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Global Competitiveness Report
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The Global Competitiveness Report (GCR)[1] is a yearly report published by the World Economic Forum. Since 2004, the Global Competitiveness Report ranks countries based on the Global Competitiveness Index,[1] developed by Xavier Sala-i-Martin and Elsa V. Artadi.[2] Before that, the macroeconomic ranks were based on Jeffrey Sachs's Growth Development Index and the microeconomic ranks were based on Michael Porter's Business Competitiveness Index. The Global Competitiveness Index integrates the macroeconomic and the micro/business aspects of competitiveness into a single index.
The report "assesses the ability of countries to provide high levels of prosperity to their citizens. This in turn depends on how productively a country uses available resources. Therefore, the Global Competitiveness Index measures the set of institutions, policies, and factors that set the sustainable current and medium-term levels of economic prosperity."[3][4]
Contents
[hide]
1 Description
2 2017–2018 rankings
3 2016–2017 rankings
4 2015–2016 rankings
5 2014–2015 rankings
6 2013–2014 rankings
7 2012–2013 rankings
8 2011–2012 rankings
9 2010–2011 rankings
10 2009–2010 rankings
11 2008–2009 rankings
12 See also
13 References
14 External links
Description[edit]
Since 2004, the report ranks the world's nations according to the Global Competitiveness Index.[2] The report states that it is based on the latest theoretical and empirical research.[5] It is made up of over 110 variables, of which two thirds come from the Executive Opinion Survey, and one third comes from publicly available sources such as the United Nations. The variables are organized into twelve pillars,[6] with each pillar representing an area considered as an important determinant of competitiveness.
One part of the report is the Executive Opinion Survey which is a survey of a representative sample of business leaders in their respective countries. Respondent numbers have increased every year and is currently just over 13,500 in 142 countries (2010).[7]
The report notes that as a nation develops, wages tend to increase, and that in order to sustain this higher income, labor productivity must improve for the nation to be competitive. In addition, what creates productivity in Sweden is necessarily different from what drives it in Ghana. Thus, the GCI separates countries into three specific stages: factor-driven, efficiency-driven, and innovation-driven, each implying a growing degree of complexity in the operation of the economy.
The report has twelve pillars of competitiveness. These are:
institutions
appropriate infrastructure
a stable macroeconomic framework
good health and primary education
higher education and training
efficient goods markets
efficient labor markets
developed financial markets
the ability to harness the benefits of existing technologies
and its market size, both domestic and international
by producing new and different goods using the most sophisticated production processes
innovation
In the factor-driven stage countries compete based on their factor endowments, primarily unskilled labor and natural resources. Companies compete on the basis of prices and sell basic products or commodities, with their low productivity reflected in low wages. To maintain competitiveness at this stage of development, competitiveness hinges mainly on well-functioning public and private institutions (pillar 1), appropriate infrastructure (pillar 2), a stable macroeconomic framework (pillar 3), and good health and primary education (pillar 4).
As wages rise with advancing development, countries move into the efficiency-driven stage of development, when they must begin to develop more efficient production processes and increase product quality. At this point, competitiveness becomes increasingly driven by higher education and training (pillar 5), efficient goods markets (pillar 6), efficient labor markets (pillar 7), developed financial markets (pillar 8), the ability to harness the benefits of existing technologies (pillar 9), and its market size, both domestic and international (pillar 10).
Finally, as countries move into the innovation-driven stage, they are only able to sustain higher wages and a higher standard of living if their businesses are able to compete by providing new or unique products. At this stage, companies must compete by producing new and different goods using the most sophisticated production processes (pillar 11) and through innovation (pillar 12).
Thus, the impact of each pillar on competitiveness varies across countries, in function of their stages of economic development. Therefore, in the calculation of the GCI, pillars are given different weights depending on the per capita income of the nation.[8] The weights used are the values that best explain growth in recent years[9] For example, the sophistication and innovation factors contribute 10% to the final score in factor and efficiency-driven economies, but 30% in innovation-driven economies. Intermediate values are used for economies in transition between stages.
The Global Competitiveness Index's annual reports are somewhat similar to the Ease of Doing Business Index and the Indices of Economic Freedom, which also look at factors affecting economic growth (but not as many as the Global Competitiveness Report).
