Learning Objectives:
Introduction
Definition of CML
Philadelphia Chromosome
Normal Granulopoiesis
Pathogenesis of CML
Aetiology
Incidence
Clinical Features
Phases of CML
Lab Diagnosis of CML
Course & Prognosis
Differential Diagnosis
Brief Overview of Treatment
This presentation is about chronic lymphocytic leukemia (CLL), its epidemiology and incidence, staging, molecular characteristics, clinical features and management.
Chronic Lypmhocytic leukemia/SLL/B-PLL/T-PLL/ATLL By SOLOMON SUasb by SOLOMON SUASB
the following presenation include
Introduction/Background
• Etiology of CLL
• Symptoms
• Test and Diagnosis
• Staging
• Prognosis
• Treatment
• B Cell diseases BPLL
• T cell diseases
T-PLL
ATLL
LGLL
Chronic myelogenous leukemia (CML) - pluripotential stem cell disease
A malignancy the treatment of which has been revolutionised over the last decade.
Here is a comprehensive discussion on the disease
Learning Objectives:
Introduction
Definition of CML
Philadelphia Chromosome
Normal Granulopoiesis
Pathogenesis of CML
Aetiology
Incidence
Clinical Features
Phases of CML
Lab Diagnosis of CML
Course & Prognosis
Differential Diagnosis
Brief Overview of Treatment
This presentation is about chronic lymphocytic leukemia (CLL), its epidemiology and incidence, staging, molecular characteristics, clinical features and management.
Chronic Lypmhocytic leukemia/SLL/B-PLL/T-PLL/ATLL By SOLOMON SUasb by SOLOMON SUASB
the following presenation include
Introduction/Background
• Etiology of CLL
• Symptoms
• Test and Diagnosis
• Staging
• Prognosis
• Treatment
• B Cell diseases BPLL
• T cell diseases
T-PLL
ATLL
LGLL
Chronic myelogenous leukemia (CML) - pluripotential stem cell disease
A malignancy the treatment of which has been revolutionised over the last decade.
Here is a comprehensive discussion on the disease
Dr. Feroze Momin presents Chronic Lymphocytic Leukemia - Review and new Insights.
To read about Dr. Feroze Momin: http://conquercancers.com/ourdoctorso1.html
To read about Cancer Treatment Center in Michigan:
http://conquercancers.com
How do we best deploy novel agents for T cell lymphoma – what have we learned from key clinical trials ? : Should they be employed upfront?
YL Kwong, MD
Lab Diagnosis of Chronic lymphoproliferative disorders (CLPD);Flowcytometric...Dr Siddartha
Lab Diagnosis of Chronic lymphoproliferative disorders (CLPD);Flowcytometric Evaluation
Basavatarakam Indo-American Cancer Hospital and Research Institute
Will detail on the historical chemotherapy, latest chemotherapy and a proposed chemotherapy for burst lymphoma. Will also detail on the pathophysiology of burnt lymphoma
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
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
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Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
2. defenition
Progressive
accumulation of matureappearing, functionally incompetent,longlived B lymphocytes in peripheral blood,
bone marrow, lymph nodes,spleen, liver
and sometimes other organs.
4. Incidence
Commonest leukaemia in Western adults (25–30%
of all leukaemias).
2.5/100,000 per year.
Age
Predominantly disease of elderly Median age at
diagnosis 65 years. (in over 70s,>20/100,000).
m:f ratio ~2:1.
Marked geographic difference e.g.
In China & Japan = 1/10 of Western world.
5. Aetiology
Unknown. No causal relationship with radiation,
chemicals or viruses.
Small proportion are familial. Genetic factors
suggested by low incidence in Japanese even after
emigration.
Lymphocyte accumulation appears to result from
defects in intracellular apoptotic pathways: 90% of
CLL cases have high levels of BCL-2 which blocks
apoptosis.
6. Clinical features and presentation
asymptomatic; lymphocytosis (>5.0 ¥ 109/L) on
routine FBC.
Lymphadenopathy:
painless,
often
symmetrical,splenomegaly (66%), hepatomegaly
BM failure due to infiltration causing
anaemia,
neutropenia and
thrombocytopenia.
