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You might be happy after reading this message to know that there are some chances when a thalasseamia patient may recover. i had one case of a 6 year boy with thalassaemia with HB-7-8% and who had blood tranfusions every 15 days. A miracle happened after prescribing homeopathic medicine. For the last 2-3 months, he only receives once a month transfusion and his HB is 9-10%.     

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Nice one Dr. Santosh
Considering the age 6 years, it is not very rational to say that he has recovered from thalassemia. There would be fluctuations in the state of body in such genetic diseases, which may make seem that the patient is improving. It cannot be assured positively until the person's levels of Hb., and oxygen saturation are maintained optimally for at least 12 - 24 months.

:-)
did you give a remedy for spleen? what did you use?
i have taken a case history by that i have given phos.1m.madam that pt ,HB is now constant to 9.3%.prior to the medicine it used to be 6-7%.

On the basis of my clinical experience of thousands of such patients i do agree with Dr Santosh z.Maurya that Phosphorus 1M is nice remedy for these cases.

regards,

Homeopathic

Dr Mumtaz Ali Riaz

 

Dr.Santosh CONGRATS!!
Thalassaemia do recovers.

There is a group (in I guess in Pune) who deals only with Thalesemia cases
They are team of Homoeopathic Drs and Hematologists
They are doing great
Find them on www.homoepathyformotherandchild.com

Do share the complete case :)
We all wil be benifited by ur experience
Yes please, I have a patient right now with thalesemia, kindly share your findings with us. thank you very much!
Pl try to provide names of remedies along with its indications for better understanding of cases.
Dr.Sahni BS
Hello dear Dr. hope you fine.
Doctor it is better if you write symptoms for the thalasseamia patient, and then suggest the homoeopathic medicine, its better for homeopathic learner like me, any way its you good achievement, best regards
To me group has not understood the Thalasemia in proper sense. May I request first understand this and we start discussing this disease.
Dr.Sahni
Retd. Dy.CMO
ONGC Hospital, Panvel, Navi Mumbai, INDIA
Dr Banerji's Website

Wikipedia | Thalassemia (also spelled thalassaemia) is an inherited autosomal recessive blood disease. In thalassemia, the genetic defect which could be either mutations or deletion results in reduced rate of synthesis or no synthesis of one of the globin chains that make up hemoglobin. Reduced synthesis or no synthesis of one of the globin chains can cause the formation of abnormal hemoglobin molecules, thus causing anemia, the characteristic presenting symptom of the thalassemias.

Thalassemia is a quantitative problem of too few globins synthesized, whereas sickle-cell anemia (a hemoglobinopathy) is a qualitative problem of synthesis of an incorrectly functioning globin.

Thalassemias usually result in underproduction of normal globin proteins, often through mutations in regulatory genes. Hemoglobinopathies imply structural abnormalities in the globin proteins themselves.[1] The two conditions may overlap, however, since some conditions which cause abnormalities in globin proteins (hemoglobinopathy) also affect their production (thalassemia). Thus, some thalassemias are hemoglobinopathies, but most are not. Either or both of these conditions may cause anemia.

The two major forms of the disease, alpha- and beta- (see below), are prevalent in discrete geographical clusters around the world - probably associated with malarial endemicity in ancient times. Alpha is prevalent in peoples of Western African descent, and is nowadays found in populations living in Africa and in the Americas. Beta is particularly prevalent among Mediterranean peoples, and this geographical association was responsible for its naming: Thalassa (θάλασσα) is Greek for the sea, Haema (αἷμα) is Greek for blood. In Europe, the highest concentrations of the disease are found in Greece, coastal regions in Turkey, in particular, Aegean Region such as Izmir, Balikesir, Aydin, Mugla and Mediterranean Region such as Antalya, Adana, Mersin, in parts of Italy, in particular, Southern Italy and the lower Po valley. The major Mediterranean islands (except the Balearics) such as Sicily, Sardinia, Malta, Corsica, Cyprus and Crete are heavily affected in particular. Other Mediterranean people, as well as those in the vicinity of the Mediterranean, also have high rates of thalassemia, including people from the West Asia and North Africa. Far from the Mediterranean, South Asians are also affected, with the world's highest concentration of carriers (16% of the population) being in the Maldives.

