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MORPHOLOGY OF PATHOLOGICAL FORMS OF PLATELETS
Khalimova Yulduz Salokhiddinovna
Assistant, Department of Clinical Sciences,
Asian International University of Bukhara, Uzbekistan.
https://doi.org/10.5281/zenodo.14879659
Abstract. Platelets are small (2-3 microns) nuclear-free, flat, colorless shaped blood cells.
They are formed by fragmentation of their megakaryocyte precursors in the bone marrow, with a
platelet lifespan of 5-9 days. For a long time, researchers have proposed various classifications of
platelet morphological forms based on variations in one parameter or another. They play an
important role in the div, performing a number of complex functions, participating in various
processes. It is on platelets that the preservation of blood in a liquid state, the dissolution of formed
blood clots and the protection of the walls of blood vessels from damage depend.
Key words: platelets, megakaryocytes, granulomer, hyalomer, thrombocytopathies.
МОРФОЛОГИЯ ПАТОЛОГИЧЕСКИХ ФОРМ ТРОМБОЦИТОВ
Аннотация. Тромбоциты — это небольшие (2–3 мкм) безъядерные, плоские,
бесцветные клетки крови. Образуются путем фрагментации своих предшественников
мегакариоцитов в костном мозге, продолжительность жизни тромбоцитов составляет
5–9 дней. Исследователи давно предлагают различные классификации морфологических
форм тромбоцитов, основанные на вариациях тех или иных параметров. Они играют
важную роль в организме, выполняя ряд сложных функций, участвуя в различных процессах.
Именно от тромбоцитов зависит сохранение крови в жидком состоянии, растворение
образовавшихся тромбов и защита стенок сосудов от повреждений.
Ключевые слова: тромбоциты, мегакариоциты, грануломер, гиаломер,
тромбоцитопатии.
Platelets are an important component of the hemostatic system: platelet adhesion to the site
of vascular injury, aggregation, secretion of coagulation factors, subsequent clot retraction, spasm
of small vessels and the formation of a white platelet thrombus stop bleeding in microcirculatory
vessels with a diameter of up to 100 nm. Activation of the coagulation system induces the
formation of fibrin on the surface of activated platelets and the formation of a full-fledged
thrombus. When platelets are activated by natural stimulants such as thrombin or collagen, which
are exposed when the vascular wall is damaged, they are able to eject the contents of their granules
containing clotting factors, peroxidase, serotonin, calcium ions – Ca2+, ADP, Willebrand factor,
platelet fibrinogen, platelet growth factor, etc. At the highest degree of activation, the platelet
surface becomes procoagulant due to the exposure of phosphatidyl serine and stimulates the
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formation of a blood clot. Platelets also play an essential role in the healing and regeneration of
damaged tissues by releasing growth factors that stimulate cell division and proliferation in the
damaged area. Hereditary platelet dysfunction encompasses a diverse group of hemorrhagic
diseases caused by congenital defects in platelet morphology and/or function in normal numbers.
Various structures can be damaged and various processes in platelets can be disrupted:
membrane receptors, intra-platelet signaling, granules, etc. This leads to various clinical
manifestations of bleeding [2-4]. Thrombocytopathies are characterized primarily by the
development of spontaneous and post-traumatic mucosal bleeding. The recognition and
differentiation of thrombocytopathies is based on the detection of microcirculatory bleeding with
impaired functional properties, morphology and biochemical characteristics of platelets. Based on
these manifestations, the modern classification of thrombocytopathies is based, which is divided
into 2 large groups – hereditary and acquired. Clinical manifestations depend on the characteristics
of qualitative and quantitative platelet defects – the severity of hemorrhagic syndrome can vary
significantly and does not depend directly on the degree of defect. With mild bleeding, there may
be a tendency to bruising with minor and minor injuries, at the site of compression with an elastic
band; periodic excessive nosebleeds, familial prolonged menstruation in women, etc. In the case
of massive hemorrhagic syndrome, life-threatening blood loss may develop. Let's look at some
thrombocytopathies in more detail.
