Дисбактериоз №2

[Tim Vetrov]

Я, вообще-то, как раз и сетовал на отсутствие контролированных исследований по терапии атопического дерматита у детей с помощью пробиотиков... Именно это толкает меня использовать методы лечения, эффективность которых не подтверждена исследованиями, которые проводились по стандарту GCP.

Я сам участвовал в проведении клинических исследований по стандарту GCP и имею соответствующую подготовку, понимаю и ценю EBM, но если таких исследований нет, а провести их сейчас я сам не могу, то я буду следовать своим личным теориям и своему личному опыту.

В Голландии, например, я так делать не мог бы. Там есть стандарты, которые не позволяют проводить бессмысленные обследования и назначать бессмысленную, хоть и безвредную терапию. А в России я могу этим заниматься. И занимаюсь. И вижу эффект, - конечно, не доказанный (в отсутствии контроля). Но и то, что эффекта нет, тоже ведь никто не доказывал? Или есть такие исследования (по коррекции биоценоза кишечника при атопическом дераматите у детей), и я просто прошел мимо них?

[Tim Vetrov]

Что-то есть и в иностранной литературе, но, в основном это доктора из Универститета Турку (побратима Спб).
[Ссылки доступны только зарегистрированным пользователям ]
[Ссылки доступны только зарегистрированным пользователям ]
Есть, правда, еще японские авторы, но их мнения разноречивы:
[Ссылки доступны только зарегистрированным пользователям ]
[Ссылки доступны только зарегистрированным пользователям ]
Но крупных контролированных исследований не было.
Это и обидно.

[Tim Vetrov]

Спасибо М. Л. Дунаевской (с форумов [Ссылки доступны только зарегистрированным пользователям ])!
Воспользовался ее ссылкой.

[Ссылки доступны только зарегистрированным пользователям ]

Guidelines of care for atopic dermatitis

Так вот, в этих рекомендациях применение пробиотиков во время беременности и после родов для профилактики атопического дерматита имеет уровень доказательности I (Properly designed randomized controlled trial).

Они ссылаются на несколько работ.

Ссылка на коллег из Турку (не те статьи, которые я приводил выше):

Kalliomaki et al., 2001
[Ссылки доступны только зарегистрированным пользователям ]

Rautava, Kalliomaki, & Isolauri, 2002
[Ссылки доступны только зарегистрированным пользователям ]

Коллеги из Копенгагена (совсем уже недалеко от Амстердама!):

Rosenfeldt et al., 2003 [Ссылки доступны только зарегистрированным пользователям ]

Так что не зря я назначаю пробиотики детям с атопическим дерматитом.

Слава богу, нашлись рекомендации, да еще и на английском языке и в американском журнале, которые считают доказанным эффект от пробиотиков в лечении атопического дерматита у детей. Ура.

А голландским детям осталось ждать недолго. Скоро и до них докатится.

[Melnichenko]

Как жаль, что Мия Львовна не появляется на нашем сайте...Имеет смысл заглянуть на Сольвей и почитать ее посты.Кого-то эта очень симпатичная доктор мне напоминает.

[Dobro]

New England Journal of Medicine 352: 2314-2324 June 2, 2005 Number 22
Hywel C. Williams, Ph. D., Atopic Dermatitis
[Ссылки доступны только зарегистрированным пользователям ]
[Ссылки доступны только зарегистрированным пользователям ]
Treatment:

