Thalassemia minor
Thalassemia Latest NEWS

Thalassemia Minor Pregnancy
Mother Thalassemia Minor + Father Normal
Result =
80% - Normal Child
10% - No child
07% - Thalassemia Minor Child
03% - Thalassemia Major Child
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Actual answer is 50% chance of having a Thalassemia minor child and 50% "Normal"

Thalassemia Minor

Thalassemia Minor
Thalassemia is a genetic disease.

Thalassemia Major is present at birth, and the child cannot outgrow it.

Thalassemia cannot be 'contracted'. It is not infectious or contagious.

Both parents need to have Thalassemia trait in order for the child to contract it.

If a person with a Thalassemia trait marries another such person, the offspring has a 25% chance of developing full blown Thalassemia.

If only one parent has the trait, the trait may be passed on to the child.

A person with a Thalassemia trait shows no symptoms except perhaps for anaemia. Iron supplements don't help, and should not be taken.

Having a Thalassemia trait does not make a person susceptible to any diseases. This trait does not harm the person in any way, and the person can live a perfectly normal life without even being aware that he has a Thalassemia trait.

A Thalassemia trait will NOT develop into the full blown disease at any stage in life.

Thalassemia Minor


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What is the difference between thalassemia minor and major?

There are two forms of beta thalassemia. They are thalassemia minor and thalassemia major (which is also called Cooley's anemia).

Thalassemia minor: The individual with thalassemia minor has only one copy of the beta thalassemia gene (together with one perfectly normal beta-chain gene). The person is said to be heterozygous for beta thalassemia.

Persons with thalassemia minor have (at most) mild anemia (with slight lowering of the hemoglobin level in the blood). This situation can very closely resemble that with mild iron-deficiency anemia. However, persons with thalassemia minor have a normal blood iron level (unless they have are iron deficient for other reasons). No treatment is necessary for thalassemia minor. In particular, iron is neither necessary nor advised.

Thalassemia Minor often coexists with other diseases such as asthma, and mood disorders

I am 25yrs old and suffreing from Thalassemia Minor. My hemoglobin count is 7grms ...We both(my husband & me) want to have a baby and we are trying from couple of months but not yet succeeded.Is Thalassemia is the reason for not getting pregnant??

Thalassemia minor is nothing to do with conception. It should be looked seperately for different causes. the only thing to know is t6hat if both husband and wife are Thalassemia carrier then in each pregnancy  there is 25% chance of having a thalassemia major child, 50% chance of having Thalassemia minor/carrier child and 25% "Normal-not even a carrier"
Dr J.S. Arora
General Secretary
National Thalassemia Welfare Society &
Federation of Indian Thalassemics

Thalassemia Latest NEWS
Thalassemia Minor is the mildest form of the illness. The individuals may be heterozygous and inheriting only one mutant or p-thal gene, which limits the synthesis of beta-peptide chains. Or they may have inherited a genetically distinct abnormality of p-globin chain which produces a milder disease. The gene for alpha chain synthesis is normal. There is usually compensatory increase in delta chain synthesis, leading to levels of Hb A2 being higher than normal. Hemoglobin A2 may be markedly reduced with co-existing iron-deficiency anemia.
Increase in the level of hemoglobin F is inconstant. Production of hemoglobin A is only slightly reduced.
Thalassemia Minor patients have only a very mild anemia, sometimes with abdominal pain and mild icteric, tinge. Thalassemia minor is often confused with iron deficiency anemia and is treated as such, till the correct diagnosis is suspected. Serum iron concentration is on the higher side and iron binding capacity is reduced. Free erythrocyte porphyrin is normal in thalassemia minor (30 microgram/dL of whole blood). This is moderately raised in iron deficiency anemia (30 to 190 ug/ dL of whole blood). This is a useful diagnostic test to differentiate iron deficiency states from thalassemia minor and lead poisoning.
The synthesis of alpha-peptide chains is suppressed. Defective alpha chain synthesis effects the production of all the normal hemoglobin viz., A, A2 and F. Four beta-peptide chains polymerise to a tetrameric form giving rise to hemoglobin H. Heterozygous alpha thalassemia is usually very mild and is often not associated with any regular alteration in the hemoglobin pattern in the adult life.
There are possibly two alleles for alpha-thalassemia gene viz., alpha-thalassemia1 causing complete inhibition of alpha chain synthesis and alpha-thai2 causing only impaired synthesis of alpha chains.
Alpha-thalassemia is most prevalent in the countries of South East Asia. The infant is usually normal at birth.

The mainstay of managing these cases is repeated blood transfusions. An attempt should be made to maintain hemoglobin level above 10-12 g/dL (by hyper transfusion) to ensure active life and adequate growth. Group and type specific, fresh, triple saline washed, packed red cell transfusions are the most desired form of component therapy. These are to be transfused at the rate of 10-15 ml/kg every 2 to 3 weeks. Blood transfusions may result in hemolytic or febrile reactions, transmission of viral infections (HIV1 & 2, Hepatitis B and C, Cytomegalovirus) and iron overload. Routine donor screening for these viral infections is a must. All thalassemics should be vaccinated with Hepatitis B vaccine before starting transfusions. Iron overload results in multiple organ dysfunction due to hemosiderosis and hemochromatosis. Chronic anemia itself is a potent stimulator of iron absorption from the gut. Iron overload can be reduced by regular chelation therapy and reducing iron absorption by keeping the hemoglobin levels high.
Neocyte transfusion
Special cell separators are available for obtaining younger cells with longer life span (neocytes). Infusion of these cells instead of the whole blood increases interval between two transfusions and decreases the transfusion requirement and hence the iron load. Simultaneous removal of older cells (gerocytes) from patient’s circulation by pheresis technique reduces iron load considerably. However, these procedurs are cumbersome, costly and need a lot of expertise.

At present only desferrioxamine is available as iron chelating agent in parenteral form. It should be given as continuous subcutaneous infusion in the dose of 25-50 mg/kg/day over a period of 8-12 hours, during the night, by specially designed microinfusion pumps, (at least 5-6 nights per week). The chelation should start by 12-14th transfusion. 100 mg of vitamin C daily should be concurrently administered. Overdose of desferrioxamine results in growth retardation, visual and auditory toxicity. Cataracts have been noted in some children on long term desferrioxamine therapy. Deferiprone (DFP) is an effective oral iron chelating agent with minimal toxicity. It is given in a dose of 75 mg/kg/day in 2-4 divided doses. The most common side-effect is arthropathy. Other oral chelators include pyridoxine hydrazine, HBED and desferrothiocine. These are still under trials.
Splenectomy is recommended in cases when the transfusion requirement exceeds 250 ml/kg/year of packed red cells. The decision should be deferred as far as possible and if required delayed beyond the age of five years.

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