Glanzmann's thrombasthenia is a hereditary disease characterized by hemorrhagic
manifestations, in which there is an elongation of bleeding time, as well as a complete absence or
a sharp decrease in the intensity of blood clot retraction against the background of a normal platelet
count per unit volume of blood [5, 6]. This is the result of a decrease in platelet aggregation
capacity. The disease was first described in 1918. Dr. Edward Glanzman. Glanzmann's
thrombasthenia gravis is a rare disease and occurs with a frequency of approximately 1 case per 1
million [7]. The manifestation of the disease occurs in early childhood. The main clinical
manifestations are cutaneous hemorrhagic syndrome, bleeding from mucous membranes,
including gastrointestinal, up to life-threatening. The formation of soft tissue hematomas of
various localization is possible. Hemorrhagic syndrome can be either post-traumatic or
spontaneous. Carrying out any surgical interventions without hemostatic therapy, including tooth
extraction, is accompanied by the development of bleeding. Currently, there are 3 types of
Glanzmann's thrombasthenia gravis: type 1 – deficiency of the GPIIb–IIIa complex of surface
glycoprotein aggregation receptors < 5% of the norm; type 2 – deficiency of the GPIIb–IIIa
complex 5-20% of the norm, type 3 – the GPIIb–IIIa complex is present in normal or almost
normal amounts, but is functionally unstable. Nevertheless, there is no correlation between the
number of GPIIb–IIIa on the platelet surface and the severity of the clinical manifestations of the
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disease [6]. The pathogenesis of this disease is based on a deficiency or dysfunction of platelet
membrane proteins, integrin aIIbb3 (GPIIb–IIIa), which form a heterodimer complex on the
platelet surface that binds fibrinogen, Willebrand factor, fibronectin and vitronectin. This
membrane complex is a necessary component of the final stage of aggregation activated by
physiological agonists [8].
Upon activation, the GPIIb–IIIa complex changes its conformation and binds fibrinogen
and other soluble adhesive proteins, which, with the participation of Ca2+ ions, mediate the
aggregation of adjacent platelets in the forming clot [9-11]. Glanzman's thrombasthenia gravis has
an autosomal recessive type of inheritance [6, 12]. Both the aIIb and β3 integrin genes are located
on the long arm of chromosome 17q21.32 and are encoded in the ITGA2B and ITGB3 genes,
respectively. Gene expression occurs independently of each other [8, 13]. Small deletions and
modifications are more common than large rearrangements of genes [14]. Despite the fact that the
ITGB3 fragment has a smaller size, due to the presence of a larger number of exons, its mutation
occurs with a higher frequency [15]. As a result of the mutation, patients with Glanzmann's
thrombasthenia may have a deficiency or disruption of the GPIIb–IIIa structure. The presence of
a molecular defect in one or two genes is sufficient for the formation of thrombocytopathy [16-
19]. The severity of the clinical picture of Glanzman's thrombasthenia does not depend on the
identified mutations and may vary within the same family.
Gray platelet syndrome. CCT (OMIM #139090) was first described by Raccuglia in 1971
[20]. It was characterized as a pathological condition accompanied by thrombocytopenia, rather
mild manifestations of bleeding and the presence of agranular platelets in peripheral blood.
Biochemical and electron microscopic methods have shown that all organelles, except for α-
granules, are unchanged and present in normal amounts [21-23]. It is assumed that the cause of
this syndrome is the inability of megakaryocytes to form specific vesicles and fill them with α-
granular components [24].
At the same time, the number of megakaryocytes in the bone marrow is usually normal
[25]. Microscopically, large, pale-colored platelets are found in the cell. Platelet dysfunction
manifests itself in a decrease in aggregation with collagen and/or thrombin. Patients with CST are
often characterized by varying degrees of macrothrombocytopenia, bleeding of the mucous
membranes, and myelofibrosis and splenomegaly develop over the course of life [26, 27]. Bleeding
is usually not life-threatening, however, with surgical interventions or serious injuries, massive
blood loss is possible that cannot be stopped by standard methods. In such patients, platelet
aggregation tests give very variable results, and no general vector of change in this indicator could
be identified [28]. In most families, there is only 1 case of CST or several siblings suffer at the
same time. The inheritance pathways and genes linked to this disease are diverse.
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There are known cases of X-linked inheritance of a mutation in GATA-1, which leads to a
general decrease in the number of granules in platelets and the appearance of defective red blood
cells [29]. In 2014, D. Monteferrario et al. [30] reported the identification of a previously unknown
nonsense mutation in the gene of transcription factor (repressor) GFI1B in a family with autosomal
dominant CT. The NBEAL2 gene is most often damaged in CST, a variety of mutations in which
were identified in 2011 by C.A. Albers et al. [31].