Topical Corticosteroids

One systematic review identified 83 randomized controlled trials of the use of topical corticosteroids in atopic dermatitis.30 Vehicle-controlled studies lasting less than one month indicate that approximately 80 percent of people report good, excellent, or clear responses with topical corticosteroids, whereas 38 percent of persons in control groups reported such responses.
Potency of topical corticosteroids is classified by the potential for vasoconstriction — a surrogate for clinical efficacy and skin thinning (Table 3). In general, only preparations that have very weak or moderate strength are used on the face and genital area, whereas those that have moderate or potent strength are used on other areas of the body.31 Lower-potency corticosteroids may be sufficient on all areas of the body in younger children. Preparations are typically used in bursts of three to seven days in order to achieve control. There is little difference in outcome between short-term use of potent preparations or longer use of weaker preparations in children with mild-to-moderate disease.32 Lichenified atopic dermatitis requires more potent preparations for longer periods.
Long-term studies of moderate-to-potent preparations in children are scarce. One study of 231 children with stabilized atopic dermatitis randomly assigned to receive twice-weekly 0.05 percent fluticasone propionate (plus emollients) or vehicle alone plus emollients for 16 weeks showed that patients in the control group were more likely, by a factor of 8, to have a relapse (95 percent confidence interval, 4.3 to 15.2).33 A four-month trial of persons 12 to 64 years of age with moderate-to-severe disease showed that the application of fluticasone to previously active and new sites of atopic dermatitis for two consecutive days each week reduced flares significantly, as compared with a group receiving an emollient only.
Reduced efficacy of topical corticosteroids may be related to disease severity rather than to glucocorticoid resistance.35 There is little evidence that the application of topical corticosteroids twice a day is more effective than once-daily applications,36 and more frequent use may cause more local side effects.
A main concern with the use of topical corticosteroids is irreversible skin thinning. Although thinning is possible, the concern on the part of patients (and parents) is often well out of proportion to the true risk.37 Although inappropriate use of potent preparations can cause skin thinning, four 16-week randomized trials did not show any clinically significant skin thinning,32,33,34,38 and a 1-year study showed no significant effect on collagen synthesis.39 A one-year study of unrestricted continual use of a potent corticosteroid on the limbs and trunk, a weak preparation on the face, or both showed that striae developed in 3 of 330 adults with moderate-to-severe atopic dermatitis.40 Similar studies in children are lacking. Other possible side effects of corticosteroids include facial telangiectasia and glaucoma from periocular use (rarely reported in adults).
Secondary adrenal suppression and the suppression of growth resulting from systemic absorption of topical corticosteroids are also concerns, although clinically relevant adrenal suppression is very rare.41 One study involving children with atopic dermatitis did not find any relationship between height velocity and the use of mild-potency as compared with moderate-potency topical corticosteroids.42 Another study showed biochemical evidence of suppression of the hypothalamic–pituitary–adrenal axis only in children with atopic dermatitis who used potent or very potent topical corticosteroids and in those who had received glucocorticoids from other routes, and not in those who had used topical corticosteroids of mild or moderate strength for a median of 6.9 years.

Emollients

There is no evidence that emollients improve atopic dermatitis directly. However, emollients are widely used because they improve the appearance and symptoms of the dry skin (xerosis) associated with this condition.30,31,43 One study has shown that emollients may reduce the need for topical corticosteroids by approximately 50 percent,44 and another study found that emollients enhanced the response to treatment with topical corticosteroids.45 There is little basis for suggesting the use of one emollient over another, and the preference of the patient is probably the most important factor.

[Dobro]

