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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, increased [[erythropoietin]] [[metabolism]], deficient [[iron]] stores, decreased [[RBC]] lifespan, and blood loss during [[phlebotomy]].
The [[pathogenesis]] of [[anemia of prematurity]] is multifactorial. [[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]].<ref name="pmid6502312">{{cite journal| author=Stockman JA, Graeber JE, Clark DA, McClellan K, Garcia JF, Kavey RE| title=Anemia of prematurity: determinants of the erythropoietin response. | journal=J Pediatr | year= 1984 | volume= 105 | issue= 5 | pages= 786-92 | pmid=6502312 | doi=10.1016/s0022-3476(84)80308-x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6502312  }} </ref><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>


===Physiological anemia in newborns===
===Physiological anemia in newborns===
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*[[Tissue hypoxia]] activates the [[oxygen sensors]] present in the [[kidney]] and [[liver]] to stimulate the [[erythropoietin]] and [[red blood cells]] production
*[[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
*[[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
*Infants have a shorter [[RBC]] lifespan and increased [[erythropoietin]] [[metabolism]] when compared to adults<ref name="pmid8847295">{{cite journal| author=Widness JA, Veng-Pedersen P, Peters C, Pereira LM, Schmidt RL, Lowe LS| title=Erythropoietin pharmacokinetics in premature infants: developmental, nonlinearity, and treatment effects. | journal=J Appl Physiol (1985) | year= 1996 | volume= 80 | issue= 1 | pages= 140-8 | pmid=8847295 | doi=10.1152/jappl.1996.80.1.140 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8847295  }} </ref>
 
===Pathological Anemia of Prematurity===
In [[preterm]] [[infants]], multiple [[physiological factors]] exaggerate and combine to result in [[pathological anemia]]. [[Hemoglobin]] levels drop rapidly to less than 10 g/dl around 4-6 weeks after birth. [[Infants]] with 1-1.5 kg of [[birthweight]] have [[hemoglobin]] levels around 8 g/dl, whereas [[infants]] with [[birthweight]] less than 1 kg have [[hemoglobin]] levels around 7 g/dl or less. The profound decrease in [[hemoglobin]] levels in [[premature infants]] produce abnormal [[signs]] and [[symptoms]] and require a [[blood transfusion]]. <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>
 
*[[Iron transport]] from [[mother]] to [[infants]] and a greater proportion of [[fetal erythropoiesis]] occur during the [[third trimester]]. So, [[infants]] born [[prematurely]] have deficient [[iron stores]] required for the [[red blood cells production]]
*[[Blood loss]] during [[phlebotomy]] is the major contributor of [[anemia of prematurity]]
*Majority of [[preterm infants]] are [[sick]] and [[critically ill]] that require frequent [[blood sampling]] for various [[laboratory investigations]] needed for their [[clinical monitoring]]. The average amount of [[blood loss]] during [[sampling]] ranges from 0.8-3.1 ml/kg/day, a significant amount that requires replacement
*[[Preterm infants]] are at increased risk of [[nosocomial infections]] that lead to [[oxidative hemolysis]]
*In [[premature infants]], [[liver]] is the major site of [[erythropoiesis]]. [[Liver]] [[EPO]] is less sensitive to anemia and tissue hypoxia<ref name="pmid9787158">{{cite journal| author=Dame C, Fahnenstich H, Freitag P, Hofmann D, Abdul-Nour T, Bartmann P | display-authors=etal| title=Erythropoietin mRNA expression in human fetal and neonatal tissue. | journal=Blood | year= 1998 | volume= 92 | issue= 9 | pages= 3218-25 | pmid=9787158 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9787158  }} </ref>
*[[Preterm infants]] have deficient [[Vitamin E]], [[Vitamin B12]], [[Folic acid]] stores required for [[red blood cells]] production
*A combination of [[blood loss]], decreased [[erythropoietin]] production, deficient [[iron stores]], increased [[erythropoietin]] [[metabolism]], shortened [[RBC]] lifespan contribute to the development of [[anemia of prematurity]]

Revision as of 10:19, 20 July 2020

Asra Firdous,M.B.B.S.[1]


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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

Incidence

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 pathogenesis of anemia of prematurity is multifactorial. 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.[2][3]

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.[3]

Pathological Anemia of Prematurity

In preterm infants, multiple physiological factors exaggerate and combine to result in pathological anemia. Hemoglobin levels drop rapidly to less than 10 g/dl around 4-6 weeks after birth. Infants with 1-1.5 kg of birthweight have hemoglobin levels around 8 g/dl, whereas infants with birthweight less than 1 kg have hemoglobin levels around 7 g/dl or less. The profound decrease in hemoglobin levels in premature infants produce abnormal signs and symptoms and require a blood transfusion. [3]

  1. Ewing's sarcoma. National cancer institute.http://www.cancer.gov/types/bone/hp/ewing-treatment-pdq#section/_1
  2. Stockman JA, Graeber JE, Clark DA, McClellan K, Garcia JF, Kavey RE (1984). "Anemia of prematurity: determinants of the erythropoietin response". J Pediatr. 105 (5): 786–92. doi:10.1016/s0022-3476(84)80308-x. PMID 6502312.
  3. 3.0 3.1 3.2 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.
  4. Widness JA, Veng-Pedersen P, Peters C, Pereira LM, Schmidt RL, Lowe LS (1996). "Erythropoietin pharmacokinetics in premature infants: developmental, nonlinearity, and treatment effects". J Appl Physiol (1985). 80 (1): 140–8. doi:10.1152/jappl.1996.80.1.140. PMID 8847295.
  5. Dame C, Fahnenstich H, Freitag P, Hofmann D, Abdul-Nour T, Bartmann P; et al. (1998). "Erythropoietin mRNA expression in human fetal and neonatal tissue". Blood. 92 (9): 3218–25. PMID 9787158.