2017–2018 rankings[edit]
This is the top 30 of the 2017–2018 report:[10]
Switzerland 5.86 (—)
United States 5.85 (+1)
Singapore 5.71 (−1)
Netherlands 5.66 (—)
Germany 5.65 (—)
Hong Kong 5.53 (+3)
Sweden 5.52 (−1)
United Kingdom 5.51 (−1)
Japan 5.49 (−1)
Finland 5.49 (—)
Norway 5.40 (—)
Denmark 5.39 (—)
New Zealand 5.37 (—)
Canada 5.35 (+1)
Taiwan 5.33 (−1)
Israel 5.31 (+8)
United Arab Emirates 5.30 (−1)
Austria 5.25 (+1)
Luxembourg 5.23 (+1)
Belgium 5.23 (−3)
Australia 5.19 (+1)
France 5.18 (−1)
Malaysia 5.17 (+2)
Ireland 5.16 (−1)
Qatar 5.11 (−7)
South Korea 5.07 (—)
China 5.00 (+1)
Iceland 4.99 (−1)
Estonia 4.85 (+1)
Saudi Arabia 4.83 (−1)
2016–2017 rankings[edit]
This is the top 30 of the 2016–2017 report:[11]
Switzerland 5.81 (—)
Singapore 5.72 (—)
United States 5.7 (—)
Netherlands 5.57 (+1)
Germany 5.57 (−1)
Sweden 5.53 (+3)
United Kingdom 5.49 (+3)
Japan 5.48 (−2)
Hong Kong 5.48 (−2)
Finland 5.44 (−2)
Norway 5.44 (—)
Denmark 5.35 (—)
New Zealand 5.31 (+3)
Taiwan 5.28 (+1)
Canada 5.27 (−2)
United Arab Emirates 5.26 (+1)
Belgium 5.25 (+2)
Qatar 5.23 (−4)
Austria 5.22 (+4)
Luxembourg 5.2 (—)
France 5.2 (+1)
Australia 5.19 (−1)
Ireland 5.18 (+1)
Israel 5.18 (+3)
Malaysia 5.16 (−7)
South Korea 5.03 (—)
Iceland 4.96 (+2)
China 4.95 (—)
Saudi Arabia 4.84 (−4)
Estonia 4.78 (—)
2015–2016 rankings[edit]
This is the top 30 of the 2015–2016 report:[12]
Switzerland 5.76 (—)
Singapore 5.68 (—)
United States 5.61 (—)
Germany 5.53 (+1)
Netherlands 5.50 (+3)
Japan 5.47 (—)
Hong Kong 5.46 (—)
Finland 5.45 (−4)
Sweden 5.43 (+1)
United Kingdom 5.43 (−1)
Norway 5.41 (—)
Denmark 5.33 (+1)
Canada 5.31 (+2)
Qatar 5.30 (+2)
Taiwan 5.28 (−1)
New Zealand 5.25 (+1)
United Arab Emirates 5.24 (−5)
Malaysia 5.23 (+2)
Belgium 5.20 (−1)
Luxembourg 5.20 (−1)
Australia 5.15 (+1)
France 5.13 (+1)
Austria 5.12 (−2)
Ireland 5.11 (+1)
Saudi Arabia 5.07 (−1)
South Korea 4.98 (—)
Israel 4.98 (—)
China 4.89 (—)
Iceland 4.83 (+1)
Estonia 4.71 (−1)
2014–2015 rankings[edit]
This is the top 30 of the 2014–2015 report:[13]
Switzerland 5.80 (—)
Singapore 5.65 (—)
United States 5.54 (+2)
Finland 5.50 (−1)
Germany 5.49 (−1)
Japan 5.47 (+3)
Hong Kong 5.46 (—)
Netherlands 5.45 (—)
United Kingdom 5.41 (+1)
Sweden 5.41 (−4)
Norway 5.35 (—)
United Arab Emirates 5.33 (+7)
Denmark 5.29 (+2)
Taiwan 5.25 (−2)
Canada 5.24 (−1)
Qatar 5.26 (−3)
New Zealand 5.20 (+1)
Belgium 5.18 (−1)
Luxembourg 5.17 (+3)
Malaysia 5.16 (+4)
Austria 5.16 (−5)
Australia 5.08 (−1)
France 5.08 (—)
Saudi Arabia 5.06 (−4)
Ireland 4.98 (+3)
South Korea 4.96 (−1)
Israel 4.95 (—)
China 4.89 (+1)
Estonia 4.71 (+3)
Iceland 4.71 (+1)
2013–2014 rankings[edit]
This is the top 30 of the 2013–2014 report:[14]
Switzerland 5.67 (—)
Singapore 5.61 (—)
Finland 5.54 (—)
Germany 5.51 (+2)
United States 5.48 (+2)
Sweden 5.48 (−2)
Hong Kong 5.47 (+2)
Netherlands 5.42 (−3)
Japan 5.40 (+1)
United Kingdom 5.37 (−2)
Norway 5.33 (+4)
Taiwan 5.29 (+1)
Qatar 5.24 (−2)
Canada 5.20 (—)
Denmark 5.18 (−3)
Austria 5.15 (—)
Belgium 5.13 (—)
New Zealand 5.11 (+5)
United Arab Emirates 5.11 (+5)
Saudi Arabia 5.10 (−2)
Australia 5.09 (−1)
Luxembourg 5.09 (—)
France 5.05 (−2)
Malaysia 5.03 (+1)
South Korea 5.01 (−6)
Brunei 4.95 (+2)
Israel 4.94 (−1)
Ireland 4.92 (−1)
