Vol 31, No 5 (2024)

Currently, medicine knows 11,800 types of different viruses (for comparison, until 2011, only 2,800 types of viruses were discovered), which, according to rough estimates by scientists, is no more than 5–10% of all existing viruses on our planet. From 95 to 100% of the population are infected with the herpes virus, and at different periods of life they become infected with at least one, and more often several types of viruses belonging to the herpesvirus family. In the second half of life, almost all people have antibodies to most human herpesviruses. Of the known human herpesviruses, herpes simplex viruses types 1 (HSV-1) and 2 (HSV-2) are the most frequently mentioned in the medical literature, since both of these viruses are associated with lesions of the skin and mucous membranes, commonly known as herpes simplex. However, only recently the role of human herpes viruses (HHVs) as copathogens causing other serious diseases has been recognized. Roseoloviruses are represented by three different types: HHV-6A, -6B, -7, genetically related to cytomegalovirus (CMV). HHVs have broad cellular tropism in vivo and, like other herpesviruses, cause lifelong latent infection in humans. It is known that all known HHVs are found in the reproductive tract. CMV and HHV-6 can contribute to the occurrence of chronic inflammatory diseases of the urogenital tract and impaired fertility in patients. Recent studies have found that HHV-6A is the cause of primary infertility in 43% of cases, and HHV-6A and -6B in some clinical cases contribute to the development of preeclampsia. The role of Epstein–Barr virus (EHV-4), as well as HHV-6, -7 and -8 in the progression of HIV infection is being actively studied. Laboratory diagnosis of HHV-6 and -7 currently has limitations. The most informative method for detecting HHV is the quantitative determination of viral DNA in the blood, other body fluids and organs using real-time polymerase chain reaction. Numerous questions about HHV-6A, -6B and -7 still remain open, particularly regarding the clinical impact and therapeutic options in immunocompromised patients.

In recent years, there has been a steady increase in the incidence of localized scleroderma (morphea). The article summarizes modern data from domestic and foreign literature on the clinical picture, course and principles of therapy of the disease. Currently, none of the methods of morphea therapy is highly specific. Ongoing scientific and clinical studies aimed at finding drugs that can affect both inflammation and the formation of fibrosis show the limited viability of therapy at the current stage of medical development and open up new possible prospects for the treatment of patients.

Stevens-Johnson syndrome and toxic epidermal necrolysis are rare and life-threatening mucocutaneous diseases that occur almost exclusively as a result of adverse drug reactions, although there are rare cases associated with infection, immunization, or malignancy. Stevens-Johnson syndrome and toxic epidermal necrolysis are often accompanied by fever, malaise, upper respiratory symptoms, difficulty swallowing, and pain or a burning sensation of the skin and mucous membranes. These symptoms may precede skin manifestations for up to 3 days. Detachment of the epidermis usually begins on the trunk, then spreads to the limbs, head and neck. In addition, more than 90% of patients have lesions of the oral mucosa, eyes or genitals. Less commonly, the mucosa of the respiratory tract and gastrointestinal tract may be affected, resulting in significant morbidity and mortality. Stevens-Johnson syndrome and toxic epidermal necrolysis usually occur between days 7 and 21 after starting treatment, increasing the dose, or changing the brand of the responsible drug. In addition, certain groups of patients are at increased risk of developing these diseases when exposed to certain medications, including patients with human immunodeficiency virus infection, patients receiving concomitant radiation therapy, and anticonvulsant medications. The article provides etiopathogenetic aspects and features of the management of patients with Stevens-Johnson syndrome and toxic epidermal necrolysis.

The International Statistical Classification of Diseases and Related Health Problems (ICD) is the basis for recording medical data and statistical information necessary for the work of clinicians and health care managers. The ICD allows the global medical community to exchange data, jointly analyze and systematize various pathologies. In the Russian Federation, the tenth revision of the ICD (ICD-10) is currently in force. Only in ICD-10 skin diseases were represented as a separate class. ICD-10 was a dynamically changing document, to which individual changes were made almost every year (these changes concerned both the addition of new codes and changes and/or deletions of individual codes). The classification of diseases of the skin and subcutaneous tissue also did not stand still and was constantly improved. It was planned to completely switch to ICD-11 by 2025. However, due to the geopolitical situation, as well as the presence of fundamental disagreements on the structure and content of individual sections of the classification, a “pause” was taken until a number of controversial and fundamental issues for the country were resolved. At present, it seems relevant to refine the existing classification, which will reflect the current needs of practicing physicians and medical concepts in such a way that it is compatible with modern information technologies while maintaining a simple structure for coding data with a high degree of detail, as well as with the possibility of timely and necessary updating of information, which will allow obtain the most accurate and useful results.

