Pesticide-induced systemic scleroderma: a case report

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BACKGROUND

Systemic sclerosis, or systemic scleroderma (SSс), is a rare autoimmune connective tissue disease characterized by generalized vasculopathy, skin fibrosis, and visceral involvement [1]. The incidence of SS is 8 to 56 cases per 1,000,000 population annually. Females are five times more likely to develop the condition than males [2].

SSс is primarily caused by genetic factors, such as TGFB1, MMP1, and MMP3 overexpression, and exogenous factors, such as organic solvents, silica dust, and viruses (Epstein–Barr virus, cytomegalovirus, etc.). This results in endothelial dysfunction due to increased expression of cell adhesion molecules, chemokines, cytokines, and growth factors [3]. Increased expression of cell adhesion molecules promotes endothelial adhesion of circulating white blood cells and platelets, facilitating infiltration by T helper 2 (Th2) and 17 (Th17) cells, macrophages, and mast cells [4, 5].

Activated endothelial cells increase the expression of endothelin-1 (ET-1), a potent endogenous vasoconstrictor that induces smooth muscle contraction and exerts a profibrotic effect by activating fibroblasts and promoting the release of endogenous cytokines [6]. Moreover, endothelial cells in SSс can activate platelets, increasing the release of thromboxane A2 (ТХА2), platelet-derived growth factor (PDGF), transforming growth factor beta (TGF-β), and thrombin. The associated intravascular fibrin deposition promotes luminal occlusion [7]. Furthermore, SSс is characterized by aberrant expression of von Willebrand factor (VWF) receptors, specifically integrin alpha-IIb and glycoprotein Ibβ [8]. An imbalance in coagulation and fibrinolysis in patients with SSс results in thrombosis, vessel wall injury, and impaired peripheral circulation, promoting inflammation and fibroblast activation [9, 10].

The clinical signs of SSс are associated with immune system disorders, vasculopathy, and fibroblast dysfunction that results in collagen overproduction. However, many pathophysiological mechanisms underlying this condition remain understudied [11].

Depending on the severity of lesions, SSс is classified as focal (with isolated skin induration), generalized with cutaneous involvement (affecting the skin of the face, arms, legs, and trunk, as well as the gastrointestinal tract, lungs, liver, heart, and blood vessels), or generalized without cutaneous involvement (affecting the internal organs).

Gastrointestinal symptoms are reported in 90% of patients with SSс [12]. Gastrointestinal dysfunction, which is common in early SSс, is caused by reduced lower esophageal sphincter tone and esophageal motility [13].

Interstitial lung disease and pulmonary hypertension are the main causes of death in patients with SSс [14]. High-resolution computed tomography detects interstitial lung disease in 50%–60% of patients with SSс [15]. Clinical signs of interstitial lung disease secondary to SSс vary. Some patients have reduced forced vital capacity, while others show normal functional test findings [16]. Pulmonary hypertension in patients with SSс is caused by diffuse vascular injury, cardiac involvement, and interstitial lung disease [17]. Primary myocardial injury in patients with SSс manifests as arrhythmia, myocarditis, pericarditis, systolic and diastolic dysfunction, and heart failure [18, 19]. According to some research, the majority of patients with SSс have myocardial injury [20].

One possible cause of SSс is exposure to chemicals, including pesticides, which are complex organic compounds extensively used in agriculture for pest, weed, and fungus management [21]. Pesticides that are especially hazardous to human health include organochlorides, organophosphates, carbamates, pyrethroids, chlorophenoxy compounds, triazines, amides, and phthalimides. According to animal studies, both short-term exposure to high doses and long-term exposure to low doses of these substances cause severe immune dysfunction [22].

SSс is not currently included in the list of occupational diseases according to Order of the Ministry of Health of Russia No. 141n of March 21, 2025, which became invalid on September 1, 2025. The updated list of occupational diseases, which came into force on September 1, 2025,¹ does not include scleroderma as a disease associated with occupational hazards. However, it includes Erasmus syndrome, a rare occupational disease that primarily affects males. The disease is caused by long-term occupational exposure to silicon dioxide (e.g., in the mining, coal, or glass industries) [23] and is characterized by a combination of silicosis and SSс. Silicosis, a well-known occupational disease, is a type of pneumoconiosis associated with fibrotic changes in the lungs caused by inhaled mineral (silica) dust. In accordance with effective legislation, silicosis is included in the list of occupational diseases,¹ making it a legally recognized occupational pathology in individuals exposed to harmful workplace factors and ensuring social support.