China 4.84 (—)
Puerto Rico 4.67 (+1)
2012–2013 rankings[edit]
This is the top 30 of the 2012–2013 report:[15]
Switzerland 5.72 (—)
Singapore 5.67 (—)
Finland 5.55 (+1)
Sweden 5.53 (−1)
Netherlands 5.50 (+2)
Germany 5.48 (—)
United States 5.47 (−2)
United Kingdom 5.45 (+2)
Hong Kong 5.41 (+2)
Japan 5.40 (−1)
Qatar 5.38 (+3)
Denmark 5.29 (−4)
Taiwan 5.28 (—)
Canada 5.27 (−2)
Norway 5.27 (+1)
Austria 5.22 (+3)
Belgium 5.21 (−2)
Saudi Arabia 5.19 (+1)
South Korea 5.12 (+5)
Australia 5.12 (—)
France 5.11 (−3)
Luxembourg 5.09 (+1)
New Zealand 5.09 (+2)
United Arab Emirates 5.07 (+3)
Malaysia 5.06 (−4)
Israel 5.02 (−4)
Ireland 4.91 (+2)
Brunei 4.87 (—)
China 4.83 (−3)
Iceland 4.74 (—)
2011–2012 rankings[edit]
This is the top 30 of the 2011–2012 report:[16][17]
Switzerland 5.75 (—)
Singapore 5.63 (+1)
Sweden 5.61 (−1)
Finland 5.47 (+3)
United States 5.43 (−1)
Germany 5.41 (−1)
Netherlands 5.41 (+1)
Denmark 5.40 (+1)
Japan 5.40 (−3)
United Kingdom 5.39 (+2)
Hong Kong 5.36 (—)
Canada 5.33 (−2)
Taiwan 5.26 (—)
Qatar 5.24 (+3)
Belgium 5.20 (+4)
Norway 5.18 (−2)
Saudi Arabia 5.17 (+4)
France 5.14 (−3)
Austria 5.14 (−1)
Australia 5.11 (−4)
Malaysia 5.08 (+5)
Israel 5.07 (+2)
Luxembourg 5.03 (−3)
South Korea 5.02 (−2)
New Zealand 4.93 (−2)
China 4.90 (+1)
United Arab Emirates 4.89 (−2)
Brunei 4.78 (—)
Ireland 4.77 (—)
Iceland 4.75 (+1)
2010–2011 rankings[edit]
This is the top 30 of the 2010–2011 report:[18]
Switzerland 5.63
Sweden 5.56
Singapore 5.48
United States 5.43
Germany 5.39
Japan 5.37
Finland 5.37
Netherlands 5.33
Denmark 5.32
Canada 5.30
Hong Kong 5.27
United Kingdom 5.25
Taiwan 5.21
Norway 5.14
France 5.13
Australia 5.11
Qatar 5.10
Austria 5.09
Belgium 5.07
Luxembourg 5.05
Saudi Arabia 4.95
South Korea 4.93
New Zealand 4.92
Israel 4.91
United Arab Emirates 4.89
Malaysia 4.88
China 4.84
Brunei 4.75
Ireland 4.74
Chile 4.69
2009–2010 rankings[edit]
This is the top 30 of the 2009–2010 report:[19]
Switzerland 5.60
United States 5.59
Singapore 5.55
Sweden 5.51
Denmark 5.46
Finland 5.43
Germany 5.37
Japan 5.37
Canada 5.33
Netherlands 5.32
Hong Kong 5.22
Taiwan 5.20
United Kingdom 5.19
Norway 5.17
Australia 5.15
France 5.13
Austria 5.13
Belgium 5.09
South Korea 5.00
New Zealand 4.98
Luxembourg 4.96
Qatar 4.95
United Arab Emirates 4.92
Malaysia 4.87
Ireland 4.84
Iceland 4.80
Israel 4.80
Saudi Arabia 4.75
China 4.74
Chile 4.70
2008–2009 rankings[edit]
This is the top 30 of the 2008–2009 report:[20]
United States 5.74
Switzerland 5.61
Denmark 5.58
Sweden 5.53
Singapore 5.53
Finland 5.50
Germany 5.46
Netherlands 5.41
Japan 5.38
Canada 5.37
Hong Kong 5.33
United Kingdom 5.30
South Korea 5.28
Austria 5.23
Norway 5.22
France 5.22
Taiwan 5.22
Australia 5.20
Belgium 5.14
Iceland 5.05
Malaysia 5.04
Ireland 4.99
Israel 4.97
New Zealand 4.93
Luxembourg 4.85
Qatar 4.83
Saudi Arabia 4.72
Chile 4.72
Spain 4.72
China 4.70
You can find the computation and structure of the GCI pp. 49–50 of the Global Competitiveness Report 2013-2013
See also[edit]
Competitiveness
List of national quality awards
World Competitiveness Yearbook
References[edit]
^ Jump up to: a b "Global Competitiveness Report 2014-2015 - Reports - World Economic Forum". Global Competitiveness Report 2014-2015.
