Ты сейчас вылечи кишечник сначала,потом будешь смотреть. А как подтвердили Бехчета?
Клещ подарил букет и покаЛечимся)
- Автор темы Ence
- Дата начала
Mitya
Почетный форумчанин
- Сообщения
- 3.378
- Лайки
- 1.485
- Баллы
- 128
Родион .. нет такой болезни, ну т.е. это очередная модель системного воспалительного ответа на хронич инфекции, в этот раз под совокупным названием болезнь бехчета
довольно таки удачная модель, стоит признать
[2020] Higher 25-hydroxyvitamin D level is associated with increased risk for Behçet's disease
Higher 25-hydroxyvitamin D level is associated with increased risk for Behçet's disease - PubMed
Previous studies showed a vitamin D deficiency in patients with Behçet's disease, suggesting potential benefits of vitamin D supplementation in the prevention and treatment of Behçet's disease. Interpretation of these studies may be limited by reverse causality or confounding bias. We aim to determine the causal association between serum 25-hydroxyvitamin D [25(OH)D] and the risk of Behçet's disease by Mendelian randomization.
...
On the basis of evidence in 7909 human beings, this study provides the newest indication that a lifelong higher 25(OH)D level is associated with an increased risk of Behçet's disease. Special attention should be paid to the potential harm of long-term or high-dose use of vitamin D supplements in clinical practice.
[2014] Vitamin D deficiency in patients with Behcet’s disease
Vitamin D deficiency in patients with Behcet’s disease
[2017] High Vitamin D Levels May Downregulate Inflammation in Patients with Behçet's Disease
High Vitamin D Levels May Downregulate Inflammation in Patients with Behçet's Disease
[2011] Vitamin D status in patients with Behcet's Disease
Vitamin D status in patients with Behcet's Disease
In patients with Behcet's Disease, 25-hydroxyvitamin D values were significantly lower than those of the healthy controls (p<0.001). Serum Ca, P, and ALP levels were similar in both groups. Serum ESR and CRP levels were significantly higher in patients than controls (p<0.05). There was no correlation between 25-hydroxyvitamin D levels and age, body mass index (BMI), disease duration, ESR, or CRP levels.
[2008] Effects of vitamin D on expression of Toll-like receptors of monocytes from patients with Behcet's disease
Effects of vitamin D on expression of Toll-like receptors of monocytes from patients with Behcet's disease - PubMed
Objectives: Recent studies have shown the immunomodulatory effect of vitamin D(3) through down-regulation of Toll-like receptor (TLR) expression in human monocytes. To understand the implication of innate immunity with the role of vitamin D affecting TLR expression in Behçet's disease (BD), we focused on the association between the TLR expression and the serum vitamin D concentration in BD.
Methods: The expression of TLR2, TLR4 and CD16 on monocytes was detected by flow cytometric analysis and RT-PCR. Serum 25-hydroxyvitamin D [25(OH)D] levels were measured in the patients with BD, psoriasis and healthy controls, and then the expression of TLRs was correlated with the value of serum 25(OH)D levels. To assess the influence of vitamin D(3) on expression and function of TLRs in vitro, human monocytes were treated with increasing concentrations of 1,25(OH)(2)D(3).
Results: We found that the monocytes of active BD patients showed higher expressions of TLR2 and TLR4 than those of controls, and serum 25(OH)D levels tended to be lower in active BD. Furthermore, 25(OH)D levels were inversely correlated with the expressions of TLR2, TLR4 and clinical indicators. In vitro analysis showed that vitamin D(3) was found to dose-dependently suppress the protein and mRNA expressions of TLR2 and TLR4. TNF-alpha synthesis was also decreased upon TLR ligand stimulation in vitamin D(3)-treated monocytes.
Conclusion: These results suggest that the inflammation triggered through TLR2 and TLR4 is important in the pathogenesis of BD. And it seems possible that vitamin D may be used as a therapeutic option by modulating TLR2 and TLR4 expression of monocytes in BD.
...