This article presents a clinical case of SSс caused by prolonged occupational exposure to cypermethrin, bromadiolone, and chlorpyrifos in an exterminator.

CLINICAL CASE DESCRIPTION

Patient Information

Patient Kh., a 42-year-old female, consulted a rheumatologist with complaints of skin discoloration in the hands when exposed to low temperatures or emotional stress, which resolved spontaneously in a warm environment. Other complaints included pain in the lower back, wrist joints, and metacarpophalangeal joints on the right; swelling and numbness in both hands during the day; non-radiating pressing retrosternal pain that lasted more than an hour and resolved spontaneously; and general weakness and fatigue.

The patient resides in the Republic of Bashkortostan and has worked as an exterminator since 2010. Her professional duties include chemical rodent and pest control in residential premises, catering facilities, child care centers, and health facilities. The chemicals used include bromadiolone, zoocoumarin, and Agran (an insectoacaricide containing 50% chlorpyrifos and 5% cypermethrin). During work, the patient wears protective gear (overalls and respiratory protective equipment). However, she transfers sprayers and insecticides (an opened bag of 1.5% zoocoumarin powder, opened paraffin blocks containing bromadiolone, and an Agran container) in her personal vehicle without protection.

Medical history. The patient considers herself ill since November 2023, when she noticed swelling of both hands. In March 2024, she developed biphasic skin discoloration in the hands when exposed to low temperatures. In April 2024, she developed non-pitting edema in both hands, with bilateral acute pain in nail walls and roots. The patient saw a surgeon. The nail walls were opened; however, no purulent discharge was obtained, and the pain did not improve. In June 2024, the patient saw a rheumatologist in her hometown (Ufa). Based on clinical and laboratory findings, she was diagnosed with SSс and Raynaud disease. The symptoms improved on treatment: there was a reduction in pain and swelling in the hands.

In June 2024, while on treatment, swelling in the hands worsened; moreover, the patient reported more frequent episodes of biphasic Raynaud disease (Fig. 1) and an increase in general weakness. She saw a rheumatologist at the Medical Research and Educational Institute (MREI), Lomonosov Moscow State University. An increase in disease activity was confirmed. On treatment, swelling in the hands resolved completely, and general weakness improved considerably; however, Raynaud disease persisted. Furthermore, the patient developed drug-induced Cushing syndrome, which necessitated glucocorticoid dose reductions.

 

Fig. 1. Biphasic Raynaud disease.

 

In September 2024, after an acute respiratory viral infection, the patient reported more frequent episodes of triphasic Raynaud disease and an increase in general weakness. In November 2024, the patient was admitted to the MREI Department of Internal Medicine to perform additional examinations and adjust the treatment strategy.

In early January 2025, the patient had an acute respiratory viral infection, which she attempted to treat with dietary supplements. Following the infection, the condition worsened again; the patient reported swelling in the hands, pain in wrist, metacarpophalangeal, and knee joints, and inflammatory pain in the thoracic spine. Moreover, she reported intermittent mild pressing retrosternal pain that lasted approximately an hour and was unrelated to exercise, as well as inflammatory pain in the thoracic spine.

Due to treatment failure and worsening of the condition, the patient was readmitted to the MREI Department of Internal Medicine in February 2025.

Diagnosis

After therapy with glucocorticoids, methotrexate, and cyclophosphan, the patient was discharged in satisfactory condition. The final diagnosis was as follows: Systemic scleroderma, diffuse, subacute: skin induration on the face, hands, and forearms (modified Rodnan skin score 28). Raynaud disease. Polyarthralgia. Capillaroscopy abnormalities (active scleroderma-related changes) and immune disorders (anti–Scl-70 antibodies 3+).

Physical Examination, Laboratory, and Imaging Findings

In June 2024, a capillaroscopy was performed by a rheumatologist in the patient’s hometown (Ufa), which revealed individual capillaries with downstream dilatation up to 0.3 mm. The majority of capillaries are narrowed; blood flow is preserved. Follow-up examination: antinuclear antibodies 1:1280, homogeneous fluorescence pattern (AC-1), anti-Scl-70 antibodies (3+++).