^ Jump up to: a b "Sala-i-Martin, Xavier and Elsa V. Artadi, "The Global Competitiveness Index", Global Competitiveness Report, Global Economic Forum 2004
Jump up ^ "Global Competitiveness Network: Frequently Asked Questions". Retrieved 2009-04-17.
Jump up ^ "Global Competitiveness".
Jump up ^ "Archived copy" (PDF). Archived from the original (PDF) on 2006-10-27. Retrieved 2006-09-27.
Jump up ^ See appendix in Page 47 of the 2011-12 report. http://www3.weforum.org/docs/WEF_GCR_Report_2011-12.pdf
Jump up ^ http://www.weforum.org/en/initiatives/gcp/FAQs/index.htm
Jump up ^ "Archived copy" (PDF). Archived from the original (PDF) on 2006-10-27. Retrieved 2006-09-28.
Jump up ^ http://www.columbia.edu/~xs23/papers/WEC_00220_00701_Snowdon.pdf
Jump up ^ "Global Competitiveness Report 2017-2018" (PDF). World Economic Forum.
Jump up ^ "Global Competitiveness Report 2016-2017" (PDF). World Economic Forum.
Jump up ^ "Global Competitiveness Report 2015-2016". Global Competitiveness Report 2015-2016.
Jump up ^ "Global Competitiveness Report 2014-2015 - Reports - World Economic Forum". Global Competitiveness Report 2014-2015.
Jump up ^ http://www3.weforum.org/docs/WEF_GlobalCompetitivenessReport_2013-14.pdf
Jump up ^ http://www3.weforum.org/docs/WEF_GlobalCompetitivenessReport_2012-13.pdf
Jump up ^ "US Competitiveness Ranking Continues to Fall; Emerging Markets Are Closing the Gap | World Economic Forum - US Competitiveness Ranking Continues to Fall; Emerging Markets Are Closing the Gap". Weforum.org. 2011-09-07. Archived from the original on 2013-05-01. Retrieved 2013-04-29.
Jump up ^ http://www3.weforum.org/docs/WEF_GCR_CompetitivenessIndexRanking_2011-12.pdf
Jump up ^ World Economic Forum. "Table 4: The Global Competitiveness Index 2010–2011 rankings and 2009–2010 comparisons" (PDF). Archived from the original (PDF) on 2010-09-22. Retrieved 2010-09-10.
Jump up ^ World Economic Forum. "Table 4: The Global Competitiveness Index 2009–2010 rankings and 2008–2009 comparisons" (PDF). Archived from the original (PDF) on 2010-10-30. Retrieved 2009-09-09.
Jump up ^ World Economic Forum. "The Global Competitiveness Index rankings and 2007–2008 comparisons" (PDF). Archived from the original (PDF) on 2009-03-24. Retrieved 2009-09-10.
External links[edit]
"Interactive Global Competitiveness Report"
Global Competitiveness Report
Top 20 countries of 2010 by competitiveness, United Explanations
http://www.imd.org/research/publications/wcy/
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Hereditary spherocytosis
From Wikipedia, the free encyclopedia
Jump to: navigation, search
This article is about aspects of spherocytosis specific to the hereditary form of the disorder. For details that apply generally to this variant as well as others, see Spherocytosis.