Topical Calcineurin Inhibitors

Topical tacrolimus and pimecrolimus have both been shown to be effective in vehicle-controlled studies. For 1 percent pimecrolimus, the rate ratio for the proportion of patients clear or almost clear of atopic dermatitis at three weeks in five vehicle-controlled trials involving 783 patients was 2.72 (95 percent confidence interval, 1.84 to 4.03).46 For 0.03 percent and 0.1 percent tacrolimus, the rate ratios for the proportion of patients who were clear or who had excellent improvement at 12 weeks were 4.50 (95 percent confidence interval, 2.91 to 6.96) and 5.62 (95 percent confidence interval, 3.67 to 8.61), respectively, in three vehicle-controlled trials involving 656 patients.46 Short-term studies suggest that 0.1 percent topical tacrolimus may be similar in strength to potent topical corticosteroids,46 whereas topical pimecrolimus is considerably weaker.
Few long-term studies compare intermittent use of topical calcineurin inhibitors with intermittent use of topical corticosteroids. A 12-month vehicle-controlled study of children with atopic dermatitis showed that early use of pimecrolimus reduced the frequency of flares from 51 percent to 28 percent,48 although early use of mild topical corticosteroids might have shown similar effects.
Topical calcineurin inhibitors do not cause skin thinning. Both tacrolimus and pimecrolimus are associated with mild burning sensations when applied to the skin (Table 3). Five-year studies show a good safety profile for these agents.49 In the United Kingdom, the National Institute of Clinical Excellence approves the use of topical tacrolimus for children older than two years of age with moderate-to-severe atopic dermatitis not controlled by topical corticosteroids, and of topical pimecrolimus as a second-line option for resistant dermatitis of the head and neck.50 In the United States, both of these topical calcineurin inhibitors are approved as second-line agents, and the site of application is not restricted for pimecrolimus.

In March 2005, the Food and Drug Administration issued an alert to health care professionals concerning a potential link between topical pimecrolimus and tacrolimus and cancer (mainly lymphoma and skin cancer) on the basis of studies in animals, case reports, and knowledge of how these drugs work.51,52 The alert emphasizes the importance of using these preparations only as labeled and when first-line treatment has failed or cannot be tolerated.

Other Topical Agents

A study of a refined-coal cream used on one side of the body in adults with mild-to-moderate atopic dermatitis as compared with 1 percent hydrocortisone used on the other side suggested similar efficacy after four weeks.53 There is insufficient evidence to conclude whether topical cromoglycate preparations are effective.30,54 Other topical treatments — such as St. John's wort cream, vitamin B12, and licorice gel — whose use is supported by single small, randomized trials require further evaluation before they can be recommended for the treatment of atopic dermatitis.

Oral Antihistamines

Evidence is lacking to support the use of antihistamines for the treatment of atopic dermatitis,55 although they are sometimes recommended for their sedative effects.56 Reports on nonsedative antihistamines are conflicting.30,56,57 The largest study failed to demonstrate any overall benefit from prolonged use of cetirizine in children with atopic dermatitis.58

Topical Doxepin

Topical doxepin produces some relief from itching within 48 hours. However, a clinically useful beneficial effect on disease severity has yet to be shown, and drowsiness may be a problem.30

Antibiotic Agents

Secondary infection with S. aureus is common (Figure 3) and usually is treated with short courses of antibiotics such as floxacillin, cephalexin, or amoxicillin–clavulanate. One randomized trial found no benefit to prescribing floxacillin continually for four weeks as compared with placebo, and methicillin-resistant strains were more common in those who were prescribed antibiotics.59 Although combinations of topical corticosteroids and antibiotics are used for atopic dermatitis, no good evidence suggests that they offer additional benefits as compared with topical corticosteroids alone.
Ultraviolet Light

Randomized clinical trials have shown that ultraviolet light (ultraviolet B, narrow-band ultraviolet B, and high-intensity ultraviolet A) is beneficial for atopic dermatitis in the short term.30 Burning and itching may occur, and carcinogenicity is a long-term concern. Phototherapy is usually used as a second- or third-line treatment.31

Immunosuppressive Agents

A brief course of oral corticosteroids (less than three weeks) may be used to control a flare of severe disease, although data from randomized clinical trials are lacking. Ongoing use of systemic immunosuppressive agents (oral corticosteroids, cyclosporine, azathioprine, mycophenolate, and interferon gamma) is limited by adverse effects and is usually reserved for people with severe disease who do not respond to other measures.
Nonpharmacologic Approaches