Physical examination at presentation to the MREI: extensive skin lesions with skin induration on the face, hands, and forearms. The skin on the back of the hands was difficult to pick. The fingertips were slightly pruney.

In 2024, the patient was admitted to the MREI Department of Internal Medicine. On examination: skin induration on the hands (scleroderma). Rodnan skin score: 27 out of 51. Triphasic Raynaud disease caused by exposure to low temperatures or emotional stress. On palpation: pain in the proximal interphalangeal joint of the middle finger of the left hand. On auscultation: accent of the second sound over the pulmonary artery. Other findings are unremarkable. Complete blood count and blood chemistry findings are normal. A slight increase in C-reactive protein up to 9 mg/mL (normal value: <5 mg/mL). Chest computed tomography: signs of interstitial lung disease. Echocardiography: left ventricular ejection fraction 60%; no areas of impaired contractility or significant valve disorders. Abdominal ultrasound: diffuse changes in the pancreas. Gastroscopy: superficial gastritis, cardial incompetence. Spirometry: no abnormalities.

Immunological tests in 2025: antinuclear antibodies 1:2560, nucleolar fluorescence pattern. Kidney ultrasound: bilateral pyelectasis. Therapy with nonsteroidal anti-inflammatory drugs and diuretics was initiated.

On examination in February 2025, when readmitted to the MREI: skin discoloration and swelling on the face (Fig. 2); skin induration and swelling on the hands (scleredema); skin induration on the arms, legs, and chest. Rodnan skin score: 28 out of 51. Tenderness on palpation in the spine (Th6), wrist and metacarpophalangeal joints on the right, temporomandibular joint on the right, and sacroiliac joint on the left. Limited range of motion in the right shoulder joint when abducting the right arm by 120°. Follow-up examination: no significant abnormalities in complete blood count, blood chemistry, and urinalysis findings. C-reactive protein 13.2 mg/mL (normal value: <5 mg/mL). Antinuclear antibodies 1:5120, nucleolar and nuclear granular fluorescence pattern. Anti-Scl-70 antibodies (3+++). C3 and C4 complement levels: normal. Echocardiography, abdominal ultrasound, and spirometry: no abnormalities. Chest computed tomography: signs of interstitial lung disease.

 

Fig. 2. Thickening and swelling of the facial skin.

 

At discharge, the Rodnan skin score was 18 points, compared to 28 points in January 2025; swelling of the hands and frequency of Raynaud disease episodes decreased.

Differential Diagnosis

Given the overlapping clinical signs, differential diagnosis is necessary between SSс and other systemic connective tissue diseases, such as eosinophilic fasciitis, undifferentiated connective tissue disease, scleromyxedema, Buschke scleredema, systemic amyloidosis, nephrogenic systemic fibrosis, porphyria cutanea tarda, progeria, and Werner syndrome, including exposure to toxic substances.

Treatment

In 2024, the local rheumatologist prescribed the following therapy: dexamethasone 1 mL IV, No. 5; methotrexate 10 mg/week; folic acid 5 mg/week; amlodipine 5 mg/day; pentoxifylline 800 mg/day; vitamin D 2000 IU/day.

In 2024, the rheumatologist at the MREI prescribed the following therapy: prednisolone 20 mg/day; methotrexate 10 mg/week; folic acid 5 mg/day; sildenafil 12.5 mg/day. Lercanidipine 10 mg/day and pentoxifylline 300 mg/day were used to improve microcirculation. When the prednisolone dose was reduced to 15 mg/day, the patient experienced recurring edema; as a result, the dose of glucocorticoids was increased to 20 mg/day. When the condition improved, the dose of glucocorticoids was reduced to 8.75 mg/day, which did not result in recurring edema.

In 2024, the patient received pulse therapy with cyclophosphamide 500 mg IV, No. 1, at the MREI Department of Internal Medicine. It was recommended that pulse therapy be performed every three weeks. Therapy with prednisolone 7.5 mg/day and sildenafil 12.5 mg/day was continued, with enalapril 2.5 mg/day and rosuvastatin 10 mg/day added to this regimen.

In 2025, the patient started taking dietary supplements containing echinacea, artichoke, milk thistle, Baikal skullcap, and other herbs, as well as mumijo.

When readmitted to the MREI, the patient received pulse therapy with cyclophosphamide 500 mg, No. 2, and methylprednisolone 250 mg, No. 1. After 6 months, due to ineffective methotrexate therapy (persistent scleroderma, arthralgia, elevated C-reactive protein), mycophenolate mofetil 1 g/day was initiated.