Hereditary spherocytosis
Peripheral blood smear from patient with hereditary spherocytos
Classification and external resources
Specialty
hematology
ICD-10
D58.0
ICD-9-CM
282.0
OMIM
182900
MedlinePlus
000530
eMedicine
med/2147
MeSH
D013103
[edit on Wikidata]
Hereditary spherocytosis (also known as Minkowski–Chauffard syndrome) abnormality of erythrocytes. The disorder is caused by mutations in genes relating to membrane proteins that allow for the erythrocytes to change shape. The abnormal erythrocytes are sphere-shaped (spherocytosis) rather than the normal biconcave disk shaped. Dysfunctional membrane proteins interfere with the cell's ability to be flexible to travel from the arteries to the smaller capillaries. This difference in shape also makes the red blood cells more prone to rupture.[1] Cells with these dysfunctional proteins are taken for degradation at the spleen. This shortage of erythrocytes results in hemolytic anemia.
It was first described in 1871 and is the most common cause of inherited hemolysis in Europe and North America within the Caucasian population, with an incidence of 1 in 5000 births. The clinical severity of HS varies from symptom-free carrier to severe haemolysis because the disorder exhibits incomplete penetrance in its expression.
Symptoms include anemia, jaundice, splenomegaly, and fatigue. On a blood smear, Howell-Jolly bodies may be seen within red blood cells. Primary treatment for patients with symptomatic HS has been total splenectomy, which eliminates the hemolytic process, allowing normal hemoglobin, reticulocyte and bilirubin levels.
As in non-hereditary spherocytosis, the spleen destroys the spherocytes. This process of red blood cells rupturing directly results in varying degrees of anemia (causing a pale appearance and fatigue), high levels of bilirubin in the blood (causing jaundice), and splenomegaly.
Acute cases can threaten to cause hypoxia through anemia and acute kernicterus through high blood levels of bilirubin, particularly in newborns. Most cases can be detected soon after birth. An adult with this disease should have their children tested, although the presence of the disease in children is usually noticed soon after birth. Occasionally, the disease will go unnoticed until the child is about 4 or 5 years of age. A person may also be a carrier of the disease and show no signs or symptoms of the disease. Other symptoms may include abdominal pain that could lead to the removal of the spleen and/or gallbladder.
Chronic symptoms include anemia, increased blood viscosity, and splenomegaly, and some symptoms are still unknown at this stage.[2] Furthermore, the detritus of the broken-down blood cells – unconjugated or indirect bilirubin – accumulates in the gallbladder, and can cause pigmented gallstones to develop. In chronic patients, an infection or other illness can cause an increase in the destruction of red blood cells, resulting in the appearance of acute symptoms, a hemolytic crisis. Spherocytosis patients who are heterozygous for a hemochromatosis gene may suffer from iron overload despite the hemochromatosis genes being recessive.[3][4]
Contents
[hide]
1 Presentation
1.1 Complications
2 Pathophysiology
3 Diagnosis
4 Treatment
5 Epidemiology
6 Research
7 See also
8 References
9 External links
Presentation[edit]
Complications[edit]
Hemolytic crisis, with more pronounced jaundice due to accelerated hemolysis (may be precipitated by infection).
Aplastic crisis with dramatic fall in hemoglobin level and (reticulocyte count)-decompensation, usually due to maturation arrest and often associated with megaloblastic changes; may be precipitated by infection, such as influenza, notably with parvovirus B19.[5][6][7]
Folate deficiency caused by increased bone marrow requirement.
Pigmented gallstones occur in approximately half of untreated patients. Increased hemolysis of red blood cells leads to increased bilirubin levels, because bilirubin is a breakdown product of heme. The high levels of bilirubin must be excreted into the bile by the liver, which may cause the formation of a pigmented gallstone, which is composed of calcium bilirubinate. Since these stones contain high levels of calcium carbonates and phosphate, they are radiopaque and are visible on x-ray.
Leg ulcer.
Abnormally low hemoglobin A1C levels.[8] Hemoglobin A1C (glycated hemoglobin) is a test for determining the average blood glucose levels over an extended period of time, and is often used to evaluate glucose control in diabetics. The hemoglobin A1C levels are abnormally low because the life span of the red blood cells is decreased, providing less time for the non-enzymatic glycosylation of hemoglobin. Thus, even with high overall blood sugar, the A1C will be lower than expected.
Pathophysiology[edit]
Hereditary spherocytosis can be an autosomal recessive or autosomal dominant trait.[9] Hereditary spherocytosis is most commonly (though not exclusively) found in Northern European and Japanese families, although an estimated 25% of cases are due to spontaneous mutations. A patient has a 50% chance of passing the mutation onto each of his/her offspring.