Recurrent
infection
due
to
acquired
hypogammaglobulinaemia: esp.Herpes zoster.
9. • Patients with advanced disease:B-symptoms:
FUO.
Night sweats.
Wt loss.
general malaise.
Autoimmune phenomena occur;
DAT +ve in 10–20% cases, warm antibodyAIHA in <50%
of these cases.
Autoimmune thrombocytopenia in 1–2%.
10. Diagnosis
FBC:
lymphocytosis >5.0
109/L
Neutropenia
anaemia,
thrombocytopenia and
absent in early stageCLL;
autoimmune haemolysis
occur at any stage.
thrombocytopenia may
11.
12.
13. Morphology:
Peripheral Blood
•Absolute lymphocytosis > 5 X 109 /L.
Mature looking lymphocytes; characteristic artefactual damage to
cells in film preparation produces numerous ‘smear cells’
(Note:absence of smear cells should prompt review of diagnosis);
•Morphological subtypes:
Atypical or mixed CLL/PLL:
> 10% & < 54% prolymphocytes.
•Morphology is usually not enough to
differentiate from reactive lymphocytosis.
spherocytes,polychromasia
Increase retics if AIHA;
14. Comparison of CLL and PLL
B-CLL
CLL-PLL
CLL
slg
CD19
CD20
CD5
PLL
+
++
++
++
++
++
++
-/+
Courtesy of Randy Gascoyne, MD.
1. Bennett JM, et al. J Clin Pathol. 1989;42:567-584.
15. Immunophenotyping
crucial
to differentiation from other
lymphocytoses
First line panel: CD20; CD5; CD19; CD23;
FMC7; SmIg, CD22 or CD79b.
CLL characteristically CD20 and FMC7 –
ve;
CD5,CD19 and CD23 +ve;
SmIg, CD22, CD79b weak;
k or l light chain restricted.
CD 38.Zab 70
16. Immunophenotype scoring
system
Scoring system for B-CLL
Points
Membrane
marker
Smlg
1
0
Weak
Moderate/strong
CD5
Positive
Negative
CD23
Positive
Negative
FMC7
Negative
Positive
CD79b (SN8)
Negative
Positive
1. Matutes E, et al. Leukemia. 1994;8:1640-1645.
2. Moreau EJ, et al. Am J Clin Pathol. 1997;108:378-382.
19. Prognosis: histologic bone
Nodular
Interstitial
Diffuse
marrow patterns
(low risk)
(low risk)
(high risk)
The
different
bone
marrow
patterns
probably
variations in amount of lymphoid accumulation
the natural course of the disease
Courtesy of Randy Gascoyne, MD.
1. Montserrat E, et al. Cancer. 1984;54:447-451.
reflect
during
20. Cytogenetics
Conventional chromosome banding can no
longer be recommended in the diagnostic
work up of CLL ( detects abnormalities in 40-50
% of CLL patients only.
21. Cytogenetics
prognostic value; abnormalities in >80% using FISH:
13q–(55%),
11q– (18%),
12q+ (16%),
17p– (7%),
6q– (7%);
11q–, 17q– veryunfavourable; sole 13q–favourable,or
6q– ,normal karotyping neutral out come ,Clonal
evolution occurs over time.
11q– and 17q– associated with advanced disease.
22. Molecular biology:
IgV genes mutational status:
Relates to stage of differentiation of malignant B-cells
Accordingly there are 2 variants of CLL :
* Pre-germinal variant :
- Naive B-lymphocytes with no IgV gene mutation
(CD38+ve)
- Unfavorable clinical outcome .
* Post-germinal Variant :
- Originates from memory B-lymphocytes,
exhibiting IgV mutation (CD38 – ve)
- Favorable clinical outcome
• bcl-2:
> 85% of B-cell cases express high levels of bcl-2 which is a potent inhibitor
of apoptosis (programmed cell death).
p53:
• The p53 tumour suppressor gene is mutated
in 8 % B-cell cases.
23. Other tests:
U&E; LFTs;
LDH;
Uric acide
b2-microglobulin;
imaging .