At discharge, it was recommended to continue mycophenolate mofetil 1 g/day, methylprednisolone 4 mg/day, rabeprazole 20 mg/day, lercanidipine 10 mg/day, and Cardiomagnyl 75 mg/day. Pulse therapy every three weeks.

Disease Course and Outcomes

The patient is currently receiving pulse therapy with cytostatics (cyclophosphamide 500 mg IV) every three weeks. On this treatment, Raynaud disease symptoms and edema of the hands have improved considerably, and the Rodnan skin score has decreased from 28 to 11. The titer of antinuclear antibodies has decreased from 1:5120 to 1:1256.

The patient reports a sustained improvement, with a decrease in edema of the hands and increased activity. The patient has changed jobs and now works from home.

Prognosis

The prognosis in SSс depends on its type, activity, and the severity of visceral involvement. Our patient was diagnosed with diffuse SSс, which has an unfavorable prognosis due to its chronic, progressive course, with a high risk of disability and decrease in life expectancy.

DISCUSSION

This article presents a case of SSс in a patient with prolonged exposure to complex chemicals (cypermethrin, chlorpyrifos, and bromadiolone).

Bromadiolone is a second-generation rodenticide with a strong anticoagulant effect, which causes lethal bleeding in rodents; moreover, long-term exposure may result in toxin-induced coagulopathies in humans.

Cypermethrin is a second-generation pyrethroid insecticide that exerts a neurotropic effect by targeting the receptor site of voltage-gated sodium channels, voltage-gated calcium channels, voltage- and ligand-gated chloride channels, and GABA receptors [24, 25]. The most typical signs of acute pyrethroid poisoning are dizziness, headache, nausea, anorexia, and chest tightness. In severe cases, impaired consciousness and seizures are possible. Long-term exposure may result in neurodegenerative diseases [26]. Cypermethrin poisoning may also be associated with pruritus, burning sensation, and blisters. When inhaled, cypermethrin may cause mucosal irritation with rhinorrhea, cough, and (in severe cases) pulmonary edema [27]. Furthermore, pyrethroids increase the risk of cardiovascular diseases [28]. Cardiotoxicity is rare and is typically reported in animal models. According to research, pyrethroids impair the prooxidant-antioxidant balance in cardiac tissues in rats [29]. Moreover, they have an arrythmogenic action [27]. Pesticides have been found to cause oxidative stress not only in the heart but also in other tissues [30]. In humans, pyrethroids have been shown to alter serum luteinizing and follicle-stimulating hormone levels in males [31]. Furthermore, pyrethroids act as estrogen receptor agonists, androgen receptor antagonists, and steroidogenesis inhibitors, ultimately reducing sperm quality [32–34]. However, according to other research, pyrethroids have no considerable effect on spermatogenesis [35, 36]. In addition to their impact on sex hormones, pyrethroids can bind to transthyretin, whose structure is similar to that of thyroid hormones, compromising the endocrine function of the thyroid gland [37]. This may affect prenatal development, resulting in developmental delays and autistic disorders [38]. The carcinogenic properties of pyrethroids are likewise not fully understood. Pyrethroids have been shown to influence DNA methylation, induce histone modifications, and increase the expression of some oncogenes [39]. All these effects disrupt the cell cycle and promote carcinogenesis [40]. Pyrethroid pesticides exert proinflammatory effects by inhibiting the activity of transcription factor Foxp3. The latter is necessary for the functioning of regulatory T cells, which suppress excessive inflammation, and the synthesis of profibrotic cytokines such as IL-4 [41]. Despite the toxic properties of permethrin insecticides, their effect on the immune system has not been studied. However, according to some research, their influence on the thyroid axis of endocrine regulation, along with oxidative stress, may result in autoimmune disorders.