Hereditary spherocytosis is caused by a variety of molecular defects in the genes that code for the red blood cell proteins spectrin (alpha and beta), ankyrin,[10] band 3 protein, protein 4.2,[11] and other red blood cell membrane proteins:[12]
Type
OMIM
Gene
Locus
HS1 182900 ANK1 8p11.2
HS2 182870 SPTB 14q22-q23
HS3 270970 SPTA 1q21
HS4 109270 SLC4A1 17q21-q22
HS5 612690 EPB42 15q15
These proteins are necessary to maintain the normal shape of a red blood cell, which is a biconcave disk. The integrating protein that is most commonly defective is spectrin which is responsible for incorporation and binding of spectrin, thus in its dysfunction cytoskeletal instabilities ensue.
The primary defect in hereditary spherocytosis is a deficiency of membrane surface area. Decreased surface area may be produced by two different mechanisms: 1) Defects of spectrin, ankyrin (most commonly), or protein 4.2 lead to reduced density of the membrane skeleton, destabilizing the overlying lipid bilayer and releasing band 3-containing microvesicles. 2) Defects of band 3 lead to band 3 deficiency and loss of its lipid-stabilizing effect. This results in the loss of band 3-free microvesicles. Both pathways result in membrane loss, decreased surface area, and formation of spherocytes with decreased deformability.
As the spleen normally targets abnormally shaped red cells (which are typically older), it also destroys spherocytes. In the spleen, the passage from the cords of Billroth into the sinusoids may be seen as a bottleneck, where red blood cells need to be flexible in order to pass through. In hereditary spherocytosis, red blood cells fail to pass through and get phagocytosed, causing extravascular hemolysis.[13]
Diagnosis[edit]
In a peripheral blood smear, the red blood cells will appear abnormally small and lack the central pale area that is present in normal red blood cells. These changes are also seen in non-hereditary spherocytosis, but they are typically more pronounced in hereditary spherocytosis. The number of immature red blood cells (reticulocyte count) will be elevated.[2] An increase in the mean corpuscular hemoglobin concentration is also consistent with hereditary spherocytosis.
Other protein deficiencies cause hereditary elliptocytosis, pyropoikilocytosis or stomatocytosis.
In longstanding cases and in patients who have taken iron supplementation or received numerous blood transfusions, iron overload may be a significant problem. This is a potential cause of heart muscle damage and liver disease. Measuring iron stores is therefore considered part of the diagnostic approach to hereditary spherocytosis.
An osmotic fragility test can aid in the diagnosis.[14] In this test, the spherocytes will rupture in liquid solutions less concentrated than the inside of the red blood cell. This is due to increased permeability of the spherocyte membrane to salt and water, which enters the concentrated inner environment of the RBC and leads to its rupture.[15] Although the osmotic fragility test is widely considered the gold standard for diagnosing hereditary spherocytosis, it misses as many as 25% of cases. Flow cytometric analysis of eosin-5′-maleimide-labeled intact red blood cells and the acidified glycerol lysis test are two additional options to aid diagnosis.[16]
Treatment[edit]
Although research is ongoing, at this point there is no cure for the genetic defect that causes hereditary spherocytosis.[12] Current management focuses on interventions that limit the severity of the disease. Treatment options include:
Splenectomy: As in non-hereditary spherocytosis, acute symptoms of anemia and hyperbilirubinemia indicate treatment with blood transfusions or exchanges and chronic symptoms of anemia and an enlarged spleen indicate dietary supplementation of folic acid and splenectomy,[17] the surgical removal of the spleen. Splenectomy is indicated for moderate to severe cases, but not mild cases.[2] To decrease the risk of sepsis, post-splenectomy spherocytosis patients require immunization against the influenza virus, encapsulated bacteria such as Streptococcus pneumoniae and meningococcus, and prophylactic antibiotic treatment. However, the use of prophylactic antibiotics, such as penicillin, remains controversial.[12]
Partial splenectomy: Since the spleen is important for protecting against encapsulated organisms, sepsis caused by encapsulated organisms is a possible complication of splenectomy.[2] The option of partial splenectomy may be considered in the interest of preserving immune function. Research on outcomes is currently limited,[2] but favorable.[18]
Surgical removal of the gallbladder may be necessary.[12]
Epidemiology[edit]
Hereditary spherocytosis is the most common disorder of the red cell membrane and affects 1 in 2,000 people of Northern European ancestry.[19] According to Harrison's Principles of Internal Medicine, the frequency is at least 1 in 5,000.[12]
Research[edit]
Experimental gene therapy exists to treat hereditary spherocytosis in lab mice; however, this treatment has not yet been tried on humans due to all of the risks involved in human gene therapy.
