Causes and treatment of acne on the forehead, face and body in men: useful tips

Pimples on the scalp in the hair are a very common occurrence. Unfortunately, it is usually not given importance, since the rashes are hidden behind the strands. As a rule, the patient turns to a specialist only when the problem becomes widespread. However, it should be remembered that treatment in this case turns out to be much more complex and lengthy.

What is acne

The content of the article

Acne occurs due to clogged sebaceous glands and excessive sebum production. This fat makes human skin more elastic, protects against drying out of the skin, promotes the process of skin thermoregulation and protects against the penetration of many viruses and infections into the body.

In the case of an increase in androgens (male sex hormones), the secretion of sebaceous secretions increases. The disease most often occurs in young men under twenty years of age. However, it can also appear at a later age due to metabolic disorders.

Skin manifestations of pathology of the digestive organs

The skin and digestive organs are in close relationship, the roots of which lie in the same origin during embryogenesis, common barrier functions, including the formation of an immune response, as well as interaction with the microflora associated with these organs. The condition of the skin largely reflects the condition of the digestive organs, however, the relationship between pathological processes in these organs can be diverse: 1) skin damage can be directly caused by dysfunction of the digestive organs; 2) skin lesions may have a common pathogenesis with diseases of the digestive organs, precisely established or suspected, and these processes occur in parallel.

The idea that dysfunction of the digestive organs naturally affects the condition of the skin, although it has been in the air for thousands of years, was first formulated in the medical literature by William Hillary in 1759 [1] and developed by A. Whitfield. The latter introduced the concept of “dermatitis colonica” in 1932 [2], and one of the first detailed reviews on the effect of impaired intestinal absorption on the skin condition was published by GC Wells only in 1962 [3].

Malabsorption of macro- and micronutrients with the development of their deficiency in the body in various diseases of the gastrointestinal tract (GIT) is obviously reflected in the condition of the skin. Most often they are observed with skin changes due to impaired intestinal absorption, which is caused by malabsorption of zinc, copper, iron, vitamins A and PP. The development of purpura can also be included in the same category as a manifestation of hemocoagulopathy due to impaired absorption of vitamin K. Selective deficiency of a particular nutrient is usually associated with a congenital defect of the corresponding intestinal transport system, while combined disorders of intestinal absorption are more often observed with generalized intestinal damage (congenital or acquired), for example, with celiac disease or short small bowel syndrome. The nature of skin damage due to deficiency of certain vitamins is given in Table. 14].

A striking clinical manifestation of the skin is impaired intestinal absorption of zinc. In general, the causes of zinc deficiency in the body can be its lack of nutrition (for example, with irrational artificial feeding), various intestinal diseases, especially those accompanied by diarrhea, as well as a congenital defect in its intestinal absorption (acrodermatitis enteropathica).

The absorption of zinc in the intestine is closely related to the nature of motility and easily develops in the case of diarrhea of ​​any origin. Thus, it has been shown that diarrhea in children under 1 year of age lasting more than 10 days is always accompanied by the development of zinc deficiency [5], and in older children, diarrhea lasting more than 14 days can lead to this condition [6]. At the same time, accelerated intestinal motility, disrupting the absorption of zinc, contributes to the loss of zinc entering the intestinal lumen with the secretions of the digestive glands. In addition, zinc deficiency leads to dysfunction of enterocytes, which in turn aggravates its malabsorption. A decrease in immune functions due to zinc deficiency favors the course of the infectious process and also aggravates diarrhea [7]. Zinc deficiency and impaired enterocyte function contribute to malabsorption of other nutrients, particularly sodium and water [8]. It is also interesting that zinc deficiency leads to a decrease in appetite as a result of a decrease in the expression of neuropeptide Y receptors in the hypothalamus and thereby contributes to a decrease in food intake [9].

Acrodermatitis enteropathica (Brandt syndrome) is characterized by a congenital disorder of zinc transport across the apical membrane of the enterocyte. The disease is transmitted in an autosomal recessive manner and is clinically manifested by a characteristic skin syndrome (skin lesions in the form of vesiculobullous rashes on the distal parts of the limbs and around natural openings), diarrhea and alopecia. The disease manifests itself after stopping breastfeeding, since human milk is an important source of zinc for the child during this period of life, with the gradual development of the main symptoms of the disease, delayed psychomotor development, and a decrease in resistance to infectious diseases. The latter is due to the significant role played by zinc in the function of the immune system, antioxidant protection, and even some direct anti-infective effects of this microelement. A condition similar to enteropathic acrodermatitis can also develop secondary to severe atrophy of the mucous membrane of the small intestine, primarily with celiac disease. In both cases, eliminating zinc deficiency requires the administration of drugs containing it.

