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==Pathophysiology of Anemia of Prematurity== | ==Pathophysiology of Anemia of Prematurity== | ||
The exact [[pathogenesis]] of [[anemia of prematurity]] is not fully understood. It is thought that [[anemia of prematurity]] is the result of a combination of decreased [[erythropoietin]] production, deficient [[iron]] stores, decreased [[RBC]] lifespan, and blood loss during [[phlebotomy]]. | The exact [[pathogenesis]] of [[anemia of prematurity]] is not fully understood. It is thought that [[anemia of prematurity]] is the result of a combination of decreased [[erythropoietin]] production, increased [[erythropoietin]] [[metabolism]], deficient [[iron]] stores, decreased [[RBC]] lifespan, and blood loss during [[phlebotomy]]. | ||
===Physiological anemia in newborns=== | ===Physiological anemia in newborns=== | ||
Normally, all the [[newborns]] experience a fall in the [[haemoglobin]] concentration during the first few weeks of life. | Normally, all the [[newborns]] experience a fall in the [[haemoglobin]] concentration during the first few weeks of life. Healthy, [[fullterm]] [[infants]] usually develop [[anemia]] around 10-12 weeks of life after birth. [[Hemoglobin]] concentration never falls below 10 g/dl in healthy infants. Physiological anemia is well tolerated by and does not require any therapy.<ref name="pmid20817366">{{cite journal| author=Strauss RG| title=Anaemia of prematurity: pathophysiology and treatment. | journal=Blood Rev | year= 2010 | volume= 24 | issue= 6 | pages= 221-5 | pmid=20817366 | doi=10.1016/j.blre.2010.08.001 | pmc=2981681 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20817366 }} </ref> | ||
*After birth, an [[embryo]] transitions from a [[hypoxic]] state in-utero to an [[infant]] in a relatively hyperoxic environment | *After birth, an [[embryo]] transitions from a [[hypoxic]] state in-utero to an [[infant]] in a relatively hyperoxic environment | ||
* | *This transition leads to an increase in [[blood oxygen]] and [[tissue oxygen]] concentration in [[newborns]] | ||
* | *Increased [[oxygen]] concentration inhibits [[erythropoietin]] production and eventually stops [[erythropoiesis]] | ||
* | *Due to the rapid growth and disproportionate RBC production, [[hemoglobin]] levels fall gradually in infants | ||
*The | *The drop in [[hemoglobin]] concentration continues until the [[tissue hypoxia]] develops which usually takes around 6-12weeks after birth | ||
*[[ | *[[Tissue hypoxia]] activates the [[oxygen sensors]] present in the [[kidney]] and [[liver]] to stimulate the [[erythropoietin]] and [[red blood cells]] production | ||
*[[ | *[[Fullterm newborns]] have enough iron stores for [[erythropoiesis]] until 20 weeks of life | ||
*Infants have a shorter [[RBC]] lifespan and increased [[erythropoietin]] [[metabolism]] when compared to adults | |||
Revision as of 07:27, 20 July 2020
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Ewing's sarcoma Microchapters |
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Diagnosis |
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Treatment |
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Case Studies |
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Sandbox:Asra On the Web |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2];Associate Editor(s)-in-Chief: Suveenkrishna Pothuru, M.B,B.S. [3];Assistant Editor(s)-In-Chief: Michael Maddaleni, B.S., Asra Firdous, M.B.B.S.
Overview
Ewing's sarcoma is the second most common malignant bone neoplasm commonly affecting children and adolescents. It usually affects patients in the second decade of life with a peak incidence around 15 years of age. It comprises 3% of all malignancies in pediatric patients and about 10-15% of childhood bone cancers. The overall incidence of Ewing's sarcoma is approximately estimated at 2.9 cases per million population in the U.S. Ewing's sarcoma is more common in males than females. It is more prevalent in whites than Africans.
Epidemiology and Demographics
- Ewing's Sarcoma is the second most common bone malignancy in children and adolescents.
