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Art of Medicine           Volume-1 

International Medical Scientific Journal        Issue-2 
10.5281/zenodo.5576350 

212 
 

 

Art of Medicine International Medical Scientific journal 

 

Founder and Publisher Pascual Izquierdo-Egea 

Published science may 2021 year. Issued Quarterly. 
Internet address: http://artofmedicineimsj.us 

E-mail: info@artofmedicineimsj.us 

11931 Barlow Pl Philadelphia, PA 19116, USA +1 (929) 266-0862 

 

 
  



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The role of endothelial dysfunction in the development of immune 

microthrombovasculitis 

Islamova Z.S., Inoyatova F.Kh., Babadjanova Sh.A., Yusupkhodjaeva Kh.S., 

Kurbonova Z.Ch. 

Tashkent Medical Academy Republic of Uzbekistan  

 

Abstract: comparative assessment of endothelial dysfunction indicators in patients 

with IMTV depending on the form of the disease and the characteristics of its course. 

Material and methods. We examined 140 patients with BMI at the age of 18-62 

years. All patients, depending on the clinical manifestations of the disease, were 

subdivided into 4 groups: 1st - 32 patients with skin, 2nd - 84 patients with skin-

articular, 3rd - 12 patients with mixed skin-articular and abdominal and 4th group - 

12 patients with generalized skin-articular and renal forms of IMTV. The control 

group consisted of 20 conditionally healthy individuals. The indices of the vascular-

platelet, coagulation link of hemostasis, the anticoagulant system were assessed 

according to generally accepted methods. Endothelial dysfunction was assessed by 

the level of endothelin 1 (ET-1), von Willebrand factor (vWF), thrombomodulin and 

adhesion molecules (sICAM-1)) by enzyme immunoassay. The digital material was 

processed by the method of variation statistics. Results. The study of the vascular-

platelet link of hemostasis in patients with IMTT showed a tendency to develop 

moderate thrombocytosis and an increase in their thrombogenic activity. The study of 

three phases of the coagulation link of hemostasis indicated pronounced 

hypercoagulation in all groups. The dynamics of changes in hemostasiological 

parameters showed their relationship with the activity and severity of IMTV. A 

pronounced endothelial dysfunction was revealed, manifested by an increase in the 

content of ET-1, vWF, sICAM-1, and thrombomodulin in the blood plasma. The 

severity of these changes is minimal in the cutaneous form of the disease and sharply 

increases in its generalized form.. Output: In patients with IMTV, depending on the 

form of the disease, dysfunction of endotheliocytes of microvessels develops with 

inhibition of anticoagulant and increased procoagulant components.  



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Keywords: immune microthrombovasculitis, vascular endothelium, endothelin 1, 

von Willebrand factor, adhesion molecules, thrombomodulin, hemostasis. 

 

Among the general human pathology, there is an increase in the incidence of 

hemorrhagic diathesis (HD). HD is characterized by widespread distribution, a 

variety of clinical manifestations, and a high incidence of severe hemorrhagic and 

thrombohemorrhagic complications, which are often fatal. In the general structure of 

HD, in terms of the frequency of its occurrence among all populations and age groups 

of the population, polymorphism and severity of the clinical course, a special place is 

given to pathologies of the primary hemostasis of an acquired nature, including 

immune microthrombovasculitis (IMTV) [3, 4, 5, 7, 21] ... The annual incidence of 

IMTV is 2 people per 10,000 population and there is an increase in the number of 

patients [6, 9]. The pathogenesis of the disease is associated with overproduction of 

low molecular weight circulating immune complexes and the deposition of granular 

IgA deposits in the vascular wall [1, 10, 13]. This leads to the activation of the 

complement system, an increase in the permeability of the vessels of the 

microvasculature and with the involvement of the hemostatic system in the process. 