Ct chest and abdomine
Pet scan(With richter transformation)
24. Poor prognostic factors
male sex.
Advanced clinical stage.
Initial lymphocytosis > 50 ¥ 109/L.
>5% prolymphocytes in blood film.
Diffuse pattern of infiltrate on trephine.
Blood lymphocyte doubling time <12 months.
Cytogenetic abnormalities 11q– or 17q–.
serum b2-microglobulin.
serum LDH.
serum thymidine kinase.
soluble CD23.
Unmutated IgVH genes.
Poor response to therapy.
25. Staging: Rai and Binet staging systems for CLL
Clinical staging systems for CLL
Stage
Value
Rai
Binet
Median survival
Lymphocytosis
(>15,000/mm3)
0
-
150 months
(12.5 years)
Lymphocytosis plus
nodal involvement
I
A
Lymphocytosis plus
organomegaly
II
B
Anemia (RBCs)
III
Hgb <11 g/dL
<3
node groups
>3
node groups
Hgb <10 g/dL
C
Lymphocytosis plus
IV
thrombocytopenia
PLT <100,000/mm3
1. Rai KR, et al. Blood. 1975;46:219-234.
(platelets)
2. Binet JL, et al. Cancer. 1981;48:198-206.
3. Binet JL, et al. Cancer. 1977;40:855-864.
PLT <100,000/mm3
101-108 months
(8.5-9 years)
60-71 months
(5-6 years)
19-24 months
(1.5-2 years)
26. Response criteria to NCI guidelines for CLL
Variable
Response criteria
CR
NCI
Physical exam
Symptoms
Lymphocytes (x 109/L)
Neutrophils (x 109/L)
Platelets (x 109/L)
Hemoglobin (g/dL)
Bone marrow lymphs (%)
Normal
None
≤4
≥1.5
>100
>11 (untransfused)
<30, no nodules
PR
Physical exam (nodes and/or liver, spleen)
Plus ≥1 of:
Neutrophils (x 109/L)
Platelets (x 109/L)
Hemoglobin (g/dL)
Duration of CR or PR
1. Cheson BD, et al. Blood. 1996;87:4990-4997.
≥50% decrease
≥1.5
>100
>11 or 50%
improvement
≥2 months
27. PD:
•Physical ex. (LN , liver , spleen):
> 50% increase or new
•Circulating lymphocytes : > 50 %
increase..
•Others: Richter’s syndrome
SD:
•All 0ther than the above.
28. Cll ttt acording to NCCN 2013
Chemotherapy reserved for patients with symptomatic or
progressive disease:
1. anaemia (Hb <10g/dL)
