Buy Cytotec Online Canada

CYTOTEC 100mg, 200mg
Active Ingredient: Misoprostol

The active ingredient of Cytotec tablets is a synthesized analogue of prostaglandin E1 produced by the body. This molecule enhances the protective properties of the gastrointestinal mucosa by stimulating the production of mucus by glandular cells of the stomach. Cytotec should be used for ulcerative lesions of the duodenum with or without bleeding, ulcerative lesions of the stomach with or without bleeding.


Residents of megacities often suffer from peptic ulcer. The reason is that they live in constant stress, eat irregularly, eat fast food. Because of this, defects appear on the mucous membrane. Excess hydrochloric acid, the action of bile and pepsin can also adversely affect the state of the stomach. This disease is chronic, so the patient periodically exacerbates. To stop them, Cytotec should be used. Due to this, the periods of remission are significantly lengthened. Sometimes an ulcer does not remind of itself for years.

The reasons:

In most cases, the cause of ulcers is the presence of the bacterium Helicobacter pylori in the stomach. When it gets into conditions favorable to it, it begins to multiply rapidly, leading to the appearance of defects on the mucous membrane. Since the bacterium is transmitted in a household way, many people are infected with it, but not everyone has an ulcer. Why does it appear for some? The point is that there are favorable factors for the development of pathology.


If a person smokes, often drinks alcohol, eats dry, every day drinks a large amount of coffee, the likelihood of the appearance of pathology increases significantly. Other risk factors include heredity, severe stress, long-term treatment with aspirin, ibuprofen, glucocorticoids. Many patients initially increased acidity of gastric juice. Because of this, they have an ulcer, because hydrochloric acid can corrode the mucous membrane.


The presence of ulcers may indicate abdominal pain after eating. They can be of different intensity. Other signs include constipation, nausea, which sometimes turns into vomiting, bringing relief, sour belching. Since eating causes an attack of pain, patients refuse to eat, not wanting to experience unpleasant sensations. This leads to weight loss. To relieve pain, you need to use Cytotec. It promotes healing of damaged areas of the mucous.


We should not think that this disease is not necessarily treated. Such a delusion sometimes leads to death, because an ulcer can cause perigastritis, penetration, perforation of the stomach wall, the appearance of serious bleeding. The patient may need immediate surgery, otherwise there is a high risk of death. Anyone who does not want to bring the situation to a dangerous one must be treated promptly.


Any patient who see a doctor is required to get tested for the presence of antibodies to Helicobacter Pylori. The doctor may prescribe a microscopic and X-ray examination of the stomach, as well as endoscopy.


The patient must follow a diet and take medications prescribed by the doctor. Experts often advise Cytotec to buy at a pharmacy to prevent the likelihood of a possible exacerbation. In addition, they prescribe medication to eliminate heartburn, destroy Helicobacter Pylori, reduce the acidity of gastric juice.

Patients can not eat spicy and very hot food, well, if they give up alcohol and coffee, irritating the mucous membrane. Thanks to the diet, they will not feel discomfort.

Ulcerative Disease in Children

Peptic ulcer and duodenal ulcer is one of the important medical and social problems of modern society, which is associated with a high level of prevalence, clinical features, high risk of early manifestation and disability, the possibility of life-threatening complications, reduced treatment efficacy and impaired quality of life of patients. According to modern concepts, peptic ulcer is a chronic recurrent polyetiological disease, which is realized as a result of the interaction of exogenous and endogenous factors. However, internal factors are leading in the development of this disease, namely: hereditary predisposition, type of nervous and endocrine systems. For a long history of studying peptic ulcer, many theories of its occurrence have been proposed. In addition, each of them represented one of the stages of studying the anatomical, physiological and neuro-humoral mechanisms of digestion.