Another selective defect is observed in Menkes disease, which is based on a violation of the cellular transport of copper in the intestine. In this case, there is a slowdown in growth, a pathology of the nervous system, as well as a characteristic curling of the hair, which is why this disease is called “curly or steel hair disease.” The disease is associated with mutations in the ATP7A gene, which encodes a Cu(2+)-transporting ATPase involved in the processes of intestinal absorption of copper.

The disease manifests itself in the neonatal period, and the first symptoms may be: hypothermia, hyperbilirubinemia, and delayed physical development. Some patients experience the formation of hair nodules (trichorexis nodosa), etc. spindle-shaped hair (monilethrix). In addition, seborrheic dermatitis may occur. During the first half of life, growth retardation, delayed psychomotor development and neurological disorders gradually progress with the loss of skills acquired in the first months of life, various types of epileptic seizures appear (focal, generalized, myoclonic) with the subsequent formation of spastic tetraparesis. Trichopolydystrophy develops: hair is matted, dull, hard, gray or ivory-colored.

The development of subdural hemorrhages and thrombotic disease is possible. Angiography in the brain, internal organs, and limbs reveals elongated, tortuous, varying-caliber arteries with alternating areas of expansion and narrowing. In addition, urinary tract diverticula may be identified, predisposing to urinary tract infections. Pathological fractures of the ribs, diffuse hypopigmentation of the skin, as well as signs of connective tissue dysplasia: hyperextensibility of the skin, hypermobility in the joints are often observed.

The diagnosis is made on the basis of a decrease in the level of copper and ceruloplasmin in the blood serum, low copper content in the liver biopsy and high copper in the intestinal mucosa and cultured skin fibroblast cells. Treatment is based on copper replacement therapy.

The following are skin diseases described in combination with celiac disease, a disease with generalized intestinal malabsorption (Table 2) [10, 11]. Some of them are due to malabsorption of macro- and micronutrients, another part is due to increased intestinal permeability against the background of the atrophic process and an increased risk of an allergic process, and the third part is due to an autoimmune process in the skin, which can be considered as a manifestation of the underlying pathological process. Dermatitis herpetiformis requires special discussion, which has much in common with celiac disease, but also has significant differences.

General mechanisms of damage to the skin and digestive organs are also observed quite often, for example, in various immunopathological processes. At the same time, dysfunction of the gastrointestinal tract and, in particular, malabsorption syndrome aggravate the course of the skin process with the participation of the mechanisms described above.

In food allergies, as a rule, several body systems are simultaneously involved: skin (atopic dermatitis), gastrointestinal tract (eosinophilic esophagitis, gastritis, enteritis, colitis), respiratory organs (allergic rhinitis, bronchial asthma) [12]. In recent years, food allergies have been given importance in the development of irritable bowel syndrome. One of the points of intersection of these diseases is visceral reception, which, on the one hand, is modulated by central nervous influences, and on the other hand, by the so-called. inflammation of low activity in the intestinal mucosa, the main role in the development of which is played by degranulation of mast cells. The latter can be caused by various mechanisms, including atopic ones [13].

In systemic autoimmune connective tissue diseases, combined damage to the skin and gastrointestinal tract is often observed. Thus, with systemic scleroderma, characteristic skin changes are combined with impaired motility of the esophagus and dysphagia, impaired motility of the small intestine and intestinal obstruction of varying severity, as well as the syndrome of impaired intestinal absorption [14–18]. With systemic vasculitis and rheumatoid arthritis, parallel damage to the arteries in various organs and systems occurs, but subsequently the malabsorption caused by this process aggravates skin changes.

Inflammatory autoimmune bowel diseases, ulcerative colitis and Crohn's disease are also characterized by skin lesions in some patients. They are often associated with erythema nodosum and pyoderma gangrenosum, which have the same pathogenesis as the main disease and are observed in approximately 3–12% of patients [19–21]. Erythema nodosum manifests itself as painless, red, subcutaneous nodules on the extensor surfaces of the extremities, and its activity corresponds to the activity of the underlying disease [22]. Biopsy reveals focal panniculitis. Erythema nodosum responds well to treatment with glucocorticoid drugs, and in resistant cases with infliximab [23, 24]. Pyoderma gangrenosum is characterized by severe ulceration, lack of parallelism with the severity of the disease and poses a serious challenge in terms of treatment therapy. A biopsy reveals a sterile abscess. Treatment requires the use of high doses of glucocorticoids, as well as cyclosporine, tacrolimus, mycofenrolate mofetil, and infliximab [23–26].