Chlorpyrifos, an organophosphorus insecticide, irreversibly inhibits acetylcholinesterase, causing acute cholinergic syndrome. Moreover, chlorpyrifos can have long-term negative effects by altering cognitive functions in both individuals exposed to this pesticide and their children in the case of prenatal and postnatal exposure [42]. Experimental studies have demonstrated that chlorpyrifos has a dose-dependent cytotoxic effect on neurons, as well as a potential influence on the thyroid axis [43]. The latter, similar to cypermethrin, may have a role in autoimmune disorders. Aside from inhibiting acetylcholinesterase, organophosphates have a number of other effects. For example, fatty acid amide hydrolase inhibition may result in neuropathy, which causes limb immobility. Moreover, this pesticide may inhibit serine hydrolases that regulate the complement system and thrombin, as well as esterases that are associated with lymphocyte membranes. Chlorpyrifos may alter the T cell subpopulation, increasing the proportion of CD5 and CD8 cells [44]. Furthermore, long-term exposure to chlorpyrifos in humans increases the levels of autoantibodies that target smooth muscles, thyroid gland, myelin, antinuclear antibodies, and other antigens [45]. Thus, organophosphates induce systemic proinflammatory effects, altering neutrophil function, T cell proliferation, macrophage production, and antibody formation [46].

Published works primarily address scleroderma-like syndromes associated with occupational exposure to pesticides, without specific autoantibodies, visceral involvement, or abnormal capillaroscopy findings. However, all these cases indicate scleroderma-like disorders. SSс is not to be confused with scleroderma-like disorders such as eosinophilic fasciitis, nephrogenic fibrosing dermopathy, or eosinophilia-myalgia syndrome [47]. Scleroderma-specific anti-centromere and anti-topoisomerase I (Scl-70) antibodies frequently play a crucial role in differential diagnosis. Scleroderma-like syndrome has been reported in a 14-year-old child after exposure to diniconazole and in an 8-year-old girl after exposure to malathion. The main symptom in both cases was skin induration on the hands, forearms, trunk, or face, with no visceral involvement or systemic manifestations. Capillaroscopy revealed no vascular anomalies, and SSс-specific autoantibodies, such as anti-Scl-70 or anti-centromere antibodies, were not detected. A histological examination of biopsy samples revealed severe perifollicular fibrosis and perivascular lymphocytic infiltrate [48]. A similar case of scleroderma-like disorder has been reported in a female farm worker with long-term exposure to various pesticides (metalaxyl, folpet, sulfur, glyphosate). The main clinical symptom was skin induration on the hands. Laboratory tests revealed elevated levels of antinuclear antibodies. Skin biopsy showed pronounced fibrotic changes in the dermis, vessel wall thickening, and perivascular lymphocytic infiltrate [49]. These findings indicate that scleroderma-like syndromes may be caused by exposure to agrochemicals. However, they are typically not associated with vascular anomalies characteristic of Raynaud disease or autoimmune disorders characteristic of SSс. The diagnosis is based on medical history, clinical signs, immunological test and capillaroscopy findings, and morphological changes.

Chemical agents are considered one of the key exogenous factors that can initiate or modulate SSс in predisposed individuals. These agents include silicon dioxide, silicone implants, organic solvents (benzene, toluene, trichloroethane), epoxy resins, vinyl chloride, and other industrial chemicals.

The clinical presentation and immune status may vary depending on a specific chemical agent. For example, silicon dioxide-induced SSс is more prevalent in men. It is typically diffuse, is frequently associated with interstitial lung disease, and anti-Scl-70 antibodies are found in up to 50% of cases [50]. There are no published data on the typical features of scleroderma induced by organic solvents such as benzene, toluene, and trichloroethane [51]. Patients exposed to organic solvents report Raynaud disease and skin induration on the hands [52]. The disease is caused by damage to endothelial cells, resulting in microvascular disorders and fibrosis of target organs [53]. Silicone breast implantation-induced scleroderma is typically associated with elevated antinuclear antibody levels, with fibrotic changes resolving after eliminating the causative factor. Epoxy resin-induced scleroderma manifests as skin induration, telangiectasis, hyperpigmentation, myalgia, arthralgia, and pulmonary involvement. However, Raynaud disease and antinuclear antibodies are frequently absent. Vinyl chloride was thought to be the primary cause of acro-osteolysis; however, systemic disorders similar to scleroderma (cutaneous and visceral fibrosis, microcirculatory disorders, thrombocytopenia) were later identified. Autoantibodies were not detected, but histological examinations showed thickened collagen fibers, aberrant elastic fiber formation, and perivascular lymphocytic infiltration [54].