Parry–Romberg progressive facial hemiatrophy is an uncommon, sporadic disorder characterized by progressive hemifacial wasting and atrophy of skin, muscle, and bone, sometimes involving the central nervous system, and manifesting as focal scleroderma. Parry–Romberg syndrome, more common in women without ethnic or geographic predilections, occurs during the first or second decades of life, leading to slow and progressive facial hemiatrophy, predominantly on the left side. The diagnosis of Parry–Romberg syndrome mainly depends on clinical history using imaging studies and histopathological correlation. The article provides data on the etiology, pathogenesis, and clinical picture of the disease. Methods for diagnosing and treating these patients are described in detail.

Alopecia areata (AA) resulting from an autoimmune attack on the hair follicle often debuts in childhood, which is one of the predictors of an unfavorable prognosis for the disease. In the case of manifestation of symptoms before puberty, half of children develop total alopecia. Currently, the treatment of children with AA does not have a generally accepted method and does not always meet expectations. The article discusses the data on current approaches to systemic and local therapy of AA published by specialists from different countries over the past few years.

Tranexamic acid (TA) has antiplasmin activity and has been shown to be effective against melasma when administered orally, for which it is considered a first-line pharmacotherapy. Several studies have shown that topical TA is also effective against melasma and skin hyperpigmentation caused by sun exposure and inflammation. When applied topically, TA acts on neutrophils and mast cells in the dermis and on the vascular system. It is unlikely that topical TA affects dermal neutrophils or mast cells, or the vascular system to form thrombi. Studies conducted to evaluate the effect of topical TA on the hyperpigmentation process show that the resulting skin «lighte-ning» mechanism involves the suppression of the production of cytokines and chemical mediators that stimulate melanin production via urokinase-type tissue plasminogen activator and dermal vascular-derived plasminogen, thereby suppressing the production of excess melanin and preventing hyperpigmentation. This article presents clinical experience with the use of topical TA-based drug «Careju» for the prevention and treatment of post-inflammatory hyperpigmentation, which has a pronounced therapeutic potential.

Components of the dermis, including fibroblasts, collagen, elastic fibers, glycosaminoglycans and proteoglycans, undergo significant changes during intrinsic and extrinsic aging processes. Previous studies have shown that increased degradation and decreased biosynthesis of collagen leads to a «net deficiency» of collagen, which is characterized by clinical changes such as wrinkles and loss of skin elasticity. Fibroblasts are resident cells of the dermis and are different from mesenchymal cells. They are responsible for the synthesis and degradation of fibrous and amorphous proteins of the extracellular matrix (ECM). Their function and interaction with the environment are important for understanding the molecular mechanism of skin aging. In young skin, fibroblasts adhere to the surrounding intact ECM, which mainly consists of type I collagen. This adherence allows fibroblasts to exert mechanical force on the surrounding ECM, as well as to spread and maintain a normal elongated shape. In aging skin, fibroblast attachment is impaired due to progressive ECM degradation, which leads to a decrease in fibroblast size, decreased elongation and collapse of morphology. Based on the data obtained, it can be assumed that the function of fibroblasts in the skin can be stimulated by enhancing the structural support of the ECM. In this case, it is rational to use collagen replacement therapy. This article describes the mechanism of action of collagen replacement therapy with Linerase and presents clinical cases of combined instrumental and injection cosmetology methods.

