- Therapie und Dosierung
(Dickdarmerkrankungen): ca. 5,6g/Tag EPA & DHA
Fachzeitschriften wurden folgende Artikel über Omega-3 publiziert.
Die Liste dieser Publikationen wurde im April 2003 kompiliert
und erhebt keinen Anspruch auf Vollständigkeit. Quelle: MEDLINE.
Die Daten dienen als Referenz für
Ärzte und Therapeuten, damit eine therapeutische Dosis für
Colitis ulcerosa festgelegt werden kann.
proctocolitis and n-3 polyunsaturated fatty acids (n-3 PUFAs):
the mucosal effect in situ.
Almallah YZ: Department of Surgery,
University of Aberdeen, United Kingdom; Ewen SW, El-Tahir A,
Mowat NA, Brunt PW, Sinclair TS, Heys SD,
J Clin Immunol 2000 Jan 20:68-76
It has been postulated that patients with ulcerative colitis
(UC) have altered reactivity of gut-associated lymphoid tissue.
In such cases there is intense infiltration of the mucosa with
immune competent cells and associated tissue damage. We have shown
previously that the dietary supplementation with the n-3 polyunsaturated
fatty acids (n-3 PUFAs), eicosapentaenoic acid (EPA), and docosahexaenoic
acid (DHA) results in significant systemic immune suppression.
The aim of this study, therefore, was to evaluate the in situ
effect of n-3 PUFAs on distal proctocolitis. Each patient received
either fish oil extract (EPA 3.2 g, DHA
2.4 g) (n = 9) or sunflower oil (n = 9) daily in a
double blind manner for six months.
Monthly assessment included: (1) disease activity using clinical,
sigmoidoscopic, and histological scores and (2) immunohistochemical
analysis (immunoglobulins, CD profiles) of rectal biopsy specimens
(before and after six months supplementation) using monoclonal
antibodies and quantitative computer-assisted video image analysis.
Prior to receiving supplementation, patients
with proctocolitis (n = 18) showed significantly higher
numbers of cells expressing CD3 (pan T cells) and HLA-DR and IgM
containing cells compared with non-colitic controls (n = 8). Six
months supplementation with n-3 PUFAs resulted in significant
reduction in the number of cells expressing CD3 and HLA and the
percentage of cells containing IgM. There was no significant
change in the CD20 nor the percentage of IgG or IgA containing
cells in either group of patients with procto-colitis. In
patients receiving n-3 PUFA supplementation, there was improvement
in the disease activity and histological scores, compared with
pretreatment evaluation. This
study has demonstrated both evidence of suppression of in situ
immune reactivity and concurrent reduction in disease activity
in patients with proctocolitis receiving n-3 PUFA supplementation.
This may have important implication for therapy in patients with
fatty acids and inflammatory diseases.
Gil A: Departamento de Bioquímica
y Biología Molecular, Facultad de Farmacia, Universidad
de Granada, Spain
Biomed Pharmacother 2002 Oct 56:388-96
Inflammation is overall a protective response, whose main
goal is to liberate the human being of cellular lesions caused
by micro-organisms, toxins, allergens, etc., as well as its consequences,
and of death cells and necrotic tissues. Chronic inflammation,
which is detrimental to tissues, is the basic pathogenic mechanism
of hypersensitivity reactions against xenobiotics. Other frequent
pathologies, for instance atherosclerosis, chronic hepatitis,
inflammatory bowel disease (IBD), liver cirrhosis, lung fibrosis,
psoriasis, and rheumatoid arthritis are also chronic inflammatory
diseases. Chemical mediators of inflammation are derived from
blood plasma or different cell-type activity. Biogenic amines,
eicosanoids and cytokines are within the most important mediators
of inflammatory processes. The different activities of eicosanoids
derived from arachidonic acid (20:4 n-6) versus those derived
from eicosapentaenoic acid (20:5 n-3) are one of the most important
mechanisms to explain why n-3, or omega-3, polyunsaturated fatty
acids (PUFA) exhibit anti-inflammatory properties in many inflammatory
diseases. Dietary supplements ranging 1-8 g per day of n-3
PUFA have been reportedly beneficial in the treatment of IBD,
eczema, psoriasis and rheumatoid arthritis. In addition, recent
experimental studies in rats with experimental ulcerative colitis,
induced by intrarectal injection of trinitrobenzene sulphonic
acid, have documented that treatment with n-3 long-chain PUFA
reduces mucosal damage as assessed by biochemical and histological
markers of inflammation. Moreover, the defence antioxidant system
in this model is enhanced in treated animals, provided that the
n-3 PUFA supply is adequately preserved from oxidation..
procto-colitis and n-3 polyunsaturated fatty acids: the mechanism(s)
of natural cytotoxicity inhibition.
