Acute graft versus host disease (GVHD) is a common complication following allogeneic hematopoietic stem cell transplantation. It occurs when the donated cells from a non-identical donor recognize the recipient's cells as foreign and attack them. GVHD is clinically graded from 1 to 4 based on its severity. Grade 1 GVHD is treated with topical steroids while grades 2-4 require systemic corticosteroids as first line therapy. For patients unresponsive to steroids, second line treatments include mycophenolate mofetil, etanercept, pentostatin, sirolimus, basiliximab, and extracorporeal photopheresis. Steroid tapering must be
Graft versus host disease (GVHD) is an immune mediated disease due to complex interaction between donor (lymphoid tissue) and recipient’s immunity occurring after transplantation.
Two types
Acute (less than 100 days)
Chronic (more than 100 days)
Graft versus host disease (GVHD) is an immune mediated disease due to complex interaction between donor (lymphoid tissue) and recipient’s immunity occurring after transplantation.
Two types
Acute (less than 100 days)
Chronic (more than 100 days)
Graft-versus-host disease (GVHD) is a complication seen in allogeneic stem cell transplantation. The incidence and severity is more in T-cell replete allograft (stem cells), donor T-cells being the principal mediators of GVHD. Acute GVHD is seen within 90 days post transplant and chronic GVHD after 90 days. Cyclosporin A (CsA) and methotrexate combination is used in prevention of acute GVHD. Corticosteroids and CsA combination is used in treatment of both acute and chronic GVHD.
This presentation is about chronic lymphocytic leukemia (CLL), its epidemiology and incidence, staging, molecular characteristics, clinical features and management.
Graft-versus-host disease (GVHD) is a complication seen in allogeneic stem cell transplantation. The incidence and severity is more in T-cell replete allograft (stem cells), donor T-cells being the principal mediators of GVHD. Acute GVHD is seen within 90 days post transplant and chronic GVHD after 90 days. Cyclosporin A (CsA) and methotrexate combination is used in prevention of acute GVHD. Corticosteroids and CsA combination is used in treatment of both acute and chronic GVHD.
This presentation is about chronic lymphocytic leukemia (CLL), its epidemiology and incidence, staging, molecular characteristics, clinical features and management.
COUNSELLING IN HIV/AIDS
Qurrot Ulain Taher
P.G Diploma in Nutrition & Dietetics
Dietetic Techniques & Patient Counseling
HIV/AIDS
HIV stands for Human Immunodeficiency Virus. AIDS stands for Acquired Immune Deficiency Syndrome. AIDS is a result of the development of the HIV virus into a more serious condition. AIDS was first recognised by the U.S. Centers for Disease Control and Prevention in 1981 and its cause, HIV, identified in the early 1980s.
Understanding HIV
HIV is a contagious infection which attacks the immune system, reducing its effectiveness and leaving the body susceptible to infections. The HIV infection damages the cells the body needs to fight illnesses. AIDS can be diagnosed when the number of immune system cells (CD4 cells) in the blood of a person with HIV drops below a certain level.
There is no cure for HIV or AIDS, but there are treatments that can slow down the disease, and help prevent the onset of AIDS. It takes around ten years for someone with HIV to develop AIDS, but it can be prevented with early detection and treatment of the HIV
PREVENTION OF Mother to child transmission
Treatment for HIV and AIDS
HAART
TYPES OF HIV TESTS
Why Is Counseling Necessary
Objectives
Whom to counsel
Characteristics of a Counselor
Skills Required in Counseling
Stages of Counseling
Risk assessment counseling
Pre test counseling
Post test counseling
Follow up counseling
Role of Counselor
Advocacy role
Health education
Referral
Clinical and therapeutic role
Special Situations in HIV Counseling
Pregnant women
Childless couples
Breast feeding positive mothers
Spouse and family members of HIV infected persons
quick review of most common genetic disorders ,, with special regards , thanks and appreciation to slide sharers who inspire me to do such ppt ,, i should give thanx to a slide sharer i dont know his name , i made the outline of my ppt from his ppt because i like it too much ,, thnx to all followers and special thanx to slideshare.net
Treatment of recurrent and resistant dermatomyositis and polymyositis in adults. prof. Adel Abdel-Salam (Rheumatology & Immunology - Mansoura School of Medicine: 2017)
Case Report on Invasive Mole. Gestational Trophoblastic Neoplasia (GTN) encom...Niranjan Chavan
Gestational Trophoblastic Neoplasia (GTN) encompasses a suite of rare but significant gynecological malignancies arising from aberrant placental trophoblast cells. As medical professionals and researchers, our comprehension of GTN's complexities is crucial for accurate diagnosis and effective treatment. This introduction serves to illuminate the key features, diagnostic procedures, and treatment protocols associated with GTN, helping to navigate the intricate landscape of this disease.
