Frequency of appearance of anemias at rheumatoid arthritis - a disease of autoimmune genesis (on the data of retrospective study)

Abdumalik N Aripov,Marif Sh Karimov,Aida A Eshmurzaeva

doi:10.1186/ar3608

Abdumalik N Aripov, Marif Sh Karimov + Show 1 more

Open Access

https://doi.org/10.1186/ar3608

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Abstract

The purpose of research is study of offenses of appearance of anemia among rheumatoid arthritis (RA) patients, revealing of their etiologic reasons, as well as the estimation of character of used anti anemia means of medicine on the basis of retrospective analysis of history of disease. Coming out of above stated histories of illness of RA patients were analyzed to presence of established as accompanying disease of anemia. Results of this analysis are represented on picture as it seen on the presented data, 33,3% of patients with RA anemia is verified as accompanying pathology. Therefore at 1/3 patients with P anemia takes place. The study of etiologic causes of anemia at these patients shows that in 76,6% cases anemia bears ferrous deficit character, 20%- anemia of chronic diseases and only in 3,4% cases - auto immune anemia. Therefore, the majority of patients of RA anemia bears ferrous deficit character. The high frequency of appearance of ferrous deficit anemia among RA patients, probably is explained by that in conditions of this disease changes of pH happen among gastro duodenal area. Besides, wide use of non steroidal anti inflammatory medicine (NAIM) at RA also may effect to pH of stomach. And in cases of destroyed reaction of ambience change of ferrous assimilation. That fact of ferrous deficit anemia may has independent character at analyzed RA patients is excluded. But on their history of illness it is impossible to determine this fact. Study of offenses of appearance of anemia at RA patients depending on age categories is evidencing on that 83,4% of patients with anemia comes to patients from 31 to 60 years old, and among patients of 31 to 40 years old appears 25% patients, from 41 to 50 years old - 26,7% and from 51 to 60 years old - 31,7%, accordingly. Results of these analysis showed that if at patients with debut RA anemia appears at 1,5% cases, than among RA patients with prolongation of anamnesis from 1 to 5 years old, from 5 to 10 years old appears in 33,3%, 28,7% and in 34,8% cases accordingly. Therefore as far as increasing of prolongation of current of RA, specific gravity of patients with anemia increases.

Highlights

Acute isolated neurological syndromes, such as optic neuropathy or transverse myelopathy, may cause diagnostic problems since they can be the first presentations in a number of demyelinating disorders including multiple sclerosis (MS) and collagen diseases
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Believing on the similarities of normal joints in humans and monkeys, we have employed a model of collagen-induced arthritis in Macaca fascicularis in an attempt to evaluate the histological alterations caused by such condition in the extracellular matrix of the articular cartilage

Summary

Introduction

Acute isolated neurological syndromes, such as optic neuropathy or transverse myelopathy, may cause diagnostic problems since they can be the first presentations in a number of demyelinating disorders including multiple sclerosis (MS) and collagen diseases. Acute Serum Amyloid A (A-SAA) is an acute phase protein strongly expressed in rheumatoid arthritis (RA) synovial tissue (ST) critically involved in regulating cell migration and angiogenesis These processes are dependent on downstream interactions between extracellular matrix and cytoskeletal components. Conclusions: These results indicate that Egr-1 contributes to IL-1mediated down-regulation of PPARg expression in OA chondrocytes and suggest that this pathway could be a potential target for pharmacologic intervention in the treatment of OA and possibly other arthritic diseases. Immune cell-derived microparticles (MPs) are present at increased amounts in synovial fluid of rheumatoid arthritis (RA) patients [1] and can activate disease-relevant signalling pathways in RA synovial fibroblasts (SF) [2,3].

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