INFO - Anemia of chronic disease

[Guest guest]

CMAJ

12 Aug 2008

" Anemia of chronic disease: a harmful disorder or an adaptive,

beneficial response? "

http://www.cmaj.ca/cgi/content/full/179/4/333

************************************

J Rheumatol. 2008 Mar;35(3):380-6. Epub 2008 Feb 1.

Anemia in early rheumatoid arthritis is associated with interleukin

6-mediated bone marrow suppression, but has no effect on disease

course or mortality.

Nikolaisen C, Figenschau Y, Nossent JC.

Department of Rheumatology, Institute of Clinical Medicine, University

of Tromsø, Tromsø, Norway.

OBJECTIVE: Anemia of chronic disease (ACD) is the most common

extraarticular manifestation of rheumatoid arthritis (RA), but there

is limited information on the cause and consequences of ACD. We

investigated the prevalence, relation with proinflammatory cytokines,

and effect on disease outcome of ACD in patients with RA.

METHODS: The presence of anemia was analyzed in a cohort of 111

consecutive patients with early RA. Anemia was related to markers of

erythropoiesis and inflammation [clinically and by levels of

erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and

serum interleukin 1beta (IL-1beta), IL-2, IL-6, IL-8, and tumor

necrosis factor-alpha]. The frequency of various disease outcomes

during the mean followup of 74 months was compared between ACD and

nonanemic patients.

RESULTS: ACD was present in 25% during the first year of disease. ACD

was associated with higher CRP (45 vs 22 g/l; p = 0.04) and ESR levels

(54 vs 33 mm/h; p = 0.002). Hemoglobin levels were inversely

correlated with serum erythropoietin (p = 0.003) in univariate

analysis, but in multivariate analysis only ESR (p = 0.005) and IL-6

(p = 0.056) remained as independent predictors of hemoglobin levels.

Presence of ACD was not associated with later development of disease

manifestations or mortality.

CONCLUSION: While ACD affected 25% of patients with RA early in the

disease course, this had no influence on disease outcome including

mortality during the following 6 years. The association between IL-6

and ACD suggests that IL-6-mediated bone marrow suppression is the

main mechanism for development of ACD in RA.

PMID: 18260177

http://www.ncbi.nlm.nih.gov/pubmed/18260177

************************************

Blood, 15 July 2002, Vol. 100, No. 2, pp. 474-482

HEMATOPOIESIS

Anemia of chronic disease in rheumatoid arthritis is associated with

increased apoptosis of bone marrow erythroid cells: improvement

following anti-tumor necrosis factor- antibody therapy

Helen A. Papadaki, Heraklis D. Kritikos, Vasilis Valatas, Dimitrios T.

Boumpas, and D. Eliopoulos

From the Departments of Hematology and Rheumatology, Clinical

Immunology and Allergiology of the University of Crete School of

Medicine, Heraklion, Crete, Greece.

Abstract

Circumstantial evidence has implicated tumor necrosis factor (TNF-)

in the pathogenesis of anemia of chronic disease (ACD) in rheumatoid

arthritis (RA). We investigated the role of TNF- in erythropoiesis of

patients with active RA (n = 40) and the effect of anti-TNF- antibody

administration (cA2). Patients with RA had lower numbers of

CD34+/CD71+ and CD36/glycophorin A+ (glycoA+) bone marrow (BM) cells

and increased proportions of apoptotic cells within the CD34+/CD71+

and CD36+/glycoA+ cell compartments, compared to healthy controls (n =

24). Erythroid burst-forming units (BFU-Es) obtained by BM mononuclear

or purified CD34+ cells were significantly lower in RA patients

compared to controls. These abnormalities were more pronounced among

patients with ACD. Increased TNF- levels in patient long-term BM

culture supernatants inversely correlated with BFU-Es and hemoglobin

levels and positively with the percentage of apoptotic CD34+/CD71+ and

CD36+/glycoA+ cells. Following cA2 therapy, a normalization was

documented in the number of CD34+/CD71+ and CD36/glycoA+ cells, the

number of BFU-Es, and the proportion of apoptotic CD34+/CD71+ and

CD36+/glycoA+ cells, which was associated with a significant increase

in hemoglobin levels compared to baseline. Recovery from anemia was

more prominent in patients with ACD. The exogenous addition of an

anti-TNF- antibody in the cultures increased BFU-E number in patients

prior to cA2 treatment but not after treatment, further substantiating

the inhibitory role of TNF- on patients' erythropoiesis. We conclude

that TNF--mediated apoptotic depletion of BM erythroid cells may

account for ACD in RA and that cA2 administration may ameliorate ACD

in these patients by down-regulating the apoptotic mechanisms involved

in erythropoiesis. (Blood. 2002;100:474-482)

*****************************

Read the full article here:

http://bloodjournal.hematologylibrary.org/cgi/content/full/100/2/474

************************************

Merck.com

" Anemia of Chronic Disease " :

http://www.merck.com/mmhe/sec14/ch172/ch172e.html

***********************************

Not an MD

[Guest guest]

dd,

If anemia is suspected, one should try to find out the cause and type of anemia.

In certain situations, treating the underlying cause will lead to

improvement in the anemia.

Not an MD

On Thu, Mar 12, 2009 at 3:02 PM, <dgd301@...> wrote:

>

> In a message dated 3/12/2009 9:55:25 A.M. Central Daylight Time,

>

> Rheumatoid.Arthritis.Support@... writes:

>

> CMAJ

> 12 Aug 2008

>

> " Anemia of chronic disease: a harmful disorder or an adaptive,

> beneficial response? "

>

> Well, this is interesting -- If anemia of chronic disease is a protective

> measure, one should expect adverse consequences associated with efforts to

> override it

>

> If this study is right, then one should know if their anemia is from chronic

> disease or some other cause. More questions for the RA doc.

>

> dd