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Biomedical subjects

S Rasković

Publications and source records attributed to S Rasković.

11 recordsLinked to original sources
PubMed1994

[Plasmapheresis in clinical practice].

Plasmapheresis is an immunomodulatory procedure with immunosuppressive effect. Plasmapheresis involves taking blood, separating off the plasma and returning the red cell-enriched fraction to the patient. In plasmapheresis improvement is due to the removal of mediators of tissue damage. Therapeutic plasmapheresis has been used in many diseases in which immunological mechanisms are proved. It has been noted that there may be a "rebound" in the level of antibodies and immune complexes after plasmapheresis, perhaps due to elimination of feedback suppressor mechanisms. For that reason, plasmapheresis is only effective when used as part of an immunosuppressive regimen which also includes steroids and/or cytotoxic agents.

Humans↗
PubMed1994

[Therapeutic use of human immunoglobulin].

Human immune globulin administered intramuscularly has been used for more than 40 years. In the last decade intravenous preparations were developed. They do not aggregate and contain IgG molecules with intact recognition and effector functions. These compounds are safe and only minor side effects were reported even when high doses were given. The mechanism by which intravenous gammaglobulin exacts its function is a combination of the Fc receptor blockade in the reticuloendothelial system, a marked increase in the suppressor cell function with down regulation of the antibody production and an intervention in the idiotype-antiidiotype network. Human immune globulin is an important therapeutic tool not only in the antibody deficiency, but also as an immunomodulatory agent in autoimmune disorders.

Humans↗
PubMedDate not supplied

[Angioedema caused by angiotensin-converting enzyme inhibitors].

Angioedema is a rare, but important effect of arterial hypertension treatment with drugs which inhibit angiotensin-converting enzyme. Usually, it develops in the first week of therapy, but some atypical cases of the development of angioedema after several months to few years after the onset of the therapy have been reported. Undesired reactions caused by these drugs are probably not allergic, but they are caused by pharmacological effect of these drugs in persons with risk of allergic reaction. In this paper we present some patients with angioedema.

Angioedema↗
PubMedDate not supplied

[Risk factors for allergic bronchial asthma].

The paper deals with the current data on aetiological factors of allergic bronchial asthma. The cause of allergic bronchial asthma is unknown. In general, endogenous and environmental factors are though to play a certain role in its development. Early contact with allergic agents, air pollution, tobacco smoking and infective agents (viruses), are considered to be environmental factors. Endogenous factors are heredity of allergic diseases and special susceptibility for bronchial asthma.

Asthma↗
PubMedDate not supplied

[The role of mononuclear phagocytes and dendritic cells in allergic inflammation].

Mononuclear-phagocytic system is a diffuse network of cells which includes monoblasts and promonocytes of the bone marrow, blood monocytes, as well as free and fixed tissue macrophage cells. In different tissues and organs macrophages acquire different morphological and functional properties under the influence of the local tissue factors. Interaction of macrophages with other cells and molecules is performed via the large number of different receptors resulting in activation of the macrophage cell, accompanied by a series of morphological and metabolic changes which potentiate all its functions. Activated macrophage cells were found in certain diseases. Macrophages and dendritic cells are associated with all aspects of immunity. Owing to their capacity to undergo phagocytosis they are of the utmost importance for unspecific defense from microorganisms. As accessory cells they also participate in cellular and humoral immunity, being at the same time effector cells owing to their capacity of antigen presentation. Moreover, they also participate in immune response regulation owing to their influence on the function of other cells, including mast cells, basophilic leukocytes and T lymphocytes, in which they may influence differentiation toward Th1 or Th2 and cytokine milieu favorable for allergic reaction. Dendritic cells are the most important antigen-presenting cells and thus, they play a major role in activation of helper T lymphocytes, and mode of antigen presentation is significant for regulation of the nature and intensity of the immune response. Pulmonary macrophage cells have been most thoroughly studied, and the observed changeability of their functional and morphological characteristics is of the utmost importance for studying of the pathogenetic properties and regulation of the chronic inflammatory response in bronchial asthma.

Asthma↗
PubMedDate not supplied

[The role of thrombocytes in allergic inflammation].