So called "Behcet’s disease" is another good example of basket-case diagnosis of a chronic, body-wide inflammation:
Behcet's disease - Diagnosis and treatment - Mayo Clinic
If you have moderate to severe Behcet's disease, your doctor might prescribe: Corticosteroids to control inflammation. Corticosteroids, such as prednisone, are used reduce the inflammation caused by Behcet's disease. Doctors often prescribe them with another medication to suppress the activity of your immune system.
____
Scientists discover how neuroactive steroids dampen inflammatory signaling in cells
Scientists discover how neuroactive steroids dampen inflammatory signaling in cells
For the first time, scientists discovered how neuroactive steroids naturally found in the brain and bloodstream inhibit the activity of a specific kind of protein called Toll-like receptors (TLR4), which have been known to play a role in inflammation in many organs, including the brain.
The effect of systemic corticosteroid therapy on the expression of toll-like receptor 2 and toll-like receptor 4 in the cutaneous lesions of leprosy Type 1 reactions
The effect of systemic corticosteroid therapy on the expression of toll-like receptor 2 and toll-like receptor 4 in the cutaneous lesions of leprosy Type 1 reactions - PubMed
We have demonstrated that the gene hARP-P0 is a suitable control gene for TLR gene expression studies in this population. The gene and protein expression of TLR2 and TLR4 were both reduced significantly during corticosteroid treatment.
____
Toll-like receptor 4 in acute viral infection: Too much of a good thing
What is TLR4 and what are its ligands?
The innate immune system recognizes pathogen-associated molecular patterns (PAMPs) of viral or bacterial intruders via pattern recognition receptors (PRRs). This includes the family of TLRs that consists of related, transmembrane proteins that play a central role in the initiation of inflammatory responses, including the secretion of cytokines and chemokines.
TLR4, which is mainly expressed on cells of the immune system—including monocytes, macrophages and dendritic cells—has long been recognized as a PRR that senses lipopolysaccharide (LPS), a component of the outer membrane of gram-negative bacteria. Activation of TLR4 by LPS, its best studied ligand, is a multistep process. The initial step involves the LPS binding protein (LBP) which extracts LPS from bacterial membranes and LPS-containing vesicles to transfer it to the TLR4 coreceptor cluster of differentiation 14 (CD14). CD14 exists in two forms, soluble and membrane-bound. Both forms are able to interact with LPS-loaded LBP. CD14 breaks down LPS aggregates and transfers monomeric LPS into a hydrophobic pocket on myeloid differentiation factor 2 (MD-2) that is part of the MD-2/TLR4 complex. The high-affinity binding of LPS leads to dimerization and activation of the MD-2/TLR4 complex [6, 7]. Activation of TLR4 results in the recruitment of the intracellular adaptor protein, myeloid differentiation primary response 88 (MyD88), and/or toll/interleukin-1 receptor (TIR)-domain-containing adapter-inducing interferon-β (TRIF), ultimately resulting in the expression and secretion of pro-inflammatory mediators [6, 7].
TLR4 has also been shown to be a sensor for damage-associated molecular patterns (DAMPs). These include a wide variety of molecules released from injured or dying tissues as well as molecules actively released in response to cellular stress from intact cells [6, 8]. In addition to bacterial PAMPs and cellular DAMPs, TLR4 also recognizes PAMPs from other pathogens including fungi, parasites, and viruses [9]. How the TLR4 complex is activated by DAMPs and non-LPS PAMPs, which vary widely in their structure—some with no structural similarities to LPS [8, 10]—remains to be determined. Resolving the structure of these complexes is a critical part toward dissecting their mechanisms of activation.
____
Potential Infectious Etiology of Behçet's Disease
Potential Infectious Etiology of Behçet's Disease
Behçet's disease is a multisystem inflammatory disorder characterized by recurrent oral aphthous ulcers, genital ulcers, uveitis, and skin lesions. The cause of Behçet's disease remains unknown, but epidemiologic findings suggest that an autoimmune process is triggered by an environmental agent in a genetically predisposed individual. An infectious agent could operate through molecular mimicry, and subsequently the disease could be perpetuated by an abnormal immune response to an autoantigen in the absence of ongoing infection. Potentia bacterial are Saccharomyces cerevisiae, mycobacteria, Borrelia burgdorferi, Helicobacter pylori, Escherichia coli, Staphylococcus aureus, and Mycoplasma fermentans, but the most commonly investigated microorganism is Streptococcus sanguinis. The relationship between streptococcal infections and Behçet's disease is suggested by clinical observations that an unhygienic oral condition is frequently noted in the oral cavity of Behçet's disease patients. Several viral agents, including herpes simplex virus-1, hepatitis C virus, parvovirus B19, cytomegalovirus, Epstein-Barr virus and varicella zoster virus, may also have some role.