Avoiding foods suspected to cause flares may be helpful in young children with severe disease, but usually is not helpful in adults.30,60 Little evidence supports dietary exclusion of milk and eggs in unselected cases.61 Some evidence supports egg-free diets in infants with atopic dermatitis who produce IgE antibodies to egg protein.60 No good evidence supports highly restrictive diets, which can sometimes cause malnutrition. Studies have failed to show clinically useful benefits from supplements such as evening primrose oil, borage oil,63 zinc, pyridoxine, or vitamin E,30 or from viable lactobacilli (probiotics).
Small randomized trials support psychological approaches such as behavior therapy (to reduce the habit of scratching) and relaxation therapy.30 Parental-education programs and demonstration of topical treatments by caregivers may be helpful.65,66 Reduction of house-dust-mite allergen can reduce severity scores for atopic dermatitis, but the clinical relevance and sustainability of such reductions is unknown.30 Impermeable mattress covers are very effective in reducing levels of mite antigens, but they have no clear clinical benefit.67

No good evidence supports the use of bandages containing zinc paste. The use of "wet wraps" (an outer dry bandage overlying an inner damp bandage used over either emollients or topical corticosteroids) has become a popular second- or third-line measure for children with resistant atopic dermatitis but is not supported by randomized trials, and enhanced systemic absorption remains a concern.41 No good data support alternative or complementary therapies such as homeopathy and bioresonance.30

Areas of Uncertainty

Randomized trials are lacking to assess the benefits of many simple interventions, such as emollients and other nonpharmacologic approaches.30 The lack of common outcome measures hinders meaningful comparisons across trials.11 Trials with active comparators are needed to inform choices among agents.47 Data on the optimal use of topical corticosteroids are needed, along with long-term data on adverse events. Data concerning the long-term safety of topical tacrolimus and pimecrolimus are also needed. The benefits of routine allergy testing require clarification. Moreover, it is unclear whether early aggressive therapy in children with atopic dermatitis alters the natural history of the disease.

[Dobro]

Studies have failed to show clinically useful benefits from supplements such as evening primrose oil, borage oil (63) zinc, pyridoxine, or vitamin E (30) or from viable lactobacilli (probiotics)(30, 64).

30.Hoare C, Li Wan Po A, Williams H. Systematic review of treatments for atopic eczema. Health Technol Assess 2000;4:1-191
[Ссылки доступны только зарегистрированным пользователям ]
64.Probiotics for atopic diseases. Drug Ther Bull 2005;43:6-8
[Ссылки доступны только зарегистрированным пользователям ]

[Tim Vetrov]

Обзор, который Вы процитировали, я уже прочитал.
В этом обзоре автор приводит ссылки на обзоры, а не на конкретные исследования. Итак, эти ссылки. Я их, естественно, посмотрел.

30.Hoare C, Li Wan Po A, Williams H. Systematic review of treatments for atopic eczema. Health Technol Assess 2000;4:1-191
[Ссылки доступны только зарегистрированным пользователям ]
Этот обзор я прочитал (он есть даже в полнотекстовом варианте), там о пробиотиках ничего нет (честное слово, не верите - проверьте [Ссылки доступны только зарегистрированным пользователям ]).


64.Probiotics for atopic diseases. Drug Ther Bull 2005;43:6-8
К сожалению, текст этого обзора я раздобыть не смог, так что мне не известно, на какие исследования опираются авторы этого обзора, делая свои выводы. Да и какие они делают выводы, из абстракта, например, непонятно. Как бы этот второй обзор раздобыть? Я даже сайт этого журнала найти не смог...

Вообще говоря, мое мнение такое - если пишешь обзор литературы, негоже ссылаться на другие обзоры (тем более, напечатанные в труднодоступных журналах).

Кроме того, процитированная Вами статья - это ведь клинический разбор, а вовсе не guideline...

