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Thalassemia is a genetic blood disorder characterized by abnormal hemoglobin production, leading to inadequate red blood cell production and anemia. It affects the body’s ability to produce hemoglobin, which is essential for transporting oxygen throughout the body. Thalassemia can range from mild to severe forms, with symptoms including fatigue, weakness, pale skin, and complications like bone deformities and organ damage. There are different types of thalassemia, including alpha and beta thalassemia, each with varying degrees of severity. Treatment may involve blood transfusions, iron chelation therapy, and in severe cases, bone marrow transplant.
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Thalassemia is a genetic blood disorder characterized by abnormal hemoglobin production, leading to inadequate red blood cell production and anemia. It affects the body’s ability to produce hemoglobin, which is essential for transporting oxygen throughout the body. Thalassemia can range from mild to severe forms, with symptoms including fatigue, weakness, pale skin, and complications like bone deformities and organ damage. There are different types of thalassemia, including alpha and beta thalassemia, each with varying degrees of severity. Treatment may involve blood transfusions, iron chelation therapy, and in severe cases, bone marrow transplant.
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Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
2. HISTORY
A 34 years old, married female
Address- Bathinda Cantt
Department- Obs & Gynae
HOPI-
An ante-natal case, G3 P1 A1 L1 (1 girl child of age 10 years)
H/o Hypothyroid in current pregnancy (TSH levels- 5)
3. No transfusion history till date
No relevant family history
Past history- H/o spontaneous abortion during 2nd pregnancy during first
abortion
General physical examination-
Pulse- 86 bpm
BP- 110/82 mm Hg
Weight- 53 kgs
Pallor- ++
Icterus- absent
Afebrile, no relevant facial features
6. Proceeding to make a diagnosis
Normal Beta-
thalassemia
Trait
Beta
Thalassemia
Intermedia
Beta-
thalassemia
Major
Hb-E
Heterozygous
Hb-E
Homozygous
Hb-F <1 Normal or may
be high if
HbA2>7
Remarkably
variable, 5-
100%.
If HbF>16.5, it
may get eluted
with LA1c or
A1c window, so
no HbF is
reported
>75%
May get eluted
with LA1c or
A1c window, so
no HbF is
reported
Normal Increased or
normal
HbA2/HbA/
HbE
HbA2 <3.5% HbA2- 4-9%
(not more than
9)
A2- reduced,
normal or
elevated.
HbA- reduced-
10-35% only
A2- reduced,
normal or
elevated.
HbA- reduced-
3% only
HbE- 30%
May elute in
HbA2 window
HbE- 85-90%
May elute in
HbA2 window
7. Proceeding to make a diagnosis
Compound
heterozygous-
HbE and Beta
Thalassemia
Sickle cell
heterozygous
Sickle cell
homozygous
Compound
heterozygous-
HbS and Beta
Thalassemia
Compound
heterozygous-
HbS and HbE
OTHERS-
HbD Punjab
HbQ India
Hb-F 15-50% 5-25% Elevated Mild elevation
HbA2/HbA/
HbE/HbS
HbE- 50-80% HbS 30-40%
Eluted with
HbA2
HbS 70-90% HbS >50%
HbA2 elevated
Botn HbS and
HbE 30-50%
8. CASE
VALUES-
Hb F- < 0.8
Hb A2- 34.3
Normal Beta-
thalassemia
Trait
Beta
Thalassemia
Intermedia
Beta-
thalassemia
Major
Hb-E
Heterozygous
Hb-E
Homozygous
Hb-F <1 Normal or may
be high if
HbA2>7
Remarkably
variable, 5-
100%.
If HbF>16.5, it
may get eluted
with LA1c or
A1c window, so
no HbF is
reported
>85%
May get eluted
with LA1c or
A1c window, so
no HbF is
reported
Normal Increased or
normal
HbA2/HbA/
HbE
HbA2 <3.5% HbA2- 4-9%
(not more than
9)
A2- reduced,
normal or
elevated.
HbA- reduced-
10-35% only
A2- reduced,
normal or
elevated.
HbA- reduced-
3% only
HbE- 30%
May elute in
HbA2 window
HbE- 85-90%
May elute in
HbA2 window
9. CASE
VALUES-
Hb F- < 0.8
Hb A2- 34.3
Normal Beta-
thalassemia
Trait
Hb-E
Heterozygous
Hb-E
Homozygous
Hb-F <1 Normal or may
be high if
HbA2>7
Normal Increased or normal
HbA2/HbA/
HbE
HbA2 <3.5% HbA2- 4-9%
(not more than 9)
HbE- 30%
May elute in HbA2
window
HbE- 85-90%
May elute in HbA2
window
10.
11. DISCUSSION
Hemoglobinopathies - Defect in any of the globin genes which
results in a structural change or an absence or decrease in the rate of
synthesis of hemoglobin
• Types:
Structural hemoglobinopathies
Thalassemias
Hereditary persistence of fetal hemoglobin
12. Structural hemoglobinopathies
• Hb S: Beta-6 Glutamic acid to Valine
• Hb E: Beta-26 Glutamic acid to Lysine
• Hb D: Beta-121 Glutamic acid to Glutamine