Hypoproliferative Anemias

Usually these types of anemia are normocytic normochromic and. Hypoproliferative anemia are characterized by a decreased production of erythropoietin (EPO) or an inadequate response to erythropoietin. Renal, metabolic and endocrine disorders are common reasons. The treatment consists of treatment of the underlying disease and occasionally the administration of erythropoietin.

Hypo proliferation is a common mechanism in anemias due to renal diseases, hypo metabolic or endocrine deficiency states (z. B. hypothyroidism, hypopituitarism) and protein deficiency. There is a relative or absolute lack of erythropoietin. In hypo metabolic conditions also the bone marrow response is limited to erythropoietin.

Usually these types of anemia are normocytic normochromic and. Hypoproliferative anemia are characterized by a decreased production of erythropoietin (EPO) or an inadequate response to erythropoietin. Renal, metabolic and endocrine disorders are common reasons. The treatment consists of treatment of the underlying disease and occasionally the administration of erythropoietin. Hypo proliferation is a common mechanism in anemias due to renal diseases, hypo metabolic or endocrine deficiency states (z. B. hypothyroidism, hypopituitarism) and protein deficiency. There is a relative or absolute lack of erythropoietin. In hypo metabolic conditions also the bone marrow response is limited to erythropoietin. Anemia in kidney disease The erythropoietin and severity of anemia correlate with the degree of renal dysfunction. Anemia occurs <45 ml / min with creatinine clearance. Glomerular kidney damage (eg., By amyloidosis, diabetic nephropathy) generally result in dependence on the degree of the excretory failure to severe anemia. The term renal anemia refers only to such disorders, which are caused by the decreased erythropoietin production, but other mechanisms may increase the severity of anemia. In uremia often leads to a weak hemolysis, whose cause is unknown. Less common is a Erythrozytenfragmentation (microangiopathic haemolytic anemia), which occurs (for. Example, in malignant hypertension, membranoproliferative glomerulonephritis, polyarteritis nodosa and acute Nierenrindennekrose) at a renovascular damage to the endothelium. The microangiopathic hemolysis in children is known as hemolytic uremic syndrome and is an acute, sometimes fatal progressive form (thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS)). The diagnosis made by detection of renal insufficiency and normozytärer anemia, peripheral reticulocytopenia and insufficient in relation to the degree of anemia hyperplasia of the erythropoiesis. The presence of fragmentocytes in the peripheral smear, particularly in accompanying thrombocytopenia, indicates the simultaneous presence of a microangiopathic hemolysis. The goal of therapy is to improve kidney function and increased erythropoiesis. After normalization of kidney function, anemia recedes slowly. In patients with long-term dialysis, the administration of erythropoietin is the treatment of choice. The starting dose is 50 to 100 I.U./kg i.v. or s.c. 3 times a week. Parallel iron supplementation should be performed. In almost all cases it comes within 8-12 weeks to the maximum increase in red blood cells. Maintenance therapy with erythropoietin can at a reduced dose (about half of the initial dose) of 1- continued to 3 times per week. Transfusion duty rarely is. The response to Erythropoetingabe must be carefully monitored to avoid unwanted effects with hemoglobin levels of> 12 g / dl. Other hypoproliferative anemia The clinical and laboratory changes in other hyperproliferative, normochromic normocytic anemia are usually weak, but can mimic the image of renal anemia. The mechanism of the development of anemia in protein deficiency is probably in general present hypometabolism. Hypometabolism leads to a reduction of the bone marrow in response to erythropoietin. However, the effect of protein deficiency on erythropoiesis is unclear.

Health Life Media Team

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