[yananshs]

[Ссылки доступны только зарегистрированным пользователям ]
Systematic review of treatments for atopic eczema.
Health Technology Assessment 2000; Vol. 4: No. 37
Executive summary
C Hoare 1
A Li Wan Po 2
H Williams 1*

1 Centre of Evidence-Based Dermatology, University of Nottingham, Queens Medical Centre NHS Trust, Nottingham, UK
2 Centre of Evidence-Based Pharmacotherapy, Aston University, Birmingham, UK

* Corresponding author

Background
Atopic eczema is the commonest inflammatory skin disease of childhood, affecting 15–20% of children in the UK at any one time. Adults make up about one-third of all community cases. Moderate-to-severe atopic eczema can have a profound effect on the quality of life for both sufferers and their families. In addition to the effects of intractable itching, skin damage, soreness, sleep loss and the social stigma of a visible skin disease, other factors such as frequent visits to doctors, special clothing andüthe need to constantly apply messy topical applications all add to the burden of disease. The cause of atopic eczema is unknown, though a genetic pre-disposition and a combination of allergic and non-allergic factors appear to be important in determining disease expression. Treatment of atopic eczema in the UK is characterised by a profusion of treatments aimed at disease control. The evidential basis of these treatments is often unclear. Most people with atopic eczema are managed in primary care where the least research has been done.

Objectives
The objectives of this scoping review are two-fold.

To produce an up-to-date coverage ‘map’ of randomised controlled trials (RCTs) of treatments of atopic eczema.


To assist in making treatment recommendations by summarising the available RCT evidence using qualitative and quantitative methods.
Methods
Data sources
Data sources included electronic searching of MEDLINE, EMBASE, the Cochrane Controlled Clinical Trials Register, the Cochrane Skin Group specialised register of trials, handsearching of atopic eczema conference proceedings, follow-up of references in retrieved articles, contact with leading researchers and requests to relevant pharmaceutical companies.

Inclusion/exclusion criteria
Only RCTs of therapeutic agents used in the prevention and treatment of people with atopic eczema of any age were considered for inclusion. Only studies where a physician diagnosed atopic eczema or atopic dermatitis were included.

Data extraction
Data extraction was conducted by two observers onto abstraction forms, with discrepancies resolved by discussion.

Quality assessment
The quality assessment of retrieved RCTs included an assessment of:

a clear description of method and concealment of allocation of randomisation


the degree to which assessors and participants were blinded to the study interventions, and


whether all those originally randomised were included in the final main analysis.
Data synthesis
Where possible, quantitative pooling of similar RCTs was conducted using the Cochrane Collaboration’s methods. Where statistical heterogeneity was found, sources of heterogeneity in terms of study participants, formulation or posology of intervention, and use of co-treatments were explored. Where pooling was not deemed to be appropriate, detailed descriptions of the study characteristics and main reported results were presented along with comments on study quality.

[yananshs]

Results
A total of 1165 possible RCTs were retrieved in hard copy form for further scrutiny. Of these, 893 were excluded from further analysis because of lack of appropriate data. The 272 remaining RCTs of atopic eczema covered at least 47 different interventions, which could be broadly categorised into ten main groups.

Quality of reporting was generally poor, and limited statistical pooling was possible only for oral cyclosporin, and only then after considerable data transformation.

There was reasonable RCT evidence to support the use of oral cyclosporin, topical corticosteroids, psychological approaches and ultraviolet light therapy.

There was insufficient evidence to make recommendations on maternal allergen avoidance for disease prevention, oral antihistamines, Chinese herbs, dietary restriction in established atopic eczema, homeopathy, house dust mite reduction, massage therapy, hypnotherapy, evening primrose oil, emollients, topical coal tar and topical doxepin.

There was no RCT evidence to support any clear clinical benefit on the use of avoidance of enzyme washing powders, cotton clothing as opposed to soft-weave synthetics, biofeedback, twice-daily as opposed to once-daily topical corticosteroids, topical antibiotic/steroid combinations versus topical steroids alone and antiseptic bath additives.