As a result, the rheological properties of blood are disturbed, platelet aggregation 

increases, and hypercoagulability syndrome with depression of the fibrinolytic 

system develops [1, 8, 10, 11]. According to the literature, the leading role in the 

development of predisposition to this pathology belongs to the polymorphism of 

genes of proinflammatory cytokines, genes of the angiotensin and endothelial 

systems [2, 16, 17]. The study of the formation mechanisms of IMTV is a priority in 

a number of large research centers of the world [12, 14, 19]. In the development of 

this multifactorial disease, an important place is given to both the individual 

characteristics of the organism, the influence of exo- and endogenous factors, the 

intensity of which largely determines the risk of its formation [15, 18, 20]. 

The expansion of innovative strategies and the introduction of high 

technologies in our Republic allow a targeted approach to the development of the 

foundations of evidence-based medicine, including such important aspects as the 



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mechanisms of formation, the development of effective methods for predicting the 

development of a severe course of the disease and the risks of developing 

complications of IMTV. The introduction of methods for determining endothelial 

dysfunction made it possible to decipher the main mechanisms of the development of 

pathological conditions, develop criteria for early and differential diagnosis and 

improve the tactics of treating various diseases manifested by endothelial 

dysfunction. However, in the literature, there are sporadic data on the presence of 

endothelial dysfunction with IMTV. 

Purpose of the study: comparative assessment of endothelial dysfunction 

indicators in patients with IMTV, depending on the form of the disease and the 

characteristics of its course. 

Material and research methods. 

The study included 140 patients with an established diagnosis of IMTV. 

Verification of the BMI diagnosis was carried out according to modern classification 

criteria. The selection of patients was carried out by the method of random sampling 

as they approached. The age of the patients with BMI ranged from 18 to 62 years 

(median age 32.1 ± 3.9 years), mostly young and mature people (86.4%). Analysis of 

the distribution of patients by age and sex showed that women predominated among 

the patients, and there were almost 2 times less men. 

All patients examined by us, depending on the clinical manifestations of the 

disease, were subdivided into the following forms of IMTV: 32 (22.8%) patients had 

a skin form (group 1), 84 (60.0%) patients had a skin-articular form (group 2 ), 12 

(8.6%) had mixed skin-articular and abdominal form (group 3) and 12 (8.6%) had 

generalized skin-articular and renal form (group 4). The control group consisted of 20 

conditionally healthy unrelated persons who did not have a history of hemostasis 

system pathology, corresponding in terms of sex and age to the examined main group 

of patients. 

The diagnosis and clinical form of the disease were established on the basis of 

complaints, history of life and disease, clinical symptoms and laboratory data. 



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Particular attention was paid to objective data and anamnesis of the disease: periodic 

appearance of small-point cutaneous hemorrhages, leaving behind 

hyperpigmentation, pain in the joints, edema, pain in the stomach during the onset of 

hemorrhages, blood in the urine and feces, general weakness, other symptoms and the 

reasons with which the patient associates the development of the disease. Upper 

respiratory tract infections (56.4%) and drug intake (22.1%) were provoking factors 

for the development of IMTT. 48.6% of patients had a history of allergic diseases, 

and 16.4% of patients noted the presence of hereditary diseases of the blood 

coagulation system. 

To assess the state of the vascular-platelet link of hemostasis, the number of 

platelets was counted according to Fonio in peripheral blood smears by the method of 

phase-contrast microscopy, the aggregation of platelets was studied using the 

hemolysate-aggregation test in dilutions 10-2, 10-6 according to ZS. Barkagan, B.F. 

Arkhipov and V.M. Kuchersky (1980), platelet adhesion on fiberglass, blood clot 

retraction in a test tube according to V.P. Baluda et al. (1980). To study the 

coagulation link of the hemostasis system, the activated partial thromboplastin time 

(APTT), prothrombin index (PTI), thrombin time (TB), soluble fibrin-monomer 

complexes (RFMK), the amount of fibrinogen) were determined on a HumaClot 

Junior coagulometer (Germany) and anticoagulant system blood by determining the 

activity of antithrombin III (AT III) and XII-α dependent fibrinolysis according to 

G.F. Eremin and A.G. Arkhipov (1982), using reagents of NPO RENAM (Russia). 