The development of erythema nodosum in Crohn's disease is due to an underlying granulomatous inflammatory process, and the development of severe pyoderma gangrenosum is due to inadequate antimicrobial protection, perhaps partly related to a decrease in the production of defensins in the skin (as is observed in the intestines).

Other cutaneous manifestations of inflammatory bowel disease include aphthous stomatitis, which usually responds well to steroid medications [27, 28].

A separate group consists of diseases in which persistent associations between intestinal pathology and changes in the skin are observed, although the mechanism of this association remains unidentified. An example of such a disease is Peutz-Jeghers syndrome.

This disease was first described by the Danish pediatrician Y. Peutz in 1921. Under his supervision there was a family whose members had a combination of skin pigmentation with polyposis of the small intestine. A similar observation was presented in 1949 by H. Jeghers [29].

Peutz-Jeghers syndrome is a congenital disease, transmitted in an autosomal dominant manner, characterized by pigmentation of the skin and mucous membranes in combination with polyps of the gastrointestinal tract. Pigment spots with a diameter of 1–5 mm usually appear in the first years of life, although they are also described in newborns, located around the mouth, nasal openings, on the buccal mucosa, on the hands and feet. Perianal and perigenital localization is less common. Interestingly, spots located around the mouth and nose do not disappear over time, while the severity of spots in other locations may decrease during puberty. Polyps are most often detected in the jejunum, but are also found in the stomach, duodenum, and colon. Polyps can cause intestinal obstruction, bleeding, and they can also become malignant. The prevalence of the syndrome is 1:120,000 live births [30], with no sex differences [31]. Its development is associated with a mutation in the STK11 (LKB1) gene localized on chromosome 19 p13.3 [32].

The STK11 gene encodes serine-threonine kinase, a modulator of cell proliferation that plays a significant role in preventing the development of tumors [33]. In this regard, the enzyme encoded by STK11 inhibits AMP-activated protein kinase and, indirectly, the mTOR signaling pathway (mammalian target of rapamycin) [34], disturbances of which have been identified in patients with Peutz-Jeghers syndrome [35].

Pigment spots are caused by an increased number of melanocytes in the area of ​​the dermoepidermal junction (dermoepidermal junction) with an increase in the content of melanin in the basal cells. Polyps of the gastrointestinal tract are hamartomas, consisting of normal tissue of an organ, but with a disturbed architecture. Polyps in this syndrome consist of glandular epithelium and smooth muscle tissue connecting to the muscularis mucosae (muscular plate of connective tissue).

Polyps are always multiple. Localized in the small intestine (64%), less often in the large intestine (53%), stomach (49%) and rectum (32%). Typically, fewer than 20 polyps are found in each case, and the size ranges from a few millimeters to 5 cm in diameter [36].

In addition to Peutz-Jeghers syndrome, hamartomatous polyps are also observed in juvenile polyposis and hamartoma tumor syndrome associated with the PTEN gene (PTEN hamartoma tumor syndrome). The latter include Cowden syndrome, Bannayan–Riley–Ruvalcaba syndrome and others caused by a mutation of this gene.

Differential diagnosis of pigmented lesions is carried out with LEOPARD, Langier–Hunziker, Carney, Cowden syndromes and normal skin condition observed in some African Americans [37, 38].

Of particular interest is the analysis of the relationship between Dühring's dermatitis herpetiformis and celiac disease. On the one hand, the pathogenesis of both diseases lies in intolerance to the cereal protein gluten with the development of atrophy of the mucous membrane of the small intestine and, as a consequence, a generalized violation of intestinal absorption. The latter is most pronounced in celiac disease, although there are a significant number of atypical forms in which the intestinal syndrome fades into the background. Atypical celiac disease often presents with iron deficiency anemia, or osteoporosis, or short stature, as well as many other extraintestinal symptoms. Dühring's dermatitis herpetiformis is not an atypical form of celiac disease, but an independent disease in which gluten-sensitive individuals develop characteristic skin lesions.

In both celiac disease and dermatitis herpetiformis, a characteristic HLA haplotype, circulating antibodies to tissue transglutaminase, and villous atrophy of the small intestinal mucosa can be identified, with a positive effect on its status of a gluten-free diet. It should be noted, however, that in approximately 20% of patients with dermatitis herpetiformis, the condition of the small intestinal mucosa remains normal [39, 40].