Higher 25-hydroxyvitamin D level is associated with increased risk for Behçet's disease - PubMed
Previous studies showed a vitamin D deficiency in patients with Behçet's disease, suggesting potential benefits of vitamin D supplementation in the prevention and treatment of Behçet's disease. Interpretation of these studies may be limited by reverse causality or confounding bias. We aim to determine the causal association between serum 25-hydroxyvitamin D [25(OH)D] and the risk of Behçet's disease by Mendelian randomization.
...
On the basis of evidence in 7909 human beings, this study provides the newest indication that a lifelong higher 25(OH)D level is associated with an increased risk of Behçet's disease. Special attention should be paid to the potential harm of long-term or high-dose use of vitamin D supplements in clinical practice.
[2014] Vitamin D deficiency in patients with Behcet’s disease
Vitamin D deficiency in patients with Behcet’s disease
[2017] High Vitamin D Levels May Downregulate Inflammation in Patients with Behçet's Disease
High Vitamin D Levels May Downregulate Inflammation in Patients with Behçet's Disease
[2011] Vitamin D status in patients with Behcet's Disease
Vitamin D status in patients with Behcet's Disease
In patients with Behcet's Disease, 25-hydroxyvitamin D values were significantly lower than those of the healthy controls (p<0.001). Serum Ca, P, and ALP levels were similar in both groups. Serum ESR and CRP levels were significantly higher in patients than controls (p<0.05). There was no correlation between 25-hydroxyvitamin D levels and age, body mass index (BMI), disease duration, ESR, or CRP levels.
[2008] Effects of vitamin D on expression of Toll-like receptors of monocytes from patients with Behcet's disease
Effects of vitamin D on expression of Toll-like receptors of monocytes from patients with Behcet's disease - PubMed
Objectives: Recent studies have shown the immunomodulatory effect of vitamin D(3) through down-regulation of Toll-like receptor (TLR) expression in human monocytes. To understand the implication of innate immunity with the role of vitamin D affecting TLR expression in Behçet's disease (BD), we focused on the association between the TLR expression and the serum vitamin D concentration in BD.
Methods: The expression of TLR2, TLR4 and CD16 on monocytes was detected by flow cytometric analysis and RT-PCR. Serum 25-hydroxyvitamin D [25(OH)D] levels were measured in the patients with BD, psoriasis and healthy controls, and then the expression of TLRs was correlated with the value of serum 25(OH)D levels. To assess the influence of vitamin D(3) on expression and function of TLRs in vitro, human monocytes were treated with increasing concentrations of 1,25(OH)(2)D(3).
Results: We found that the monocytes of active BD patients showed higher expressions of TLR2 and TLR4 than those of controls, and serum 25(OH)D levels tended to be lower in active BD. Furthermore, 25(OH)D levels were inversely correlated with the expressions of TLR2, TLR4 and clinical indicators. In vitro analysis showed that vitamin D(3) was found to dose-dependently suppress the protein and mRNA expressions of TLR2 and TLR4. TNF-alpha synthesis was also decreased upon TLR ligand stimulation in vitamin D(3)-treated monocytes.
Conclusion: These results suggest that the inflammation triggered through TLR2 and TLR4 is important in the pathogenesis of BD. And it seems possible that vitamin D may be used as a therapeutic option by modulating TLR2 and TLR4 expression of monocytes in BD.
...
So called "Behcet’s disease" is another good example of basket-case diagnosis of a chronic, body-wide inflammation:
Behcet's disease - Diagnosis and treatment - Mayo Clinic
If you have moderate to severe Behcet's disease, your doctor might prescribe: Corticosteroids to control inflammation. Corticosteroids, such as prednisone, are used reduce the inflammation caused by Behcet's disease. Doctors often prescribe them with another medication to suppress the activity of your immune system.