Palmoplantar keratodermas are a heterogeneous group of inherited keratinization disorders of varying severity. Olmsted syndrome (OS) is one of the rarest diseases in this group, which is manifested by progressive mutilating keratoderma of the palms and soles, periorificial hyperkeratosis, and alopecia of varying severity. Most cases of OS arise as a result of pathogenic variants in the TRPV3 gene. In keratinocytes, TRPV3 forms a signaling complex with the epidermal growth factor receptor, which in turn leads to the activation of many downstream kinases, including serine-threonine kinase (mTOR), which is the main regulator of cell growth and proliferation. Enhanced activation of the mTOR pathway leads to various inflammatory, hyperproliferative and neoplastic diseases of the skin, including OS. There is currently no effective treatment for OS; topical, physiotherapeutic and medicinal agents do not have a significant clinical effect. The search for new pathogenetically substantiated treatment methods is an important task of modern dermatology. The article describes a clinical example of the first successful use of sirolimus in in a patient with OS in Russia.

Background. Analysis of clinical symptoms in patients has an important diagnostic and prognostic value; for HIV-infected patients, the role of clinical symptoms is difficult to overestimate. At the same time, dermatological symptoms and their dynamic changes are a key component of many clinical symptoms and often indicate the features of the course of both somatic and infectious pathology. Evaluation of homeostasis parameters on modern laboratory equipment allows to accurately determine many metabolic disorders, deviations in the functioning of the immune system, as well as other changes in the stability of the patient’s state, while the process is time consuming and requires material costs. Many researchers believe that skin symptoms in HIV-infected patients suffering from psoriasis are a common pathology and are not used enough to assess the condition of these patients. At the same time, studies on the involvement of the immune directions Th1, Th2 and others in the development of psoriasis and the activity of these directions at various stages of the pathogenesis of HIV infection have shown that these diseases have a large number of intersecting pathogenetic links. This fact allows to compare clinical and laboratory parameters for a more complete understanding of the mutual influence of these diseases and the widespread use of dermatological symptoms to assess the condition of HIV-infected patients.

Objective. Evaluation of the role of psoriasis in HIV-infected patients in the development of systemic inflammation, using the indicators of the systemic immune inflammation index (SII) and acute phase proteins (CRP) against the background of genetic engineering biological therapy.

Methods. The study included 180 HIV-infected patients aged 20 to 45 years, of whom 90 had a verified diagnosis HIV infection and psoriasis (group 1). Depending on the severity of psoriasis (Psoriasis Area and Severity Index – PASI), patients in group 1 were divided into subgroups: 1a (n=30) – mild psoriasis – PASI ≤10 points; 1b (n=30) – moderate-to-severe psoriasis – PASI 11 to 20 points; 1c (n=30) – severe psoriasis – PASI >20 points. In order to control the indicators of systemic inflammation, comparison group 2 was selected. This group included 90 people only with HIV infection, without psoriasis. Group 2 was selected using the «pair selection method» (paired groups) to group 1 (taking into account gender characteristics, age, HIV stage, antiretroviral therapy [ART] regimen). The group was divided into subgroups of 30 patients – 2a, 2b, 2c. In total, there were 106 men (58.9%) and 74 women (41.1%) in both groups. All patients in both groups had been receiving ART for at least 3 months at the time of inclusion in the study. Systemic immune inflammation (systemic immune-inflammation index – SII) was assessed using the formula: SII = P × N / L. Where: P is the absolute value of the platelet count, N is the absolute number of neutrophils, and L is the number of lymphocytes in the peripheral blood. C-reactive protein (CRP) levels were determined by generally accepted laboratory methods, with a value of 5 mg/L taken as the norm. To assess the correlation coefficient in subgroups 1a, 1b, 1c of psoriasis severity with the values of systemic immune inflammation indices (SII) and CRP levels, the Pearson correlation coefficient was used, with the calculation of the covariance ratios of two variables and the product of their standard deviations. Therapy for psoriasis in patients with its mild course consisted of topical use of an ointment containing, per 100 g: betamethasone dipropionate – 0.05; salicylic acid – 3.0; patients with moderate and severe psoriasis additionally received the drug netakimab subcutaneously according to the scheme attached to the instructions for the drug.