Determination of indicators of endothelial dysfunction (endothelin 1 (ET-1), 

von Willebrand factor (vWF), thrombomodulin and adhesion molecules (sICAM-1)) 

was determined on a HumaReader HS (Human) enzyme immunoassay analyzer using 

commercial ELIZA kits from Human. All statistical analyzes were performed using 

SAS software. Quantitative variables were presented as mean ± standard deviation. In 

addition, when analyzing the correlations, the Spearman rank test was used. P <0.05 

was considered statistically significant. 

Results and its discussion 



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Symmetrical petechial hemorrhagic rashes on the legs up to the knee were 

present in 32.3% of patients in group 1 with the cutaneous form of BMI, in 29% - 

also petechiae on the hips and buttocks, in 29% - in most parts of the body. In severe 

cases, maculopapular rash with necrotic changes in the skin in the center and the 

appearance of small ulcers was observed in 16.1% of patients. At first, rashes 

appeared on the feet and legs, later they spread higher, the abundance of rashes 

correlated with the severity of BMI. The duration of the disease in patients with the 

cutaneous form was the shortest and amounted to 15.0 ± 2.3 days. 

In group 2 patients, along with skin lesions in the form of a symmetrical 

hemorrhagic rash, joint damage was also observed. The articular syndrome was 

expressed by pain and periarticular swelling, redness, disorder of motor functions, 

mainly in large joints. Basically, 61.9% of patients had ankle joint damage, in 22.6% 

of cases - ankle and knee joint damage, in 15.5% of cases other joints were also 

affected. Symmetrical involvement of the joints was observed; joint deformities with 

impaired function were not observed. The duration of the disease in patients with 

skin-articular form averaged 8.7 ± 1.8 months. 

In group 3 patients with a mixed skin-articular and abdominal form of the 

disease, in addition to damage to the skin and joints, damage to the gastrointestinal 

tract was also observed, resulting from hemorrhage in the intestinal wall and 

mesentery. Patients complained of vomiting, cramping abdominal pains like intestinal 

colic, tension and tenderness of the abdomen on palpation, but they could not 

pinpoint the location of pain. In 25% of patients, vomiting, abdominal pain preceded 

skin-articular symptoms, which made diagnosis difficult. During 

esophagoduodenoscopy in patients of this category, petechial rashes were observed in 

the mucous membranes of the stomach and duodenum 12. In 16.6% of patients, the 

abdominal form was complicated by intestinal bleeding, simulating acute surgical 

diseases of the abdominal cavity. The duration of the disease with a mixed skin-

articular and abdominal form of IMTV was more than 2 years, proceeded with 

relapses in case of violation of the diet. 



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In group 4 of patients with a mixed skin-articular and renal form of IMTV, 

there was kidney damage of varying degrees: in 50% of patients there was short-term 

unstable hematuria up to 2-3 days, in 33.3% - persistent but unexpressed hematuria 

up to 5-7 days, and 16.7% had pronounced gross hematuria for more than 10.0 ± 0.7 

days. Chronic renal failure was established in 16.7% of patients in this group. The 

duration of the course of this form of IMTV was about 1.5 years. 

The study of the vascular-platelet link of hemostasis in patients with IMTV 

showed a tendency to develop moderate thrombocytosis (from 308 ± 32.3 x 109 / L 

to 453 ± 56.1 x 109 / L), an increase in thrombocrit from 0.26 ± 0.02% to 0 ,  45 ± 

0.02%. The study of the functional activity of platelets showed an increase in 

thrombogenic activity of platelets, manifested by an increase in the adhesive and 

aggregation properties of platelets by 18.6-42.7%, a shortening of the retraction time 

of a blood clot by 12.5-25.0%.  

Analysis of the plasma link of hemostasis showed a pronounced shortening of 

the blood coagulation time and APTT, prothrombin time, thrombin time, INR, an 

increase in the prothrombin index, the amount of fibrinogen, and plasma tolerance to 

heparin. The study of the three phases of the coagulation link of hemostasis indicated 

pronounced hypercoagulation in all groups in relation to the control group. The 

dynamics of changes in hemostasiological parameters showed their relationship with 

the activity and severity of IMTV. 