____
Scientists discover how neuroactive steroids dampen inflammatory signaling in cells
Scientists discover how neuroactive steroids dampen inflammatory signaling in cells
For the first time, scientists discovered how neuroactive steroids naturally found in the brain and bloodstream inhibit the activity of a specific kind of protein called Toll-like receptors (TLR4), which have been known to play a role in inflammation in many organs, including the brain.
The effect of systemic corticosteroid therapy on the expression of toll-like receptor 2 and toll-like receptor 4 in the cutaneous lesions of leprosy Type 1 reactions
The effect of systemic corticosteroid therapy on the expression of toll-like receptor 2 and toll-like receptor 4 in the cutaneous lesions of leprosy Type 1 reactions - PubMed
We have demonstrated that the gene hARP-P0 is a suitable control gene for TLR gene expression studies in this population. The gene and protein expression of TLR2 and TLR4 were both reduced significantly during corticosteroid treatment.
____
Toll-like receptor 4 in acute viral infection: Too much of a good thing
What is TLR4 and what are its ligands?
The innate immune system recognizes pathogen-associated molecular patterns (PAMPs) of viral or bacterial intruders via pattern recognition receptors (PRRs). This includes the family of TLRs that consists of related, transmembrane proteins that play a central role in the initiation of inflammatory responses, including the secretion of cytokines and chemokines.
TLR4, which is mainly expressed on cells of the immune system—including monocytes, macrophages and dendritic cells—has long been recognized as a PRR that senses lipopolysaccharide (LPS), a component of the outer membrane of gram-negative bacteria. Activation of TLR4 by LPS, its best studied ligand, is a multistep process. The initial step involves the LPS binding protein (LBP) which extracts LPS from bacterial membranes and LPS-containing vesicles to transfer it to the TLR4 coreceptor cluster of differentiation 14 (CD14). CD14 exists in two forms, soluble and membrane-bound. Both forms are able to interact with LPS-loaded LBP. CD14 breaks down LPS aggregates and transfers monomeric LPS into a hydrophobic pocket on myeloid differentiation factor 2 (MD-2) that is part of the MD-2/TLR4 complex. The high-affinity binding of LPS leads to dimerization and activation of the MD-2/TLR4 complex [6, 7]. Activation of TLR4 results in the recruitment of the intracellular adaptor protein, myeloid differentiation primary response 88 (MyD88), and/or toll/interleukin-1 receptor (TIR)-domain-containing adapter-inducing interferon-β (TRIF), ultimately resulting in the expression and secretion of pro-inflammatory mediators [6, 7].
TLR4 has also been shown to be a sensor for damage-associated molecular patterns (DAMPs). These include a wide variety of molecules released from injured or dying tissues as well as molecules actively released in response to cellular stress from intact cells [6, 8]. In addition to bacterial PAMPs and cellular DAMPs, TLR4 also recognizes PAMPs from other pathogens including fungi, parasites, and viruses [9]. How the TLR4 complex is activated by DAMPs and non-LPS PAMPs, which vary widely in their structure—some with no structural similarities to LPS [8, 10]—remains to be determined. Resolving the structure of these complexes is a critical part toward dissecting their mechanisms of activation.
____
Potential Infectious Etiology of Behçet's Disease
Potential Infectious Etiology of Behçet's Disease
Behçet's disease is a multisystem inflammatory disorder characterized by recurrent oral aphthous ulcers, genital ulcers, uveitis, and skin lesions. The cause of Behçet's disease remains unknown, but epidemiologic findings suggest that an autoimmune process is triggered by an environmental agent in a genetically predisposed individual. An infectious agent could operate through molecular mimicry, and subsequently the disease could be perpetuated by an abnormal immune response to an autoantigen in the absence of ongoing infection. Potentia bacterial are Saccharomyces cerevisiae, mycobacteria, Borrelia burgdorferi, Helicobacter pylori, Escherichia coli, Staphylococcus aureus, and Mycoplasma fermentans, but the most commonly investigated microorganism is Streptococcus sanguinis. The relationship between streptococcal infections and Behçet's disease is suggested by clinical observations that an unhygienic oral condition is frequently noted in the oral cavity of Behçet's disease patients. Several viral agents, including herpes simplex virus-1, hepatitis C virus, parvovirus B19, cytomegalovirus, Epstein-Barr virus and varicella zoster virus, may also have some role.