It has been established that when exposed to exogenous adverse factors, such as Helicobacterpylori infection, constant nutritional error, exposure to acute and chronic stress, as well as exposure to bad habits, hereditary predisposition to the development of erosive-ulcerative lesions of the gastrointestinal tract is realized. Genetic predisposition is one of the dominant causes of the development of gastric ulcer and duodenal ulcer. To date, genetic predictors have been identified, the presence of which contributes to the occurrence of destructive-inflammatory diseases of the gastrointestinal tract. The most important of them are: the hereditary increase in the mass of occipital cells and their hypersensitivity to gastrin, increased formation of pepsinogen-1, congenital deficiency of mucus fukoukoproteidov, insufficient production of secreted IgA and prostaglandins, as well as the first blood group and the presence of HLA antigens B5, B15, B35.

Among exogenous factors, there are so-called “background” situations that often accompany a child’s life: neuro-emotional stress, disruption of the day and diet, abuse of foods containing dyes and preservatives, dominance in the diet of refined foods that do not have sufficient buffering capacity, poor chewing food, etc. Of great importance is the unbalanced intake of vitamins and minerals from food. In addition to the above, the long-term use of drugs from the group of nonsteroidal anti-inflammatory drugs, tetracycline antibiotics, salicylates and sulfonamides has a negative effect on the state of the gastric mucosa. Such etiological factors play an important role, such as a decrease in the immunological reactivity of the child's body after acute viral infections and against the background of chronic, in particular, helminthic invasions. At present, according to most domestic and foreign authors, Helicobacterpylori infection, which was discovered in 1983 by Australian researchers R. Warren and B. Marshall, plays the most important etiological role in the development and course of peptic ulcer. H.p. is a gram-negative anaerobic bacterium. It is established that H.p. can stimulate both local and systemic defenses of the body. Leukocytes and macrophages phagocytic H.p. with the formation of IgA, IgG, IgM-antigens that activate complement and cytokine system. As a result, neutrophilic infiltration occurs in the mucosa. At the same time, interleukin-8 is of primary importance, which, modulating the chemotaxis and release of lysosomal enzymes from leukocytes, is aimed at neutralizing H.p.


However, activated leukocytes, seeking to penetrate the epithelium, damage the intercellular spaces. In addition, they secrete enzymes and oxygen free radicals, which violate the integrity of the epithelium and form a surface defect. In turn, H.p. stimulates apoptosis and enhances cell death along the periphery of the ulcer. Thus, NR, interfering with the processes of reparation, causes the development of chronic ulcers. However, the role of H.p. in the formation of gastric ulcer and duodenal ulcer in children remains controversial and the subject of numerous scientific debates and debates. First of all, this is due to the fact that not every patient infected with H.p. has a peptic ulcer, and moreover, not all cases of peptic ulcer are associated in childhood with H.p. Despite years of anti-Helicobacter therapy, the prevalence of peptic ulcer in our country, as in most countries of the world, is not decreasing, which contradicts the statement about the leading role of H.p. in the pathogenesis of peptic ulcer disease. Even apologists of the infectious theory of the origin of peptic ulcer are forced to admit that in some cases none of the reliable methods for identifying Helicobacterpylori, even with the simultaneous use of two or three diagnostic tests, can detect this infectious agent in the gastric and / or duodenal mucosa in patients with ulcerative diseases. It should be noted that the number of such cases is steadily increasing. Based on the above, it becomes obvious that a peptic ulcer should be considered as a polyetiological and polypathogenetic disease, and HP infection - as one of the most important, acting mainly locally, but not the only one. Given the multifactorial nature of peptic ulcer disease, as evidenced by numerous scientific medical works, it is currently difficult to imagine the development of this pathology among children, based on one ultirogenic factor alone.