2. Thrombocytopenia (<100 ¥109/L),
3. Constitutional Symptoms Due To CLL (>10% Weight
Loss In 6 Months, Fatigue, Fever, Night Sweats),
4. Progressive Lymphocytosis: Doubling Time <6 Months,
5. SymptomaticLymphadenopathy>10cm
splenomegay>6cm
BCM,
Autoimmune
Disease
Refractory To Steroids,
6. Repeated Infections Hypogammaglobulinaemia.
30. Cll patients indicated to ttt
Fish
T(11,14)
Del 13
Del11
Del17
1-cll without del
17p,11q
2-cll with del17p
3-cll with del 11q
31. Cll without del 17p,11q
>70 years
,significant
comorbidiyy
Chlorampucil ±rituximab
bendamastine
Cyclophosphamide,predni
slone±R
Rituximab
Alemtuzumab
Fludarabine±R
Cladripine
Lenalidomide
<70 years , no
significant
comorbidiyy
FCR
FR
PCR(Pentostatin)
bendamastine±R
32. Cll without del 17p,11q
Relapse, no response
>70 years
,significant
comorbidiyy
Reduced dose FCR,PCR
Bendamastine±R
Chlorampucil
±rituximab
Alemtuzumab±R
Lenalidomide±R
HDMP+R
<70 years , no
significant
comorbidiyy
FCR
PCR(Pentostatin)
bendamastine±R
F+Alemtuzemab
Alemtuzemab±R
R-CHOP
OFAR
R-HYPER CVAD
Lenalidomide±R
Then allogenic SCT
33. Cll with del 17p
short term
relapse,no
response
First line
therapy
FCR
FR
Alemtuzumab±R
HDMP+R
Then allogenic SCT
Alemtuzumab±R
RCHOP
CFAR
OFAR
HDMP+R
R±hyper CVAD
Lenalidomide±R
Then allogenic SCT
34. Cll Without Del 11q
>70 years
,significant
comorbidiyy
Chlorampucil ±rituximab
Bendamastine
Cyclophosphamide,predni
slone±R
Rituximab
Alemtuzumab
Fludarabine±R
Cladripine
Lenalidomide
<70 years , no
significant
comorbidiyy
FCR
PCR(Pentostatin)
bendamastine±R
Then allogenic SCT with
PR,opserve With CR
35. Cll without del 11q
Relapse, no response
>70 years
,significant
comorbidiyy
Reduced dose FCR,PCR
Bendamastine±R
Chlorampucil
±rituximab
Alemtuzumab±R
Lenalidomide±R
HDMP+R
<70 years , no
significant
comorbidiyy
FCR
PCR(Pentostatin)
bendamastine±R
F+Alemtuzemab
Alemtuzemab±R
R-CHOP
R-HYPER CVAD
Lenalidomide±R
Then allogenic SCT
36. Treatment of CLL
CHLORAMBUCIL:
•Still the primary therapy of choice for older patients.
•CR rates: 8-13%.
•Addition of steroids: No advantage except in
autoimmune cytopenias.
•Dose: 0.4 mg/kg day 1 (repeat every 2 weeks)
or 0.1 mg/kg day 1-14 (repeat every 4 weeks)
•For how long?: Till max. response (may take months).
•Maintenance treatment: No advatage in CLL.
•Progress after 12 months of max. response: You may
repeat the same dose.
37. Treatment of CLL
FLUDARABINE (Purine analog):
•Salvage treatment in older patients.
•Primary treatment in young patients who will
receive stem cell transplantaion.
•It is the most active single agent in CLL.
•CR rates: 25% (up to 20 months duration) even if
strict NCI WG criteria are used.
•Most CR cases occur in the first 3 months of
• treatment. Dose:
25 mg / m2 D 1-5 repeated every 4 weeks for 3 - 6 cycles.
Side effects:•Lymphocytopenia + opportunistic infections.
•AIHA (contraindicated if AIHA is already present).
•Tumour lysis syndrome in the first cycle if counts are very high
due to rapid response.
•Transfusion-associated GVHD (irradiate blood components).
38. Treatment of CLL
CLADARABINE (2CdA, Leustatin)
•Purine analog
•Same effect in CLL as Fludarabine
•Dose:
0.1 mg / kg D 1-7 repeated every 4 weeks
for 3-6 cycles.
•Side effects:-
Almost the same like Fludarabine.
39. Treatment of CLL
(MONOCLONAL AB)
2- Campath-1H
Anti CD 52 antibody
(CD 52 present on most B &T cells )
Response rates 50 %
Toxicities : rigors,chills, fever,immunosuppression & lymphocytopenia .
CMV re-activation is a problem
3- Rituximab ( anti-CD20)
In CLL CD 20 is moderately expressed on the cells ( possible reason for
low response rates )
With high counts (TLC > 50,000) patient may develop “cytokine
release syndrome” (fever, rigor, skin rash , nausea, vomiting,
hypotension, & dyspnea )
40.
41. Stem Cell
Transplantation
• The only treatment modality that
resulted in PCR-negative CRs in
a substantial number of patients.
• Minitransplants can be applied to a
higher age range group.
Cll with del 17p after first crif patient eligible with doner
Cll with del11q after first pr if patient eligible with doner
Cll with relapse after receiving high dose chemotherapy
42. Complications of cll
Recurrent infection(neutropenia,immunoparesis)
Ivig
Antimicrobial agent
Anti infective prophylaxis
Herpes
Sulfa(neumocystic)
CMV(alemtuzemab)
Autoimmune disease
ITP,AIHA,PRCA
steriod,rituximab,cyclosporine,splenectomy
Fludarabine is contraindicated with AIHA