The platelet has traditionally been associated with haemostasis. Participation of platelets in defence mechanisms is presentiment by the knowledge that primary haemostasis may be phylogenetic vestige retained from the behaviour of primitive leukocytes. Platelets have the ability to undergo shape change with pseudopod formation, chemotaxis, diapedesis, and phagocytose. Platelets contain a wide range highly potent inflammatory factors that are capable of inducing or augmenting certain inflammatory responses. Different surface molecules have been detected on the plasma membrane, highlight the platelets ability to bind a variety of biologic surfaces, including those of other cells, resulting in close apposition of platelets and their targets. They can interact with parasites, viruses and bacteria. Studies from several groups suggest an important role of the platelet in allergic processes. Platelets possess receptor for immunoglobulin E. Numerous clinical reports are describing the modification of biologic activity of platelets from allergic patients as compared to healthy subjects. The incidence of abnormal platelet responsiveness is in higher among patients having high serum IgE titres. Platelet depletion decreased the anaphylactic response and protects against the lethal consequences of the antigen provocation. Evidence now exists in support of primary role of the platelet in the pathogenesis of bronchial asthma. Platelets can participate in allergic asthma by acting as inflammatory cells, by releasing spasmogens and by interacting with other inflammatory cells. Thrombocytopenia and the increased plasma levels of platelet-derived markers occurred in parallel with bronchoconstriction induced by antigen provocation of allergic astmatics. Platelet depletion inhibits the ability of antigen to induce late onset airways obstruction and airway hyperresponsiveness. Platelet apheresis in human resulted in a positive clinical effect. Platelets respond to aspirin or other NSAIDs in acetyl salicylic acid sensitive asthmatics and these findings provide further evidence for role of the platelet in this form of bronchial asthma.

Asthma↗
PubMedDate not supplied

[T lymphocytes in allergic inflammation].

T lymphocytes are the crucial cells in immunopathogenesis of allergic diseases since they regulate the occurrence of allergic sensitisation, synthesis of immunoglobulin E and allergic inflammation. The importance of lymphocyte T is reflected on the fact that after activation by a specific antigen they are able to produce different cytokines responsible for activation and aggregation of specific inflammatory cells in target tissues, promoting the occurrence and maintenance of allergic inflammation. Discovery of functional dichotomy of activated lymphocytes T CD4+ capable of suppressing synthesis of immunoglobulin E (Th1) or stimulate immunoglobulin E and allergic inflammation (Th2) is an important element in elucidation of pathogenesis of allergic inflammation and inadequate synthesis of immunoglobulin E. The immunoglobulin synthesis is regulated by a complex combination of factors and signals where lymphocytes CD4+ play the central regulatory role.

Humans↗
PubMedDate not supplied

[Leukotrienes in allergic inflammatory reactions].

Production of leukotrienes, lipooxygenase products of arachidonic acid metabolism, plays an important role in inflammatory reactions, particularly well studied in bronchial asthma. Lipooxigenase-5 and lipooxygenase-activating protein-5 are crucial in the production of leukotrienes with potent biological activities. Leukotriene B4 is a leukocytic chemoattractant and it induces aggregation and adherence of leukocytes to endothelial vasculature. Sulfidopeptid leukotrienes (C4, D4 and E4) are potent bronchoconstrictors, producing mucous secretion in the airways and increasing vascular permeability. Leukotrienes participate in the process of inflammation, as well as in early and late asthmatic responses. They are found in the blood, liquid obtained upon bronchoalveolar lavage as well as in the urine, irrespectively whether bronchospasm developed spontaneously or it was induced by an allergen. Administration of the specific leukotriene receptor antagonists or leukotriene synthesis inhibitors ameliorates the symptoms and signs of bronchial asthma.

Asthma↗
PubMedDate not supplied

[The role of prostaglandins in allergic inflammation].

Prostaglandins likewise leukotriens are proinflammatory mediators resulting from metabolic degradation of the arachidonic acid originating from membrane phospholipids. The most important products of enzyme cyclooxygenation of arachidonic acid are prostaglandins D2, E2, F2a, tromboxane A2 and prostacyclin. Prostaglandins express their tissue effects via the five basic receptor types. Within the allergic inflammation activated mast cell synthesizes prostaglandin D2 (first lipid mediator) which has bronchoconstrictive and vasodilating effects and attracts neutrophilic leukocytes. Moreover, it also participates in the late phase reactions, six hours subsequent to the exposure to the allergen. This mediator is also important in pathogenesis of urticaria, allergic rhinitis and allergic bronchial asthma. In addition to prostaglandin D2, prostaglandin F2a and tromboxane A2 also have bronchoconstrictive actions, while prostacyclin and prostaglandin E have bronchodilating effects. Inhalation of prostaglandin E prevents asthmatic attacks caused by allergens, strain, metabisulfite and ameliorates attacks of aspirin asthma, which confirms the hypothesis that aspirin asthma is based on cyclooxigenase inhibition and increased leukotriene production. In patients with atopic dermatitis, prostaglandin E has suppressive effects on Interferon gamma production by Th1 helper cells and increases production of Interleukin 4 by the Th2 cells. Tromboxane A2 plays a certain role in the development of bronchial hyperreactivity and late asthmatic response. Prostaglandins are also important mediators in the pathogenesis of allergic conjunctivitis. Most of nonsteroidal antiinflammatory drugs inhibit the enzyme cyclooxygenase and thus also prostaglandin biosynthesis and release.

Animals↗