It is known that in the development of peptic ulcer significant role belongs to changes in the functional activity of the immune system, implemented by T-and B-lymphocytes, in particular, cytokines. Along with the nervous and hormonal networks, the cytokine network constitutes an independent system of regulation of body functions. Being a communicator that links between neuroendocrine, immune, hematopoietic, and other systems, it serves to involve them in the organization and regulation of a single defensive response. Interleukins play an important role in the development and chronicity of diseases of the digestive system in children. In pathological conditions, there is a sharp increase in the values ​​of some interleukins against the background of a decrease in the indicators of others. According to literature data, cytokine imbalance is observed in the blood serum of patients younger than 18 years old with erosive and ulcerative lesions of the gastrointestinal tract, which is a manifestation of a systemic inflammatory process in this pathology. A review of immunological studies made it possible to summarize that peptic ulcer disease in children is accompanied by an increase in the content of pro-and anti-inflammatory interleukins in peripheral blood, expressed to varying degrees depending on the course of the disease, the stage of the inflammatory process and the effectiveness of the therapy. At the same time, changes in the content of cytokines in the blood of children with peptic ulcer disease are characterized by a significant increase in the ratios of concentrations of pro- and anti-inflammatory (IL-4) interleukins. The maximum increase in concentration is detected in children with newly diagnosed peptic ulcer.

Meanwhile, cytokines, in the first place, regulate the development of local inflammatory, immune reactions in tissues. It can be assumed that the assessment of the characteristics of changes in the cytokine profile directly in the inflammatory focus is more informative to determine the nature and direction of changes in immunopathological changes.

When studying the local inflammatory response in patients with peptic ulcer disease associated with N. p., It was found that the pathogen stimulates the production of proinflammatory cytokine - interleukin 8 (IL-8), both by cells of the gastric epithelium and by activated macrophages. This interleukin is a powerful cytokine produced by monocytes, lymphocytes, and endothelial cells. It attracts neutrophils and T-lymphocytes to the site of damage, regulates leukocyte adhesion. An important role in the launch and stimulation of the production of IL-8 is played by the cell wall lipopolysaccharide N. p. This reveals a direct correlation between the neutrophilic infiltration of the gastric mucosa and the level of secretion of IL-8. By activating neutrophils, IL-8 degrades them, providing a release of lysosomal enzymes, leukotrienes and reactive oxygen metabolites, which have a damaging effect on the mucous membrane. In turn, activated neutrophils begin to produce IL-8, which leads to the development of a "vicious circle of inflammation" and further exacerbate existing disorders. In addition, it was found that, in addition to the chemotactic effect on microphages, IL-8 also stimulates the release of gastrin by G-cells, and, consequently, contributes to the increase in acid production. H. pylori also induces the production of TNF-α and IL-6 by macrophages.

IL-1β plays an equally important place in the cytokine regulation ensemble for peptic ulcer disease. The inhibitory ability of IL-1β on gastric acid formation is realized both directly, through exposure directly to the parietal cells, and indirectly. E. Saperas et al. Found that the inhibitory effect of IL-1β is realized through the stimulation of the synthesis of prostaglandin E2, which is a potent inhibitor of hydrochloric acid. A direct inhibitory effect on acid formation, as suggested by W. Schepp et al., Can be accomplished through receptors that are complementary to IL-1β, located on the parietal cells. According to the medical literature, IL-1β is one of the leading immunological factors that can inhibit the production of hydrochloric acid. In addition, the activation of interleukin-1β leads to the launch of a cascade of both pro- and anti-inflammatory cytokines, which can be a factor in the progression of the pathological process, exerting a direct damaging effect on cells and tissues, inducing alteration, disturbance of the integrity of the vascular wall, strengthening and chronization of the inflammatory process . Thus, summarizing the data from the medical literature, it can be argued that the local immune response, as well as the systemic one, is pro-inflammatory. Of the two classes of T-lymphocyte-helper cells (CD4 +), ulcers with YB are dominated by the Th phenotype, which is characterized by the secretion of pro-inflammatory cytokines, such as IL-1, IL-8, TNFα. At the same time, cytotoxic T-lymphocyte suppressors (CD8 +) are expressed with the development of immune inflammation in the gastric mucosa. Ultimately, an ulcerative defect is formed as a result of an increase in the aggressiveness of the gastric juice and a weakening of the protective factors of the gastric mucosa. However, the question of whether the triggering factor for the development of an ulcer defect is presently still debatable: the presence of a pathogenic microbe that alters local immunity, or, nevertheless, the cause of peptic ulcer disease is genetic polymorphism that has arisen during ontogeny, as a process of adaptation to changing external conditions and the internal environment of the body. There is no doubt the fact that "the plague is a local expression of some common violations." Considering the pathogenesis of peptic ulcer, it is necessary to understand that its formation, both in the gastric mucosa and in the duodenum, is associated with an imbalance of local factors of "protection" and "aggression". At the same time, the role of H.p in the occurrence and progression of this disease is far from ambiguous.