Clinically, dermatitis herpetiformis manifests itself as herpetiform grouped polymorphic elements (vesicles, blisters, pustules, papules and papulovesicles) on unchanged or swollen erythematous areas of the skin, appearing simultaneously or at short intervals. The bladder cover is dense. The contents of the bubble are initially transparent, then cloudy. Blisters can turn into pustules, open with the formation of erosions, on the surface of which crusts form, followed by epithelization. Blisters may appear along the periphery of such areas. The rash is usually located symmetrically and is grouped in the form of rings, half rings or garlands (herpetiform grouping). Typical sites of localization are the extensor surfaces of the limbs and the buttocks. The appearance of a rash is often preceded or accompanied by general malaise, headaches, insomnia, dyspeptic symptoms, and an increase in temperature from 37.5 to 40 °C. The itching is usually severe, and sometimes a burning sensation is possible. The exacerbation of the disease continues for several weeks, and in some areas the rash resolves, passing through the stage of secondary elements (erosion, scales, crusts, hyper- or hypopigmentation), while in others fresh rashes appear. There are no rashes on the scalp. In children, the mucous membranes are quite often affected [41], and there is an increased tendency to form pustules.

The pathogenesis of both diseases remains completely unsolved. At the same time, the nature of the pathological process in the skin differs from that in the small intestine and is characterized by the presence of an inflammatory infiltrate, predominantly consisting of neutrophils, localized in the dermal papillae, where IgA deposits are also found [42]. The importance of neutrophils in the pathological process is confirmed by the positive effect on skin changes of the administration of dapsone, which suppresses the activity of neutrophils. This is also indicated by increased expression of CD11b, a slight decrease in L-selectin, and increased function of FcIgA receptors [43]. At the same time, in the small intestine, both in celiac disease and in dermatitis herpetiformis, a predominantly mononuclear reaction is observed.

It is also noteworthy that a gluten-free diet, effective for celiac disease, is not effective enough for dermatitis herpetiformis, which requires additional prescription of specific drugs.

Thus, the relationship between the skin and intestinal processes in dermatitis herpetiformis remains unclear, although the parallelism of these disorders is obvious.

In recent decades, the infection Helicobacter pylori (H. pylori), initially associated with the development of chronic gastritis and peptic ulcers, has attracted particular attention. Subsequently, the possible role of this infectious agent in the development of a significant number of diseases, including skin diseases, was established (Table 3) [44].

A significant number of studies have been devoted to studying the relationship between H. pylori infection and chronic urticaria, which is a chronic skin disease characterized by recurrent itchy blisters without a clear connection with physical and nutritional factors. The nature of this relationship has not been fully established. One hypothesis suggests an increase in intestinal permeability against the background of Helicobacter pylori infection to various agents that can cause mast cell degranulation [45]. Other hypotheses attribute immunomodulatory effects to H. pylori. In particular, IgG and IgA antibodies to the H. pylori-associated 19-kDa lipoprotein were detected in the blood serum of patients with chronic urticaria [46, 47]. Autoantibodies of the IgG class to IgE and Fc-εRiα are also detected, and the possibility of production of antibodies during Helicobacter pylori infection due to molecular mimicry is assumed [48]. Studies evaluating the effectiveness of H. pylori eradication in chronic urticaria are controversial. However, a carefully designed study by E. Magen et al. showed a significant decrease in process activity in patients who received treatment compared with those who did not receive treatment [49].

In this regard, the importance of H. pylori in the development of atopic dermatitis is discussed. Thus, G. Corrado et al. showed a positive association of food allergy with Helicobacter pylori infection in a group that included 30 children with various gastrointestinal complaints [50]. In a study by IH Galadari et al. the frequency of detection of H. pylori in patients with atopic dermatitis was significantly higher compared to controls [51]. K. Murakami et al. described a case of successful treatment of atopic dermatitis in a 14-year-old girl who underwent H. pylori eradication [52]. However, many aspects of this relationship remain controversial.

It is also assumed that Helicobacter pylori infection may be a trigger for the development of psoriasis [54–56], but the mechanisms of its development are unknown.

Thus, diseases of the digestive system have a significant impact on the condition of the skin, and symptoms of its damage may indicate damage to the gastrointestinal tract. The mechanisms of this relationship may be different, and in some cases remain completely unknown. However, with the development of a skin pathological process, diseases of the digestive system should be excluded, and with gastroenterological pathology, the condition of the skin should be closely monitored, which may be important for assessing the activity of the process, its prognosis and prescribing adequate therapy in both gastroenterological and dermatological practice .