There was complete absence of RCT evidence on short bursts of potent versus longer-term weaker topical steroids, dilution of topical corticosteroids, oral prednisolone and azathioprine, salt baths, impregnated bandages, wet-wrap bandages, water softening devices, allergy testing, and different approaches to organisation of care.

Conclusions
Coverage
The evidence base for the prevention and treat-ment of atopic eczema has many limitations. It is characterised by a profusion of short-term trials of ‘me too’ products, a lack of common outcome measures which measure things that are important to patientsý poor standards of clinical trial reporting, and a lack of data on questions that physicians and people with atopic eczema deem to be important. Little research has evaluated commonly used treatments compared with each other or in combination. This mismatch is probably due to a combination of the questions not being asked coupled with a lack of independent investment in primary atopic eczema research.

Recommendations for research
Urgent primary research priorities include RCTs of wet-wrap treatments, the clinical benefit of allergy testing, the use of water softeners, the role of specialist nurses, comparisons of tacrolimus and ascomycin against topical corticosteroids, studies of disease prevention, and the use of emollients in preventing disease relapse. Such RCTs should ideally be pragmatic and simple in design, with a few outcome measures that doctors and patients find easy to understand. They should ideally be of 4 months’ or more duration in order to capture the chronicity of disease as well as short-term effects. If such trials are intended to inform primary care, where patients may have milder disease, then they should be conducted in a primary care setting.

This review suggests that there is some scope for further secondary research by systematically reviewing some of the major treatment groups such as antihistamines and essential fatty acids in more detail, and some of these are already underway within the Cochrane Skin Group.

Future methodological research is needed to increase the clinical relevance and reliability of outcome measures for atopic eczema. The RCT database contained within this report also provides a good opportunity to conduct some general research into the relationship between study quality and treatment benefit. There is much scope for improving the standard of clinical trial reporting in atopic eczema by dermatology journals adopting rigorous checks on clinical trial reporting and by registering ongoing trials with the Cochrane Skin Group.

Publication
Hoare C, Li Wan Po A, Williams H. Systematic review of treatments of atopic eczema. Health Technol Assess 2000;4(37).

NHS R&D HTA Programme
The NHS R&D Health Technology Assessment (HTA) Programme was set up in 1993 to ensure that high-quality research information on the costs, effectiveness and broader impact of health technologies is produced in the most efficient way for those who use, manage and provide care in the NHS.

Initially, six HTA panels (pharmaceuticals, acute sector, primary and community care, diagnostics and imaging, population screening, methodology) helped to set the research priorities for the HTA Programme. However, during the past few years there have been a number of changes in and around NHS R&D, such as the establishment of the National Institute for Clinical Excellence (NICE) and the creation of three new research programmes: Service Delivery and Organisation (SDO); New and Emerging Applications of Technology (NEAT); and the Methodology Programme.

This has meant that the HTA panels can now focus more explicitly on health technologies (‘health technologies’ are broadly defined to include all interventions used to promote health, prevent and treat disease, and improve rehabilitation and long-term care) rather than settings of care. Therefore the panel structure has been redefined and replaced by three new panels: Pharmaceuticals; Therapeutic Procedures (including devices and operations); and Diagnostic Technologies and Screening.

The HTA Programme will continue to commission both primary and secondary research. The HTA Commissioning Board, supported by the National Coordinating Centre for Health Technology Assessment (NCCHTA), will consider and advise the Programme Director on the best research projects to pursue in order to address the research priorities identified by the three HTA panels.

The research reported in this monograph was funded as project number 96/17/01.

The views expressed in this publication are those of the authors and not necessarily those of the HTA Programme or the Department of Health. The editors wish to eme that funding and publication of this research by the NHS should not be taken as implicit support for any recommendations made by the authors.

Criteria for inclusion in the HTA monograph series
Reports are published in the HTA monograph series if (1) they have resulted from work commissioned for the HTA Programme, and (2) they are of a sufficiently high scientific quality as assessed by the referees and editors.