The thalassemia trait may confer a degree of protection against malaria, which is or was prevalent in the regions where the trait is common, thus conferring a selective survival advantage on carriers, and perpetuating the mutation. In that respect the various thalassemias resemble another genetic disorder affecting hemoglobin, sickle-cell disease(ref?).

Medicine.net
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 major (Cooley's anemia): The child born with thalassemia major has two genes for beta thalassemia and no normal beta-chain gene. The child is homozygous for beta thalassemia. This causes a striking deficiency in beta chain production and in the production of Hb A. Thalassemia major is, therefore, a serious disease.

The clinical picture associated with thalassemia major was first described in 1925 by the American pediatrician Thomas Cooley. Hence, the name Cooley's anemia in his honor.

At birth the baby with thalassemia major seems entirely normal. This is because the predominant hemoglobin at birth is still fetal hemoglobin (Hb F). Hb F has two alpha chains (like Hb A) and two gamma chains (unlike Hb A). It has no beta chains so the baby is protected at birth from the effects of thalassemia major.

Anemia begins to develop within the first months after birth. It becomes progressively more and more severe. The infant fails to thrive (to grow normally) and often has problems feeding (due to easy fatigue from lack of oxygen, with the profound anemia), bouts of fever (due to infections to which the severe anemia predisposes the child) and diarrhea and other intestinal problems.

Lab tests online

The world distribution of haemoglobinopathies overlaps the geographic distribution of malaria. The prevalence has increased in previously non-endemic areas as a consequence of historical and recent immigration flows, slave-trade, trading activities and colonization. In all these regions there is a high prevalence of a thalassaemia. It is believed that carriers of α thalassaemia are protected against malaria and that natural selection is responsible for elevating and maintaining their gene frequencies.
OJRD Journal http://www.ojrd.com/content/5/1/13

Nature.com | Gene-therapy hope for β-thalassaemia patients

Gene therapy for a form of β-thalassaemia, a genetic disorder whose sufferers require frequent blood transfusions because they cannot properly produce red blood cells, seems to have been successful in a patient who, three years after treatment, no longer requires transfusions1. Doubts remain, however, over whether a set of lucky circumstances is behind the success.

Patients with β-thalassaemia carry faulty copies of the genes needed to produce the β-globin chain of haemoglobin, sometimes lacking the genes altogether. This leads to a shortage of red blood cells, the body's oxygen carriers.

Sufferers must have regular blood transfusions throughout their lives, an inconvenient and debilitating regime that ultimately shortens life expectancy. The only known cure is stem-cell transplantation, but few patients are able to find a suitable donor.

Because of the gruelling nature of this treatment, the development of gene therapies for β-thalassaemia is seen by many as an exciting prospect. The subject of the latest trial was an 18-year-old man with βE/β0-thalassaemia — in this form of the disease, one copy of the β–globin gene produces unstable β-globin and the other copy is non-functional.

Around half of the patients with this form of β-thalassaemia are dependent on transfusions, and the patient concerned had received blood transfusions since the age of three

Northern California Comprehensive Thalassemia Center

Thalassemia is the most common, inherited single gene disorder in the world. Early comprehensive treatment has changed thalassemia from a fatal pediatric disease to one in which patients live productive lives throughout adulthood.

Oxford Journals | Can Homeopathy Bring Additional Benefits to Thalassemic Patients on Hydroxyurea Therapy? Encouraging Results of a Preliminary Study

Much tanks Dear Dr.

To provides this useful information.

Blessing

fahim

This will boost up all the Homoeopaths to do more miracles.... Best of luck......

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