Almallah YZ: Department of Surgery,
University of Aberdeen, UK; El-Tahir A, Heys SD, Richardson S,
Eur J Clin Invest 2000 Jan 30:58-65
BACKGROUND: Altered natural killer (NK) and lymphokine-activated
killer (LAK) cell activities have been reported with ulcerative
colitis (UC). Previously, we have shown that in patients with
UC, the n-3 polyunsaturated fatty acids (PUFAs), eicosapentaenoic
acid (EPA) and docosahexaenoic acid (DHA), specifically inhibit
natural cytotoxicity with clinical improvement in disease activity.
The aim of this study therefore was to evaluate the possible mechanism(s)
involved in this inhibition, and in particular the alteration
of production of interleukin 2 (IL2) and the arachidonic acid
metabolite leukotriene B4 (LTB4), both known to modulate NK cell
activity. MATERIALS AND METHODS: Each patient with procto-colitis
received either fish oil extract (EPA 3.2 g, DHA 2.4 g; n = 9)
or placebo (n = 9) daily for 6 months. Monthly assessment
included disease activity using clinical and sigmoidoscopic scores.
Peripheral blood mononuclear (PBMN) cells were isolated and NK
cell cytotoxic activity in vitro was measured. Monthly serum samples
were analysed for LTB4, IL2 and soluble IL2 receptors (sIL2R).
RESULTS: The n-3 PUFAs group had significantly reduced NK cell
activity, compared with the placebo group (P < 0.05, Mann-Whitney
U-test). In the n-3 PUFA group, incubation of PBMN cells for
72 h with recombinant interleukin 2 (rIL2) reversed the NK inhibition.
In patients with active proctocolitis, serum levels of LTB4 correlated
positively with NK cell cytotoxicity (r = 0.873, P < 0.05,
Kendall's correlation coefficient). After six months of n-3 PUFAs
supplementation, serum levels of LTB4 were undetectable with concurrent
significant reduction in NK cell cytotoxic activity. The latter
was associated with significant reduction of serum IL2 and sIL2R
levels (P < 0.05). CONCLUSION: This study has demonstrated
both evidence of suppression of immune reactivity and concurrent
reduction in disease activity in patients with proctocolitis receiving
n-3 PUFAs supplementation. This may have important implications
for therapy in patients with UC.
and mucosal fatty acid pattern in colectomized ulcerative colitis
Esteve M: Department of Gastroenterology,
Hospital Universitari Germans Trias i Pujol, Badalona, Catalonia,
Spain; Navarro E, Klaassen J, Abad-Lacruz A, Gonzalez-Huix F,
Cabre E, Ramos E, Condom E, Fernandez-Bajares F,
Pastor C, Humbert P, Marte-Rague J, Gassull MA
Dig Dis Sci 1998 May 43:1071-8
Patients with inflammatory bowel disease (IBD) have increased
plasma n3 polyunsaturated fatty acids (PUFAs), which in ulcerative
colitis (UC) patients persists six months after colectomy, suggesting
a primary abnormality in fatty acid (FA) metabolism in IBD. This
finding needed to be confirmed in a larger series of UC long-term
colectomized patients. We aimed to assess the plasma FA pattern
in UC colectomized patients with either Brooke's ileostomy (UC-BI)
or ileal pouch anal anastomosis (UC-IPAA) and the mucosal FA pattern
in the ileal reservoir of the UC-IPAA patients. Plasma FAs were
assessed in 63 UC colectomized patients (31 with BI and 32
with IPAA) and 30 controls. In 26 UC-IPAA (8 with pouchitis
and 18 without pouchitis) and in 13 healthy controls gut mucosal
FAs were also investigated. FAs were detected by capillary column
gas-liquid chromatography. Increased levels of saturated fatty
acids (SFAs) and decreased percentages of monounsaturated fatty
acids (MUFAs) were observed in both groups of patients. There
were no changes in plasma n3 and n6 PUFAs. The mucosal FA pattern
of the ileal reservoir consisted of increased long-chain PUFAs,
specially n6 PUFA, and a decrease of their essential precursors.
High percentages of SFAs and low percentages of MUFAs were also
seen. The plasma FA profile previously described in IBD is
not observed long-term after colectomy in UC, suggesting that
it is related with the presence of inflamed intestine. High
concentrations of SFAs and decreased percentages of MUFAs might
represent early events in disturbed FA metabolism in IBD.
The changes in FAs of the ileal reservoir, which closely resemble
those found in human and experimental IBD, probably represent
a common pattern of intestinal inflammation.