Prophylaxis and treatment of opportunistic infections in HIV patients - Toxoplasmosis .
Updated guide lines for treatment of Toxoplasmosis in HIV patient accodring to DHHS guide lines 2013 and other recommendations
Prophylaxis and treatment of opportunistic infections in HIV patients - Toxoplasmosis .
Updated guide lines for treatment of Toxoplasmosis in HIV patient accodring to DHHS guide lines 2013 and other recommendations
Precision medicine is a rapidly growing field of medicine that proposes individually customized diagnostics and therapeutics based upon molecular and genetic profile of individual patients. The main goal of precision medicine is to minimize harmful side effects and maximize benefits. In particular, hematological malignancies were seen as the most direct candidates of the most promising applications of precision medicine. However, Precision medicine approaches face multiple challenges. Despite these challenges and limitations, continuous effort is carried out to use these molecular findings as disease biomarkers and targets for therapeutic intervention. In the last decade the hemato-oncology witnessed a major revolution in the understanding of the molecular pathogenesis of hematological malignancies. While the therapeutic research for hematologic malignancies is continuously expanding, some medicines have been approved in hematological malignancies patients’ therapeutic algorithm and many are still under investigation.
Recent advancement in prevention and management of GVHD.pptxroysudip900
advances in prevention of GVHD by different investigational and approved methods of graft modulating, drugs, chemotherapy, analysis of published data, improved survival, future direction. different sources of stem cell and strategies to prevent mortality and morbidity
Similar to Management of acute graft versus host disease (20)
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Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
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- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
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NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
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In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Title: Sense of Taste
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 structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Basavarajeeyam - Ayurvedic heritage book of Andhra pradesh
Management of acute graft versus host disease
1. MANAGEMENT OF
ACUTE GRAFT VERSUS HOST
DISEASE (GVHD)
Mahmoud A. Hashim Ahmed Khalaf
Visiting Students
UAB School of Medicine
Hem-Onc Department
Bone Marrow Transplantation Unit
2. DEFINITION
Multisystem Disorders due to immune
reaction caused by transplanted cells from a
non-identical donor (the graft) that
recognize recipient cells
(the host) as foreign, thus disease is caused
in the recipient organs.
It can be fatal in up to 15% of HSCT
recipients.
4. CLASSIFICATION
Patients with GVHD are sub classified based upon the timing of presentation and the features
present:
Classic acute GVHD
Cases present within 100 days of hematopoietic cell transplant (HCT).
Shows features of acute GVHD.
Diagnostic features of chronic GVHD are absent.
Persistent, recurrent, late onset acute GVHD
Cases present greater than 100 days post-HCT.
Shows features of acute GVHD.
Diagnostic features of chronic GVHD are absent.
Classic chronic GVHD
Cases may present at any time post-HCT.
Diagnostic features of chronic GVHD are present.
There are no features of acute GVHD.
Overlap syndrome “Acute on Chronic GVHD”
Cases may present at any time post-HCT .
Shows features of both chronic GVHD and acute GVHD.
5. CLINICAL MANIFESTATIONS AND GRADING
I. Maculopapular rash. “ 1st and most common symptom”
II. GI Symptoms “ 2nd commonest symptoms”
Diarrhea with or without Abd. Pain.
Persistent nausea and/or emesis.
III. Jaundice
“Glucksberg Criteria”
7. DIAGNOSES
I. Clinical Evaluation
The diagnosis of aGvHD is
predominantly based on clinical
findings.
II. Histological Tests
A. Skin Biopsy is important in absence
of the classic symptoms.
Skin biopsy was not found to be
useful in predicting severity of
disease.
B. Rectosigmoid Biopsy was found to
be the most informative.
C. Transjugular liver biopsy can show
Endothelialitis, Lymphocytic
infiltration of the portal area,
pericholangitis and Bile duct
obstruction.
III. Imaging
upper GI endoscopy as well as lower
endoscopic biopsy may show
Luminal Dilatation and Thckening of
small bowel wall.
IV. Biomarkers
There are many candidate biomarkers
but none are ready for clinical
application.
8. MANAGEMENT
The choice of initial therapy for patients with acute graft-verus-host
disease (GVHD) depends upon :
Overall grading of Acute GVHD.
Grade 1 GVHD Management
A. Topical steroids are the most commonly used skin-directed
therapy for acute GVHD.