See also[edit]
Spherocytosis
Anemia
Hematology
References[edit]
Jump up ^ Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease. St. Louis, Mo: Elsevier Saunders. p. 625. ISBN 0-7216-0187-1.
^ Jump up to: a b c d e Bolton-Maggs, P. H. B.; Stevens, R. F.; Dodd, N. J.; Lamont, G.; Tittensor, P.; King, M. -J.; General Haematology Task Force of the British Committee for Standards in Haematology (2004). "Guidelines for the diagnosis and management of hereditary spherocytosis". British Journal of Haematology. 126 (4): 455–474. doi:10.1111/j.1365-2141.2004.05052.x. PMID 15287938.
Jump up ^ J L Rasmussen; D A Odelson; F L Macrina (1987-08-01). "Complete nucleotide sequence of insertion element IS4351 from Bacteroides fragilis. - UKPMC Article - UK PubMed Central". UKPMC Article. Archived from the original on 2012-12-23. Retrieved 2012-07-03.
Jump up ^ Paula Bolton-Maggs (September 2011). "Guidelines for the Diagnosis and Management of Hereditary Spherocytosis" (PDF). The British Committee for Standards in Haematology. Retrieved 2 July 2012.
Jump up ^ Fjaerli, H. O.; Vogt, H.; Bruu, A. L. (1991). "Human parvovirus B19 as the cause of aplastic crisis in hereditary spherocytosis". Tidsskrift for den Norske laegeforening : tidsskrift for praktisk medicin, ny raekke. 111 (22): 2735–2737. PMID 1658972.
Jump up ^ Beland, S. S.; Daniel, G. K.; Menard, J. C.; Miller, N. M. (1997). "Aplastic crisis associated with parvovirus B19 in an adult with hereditary spherocytosis". The Journal of the Arkansas Medical Society. 94 (4): 163–164. PMID 9308316.
Jump up ^ Servey, J. T.; Reamy, B. V.; Hodge, J. (2007). "Clinical presentations of parvovirus B19 infection". American Family Physician. 75 (3): 373–376. PMID 17304869.
Jump up ^ Kutter, D; Thoma, J (2006). "Hereditary spherocytosis and other hemolytic anomalies distort diabetic control by glycated hemoglobin". Clinical laboratory. 52 (9-10): 477–81. PMID 17078474.
Jump up ^ Eber S, Lux SE (April 2004). "Hereditary spherocytosis--defects in proteins that connect the membrane skeleton to the lipid bilayer". Semin. Hematol. 41 (2): 118–41. doi:10.1053/j.seminhematol.2004.01.002. PMID 15071790.
Jump up ^ Gallagher PG, Forget BG (December 1998). "Hematologically important mutations: spectrin and ankyrin variants in hereditary spherocytosis". Blood Cells Mol. Dis. 24 (4): 539–43. doi:10.1006/bcmd.1998.0217. PMID 9887280.
Jump up ^ Perrotta S, Gallagher PG, Mohandas N (October 2008). "Hereditary spherocytosis". Lancet. 372 (9647): 1411–26. doi:10.1016/S0140-6736(08)61588-3. PMID 18940465.
^ Jump up to: a b c d e Anthony S. Fauci; Eugene Braunwald; Dennis L. Kasper; Stephen L. Hauser; Dan L. Longo; J. Larry Jameson; Joseph Loscalzo (2008). Harrison's principles of internal medicine (17th ed.). New York: McGraw-Hill Medical. pp. Chapter 106. ISBN 978-0071466332.
Jump up ^ Chapter 12, page 425 in: Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson. Robbins Basic Pathology. Philadelphia: Saunders. ISBN 1-4160-2973-7. 8th edition.
Jump up ^ Won DI, Suh JS (March 2009). "Flow cytometric detection of erythrocyte osmotic fragility". Cytometry Part B. 76 (2): 135–41. doi:10.1002/cyto.b.20448. PMID 18727072.
Jump up ^ Goljan. Rapid Review Pathology. 2010. Page 213.
Jump up ^ Bianchi, P.; Fermo, E.; Vercellati, C.; Marcello, A. P.; Porretti, L.; Cortelezzi, A.; Barcellini, W.; Zanella, A. (2011). "Diagnostic power of laboratory tests for hereditary spherocytosis: A comparison study in 150 patients grouped according to molecular and clinical characteristics". Haematologica. 97 (4): 516–523. doi:10.3324/haematol.2011.052845. PMC 3347664  . PMID 22058213.
