In severe tissue parasitosis in tropical areas, those that evolve towards cachexia and exitus, especially in children, are probably involved several factors: direct action of parasitic metabolic products, the action of the immune system by cytokines (TNF, IFN) and indirect immunological action by cross-reactivity (examples – chronic heart disease, esophagitis and megacolon in Chagas disease, resulting in cross-reactivity between Irypanosoma cruzi and neuron structures; oncercus volvulus ossifies a cross-reactivity antigen with the retina.
\nThe main immunological mechanism of parasite defense seems to be the TH1 line (IFN and TNF\u03b1) involved, especially in the larval forms and the TH2 line (IL3, IL4, IL5), in helminthiasis forms.
\nIn Europe, the evolution of parasitosis is much better. The sharing of tapeworms can extend over a period of years without affecting the general condition, while African filariasis causes cachexia and lethargy. Treatment regimens in Europe are much shorter and more effective, so there is probably a degree of immunodeficiency in Africa, especially in children.
\nAccording to the observations of immunologists, in filariasis, TH1 has a defect of activation and proliferation in cellular immunity, while the humoral response increases, especially on the Ig G4 line. Filariasis can secrete prostaglandin depressive cures on the inflammatory reaction.
\nIn tropical areas, where exposure to U.V radiation is high, there may be a degree of immunodeficiency resulting from an excess of vitamin D3 (cholecalcifera). In these areas, the incidence of autoimmune diseases is lower, as vitamin D3 has a modulating role in rheumatoid arthritis, multiple sclerosis and insulin-dependent diabetes. Vitamin D has been proposed to be associated with glucocorticoid regimens because it has an immunomodulatory effect.
\nThe combination of active vitamin D3 + Dexamethasone, placed in a culture medium with monocyte-derived dendritic cells, reveals a synergistic effect of inhibiting dendritic cell maturation.
\nVitamin D functions as a regulator of the immune response; Vitamin D (VDR) receptors are found on the surface of mononuclear blood cells. Supplementation with the hydroxylated active form 1,25 dihydroxycholecalciferol [1,25 – (OH) 2D3] has a beneficial role in rheumatoid arthritis, juvenile diabetes and allergic encephalomyelitis.
\nAnd the TH lymphocyte has VDR; Vitamin D3 has an inhibitory action on the TH1 lymphocyte and a stimulatory action on the TH2. Vitamin D may be a regulator of TH cytokine transcription.
\nPatients in these areas may also have an imbalance of essential fatty acids. They are known to have immunomodulatory properties, but it is important that the essential fatty acids be of plant origin. They can be obtained in vegetarian diets by converting linoleic acid (from sunflower) to arachidonic acid.
\nSources of essential fatty acids 3 are more difficult to access (flaxseed and soybean oil) but they can be obtained from sunflower oil by transformation (conversion occurs easily if the diet is vegetarian).
\nIn Europe, where it consumes a lot of sunflower oil, the degree of immunodeficiency is not as high as in Africa. Butylcarbamazine has been discontinued in some Eastern European countries. Although it is an effective antiparasitic, it is more immunomodulatory and probably in this regime, the immune system is more competent.
\nIn parasitosis, it seems that the cure with pumpkin seeds is effective, probably due to the content of polyunsaturated fatty acids. The equivalent of one kilogram of pumpkin seeds \/ day is required to prove effectiveness. Essential polyunsaturated fatty acids also have an anticasectic role and an anti-inflammatory and immunomodulatory effect. Casexia is also produced by metabolic changes produced by proinflammatory cytokines.
\nParasitic antigens are of two types:
\n– somatic (polysaccharides, glycoproteins, hypoproteins, proteins) – their immunogenicity is lower than metabolic ones; sometimes, they are coupled with haptens to various structures and often give cross-reactions, responsible for some of the symptoms;
\n– metabolic antigens – products of secretion and excretion resulting from metabolism; they have structures close to proteolytic and lipolytic enzymes and are strongly immunogenic.
\nGlycolytic structures are not described, which confirms the observation in Romanian folk medicine that the evolution is much improved if sugar and dairy products are removed from the diet. It seems that parasites use harder glucose from starch, so the combination of diabetes with the treatment greatly improves the evolution and can save fatal cases. It should be mentioned that starvation, hypoglycemic cures are not effective, but, on the contrary, a carefully chosen vegetarian diet.