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N. G. Korotky, Doctor of Medical Sciences, Professor N. M. Narinskaya S. V. Belmer1, Doctor of Medical Sciences, Professor

GBOU VPO RNIMU im. N. I. Pirogova Ministry of Health of the Russian Federation, Moscow

1 Contact information

Abstract. Alimentary organ diseases have strong impact on skin condition and the symptoms of its affection may indicate affection of alimentary organ. The article covers relations between bowel pathology and changes of cutaneous covering in cases of Brandt's syndrome, Peutz–Jeghers' syndrome, Crohn's disease, interconnection of dermatitis herpetiformis and celiac disease. Authors also analyze the role of H. pylori in the development of atopic dermatitis.

Causes of acne in men

The main reason is hormonal changes in the body, nothing can be done about it - nature. But nutrition and personal hygiene are also important factors. Poor diet contributes to the production of toxins in the body, which leads to discharge on the skin, rashes can be located in small areas throughout the body.

If hygiene is insufficient, ulcers will appear in ninety percent of cases, they will spread over a large area, it is important to stop this spread in time.

How to deal with acne

First of all, you need to visit a dermatologist, but if this is not possible, you can use the tips below.

In the case of nutrition, everything is simple, a properly selected diet is enough, it’s not difficult to create it yourself. You need to give up high consumption of flour, soda and other junk foods.

Hygiene is more difficult. Those areas where acne has appeared must be washed with running water at least 3 times a day, and you will also have to use various ointments and lotions to wipe the affected areas. You should not use regular soap (replace with foam), and do not try to dry the skin with alcohol-containing products or acids (salicylic). Dry, cracked skin makes it easier for bacteria to penetrate.

If acne does not go away by following these rules, then you need to go to the clinic to see a dermatologist and, through laser treatment, say goodbye to this disease once and for all. The laser is effective because it destroys the porphyrin in propionbacteria, therefore killing them.

Treatment methods

If acne is only a consequence of dysfunction of the digestive system, the doctor will prescribe therapy for the underlying disease. Both specific drugs and symptomatic therapy may be required. For chronic constipation, a specialist will prescribe laxatives.

A therapeutic diet is required. It is important to adhere to a healthy diet, limiting intake of foods rich in carbohydrates and fats, as well as dairy products. Studies show that in functional disorders of the gastrointestinal tract associated with dysbiosis, probiotics and prebiotics demonstrate quite high effectiveness. They allow you to restore the normal balance of microflora after intestinal cleansing measures.

In some cases, colon hydrotherapy may be recommended in a clinic setting. This is intestinal lavage using a stream of physiological fluid. There are two ways to carry out the procedure: underwater rinsing, irrigation according to the Lensky method. As a result, it is possible to remove toxic substances, stagnant feces and improve overall well-being.

Underwater washing involves the use of a special apparatus. The procedure is carried out in a bath. Water heated to 37 °C is gradually supplied to the intestines. Feces are removed using a special suction device. Complete cleansing of the body requires several sessions.

Irrigation according to Lensky involves inserting a probe into the anus. The other end of the tube is located in a vessel with irrigating liquid. Water flows out through a special tube. The procedure takes about half an hour, it is recommended to repeat it after 2 days.

It is important to remember that both home cleansing (enemas, laxatives) and procedures in the clinic must be agreed upon with the attending physician. Such measures are necessary for patients suffering from constipation and other disorders. However, they also have contraindications.

What to do if acne appears

Acne is not as simple as it might seem; you can get it at any age. Of course, there is nothing terrible about it, but you shouldn’t leave everything to the will of fate - it could cost you your natural beauty!

It is necessary to take hormone tests every six months, then there will be no problems with this.

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Diagnostic features

Before you start taking colon cleansing medications, it is important to understand the causes of acne. If you feel discomfort and notice problems with digestion, it is advisable to visit a therapist or gastroenterologist. Treatment of the underlying disease can significantly improve the condition of the skin.

Diagnosis of the gastrointestinal tract condition is carried out using different methods:

• Ultrasound of the abdominal organs;
• gastroscopy;
• probing and microscopic examination of bile;
• colonoscopy;
• laboratory tests: microflora studies, coprogram, general blood tests, urine tests, etc.

Based on the examination, the doctor makes an accurate diagnosis and develops a treatment plan.