B. Antihistamines may be used as supportive therapy for
patients with pruritus.
C. In Resistant grade 1 aGVHD,
Topical Tacrolimus may be useful.
D. Optimizing prophylactic agents
When acute GVHD of any grade develops, to ensure a
therapeutic level.
For those no longer receiving prophylaxis, the prior
prophylactic agent should be restarted again.
9. GRADE 2-4 GVHD
Patients with grade 2-4 disease are likely
to require addition of Systemic agents to
achieve a response and Optimizing
prophylactic calcineurin inhibitors
agents.
A. First Line of Treatment:
Corticosteroids
Most centres used 2 mg/kg /day of
methylprednisolone to be the standard
primary dose.
Oral beclomethasone, a non-
absorbable glucocorticoid, is added
for most patients with GI involvement.
Topical steroids can be added for
further control of Skin lesions.
Steroids are continued for several weeks in
responders and then gradually tapered over
a period of several months.
Patients who shows progression of disease
by day 5 or non-response by day 7 are
considered to have corticosteroid resistance.
Use of Steroids results in complete response
rates ranging from 25 to 40 %.
10. HOW TO TAPER THE STEROIDS AFTER INITIAL RESPONSE?
Conclusion
I. Tapering of steroid doses should begin as soon as GVHD
manifestations show major improvement.
II. Inappropriately rapid taper rates carry a risk of GVHD
exacerbation or recurrence, while inappropriately slow taper rates
increase the risk of steroid-related complications.
III. Doses should be gradual reduced 0.2 mg/kg/day every 3–5 days,
after prednisone doses are decreased to less than 20–30 mg/day,
slower tapering rate is required.
11. B. Second Line of Treatment:
Given in Patients who fail to respond
to
2 mg/kg/day Methylprednisolone for
5 d or progressive symptoms after 72
h.
There is nostrong comparative data
showing superior efficacy for any
particular agent over others, so the
choice of a second-line regimen
should be guided by
1. Considerations of potential toxicity,
interactions with other agents
2. Expense
3. The familiarity of the physician with
the agent
4. The prior experience of the
physician
Includes:
1. Mycophenolate mofetil (MMF)
2. Etanercept “ Anti TNF Antibodies”
3. Pentostatin
4. Sirolimus
5. Basiliximab
6. Extracorporeal Photopheresis
12. I. MYCOPHENOLATE MOFETIL (MMF)
Mechanism of Action:
I. MMF is a prodrug of mycophenolic acid (MPA), an inhibitor of inosine monophosphate
dehydrogenase (IMPDH).
This is the rate-limiting enzyme in de novo synthesis of guanosine nucleotides.
T- and B-lymphocytes are more dependent on this pathway than other cell types are.
II. MPA can induce apoptosis of activated T-lymphocytes.
III. MMF dose in Adults is 2 gm/kg/day.
Side Effects
Dose related Cytopenia and gastrointestinal toxicity.
Moderate High possibility of Viral reactivation.
13. II. ETANERCEPT
A recombinant human TNF-alpha
receptor fusion protein.
Given SC at a dose of 0.4 mg/kg
per dose, Twice/ week.
(maximum dose, 25 mg/week).
Mechanism
A purine analog, a potent inhibitor
of adenosine deaminase.
T and NK Cells Death occurs due to
accumulation of 2-deoxyadenosine
5-triphosphate.
Dose: 1.5 mg/m2 IV /day for three
days.
Pentostatin should be used with
caution in patients with
renal insufficiency.
A 50 % dose reduction has been
suggested for patients with an
estimated creatinine clearance of
30 to 50 mL/min/1.73 m2
III. Pentostatin
14. IV. SIROLIMUS
(RAPAMYCIN)
Mechanism
Exerts its immunosuppressive effect through
inhibition of mTOR.
Loading dose of 6 mg/m2 followed by a daily
dose of 3 mg/m2 daily for 13 days .
At a dose of 4 -5 mg/m2 without a loading
dose for 14 days.
Reversible cytopenia, hypertriglyceridemia,
and nephrotoxicity (HUS) and neurotoxicity
when combined with calcineurin inhibitors.
The use of Sirolimus has also been associated
with sinusoidal obstruction syndrome (SOS)
following conditioning regimens especially,
Busulfan.
Mechanism
Humanized monoclonal antibodies
directed against the interleukin-2
receptor leading to prevention of T-
cell proliferation.
V. BASILIXIMAB
VI. DENILEUKIN
DIFTITOX
Mechanism
Recombinant fusion molecule of
human IL-2 and diphtheria toxin
that binds to the IL-2R-α and
triggers apoptosis in activated T
cells.
