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Systemic Lupus Erythematosus blood system damage _99119


									?Systemic Lupus Erythematosus
blood system damage


Systemic Lupus Erythematosus (SLE) can produce a variety of
autoantibodies, selective targeting of peripheral blood cells or bone
marrow hematopoietic cells, leading to changes in the blood system.
At the same time, renal failure, iron deficiency, infection and drugs,
and other factors can cause damage to the blood system. Almost all of
Lupus patients can be in the course of a stage show or hematological
abnormalities. Blood system exception can occur in Lupus Symptoms,
can also be in a typical Lupus occurs

Haematological anomalies are often the first published now SLE, or
prompt the deterioration. It is a sign of disease activity, reflects
the disease on bone marrow function and effects of peripheral blood
cell survival. Liaoning Provincial Academy of traditional Chinese
medicine Rheumatology immune branch chenyan pine

1982 United States Rheumatism Association (ARA) revised the
classification criteria for diagnosis of SLE

Haematological anomalies

Hemolytic anemia: Hematocrit < 35%, with increased reticulocyte count;

Leukopenia: 2 or 2 + determination "4 `9 10/L

Lymphopenia: 2 or 2 + determination "1.5 `9/L 10;

Thrombocytopenia: unused and thrombocytopenia-related medication
measured less than 100 `9/L 10.

57%-78% of patients with systemic lupus erythematosus suffer from
anaemia, more moderate anemia.
Its mechanism: erythropoiesis blocked, factors such as RBC detained
arising from the peripheral damage; adults are pigment is cell anemia;
children mainly jaundice, reticulocyte count number of red blood
cells, bone marrow hyperplasia, etc.

Anemia causes fall into non-immune factors and immune factors.

Non-immunological factors: chronic anemia, iron deficiency anemia,
anemia, kidney sideroblasts-cell anemia, drug-induced and secondary
to other disease anemia.

Immunological factors: Autoimmune hemolytic anemia, drug-induced
hemolytic anemia, aplastic anemia, pure red cell Aplasia and
pernicious anemia, etc.

Hormones are the main treatment for anemia drugs, efficiency 75%; for
seriously ill and rapidly, methylprednisolone pulse therapy. You can
also use azathioprine, not satisfied with the hormone effect,
available Splenectomy, Splenectomy rarely obtain long-term efficacy.
Therefore, the treatment of anemia caused by SLE or to treat primary

50%-60% of SLE patients can appear leukopenia, and multiple skin rash,
lymphopenia, etc.

Pathogenesis: 1. antibody-mediated: such as anti-myeloid, monocyte
antibodies; 2. drug-induced; 3. bone marrow dysfunction; 4.
peripheral damage;: hypersplenism; immune complex specific antibody-
induced condensation reaction, etc.

At the same time can be accompanied by neutrophils and lymphocytes.

7%-52% of the SLE can appear abnormal platelet count. In particular,
Idiopathic Thrombocytopenic Purpura (ITP), 7%-26%. Less than 20
`109/L of severe thrombocytopenia is common, but mild
thrombocytopenia occurs in no bleeding tendency of SLE deterioration.

With regard to the SLE patients in serious immune thrombocytopenia,
and hormone therapy. Adrenal corticosteroids for the treatment of
invalid or difficult to decrement of patients, you can take high-dose
methylprednisolone, vincristine, azathioprine, cyclophosphamide,
cyclosporin, high-dose intravenous immunoglobulin treatment or
Splenectomy, etc.
Hematological abnormalities are the most common manifestations of SLE,
hematological abnormalities, particularly women of reproductive age
and should be carried out in patients with SLE of screening. For the
diagnosis of autoimmune hemolytic anemia or Idiopathic
Thrombocytopenic Purpura patients, should be alert to the possibility
of simultaneous presence of SLE, some patients with autoimmune
hemolytic anemia as.

SLE blood system damage attributable to the Chinese "blood" and
"edema" or "Virtual Lab" category. Clinical management requires
differentiation, differentiation and argue with treatment. ?


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