At present, there is a shift of attention from the immune to the immunogenetic basis of diseases, while peptic ulcer is not an exception. In the past decade, evidence has emerged that not so much the properties of the bacteria determine the development of reactive changes in the gastric mucosa, but many genetic factors, in particular, immune inflammation genes, coordinating the direction and severity of immunological reactions. The effect of the polymorphisms of the IL-1β genes (encoding IL-1β) and IL1RN (an IL-1β receptor antagonist) on the character of immune inflammation is as follows: the carriage of wild alleles of genes is associated with moderate production of the corresponding proteins; while in carriers of mutant alleles, there is a genetically determined advantage in favor of increased production of IL-1β and the development of pronounced immune inflammation.

Equally important in the immune response system for ulcer are polymorphisms of the IL-1RA genes (IL-1 receptor antagonist). It has been proven that in carriers of a genetically determined bias towards the production of IL-1RA, the inflammatory response is more continual, which may cause chronic inflammation. The plasma level of IL-1RA is known to be dependent and jointly regulated by the IL-1β and IL1RN genes, and the carrier state of IL1RN * 2 is responsible for the elevated levels of both circulating IL-1RA and IL-1β, the increased activation of expression and production of which is a consequence over-production IL-1RA. According to this version, when implementing an inflammatory response in carriers of a genetically determined overbalance towards the production of IL-1RA, the amount of IL-1 receptor antagonist is greater than is necessary for adequate realization of inflammation, which causes a compensatory increase in IL-1β synthesis. At the same time, IL-1RA, in response, begins to be produced in larger quantities. Thus, the carriage of combinations of the IL1B and IL1RN genes, which determine an advantage in the direction of IL-1RA production, leads to a longer inflammatory response. It is proved that polymorphic variants of the gene IL-1β with peptic ulcer are highly producing. In individuals who are homo- or heterozygous for the high-producing IL-1β allele, there is an increase in the synthesis of this cytokine by 2–4 times higher than in patients who have a wild allele in a homozygous state. It can be assumed that high rates of pro-inflammatory cytokines are beneficial for the macroorganism. However, in the presence of a polymorphic variant of IL-1β, further inhibition of acid production occurs with further colonization of H. pylori and the progression of inflammatory changes in the body of the stomach. At the same time, the level of acid production decreases and, over time, the glands lose, that is, atrophy of the gastric mucosa begins. It should be noted that the immunogenetic aspects of the etiopathogenesis of peptic ulcer are highlighted for advantage in persons over 18 years of age. At the same time, it is impossible to put an equal sign between those gene-phenotypic associations found in adult patients with peptic ulcer and children. This is primarily due to the “functional immaturity” of the immune mechanisms in childhood, as well as the presence of so-called “critical periods of immunity development”, when an inadequate response of the body in response to typical inflammation and the lack of full realization of the phenotypic manifestation of the genetic polymorphism being studied can occur the course of the disease. Thus, the study of gene-mediators of immune inflammation, with destructive-inflammatory diseases of the gastroduodenal zone in children, is one of the priorities in uncovering the pathogenetic aspects of the development and course of peptic ulcer, as well as to identify genetic risk factors for complications of the disease.

Today, gastric ulcer and duodenal ulcer is a systemic multifactorial disease with a polygenic variant of inheritance, while HP infection can be considered as one of the important, but mainly locally acting, factors of the pathogenesis of peptic ulcer, and as an indicator of the risk of its recurrence. At the same time, the study of the genetic basis of the immune response in peptic ulcer disease in children, in particular, the polymorphisms of the IL-1β, IL-8, TNFα genes, allows extending the etiopathogenetic ideas about the disease and revealing the genetic risk factors of certain complications.


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