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Eosinophil cationic protein increase is one of the reasons for the cerebrovascular diseases and related neurological disorders

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Reasons for increase in ECP

*The section will contain fewer references to literature and more personal observations (considering «forking» of reasons and their individuality), the information may be updated and expanded*

The reasons for increase in ECP may be quite individual, so finding one reason, relevant for all patients, is not the purpose of this section. An increase in ECP may result from a multitude of factors, and they are unfortunately not always evident.
The following main reasons for an increase in ECP are enumerated most often in literature/on the Internet:

  • parasitic invasions;
  • allergic reactions;
  • bacterial infections;
  • bronchial asthma;
  • autoimmune processes.

Less often ulcers and intestinal inflammation are added to the list.

Let us consider the main reasons in detail (on the author’s experience). While reading, it may be noticed that some reasons for ECP increase in literature are already associated with different neurological disorders (despite the fact that increase in ECP is not mentioned in that cases). That is, increased ECP level unites different diseases which may result in neurological disorders.

Parasitic invasions

Parasitic invasion was the author’s first version (it was not confirmed later on). ECP is toxic for parasites [Soroka, 1995] and its level increases with the majority of parasitic invasions. It is interesting to note that both leading and ordinary employees of the Martsinkovsky Parasitology Center (Moscow) were not surprised at a possible connection between neurological disorders and parasites. Neurological disorders caused by invasions are quite well-known and evident for parasitologists. It is important that this effect is produced not only by rare parasites, located right in the brain, but also all of the most widespread kinds. The concomitant neurological disorders are usually connected with their toxic influence on the body.

Thus, the first thing to be tested in case of an increased ECP (especially in children) is the presence of the most widespread parasites.

Allergic reactions

The author’s next version was hidden allergic reaction. The main allergens (respiratory and food panels) were tested, but the result did not give any reasons to talk about allergy.

However, it was found out later that food panels do not allow to precisely define one of the widespread food allergies, sensitivity to gluten. Sensitivity to gluten is determined by a whole number of specific tests. Russian laboratories use about 6 tests, while there are about 24 of them in the Western practice (CYREX array 3). Probably this is the reason why gluten-sensitive enteropathy is diagnosed much more frequently in the western countries. Besides, it should be noted that, in accordance with present day knowledge of gluten-sensitive enteropathy, this disease is no longer considered to be rare, and distribution of its hidden forms may achieve 1:100 [Парфенов, 2013], and according to some data — 1:3 [Perlmutter, 2013 / Перлмуттер, 2014]. Also, hidden forms of gluten-sensitive enteropathy often disguise as other diseases.
It turned out that the connection between sensitivity to gluten and neurological disorders had been already described, for example, in [Perlmutter, 2013 / Перлмуттер, 2014]. However, in [Perlmutter, 2013 / Перлмуттер, 2014] another mechanism of influencing the brain is presupposed, without participation of ECP or vascular spasms.

Thus, increased ECP also requires taking gluten sensitivity assays and, if necessary, sensitivity to other allergens (food and respiratory panels).

The question of whether the website author is sensitive to gluten still remains open. Five out of six tests are within reference values, and one is permanently increased (deamidated gliadin peptide antibodies, IgA). However, a biopsy did not confirm gluten-sensitive enteropathy, and the results of genetic studies also testify to its low probability. Gluten-free diet did not influence dynamics of ECP and deamidated gliadin peptide antibodies, though there are notable details described in the section «Additional comments».

Intestines inflammation (as a result of dysbacteriosis)

At the same time, a biopsy revealed inflammation of intestines (chronic duodenitis and colitis), supposedly of a bacterial nature (tests showed the development of opportunistic pathogenic and pathogenic microflora). Inflammation of intestines may also lead to increased ECP, and this is the author’s current version (regarding the reason for ECP increase in the case of the author).

The following observations should be provided here:
— the author observed the longest remission period in the middle of 2014 (complete absence of neurologic disorders). At that moment, the author had no version about spasms or ECP, but it was noted that it had happened after a course of antibiotics (in connection with another disease);
— at the end of 2014, the author experienced a period of the most frequent, severe and continuous neurological disorders. Supposedly, after treatment with antibiotics in the middle of the year, the intestinal microflora were not completely restored, whereas a shortage of useful microflora leads to the development of pathogenic microflora;
— in August of 2016, after treatment of another disease with antibiotics, ECP fell notably, but it restored over the following weeks (see the diagram below);
— in November of 2016, after duodenitis and colitis were diagnosed, treatment with antibiotics also resulted in falling ECP, but its level also restored over the following weeks;
— in April of 2017, taking Natamycin antimycotic agent (against Candida fungi whose development was discovered in dysbacteriosis analysis), which is active only in intestines, also resulted in a sharp decrease in ECP. However, it is possible that the decrease was connected not so much with elimination of Candida fungi but more with ECP withdrawal from the intestines as a result of Natamycin’s side effects; either way, the connection between ECP and intestines is quite visible.