- 10-15% of childhood bone cancers are Ewing's Sarcoma.
- Ewing's Sarcoma constitutes about 4% of pediatric cancers.
- 200-250 new cases of Ewing's sarcoma are reported each year in the United States.
- Nearly, 60% of the Ewing Sarcoma cases have long-term disease-free survival.
Incidence
- The incidence of Ewing's sarcoma has remained unchanged for 30 years.[1]
- In the United States, the overall incidence of Ewing's sarcoma is 1 cases per million individuals.
- During 1973-2004, the average annual incidence of Ewing's Sarcoma was estimated to be 2.9 cases per million population in the United States.
- The incidence of Ewing's Sarcoma, in the United States, is estimated to be 200-250 cases annually.
Mortality/Morbidity
The overall 5-year survival rate for patients with Ewing's Sarcoma is approximately 70% in primary lesions and 30% in metastatic disease.
Race
- Ewing's Sarcoma is more prevalent in Caucasians than Asians or Hispanics.
- African Americans and Africans are less likely to develop Ewing's Sarcoma.
- The incidence in the Caucasians is 1.5 cases per million population.
- The incidence in the Asians is 0.8 cases per million population.
- The incidence in Africans is 0.2 cases per million population.
Age
- Ewing's Sarcoma commonly affects children and adolescents between 10 and 20 years of age.
- The median age at diagnosis is 15 years
- In patients younger than 5 years, diagnosed in about 0.6 cases per million population.
- In patients aged 10-14 years, diagnosed in about more than 5 cases per million population.
Gender
- Males are more commonly affected than females. The male to female ratio is around 3:2.
Reference
Anemia of Prematurity Symptoms
The majority of patients with Anemia of Prematurity are asymptomatic. In premature infants with severe disease, symptoms are usually vague or non-specific.
- Common symptoms of Anemia of Prematurity include
- Tachycardia
- Tachypnea
- Decreased activity or lethargy
- Difficulty feeding
- Pallor
- Less common symptoms of Anemia of Prematurity include
- Poor weight gain despite adequate calorie intake
- Breathing difficulties
- Metabolic acidosis due to increased lactic acid production from anaerobic metabolism in the cells
- Heart murmurs
Pathophysiology of Anemia of Prematurity
The exact pathogenesis of anemia of prematurity is not fully understood. It is thought that anemia of prematurity is the result of a combination of decreased erythropoietin production, increased erythropoietin metabolism, deficient iron stores, decreased RBC lifespan, and blood loss during phlebotomy.
Physiological anemia in newborns
Normally, all the newborns experience a fall in the haemoglobin concentration during the first few weeks of life. Healthy, fullterm infants usually develop anemia around 10-12 weeks of life after birth. Hemoglobin concentration never falls below 10 g/dl in healthy infants. Physiological anemia is well tolerated by and does not require any therapy.[2]
- After birth, an embryo transitions from a hypoxic state in-utero to an infant in a relatively hyperoxic environment
- This transition leads to an increase in blood oxygen and tissue oxygen concentration in newborns
- Increased oxygen concentration inhibits erythropoietin production and eventually stops erythropoiesis
- Due to the rapid growth and disproportionate RBC production, hemoglobin levels fall gradually in infants
- The drop in hemoglobin concentration continues until the tissue hypoxia develops which usually takes around 6-12weeks after birth
- Tissue hypoxia activates the oxygen sensors present in the kidney and liver to stimulate the erythropoietin and red blood cells production
- Fullterm newborns have enough iron stores for erythropoiesis until 20 weeks of life
- Infants have a shorter RBC lifespan and increased erythropoietin metabolism when compared to adults
- ↑ Ewing's sarcoma. National cancer institute.http://www.cancer.gov/types/bone/hp/ewing-treatment-pdq#section/_1
- ↑ Strauss RG (2010). "Anaemia of prematurity: pathophysiology and treatment". Blood Rev. 24 (6): 221–5. doi:10.1016/j.blre.2010.08.001. PMC 2981681. PMID 20817366.