\nAlbendazole treatment also works to reduce the use of glucose through microtubules: it binds to microtubules and inhibits the polymerization and assembly of microtubules, so the combination with a sweet and dairy-free glucose-free diet brings superior results. The regime must be maintained for years to come, probably for life.
\nSometimes antiparasitic regimens also contain associated glucocorticoids (example: in ocular toxocarosis the standard scaffold includes Albendazole and glucocorticoids for 5-20 days). A standard combination of Saprosan 3% and Triamcinolone acetonide 0.10% in Triamcinolone S (topical ointment) greatly increases the effectiveness of the antifungal. Efficacy-enhancing combinations are common with ointments and less with oral medication, but this is probably the case with glucocorticoid + vitamin D3, glucocorticoid + albendazole regimens in ocular toxocarosis, glucocorticoids + antituberculostatic in TB pleurisy (not in pneumonia is TB). also intense), glucocorticoids + myostin in the standard 15 mg Prednisone regimen (3 times basal adrenal secretion) in myasthenia gravis.
\nAnother type of regimen has been proposed by some authors with the administration of Prednisone before chemotherapy (in viral hepatitis in the idea of \u200b\u200bactivating the liver virus at a level at which it is more sensitive to the action of interferon). The scheme was also tested in parasitology (Prednisone before Albendazole), without superior effects. It seems that the maximum efficacy is only when the standard scheme of ocular toxocarosis is combined with Albendazole concomitantly with Prednisone for 5-20 days.
\nAccording to allergists, Prednisone in vitro can sometimes have the opposite effect of immunostimulation, like Cyclophosphamide. Cyclophosphamide, at very low doses, can inhibit Ts lymphocyte (dose-dependent inhibition) by producing stimulation. The effect is similar to that of BCG vaccination.
\nIn parasitosis, the duration and concentration of the chemotherapeutic should be adjusted according to the development cycle of the parasite. In dormant parasites, anti-metabolic parasites are not very active and prolonging the duration of treatment can lead to resistance (the parasite chronically swallowing the drug can develop resistance so it is important to establish the optimal duration of treatment as short as possible).
\nSome infectious disease and parasitologists in Iasi, Romania, treated a case of urticaria and angioedema in toxocarosis with short Albendazole regimens of 5-7, respectively, 10 days. Psychiatrists have reported positive antisepocara canis antibodies during treatment with Risperidone in patients with psychosis (parasitic disillusionment). They are probably asymptomatic carriers of dormant parasites with cerebral localization (Risperidone has tropism for the central nervous system and may also act in parasites of the central nervous system inversely than Ivermectin which does not cross the blood-brain barrier and acts only in tissue parasites.
\nIn Romania, a case of toxocarosis was also positive with clinical manifestations of marked asthenia (chronic fatigue syndrome, diagnosed with the criteria Gay Holmes – Atlanta, 1988). Canis antitoxocara antibodies were initially undetectable but subsequently tested positive with Albendazole in parallel with the improvement in clinical symptoms. It appears to have been a case of chronic fatigue syndrome with cerebral toxocarosis with undetectable antibodies. There are several mechanisms by which parasites evade the immune system’s defense systems:
\n\u2022 parasitic dormancy (not very expressive of metabolic antigens and somatic antigens are not very immunogenic; the cuticle of some parasites may be devoid of antigenicity but may become immunogenic by conjugation with other components of the parasites);
\n\u2022 immunodeficiency (in macrophage B and T lymphocytes, deficiencies of the complement system that lead to altered immune system function).
\nIn conclusion, balancing the hygienic-dietary regime by respecting exposure to UV radiation (it seems that morning radiation is beneficial in strengthening the immune system) and introducing a vegetarian diet, without sweet and dairy foods, could have beneficial effects in the treatment of tropical parasites, thus being able to save severe cases.<\/p>\n
Mihaela Ghimpu
\nClinical Immunology Specialist
\nand Allergology<\/p>\n","protected":false},"excerpt":{"rendered":"
In severe tissue parasitosis in tropical areas, those that evolve towards cachexia and exitus, especially in children, are probably involved several factors: direct action of parasitic metabolic products, the action of the immune system by cytokines (TNF, IFN) and indirect immunological action by cross-reactivity (examples – chronic heart disease, esophagitis […]<\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[41],"tags":[],"class_list":["post-128","post","type-post","status-publish","format-standard","hentry","category-therapeutic-perspectives"],"yoast_head":"\n