One of the most well-known cases of scleroderma-like disease induced by chemical agents is the toxic oil syndrome (TOS) outbreak in Spain in 1981. This massive outbreak was caused by the consumption of contaminated rapeseed oil that had not been properly purified to remove aniline, a toxic chemical intended for industrial use. Consumption of aniline and its derivatives resulted in symptoms such as scleroderma-like skin induration, muscle spasms, Raynaud disease, and pulmonary hypertension [54]. However, histologically, the condition was more like eosinophilic fasciitis [55]. Moreover, scleroderma-like syndromes induced by carbidopa, L-tryptophan, bleomycin, and cocaine have been reported [56].

These findings highlight the heterogeneity of induced scleroderma, in which the clinical presentation, laboratory findings, and histology may vary considerably depending on the specific chemical, dose, and duration of exposure, necessitating comprehensive diagnostic workup.

CONCLUSION

This article presents a clinical case of SSс induced by long-term occupational exposure to aggressive chemicals.

When taking a patient’s life history, the working condition and occupational history must be thoroughly assessed to identify potential harmful workplace factors. If such factors are confirmed, a consultation with an occupational physician is required to assess the potential relationship between the disease and professional activities, as well as to determine prevention and treatment strategies.

ADDITIONAL INFORMATION

Author contributions: O.A. Georginova: conceptualization, investigation, visualization, writing—original draft; E.A. Grishanina: investigation, writing—original draft, writing—review & editing; A.A. Michurina: investigation, writing—original draft; E.A. Makarova: conceptualization, formal analysis, writing—review & editing; V.G. Avdeev, E.M. Seredinina, T.N. Krasnova: conceptualization, investigation; L.A. Strizhakov: conceptualization Thereby, all authors provided approval of the version to be published and agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Consent for publication: Written informed consent was obtained from the patient for the publication of personal data, including photographs (with face obscured), in a scientific journal and its online version (signed on April 15, 2025). The scope of the published data was approved by the patient.

Funding sources: The study had no sponsorship.

Disclosure of interests: The authors declare that they have no competing interests.

Statement of originality: The authors did not use previously published information (text, illustrations, data) while conducting this work.

Data availability statement: All data obtained in this study are available in this article.

Generative AI: Generative AI technologies were not used for this article creation.

 

¹ Order of the Ministry of Health of Russia No. 141n of March 21, 2025, On Approval of the List of Occupational Diseases (Reg. No. 81893 of April 18, 2025). Available at: https://docs.cntd.ru/document/1312512294?ysclid=mjh4yjcitq786422672. Accessed on: December 15, 2025.

About the authors

Olga A. Georginova

Lomonosov Moscow State University

Email: olga.georginova@gmail.com
ORCID iD: 0000-0002-7542-8189
SPIN-code: 8331-3656

MD, PhD, Assistant Professor

Russian Federation, Moscow

Ekaterina A. Grishanina

Lomonosov Moscow State University

Author for correspondence.
Email: grishanina-2000@mail.ru
ORCID iD: 0009-0007-8265-6802
SPIN-code: 8220-7129
Russian Federation, Moscow

Antonina A. Michurina

Lomonosov Moscow State University

Email: michurinaa6@gmail.com
ORCID iD: 0000-0002-6563-5598
Russian Federation, Moscow

Egor A. Makarov

Lomonosov Moscow State University

Email: embrevas1507@gmail.com
ORCID iD: 0000-0002-2387-9930
SPIN-code: 8847-1318

MD, PhD

Russian Federation, Moscow

Vladimir G. Avdeev

Lomonosov Moscow State University

Email: avdeevvg@gmail.com
ORCID iD: 0000-0001-7901-6635
SPIN-code: 9387-0270

MD, PhD, Assistant Professor

Russian Federation, Moscow

Leonid A. Strizhakov

Lomonosov Moscow State University

Email: strizhakov76@mail.ru
ORCID iD: 0000-0002-2291-6453
SPIN-code: 3539-7327

MD, PhD, Professor

Russian Federation, Moscow

Tatyana N. Krasnova

Lomonosov Moscow State University

Email: krasnovamgu@yandex.ru
ORCID iD: 0000-0001-6175-1076
SPIN-code: 5524-6595

MD, PhD

Russian Federation, Moscow

Elena M. Seredenina

Lomonosov Moscow State University

Email: e.m.seredenina@gmail.com
ORCID iD: 0000-0002-1490-2078
SPIN-code: 8240-1733

MD, PhD

Russian Federation, Moscow

References

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