Conclusion. Psoriasis in HIV-infected patients, depending on its severity, had a pronounced effect on the parameters of systemic inflammation, as indicated by the levels of the median SII index (Me SII1a=362.8 U; Me SII1b=638.2 U) and acute phase proteins CRP (Me CRP1a=15.6 mg/l; Me CRP1b=241.3 mg/l). The SII levels in these patients were linearly associated with the psoriasis severity and significantly improved against the background of biological therapy with Netakimab (Me 0week1b=638.2 U; Me 5week1b=394.7 U; p<0.01). The increase in CRP levels depended on the severity of psoriasis and was significantly reduced by the use of genetically engineered biological therapy (Me 0week 1v=241.3 mg/l; Me 5week 1v=32.9 mg/l; p<0.001).

Psoriasis is a common chronic immune-mediated disease that causes a significant burden on 125 million people worldwide. A growing body of research has led to the recognition that psoriasis is often associated with other conditions beyond the skin. Much research into the comorbidity of psoriasis has focused on the association with cardiovascular disease, cancer, infections, and psychiatric disorders, and recently there have been increasing reports of a correlation between psoriasis and kidney damage. Repeated studies have found an increased prevalence of microalbuminuria and renal failure in patients with psoriasis, and there has been a direct and inverse correlation between psoriasis, chronic kidney disease (CKD), and renal failure. Mechanisms of kidney damage may be immune-mediated, non-immune, or drug-related. The incidence, prevalence, and progression of CKD vary by race and social determinants of health, it affects ~11% of the population, and people with CKD are 5 to 10 times more likely to die prematurely than before progression to end-stage renal disease (ESRD). Additionally, psoriasis severity was associated with an increased risk of CKD and ESRD. Also, the risks of kidney damage increased in patients with other comorbid conditions (for example, psoriatic arthritis, diabetes mellitus, hypertension), which reflects the general background of systemic inflammation. In patients with psoriasis in the pediatric population, the relationship between psoriasis and kidney disease has not yet been proven.

This article presents a case of clinical observation of a patient with a rare form of deep streptostaphyloderma - chronic ulcerative pyoderma. This disease is characterized by ulcerative areas of skin lesions with histological features of pseudoepitheliomatous hyperplasia and chronic granulomatosis. The causative agents of the disease are most often Staphylococcus aureus and group A streptococci. Dermatosis often develops in patients with ulcerative colitis, alcoholism, lymphoma and other immunodeficiency conditions. Deficiency of the T-immune system, decrease in chemotaxis and phagocytic activity are detected in patients. Diagnosis of this disease is based on clinical, histological and microbiological research methods. Clinical observation of this case is of interest to practicing dermatovenerologists.

Background. Halo nevus (Sutton`s nevus) and vitiligo are multifactorial diseases with a hereditary predisposition and with the leading role of autoimmune mechanism of melanocyte destruction in their development. Each of these conditions as an independent pathology is a well-studied disease from the group of dyschromias, their clinical signs are described in detail, a sufficient amount of data on dermatoscopic and immunohistochemical pictures has been accumulated. The incidence of the combination of vitiligo and Sutton nevus (SN), according to the literature, varies from 18 to 26% of cases, since SN is not always considered as a separate nosology. The high frequency of association of these dyschromias is attributable to common cell-mediated autoimmune mechanisms of their development. Their long-term chronic progressive course significantly reduces the quality of life of patients, often leading to deep psychosocial experiences, especially when exposed areas of the skin (face, hands) are affected. When SN appears against the background of existing vitiligo, as well as when halo nevus-associated leukoderma appears, difficulties in making a diagnosis arise, which requires differential diagnostics based on clinical and dermatoscopic pictures of the disease to determine the tactics of patient management.

Description of the clinical case. The article presents author’s own clinical observation of the long-term existence of a combination of vitiligo and multiple SN in a 22-year-old patient. Multiple SN began to form sequentially around congenital nevi a year after the onset of vitiligo. Dermatoscopic examination revealed that the vitiligo foci were at different stages of development, while the SN had the same structure. The absence of spontaneous regression or partial repigmentation of SN over a long period of time is a reason for regular clinical and dermatoscopic monitoring of the patient.

Conclusion. The presented case raises physicians’ awareness of the possibility of combining vitiligo and SN and the nuances of differential diagnosis of these dyschromias based on clinical and dermatoscopic criteria.