Bernard–Soulier syndrome is a hereditary thrombocytopathy caused by a genetic defect or
a decrease in the functional activity of the GPIb-IX–V platelet complex. This complex is a
Willebrand factor receptor, and is also necessary for thrombin fixation on the platelet surface. From
a functional point of view, platelet adhesion to the vascular subendothelial matrix is impaired,
which is also characteristic of Willebrand's disease. The main diagnostic criteria for this pathology
are macrothrombocytopenia and the absence of Willebrand factor-dependent aggregation with
ristocetin, with a normal amount and normal activity of the factor itself. There may also be a
decrease in aggregation with thrombin against the background of normal aggregation with other
agonists. Deficiency of the GPIb-IX–V surface glycoprotein complex can be confirmed by flow
cytofluorometry and by genetic analysis of the GPIBA, GPIBB and GP9 genes.
Bernard–Soulier syndrome is manifested by significant bleeding of microcirculatory and
mixed type, which manifests itself immediately after birth. Inheritance is autosomal recessive [32].
Wiskott–Aldrich syndrome. Microthrombocytopenia and impaired platelet aggregation indicate
the presence of a qualitative or quantitative defect in the specific WASP protein (Wiskott–Aldrich
syndrome protein). The classical form of CBO is characterized by a complex of disorders, which
includes increased bleeding, recurrent bacterial, viral and fungal infections, as well as skin eczema.
There is a milder form of the disease – X-linked thrombocytopenia. The disease is
characterized by the absence of pronounced signs of immunodeficiency and eczema. In order to
verify the diagnosis of this group of patients, bone marrow puncture and myelogram analysis
should be performed. A normal number of unchanged megakaryocytes is noted in the myelogram
during CBO. Immunological defects in patients with CBO are the result of a violation of
lymphocyte homeostasis, manifested in a sharp decrease in the proportion of T and B lymphocytes.
When studying functional disorders of platelets in patients with CBO, increased expression of
phosphatidylserine and the formation of microparticles in response to a stimulus are detected. A
probable mechanism for the development of thrombocytopenia is increased removal of platelets
expressing phosphatidylserine by spleen macrophages. To confirm the diagnosis of Wiskott–
Aldrich syndrome and X-linked thrombocytopenia, it is necessary to analyze protein expression
and determine the WASP gene mutation [33].
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The MYH9 group of syndromes. The presence of large basophilic inclusions (Dele bodies)
in granulocytes and monocytes in a blood smear during Romanovsky-Giemse staining is a marker
of the MYH9 group of syndromes.
This group of syndromes includes the May–Hegglin anomaly, Fechtner, Epstein, and
Sebastian syndromes. The May–Hegglin anomaly was described by the German physician R. May
(1863-1937), and later by the Swiss physician R.M. Hegglin (1907-1969). The pathology is based
on a mutation of the MYH9 gene encoding the non–muscular myosin IIA heavy chain (NMMHC-
IIA). It is asymptomatic in most cases, but in some patients it is manifested by increased bleeding.
The type of inheritance is autosomal dominant. It is accompanied by thrombocytopenia, kidney
damage (nephritis), neuro-sensory hearing loss and cataracts, but the presence of these pathologies
is not mandatory, especially in children. Platelet aggregation with collagen is often disrupted in
patients with May–Hegglin anomaly during normal aggregation with other agonists, especially
with ristocetin. The detection of NMMHC–IIA aggregates in neutrophils by immunofluorescence
confirms the diagnosis of this group of syndromes. In order to determine a specific mutation, a
genetic analysis is recommended [34].
Storage pool deficiency syndromes. These include the Hermansky–Pudlak and Chediaka–
Higashi syndromes. They are inherited in an autosomal recessive way. These syndromes include
albinism, frequent infections, pulmonary fibrosis, granulomatous colitis, prolonged bleeding time,
and minor blood clotting disorders. The cause of the disease is a deficiency in the contents of dense
granules or themselves. Studies of platelet function reveal a violation of aggregation in reaction
with ADP, adrenaline, ristocetin and collagen. In Chediak–Higashi syndrome, dense granules
detected by electron microscopy are larger than normal and similar in size to granules of
melanocytes, leukocytes, and fibroblasts [35].
Scott syndrome. Thrombocytopathy, inherited by autosomal recessive type, caused by a
defect in phosphatidylserine release during platelet activation and, as a result, a violation of platelet
interaction with plasma coagulation factors. In this case, defective complexes of coagulation
factors Va–X and VIII–IXa are formed on the membrane. Defects in the binding of these
complexes lead to incomplete activation of factor X and prothrombin, as well as to impaired
activity of platelet factor 3 [36].
Thus, the recognition and differential diagnosis of thrombocytopathies should be based on
a comprehensive study of hemostasis, the study of platelet morphology by light and electron
microscopy, the assessment of functional activity by flow cytofluorometry, as well as genetic
analysis to identify mutations correlating with various types of thrombocytopathies.
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