Currently, the immunocomplex nature of IMTV has been proven, in which 

aseptic inflammation develops in microvessels with wall destruction, thrombosis and 

the appearance of purpura of various localization due to the damaging effect of 

circulating immune complexes and activated components of the complement system 

[2, 11, 20]. Expression of such pro-inflammatory cytokines as tumor necrosis factor-α 

(TNF-α) and interleukin-6 (IL-6) leads to an increase in the synthesis of vascular 

growth factor (VEGF) by endothelial cells during the acute phase of the disease [3, 6, 

21] ... In this regard, we investigated the indicators of the functional activity of the 

endothelium showed the development of its dysfunction (Table 1). Thus, 



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dysregulation of vascular tone during IMTV is associated with an increase in the 

production of endothelial peptides, in particular ET-1, the content of which in the 

blood serum of patients increases statistically significantly increases depending on 

the form of the disease. If in the cutaneous form of BMI the content of ET-1 exceeds 

the standard level by 15.8%, then in the cutaneous-articular, abdominal and renal 

forms this excess was 28.5; 30.2 and 67.1%, respectively, groups, indicating the 

development of vasoconstriction in patients. It should be said that at low 

physiological concentrations, ET-1 has an effect on endothelial receptors, causing the 

release of relaxation factors. At the same time, at high concentrations, it activates 

smooth muscle cell receptors and causes persistent vasoconstriction.  

Table 1 

Indicators of endothelial dysfunction in patients with IMTV, M ± m 

Groups Von Willebrand 

factor, % 

Endothelin-

1, pg / ml 

Thrombomod-

lin, pg / ml 

sICAM-1, pg / 

ml 

Control group, 

n = 20 

89,89±2,56 4,10 ± 0,24 3,54±0,28 55,69±4,44 

ИМТВ 

Skin form, n = 

8 133,75±7,46* 4,75±0,54 2,44±0,22** 69,95±4,94* 

Skin-articular 

form, n = 18 145,17±5,60** 5,27±0,36* 2,18±0,12*** 86,00±7,04*** 

Abdominal 
form, n = 12 188,00±3,29*** 5,34±0,53* 1,93±0,17*** 110,80±11,66** 

Renal form, n = 

7 191,41±5,52*** 6,85±0,52** 1,56±0,15*** 146,83±12,86*** 
Note: * - the differences between the indices of the control group of the examined and the 

patients with IMTV are significant (P <0.05), ** - P <0.01 and *** - P <0.001. 

 

Along with this, we also revealed the content of vWF: exceeding the standard 

values by 48.8; 61.5; 109.1 and 112.9% in groups of patients with skin, skin-articular, 

abdominal and renal forms of the disease, respectively groups. This factor is a carrier-

stabilizer for the procoagulant protein FVIII: C circulating in the serum in the form of 

a non-covalently bound complex, and is an adhesion protein during hemostasis [11]. 

Therefore, elevated vWF levels are an indicator of endothelial damage. On the other 



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hand, the increased formation of collagen in the vascular wall leads to a loss of their 

elasticity, the ability of the vessels to dilate decreases, which is manifested by the 

inhibition of anticoagulant and increased procoagulant properties [3, 5]. The 

pathogenesis is based on the formation of immune complexes and the activation of 

components of the complement system, which have a damaging effect on the vascular 

wall [4, 6]. The main initiators of endothelial damage in PSG are cytokines, which 

are involved in the activation of neutrophils. IL-8, which activates neutrophil 

epithelial protein (ENA-78), and T-lymphocytes are involved in providing 

chemotaxis of neutrophils to sites of inflammation [3, 5, 20]. Circulating immune 

complexes cause vasculitis, which is accompanied by perivascular edema, 

microcirculation disorders, and hemorrhages. Damage to the vascular wall leads to 

activation of the hemostasis system: functional activity of platelets, hypercoagulation, 

a decrease in the level of antithrombin III [3, 5]. 