Thus, if ECP exceeds the norm, one should take dysbacteriosis assay (it worth be noted that in Western practice a term «Intestinal Bacterial Overgrowth» is used to describe dysbacteriosis which underlines the proliferation of pathogenic microorganisms). If development of opportunistic pathogenic and pathogenic microflora is found, the patient needs to consult a gastroenterologist first. Before the microflora balance is restored, one can reduce the influence of ECP (and endotoxins associated with development of pathogenic microflora) by taking enterosorbents (for example, polymethylsiloxane polyhydrate). Also it should be always kept in mind that the use of antibiotics requires complete recovering of microflora in the intestines and ensuring its state even in absence of complaints about GIT functioning.

It was found later that the connection of intestinal microflora with the brain had been also described [Perlmutter, 2015 / Перлмуттер, 2017], but with a different mechanism of connection with the brain (without involvement of ECP and vascular spasms).

Intestines inflammation (as a result of gastrointestinal tract organs disease)

At the same time, development of microflora may only result from intestinal inflammation rather than cause it. Another possible reason of intestinal inflammation is the diseases of GIT organs, including liver and biliary tracts. It is noticeable that there is a separate term which connects brain disorders with liver diseases, hepatic encephalopathy. The concomitant neurologic disorders are also connected with increased content of toxic substances in the blood. Therefore, the patient also needs to take the relevant tests: ALAT, ASAT, Gamma GT, Bilirubin.

The author’s assays listed above are also within the normal range (the only analysis outside reference values is bile acids, but the «diagnostic value» of this test has not been established yet).

Despite the fact that the author still fails to find out the reason for intestinal inflammation, the dependence of ECP level on the state of the intestines is quite evident (in the case of the author).

Other reasons

Other possible reasons for increased ECP:

  • other gastrointestinal tract diseases (including intestinal ulcer);
  • other bacterial infections (e.g. in nasopharynx);
  • other allergic reactions;
  • bronchial asthma;
  • autoimmune diseases.

As the reasons are quite individual, additional hypotheses probably should base on the patient’s anamnesis.

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Additional comments

* The information may be updated and expanded *

  • Eosinophils were normal over the whole period of observations. ECP ranged within 24-50 ng/ml (with the normal value of <24 ng/ml). That is, the described case is not one of the quite rare hypereosinophilic syndromes. This is important in terms of extent of such diseases spreading.
  • During practically the whole period of observations, the level of uric acid was increased (and it fell after duodenitis and colitis treatment). It is interesting to note that there is information about the protective influence of uric acid in case of brain ischemia [Mattson M. et al., 2000].
  • Within the whole blood assays (a very large list) only consistent elevation of ECP, uric acid and deamidated gliadin peptide antibodies IgA was observed. The liver biochemistry samples has normal values (except for biliary acids). The thyroid gland is functioning normally.
  • Dynamics of deamidated gliadin peptide antibodies IgA was not fully explained by the diet. The result could be quite low with consumption of gluten-containing products and quite high when a diet was followed. Probably sensitivity to gluten may also be connected with the state of intestinal microflora [Barcik W. et al., 2016; Caminero A. et al., 2015]. According to the author’s observations, the state of microflora in the intestines predetermined the results of other analyses. In several cases, when the test for dysbacteriosis did not reveal any abnormalities, ECP, uric acid, deamidated gliadin peptide antibodies IgA and biliary acids showed normal values.
  • The results of dysbacteriosis test were unstable in time and changed significantly even over one week. However, it was noticed that a deterioration of state and increase in ECP was possible without excessive growth of gram-negative bacteria. This fact supports the idea that the impact of intestinal microflora on the brain is connected not only with lipopolysaccharides (which result from the decay of gram-negative bacteria).
  • Despite the fact that the author did not manage to reach stable lowering of ECP yet, the overall state has been radically improved due to treatment with nimodipine (Nimotop, BAYER), control of trigger-factors and diet correction. It is quite possible that the average level of ECP as for the end of 2014 (when the most severe symptoms were observed) was significantly higher, but unfortunately it cannot be proved now.

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