. It is not always that the medula degenerates and becomes air-containing; this can be observed in thicker hair.

In the cortical part of the hair, cystine chains arise as a result of the sulfhydryl reaction. In hair, unlike the superficial epidermis and hair receptacle, keratohyaline granules do not always appear.

The hair cuticle consists of 5–10 layers layered on top of each other, each 350–450 microns thick. As the hair emerges from the surface of the skin, the cuticle gradually becomes jagged and suddenly breaks. The outer part of the hair has a layer with a high sulfur content. External influences on the cuticle cells of the hair shaft lead to premature breakage through chemical and physical insults.

The purpose of the study is to increase the effectiveness of therapy for patients with various forms of alopecia by adding to the treatment complex a drug that is a source of sulfur and has a positive effect on the structure of the skin and its appendages.

We observed 22 patients aged from 14 to 36 years with various hair diseases (10 patients with focal alopecia, 2 patients with anagen effluvium, 2 with telogen effluvium, 5 with androgenetic alopecia, 1 was diagnosed with trichorrhexis nodosum, in 2 the duration of the pathological process in patients did not exceed 3 years, such qualitative characteristics of hair as thickness, fragility, elasticity, and dullness were assessed.

The drug “Natubiotin” was added to the therapy algorithm, which has a significant effect on the hair structure.

"Natubiotin" primarily compensates for the deficiency of sulfur-containing amino acids in the body. Activation of metabolism changes intracellular redox processes in the cells of the hair follicle, which leads to a decrease in the susceptibility of the receptor apparatus of follicle cells to negative endogenous influences.

The following active components are known in Natubiotin : biotin, lactose, crospovidone, povidone K30, magnesium stearate. Biotin (vitamin H, vitamin B7) is a water-soluble B vitamin.

In the body, biotin plays an important role in the metabolism of carbohydrates, fats, proteins and is vital for normal cell growth and development. Biotin is a vital substance for cell development and growth.

It should be remembered that the cells of the hair follicle must be in a process of constant growth and renewal. Biotin also helps stabilize blood sugar and improves the function of the nervous system.

Biotin is a synergist with other B vitamins - folic acid, pantothenic acid, cyanocobalamin.

There is evidence of the participation of biotin in the synthesis of purine nucleotides; it is also a source of sulfur involved in the synthesis of protein - collagen and, thus, has a positive effect on the structure of the skin and its appendages (hair, nails). In this material, we quite clearly described the role of sulfur in building a normal hair structure.

As a coenzyme, biotin plays an important role in gluconeogenesis, lipogenesis, biotransformation of propionates, synthesis of fatty acids in the breakdown of leucine. Biotin deficiency can occur due to an unbalanced diet. Biotin deficiency also manifests itself as a reaction on the skin and appendages, and it can become one of the components of hair diseases.

Natubiotin is a reasonable drug in the treatment algorithm for a number of hair shaft diseases (trichoptilosis, tricoshiasis, trichothiodystrophy, trichorrhexis nodosum, moniletrix, trichoclasia), in which sulfur deficiency plays an important role. The occurrence of pathology of the hair structure remains, unfortunately, beyond the attention of the dermatologist. And at the same time, it is precisely these diseases that require the use of a systemic drug such as Natubiotin. Natubiotin is prescribed for 4–6 months, 1 tablet 5 mg 1–2 times a day.

Research results . For anagen alopecia, the drug was prescribed simultaneously with detoxification therapy. Patients took the drug for 1–4 months.

For patients with alopecia areata , Natubiotin was prescribed along with physiotherapy and cryotherapy. This course justified itself, and in the dynamic observation a stable positive effect was noted.

Three patients with total alopecia were prescribed Natubiotin in justified systemic therapy along with small doses of methylprednisolone.

For androgenetic alopecia, Natubiotin helped strengthen the structure of miniaturized hair.

The use of Natubiotin in complex therapy has made it possible to obtain significant positive results in the treatment of disorders of the hair shaft structure. This was a sick 15-year-old girl, who, during a detailed examination (clinical picture, trichoscopy, hair microscopy), was diagnosed with trichorexis nodosum. After a 2-month course of “Natubiotin” with topical use of emollient therapy, hair fragility stopped. Microscopy of the hair significantly improved the structure (splitting and unevenness of the surface disappeared).

Conclusions. The use of “Natubiotin” in combination with emollient external agents and shampoos allowed us to obtain a positive result in the form of strengthening hair, restoring its quantity in case of telogen effluvium and anagen effluvium. This indicates the effect of “Natubiotin” on improving hair structure and allows us to recommend involving in the treatment of patients not only with various clinical forms of alopecia, but also with trichotylomania. This position is based on the fact that ordinary hair pulling is certainly stressful for the hair follicle and the disease requires systemic support, since Natubiotin has a neurostabilizing effect. Thus, knowledge of hair pathology and the ability to make a differential diagnosis allow the doctor to plan reasonable, adequate treatment for hair diseases.