According to the literature, with thrombophilia, the content of homocysteine in 

the blood plasma increases [3, 6]. According to B.I. Kuznik et al. (2012), 

hyperhomocysteinemia is the leading pathogenetic mechanism of endothelial 

dysfunction [6]. Its oxidized form activates the formation of free radicals, inhibits the 

synthesis of antioxidant enzymes in endothelial cells. As a result, there is damage to 

the endothelial lining of blood vessels, proliferation of smooth muscle cells, 

activation of platelets and a decrease in the content of heparan sulfate, which is an 

antithrombin III receptor (AT-III). At the same time, the binding of AT-III to 

endothelial cells decreases, which disrupts the atrombogenicity of the inner layer of 

the endothelium [3, 6]. Along with this, the activation of leukocytes, the release of 

cyto- and chemokines, and the expression of adhesion molecules are noted.  

In this regard, we also studied the content of serum sICAM-1. Studies have 

shown an increase in its content by 26 and 54.4% in cutaneous and skin-articular 

forms of IMTV. In the generalized form of BMI, the level of sICAM-1 increases 

more pronounced: in the abdominal form by 99.89%, in the renal form - by 163.7% 

relative to the values of practically healthy individuals. These indicators were 



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significantly higher than the values of groups with skin and skin-articular forms of 

IMTV. Therefore, we can say an increase in the adhesive properties of leukocytes. 

Under physiological conditions, the endothelial cell does not express adhesion 

molecules. An increase in the concentration of the latter on the surface of endothelial 

cells occurs under the action of various damaging factors: an increase in the linear 

shear stress in a certain part of the artery, the accumulation of oxidized lipids and 

lipoproteins in the subendothelial space [3, 6]. sICAM-1 of fibroblasts and 

endothelial cells is induced by inflammatory mediators. The interaction of leukocyte 

β2-integrin with sICAM-1 accelerates the adhesion of leukocytes and their 

transendothelial migration. 

It should be said that vascular endothelial dysfunction leads to a decrease in the 

activity of protein C (PC) and protein S (PS), a decrease in the affinity of 

thrombomodulin for thrombin, leading to a sharp drop in the activity of natural 

anticoagulants [3]. Thrombomodulin is a receptor for thrombin expressed on 

endothelial cell membranes. When interacting with thrombin, the resulting 

thrombomodulin / thrombin complex activates protein C, i.e. thrombomodulin carries 

out anticoagulant regulation, since active protein C inactivates factors fVa, fVIIIa, 

fXa and fXIIIa, inhibits the conversion of fibrinogen to fibrin, accelerates thrombin 

inactivation by antithrombin III. 

In this regard, we also studied the content of thrombomodulin in the blood 

plasma of patients with IMTV. Studies have shown a decrease in its content by 31.1; 

38.4; 45.5 and 55.9%, respectively, in the groups with cutaneous, skin-articular, 

abdominal and renal forms of BMI. It should be said that the concentration of 

thrombomodulin increases with an increase in the ratio of the surface of the vessels to 

the volume of blood. This ratio changes more than 1000 times when moving from 

large vessels to microcirculation. In microcirculation, almost all thrombin is 

associated with CD141, its clotting activity is suppressed and activation is increased. 

The concentration of the level of thrombomodulin in plasma indicates damage to the 

vascular endothelium. 



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Thus, the conducted studies have shown dysfunction of the vascular 

endothelium in patients with IMTV. The severity of these changes is minimal in the 

cutaneous form of the disease and sharply increases in its generalized form. In 

patients with a severe form of IMTV, it is indicative of a hypercoagulable syndrome 

due to dysfunction of endothelial cells of microvessels with inhibition of 

anticoagulant and an increase in procoagulant components. Our data demonstrate the 

importance of studying specific inducers of platelet aggregation, indicators of the 

functional activity of the vascular endothelium in patients with IMTV.  

Conflicts of Interest. The authors declare no conflicts of interest. 

Sources of financing. The study was not sponsored. 

Authors' contributions. Concept and design: all authors. Collection and 

processing of data: all authors. Submission of research materials: all authors. Data 

Analysis and Interpretation: All Authors. Manuscript preparation: all authors. Final 

approval of the manuscript: F.Kh. Inoyatova. 

 

  



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