Reviews in Health Technology Assessment are termed ‘systematic’ when the account of the search, appraisal and synthesis methods (to minimise biases and random errors) would, in theory, permit the replication of the review by others.

HTA Programme Director: Professor Kent Woods
Series Editors: Professor Andrew Stevens, Dr Ken Stein and Professor John Gabbay
Monograph Editorial Manager: Melanie Corris

[yananshs]

По-моему, статья, приведенная Валентином Александровичем, относится к категории "cистематический обзор", а не "клинический разбор".
New England Journal of Medicine 352: 2314-2324 June 2, 2005 Number 22
Hywel C. Williams, Ph. D., Atopic Dermatitis
[Ссылки доступны только зарегистрированным пользователям ]
[Ссылки доступны только зарегистрированным пользователям ]

[yananshs]

Systematic review of treatments for atopic eczema.
Health Technology Assessment 2000; Vol. 4: No. 37
[Ссылки доступны только зарегистрированным пользователям ]
[Ссылки доступны только зарегистрированным пользователям ]

[Tim Vetrov]

Яна, Вы читали эти обзоры?

Речь ведь о том, что авторы статьи, которую пространно цитирует Валентин Александрович (пусть будет систематический обзор, хотя к чему тогда там 10-летняя девочка?), утверждая, что эффект пробиотиков при атопическом дерматите не доказан, ссылаются на 2 других обзора, ссылку на один из которых вы привели в последнем посте. Только эту ссылку я уже приводил (http://forums.rusmedserv.com/showpos...4&postcount=24) и обзор этот уже читал, и ничего там про эффективность/неэффективность пробиотиков нет.
Второй обзор, к сожалению, доступен только в виде абстракта. И из этого абстракта неясно мнение авторов (пожелавших остаться неизвестным).

К чему Вы привели эту огромную выдержку? Разве в ней есть что-либо про неэффективность пробиотиков? Если есть, значит, я проглядел (хотя смотрел 3 раза очень внимательно), ну, выделите жирным, пожалуйста...

Вы специально игнорируете мои посты? А если нет, зачем по второму и третьему разу приводите источники, не имеющие отношение к делу?

[Aminazinka]

Уважаемый Tim Vetrov!
Немного офaтоп, но касательно методологии. Вас удивляет, что нет работ о пробиотиках в лечении атопического дерматита? Знаете, меня удивляет, почему нигде в работах по депрессии не упоминаются антибиотики. Странное дело, может мне начать исследовать? В России это вроде позволено.. Вы как думаете, смысл будет? Ну как же, была же теория инфекционной шизофрении. Вдруг по мне Нобелевская плачет?
Ваше упорство найти пробиотики в лечении дерматита атопического - хорошее чувство. Но на чем основано это упорство? Давайте вернемся к процессу (атопическому дерматиту), вдруг выяснится, что состояние кишечника и "флоры его" никакого влияния на течение дерматита не оказывает?

[Tim Vetrov]

Уважаемая Ирина Геннадиевна!

Я уже много чего нашел, в том числе и гайдлайн по атопическому дерматиту, который признает эффективность пробиотиков при этом заболевании, опираясь на ряд двойных слепых плацебо контролируемых исследований... Эти исследования я также нашел, и ссылки на них в этом топике есть.

Так что Ваше предположение вряд ли верно: есть довольно убедительные данные, свидетельствующие об эффективности пробиотиков при атопическом дерматите.

Посмотрите вот здесь
[Ссылки доступны только зарегистрированным пользователям ]

Эта ссылка, между прочим, уже была приведена в данном топике.
http://forums.rusmedserv.com/showpos...5&postcount=19

Почему бы Вам не прочитать топик с начала до конца и не посмотреть те ссылки, которые приводятся? Может, тогда Вы поймете, на чем основано мое упорство?