Mitya
Почетный форумчанин
- Сообщения
- 3.378
- Лайки
- 1.485
- Баллы
- 128
Нет такой болезни... Это да, это мощно. И лечить не надо, раз болезни нет. Как удобно.
хахахаха Вам уже выдали нобелевку за первый случай вылечивания бехчета?
вы пишите осторожнее, а то нубы могут действительно поверить что вы своей фармой че-то там "вылечиваете"
Болезнь Бехчета - Нарушения со стороны скелетно-мышечной и соединительной ткани - Справочник MSD Профессиональная версия
Болезнь Бехчета — этиология, патофизиология, симптомы, признаки, диагностика и прогноз в справочниках СПРАВОЧНИКИ MSD Профессиональная версия.
Лечение преимущественно симптоматическое, но при более тяжелом течении заболевания могут назначаться глюкокортикоиды как монотерапия или в сочетании с иммунодепрессантами.
ой, какой сюрприз, опять кортикоиды повылезали, какое совпадение не правда ли? на любую из бед - один ответ
Svetlana
Известный человек
- Сообщения
- 683
- Лайки
- 253
- Баллы
- 58
Лечила Энтеролом, Смектой, Ципролетом максимум 7 дней (от него связки заболели).
MiaMagic
Известный человек
- Сообщения
- 672
- Лайки
- 221
- Баллы
- 58
Маргарита, день добрый!
Подскажите, пожалуйста, Вы употребляли кору вяза скользкого вместе в антибиотиками?
Если да, то на сколько разносили прием вяза с антибиотиками и другими препаратами?
Маргарита Фрост
Уважаемый форумчанин
- Сообщения
- 1.810
- Лайки
- 690
- Баллы
- 128
Добрый день, нет, я кору пила до аб.Во время аб максилак только.
Добрый день
Каких антов?
Больше предназначен для лечения эрозивных поражений,препарат выбора.
Белла59
Читатель
- Сообщения
- 26
- Лайки
- 7
- Баллы
- 3
В данный момент я стала принемать профилактический курс аб. амоксициллин, после укуса клеща, Чем лучше защитить желудок, кишечник?
Спасибо.
Тут надо пробиотики пить,а не ингибиторы для снижения кислотности,иначе будут проблемы по флоре из-за.смещения ph и отсутствия антогонизма.
Белла59
Читатель
- Сообщения
- 26
- Лайки
- 7
- Баллы
- 3
Спасибо!
Добавьте энтерол по 1 капсуле 2 раза в день. Принимать за час до еды. И максилак 1 капсула в день с крайним приемом пищи. Курс обоих препаратов 10 дней. Противогрибковые не принмать,если назначали.
Белла59
Читатель
- Сообщения
- 26
- Лайки
- 7
- Баллы
- 3
Нет, противогрибковые не назначили. Хорошо, я начну принемать пробиот. Я недавно закончила эрадикацию ХЕЛИКА и теперь снова приходиться пить антиб. из-за этого мерзкого клеща... называется невезуха... Хорошо, спасибо Вам. 🙂
Хелик не лечат аб)так на будущее
Белла59
Читатель
- Сообщения
- 26
- Лайки
- 7
- Баллы
- 3
Ха.. Правда? Может я не так выразилась... хеликобактер.. 🙂
Хеликобактер не лечат аб,если нет язвы. И в некоторых случаях даже при язве не назначают,если нет температуры.
Это бактерия живет в кислоте,нет кислоты-нет хелика. Так что обходятся ипп в дозировке 20-40 мг в сутки в зависимости от ситуации. Обычно 20мг достаточно в течении 2 недель и соблюдение диеты в течении месяца.
Амоксицилин не зацепит коифекции клещевые!!! А Юнидокс салютаб в этом случае лучше для профилактики и на боррелий он лучше действует!
Ну потому что были диспепсические явления и рефлюкс,их не лечат аб. Можно денол и ипп,чтоб только воспаление снять от заброса.
Ну это уже осложнения от аб. Потеря веса при срк это редкость,колит надо исключать.