Jump up ^ Bolton-Maggs PH, Stevens RF, Dodd NJ, Lamont G, Tittensor P, King MJ (August 2004). "Guidelines for the diagnosis and management of hereditary spherocytosis". Br. J. Haematol. 126 (4): 455–74. doi:10.1111/j.1365-2141.2004.05052.x. PMID 15287938.
Jump up ^ Buesing, K. L.; Tracy, E. T.; Kiernan, C.; Pastor, A. C.; Cassidy, L. D.; Scott, J. P.; Ware, R. E.; Davidoff, A. M.; Rescorla, F. J.; Langer, J. C.; Rice, H. E.; Oldham, K. T. (2011). "Partial splenectomy for hereditary spherocytosis: A multi-institutional review". Journal of Pediatric Surgery. 46 (1): 178–183. doi:10.1016/j.jpedsurg.2010.09.090. PMID 21238662.
Jump up ^ https://ghr.nlm.nih.gov/condition/hereditary-spherocytosis#genes
External links[edit]
An online HS resource from The University of Texas Southwestern Medical Center
A short article from WebMD
A picture of spherocytes from Medline
[show]
v
t
e
Diseases of red blood cells (D50–69,74, 280–287)
↑
Polycythemia
Polycythemia vera
↓
Anemia
Nutritional
Micro-: Iron-deficiency anemia
Plummer–Vinson syndrome
Macro-: Megaloblastic anemia
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(mostly normo-)
Hereditary
enzymopathy: G6PD
glycolysis
PK
TI
HK
hemoglobinopathy: Thalassemia
alpha
beta
delta
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membrane: Hereditary spherocytosis
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[show]
v
t
e
Cytoskeletal defects
Microfilaments
Myofilament
Actin
Hypertrophic cardiomyopathy 11
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DFNA20
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DFN A3, 4, 11, 17, 22; B2, 30, 37, 48
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Hypertrophic cardiomyopathy 7, 2
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Tropomyosin
Hypertrophic cardiomyopathy 3
Nemaline myopathy 1
Titin
Hypertrophic cardiomyopathy 9
Other
Fibrillin
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Filamin
FG syndrome 2
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IF
1/2
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Striate palmoplantar keratoderma 3
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IHCM
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KRT4 (White sponge nevus)
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KRT10 (Epidermolytic hyperkeratosis)
KRT12 (Meesmann juvenile epithelial corneal dystrophy)
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KRT18 (Familial cirrhosis)
KRT81/KRT83/KRT86 (Monilethrix)
Naegeli–Franceschetti–Jadassohn syndrome
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3
Desmin: Desmin-related myofibrillar myopathy
Dilated cardiomyopathy 1I
GFAP: Alexander disease
Peripherin: Amyotrophic lateral sclerosis
4
Neurofilament: Parkinson's disease
Charcot–Marie–Tooth disease 1F, 2E
Amyotrophic lateral sclerosis
5
Laminopathy: LMNA
Mandibuloacral dysplasia
Dunnigan Familial partial lipodystrophy
Emery–Dreifuss muscular dystrophy 2
Limb-girdle muscular dystrophy 1B
Charcot–Marie–Tooth disease 2B1
LMNB
Barraquer–Simons syndrome
LEMD3
Buschke–Ollendorff syndrome
Osteopoikilosis
LBR
Pelger–Huet anomaly
Hydrops-ectopic calcification-moth-eaten skeletal dysplasia
Microtubules
Kinesin
Charcot–Marie–Tooth disease 2A
Hereditary spastic paraplegia 10
Dynein
Primary ciliary dyskinesia
Short rib-polydactyly syndrome 3
Asphyxiating thoracic dysplasia 3
Other
Tauopathy
Cavernous venous malformation
Membrane
Spectrin: Spinocerebellar ataxia 5
Hereditary spherocytosis 2, 3
Hereditary elliptocytosis 2, 3
Ankyrin: Long QT syndrome 4
Hereditary spherocytosis 1
Catenin
APC
Gardner's syndrome
Familial adenomatous polyposis
plakoglobin (Naxos syndrome)
GAN (Giant axonal neuropathy)
Other
desmoplakin: Striate palmoplantar keratoderma 2
Carvajal syndrome
Arrhythmogenic right ventricular dysplasia 8
plectin: Epidermolysis bullosa simplex with muscular dystrophy
Epidermolysis bullosa simplex of Ogna
plakophilin: Skin fragility syndrome
Arrhythmogenic right ventricular dysplasia 9
centrosome: PCNT (Microcephalic osteodysplastic primordial dwarfism type II)
See also: cytoskeletal proteins
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