15. VII.EXTRACORPOREAL PHOTOPHERESIS
Infusion of ultraviolet-A irradiated
autologous peripheral lymphocytes
which have been collected by
apheresis and incubated with 8-
methoxypsoralen.
ECP induces apoptosis of all
leucocytes (including activatedn T-
cells) within 24 h of return.
Several studies have suggested that
ECP may have a role in the treatment
of acute GVHD.
Better results are expected in patients
with disease limited to the skin.
Side effects is mild including
hypotension, fevers and reduced
hemoglobin level.
17. REFERENCES
I. Advances in graft-versus-host disease biology and therapy,2013,
Bruce R. Blazar, William J. Murphy, and Mehrdad Abedi
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3552454/
II. Diagnosis and management of acute graft-versus-host disease,
2012, Fiona L. Dignan et al.
http://www.bcshguidelines.com/documents/bjh_9129_Rev_EV.pdf
III. First and Second-Line Systemic Treatment of Acute Graft-versus-
host Disease: Recommendations of the American Society of Blood
and Marrow Transplantation, Paul J. Martin et al.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3404151/
IV. Management of Acute GVHD, Uptodate.com
V. Extracorporeal photopheresis in the management of graft-versus-
host disease, Bredeson C et al.
http://www.ncbi.nlm.nih.gov/pubmed/24764713
Editor's Notes
Steps of Transplantation :
Conditioning
Stem cell infusion
Neutropenic Phase
Engraftment Phase
Post- Engraftment Phase
Overall aGVHD cascade
Initiation and maintenance of aGVHD has been conceptualized into 4 phases with feedback loops that self-sustain the process. Although the effect of conditioning phase in aGVHD is not absolutely necessary, in many of the models it activates APCs, via tissue destruction, and improve APC capacity. It also, through release of gut bacteria, PAMPS and chemokines, can activate cellular components of innate immune system that can participate in direct tissue damage and contribute in cytokine storm. Host hematopoietic APCs have perhaps the most important role in initiation of GVHD, but this may depend on the model and the potential role of recipient APCs as well host non-hematopoietic APCs should not be ignored. Following antigen presentation, a strong cytokine response is initiated, promoting greater antigen presentation and recruitment of Teffs, and innate immune cells further contributing to the inflammatory cytokine milieu. Finally, the Teff cells, NK cells, macrophages and pro-inflammatory cytokines (e.g. TNF-α), will result in end organ damage, clinically recognized as aGVHD in the skin, lung, gut and liver. The resulting tissue damage, if not treated, will further escalate the disease, spiraling up the process to higher and more severe stages of GVHD pathology, which is extremely difficult to control.
Although initial definitions of acute GVHD required an onset of symptoms before 100 days post transplantation, the current National Institutes of Health (NIH) consensus criteria use clinical findings, rather than a set time period, to differentiate between acute and chronic GVHD.
Scale Index allows patients to be classified as to their functional impairment
40Disabled; requires special care and assistance.
30Severely disabled; hospital admission is indicated although death not imminent.
20Very sick; hospital admission necessary; active supportive treatment necessary.
10Moribund; fatal processes progressing rapidly.
0Dead
Liver biopsy is poses a significant risk of major bleeding since most patients are thrombocytopenic at the time of presentation with GVHD. Transjugular liver biopsy is a safer alternative if it can be adequately performed.
In Grade 1: No systemic Steroids is used.
the most common prophylaxis regimen is the combination of cyclosporine and methotrexate. The cyclosporine is administered to reach a therapeutic target concentration, which varies according to the time from transplantation. A target concentration of 200 to 300 mcg/L is used during the first three to four weeks post transplant; then, if there is no GVHD, the target concentration is decreased to 100 to 200 mcg/L until three months after transplantation, and then tapered further. Patients who develop GVHD of any grade should have their cyclosporine dose adjusted to ensure a therapeutic level
The mechanism of prednisolone their effects may because of lympholytic effects and anti-inflammatory properties
Gradual tapering is important to prevent a flare of GVHD.
These efficacy and toxicity data suggested the use of mycophenolate plus glucocorticoids as the most promising combination
Day 28 post initiation of treatment complete response rates for methylprednisolone plus either etanercept, or mycophenolate, or denileukin, or pentostatin were 26, 60, 53, and 38 %, respectively.
9 month overall survival rates for these four treatment regimens were 47, 64, 49, and 47 percent, respectively.
Cumulative incidences of severe infection were 48, 44, 62, and 57 percent, respectively.
Etanercept plus methylprednisolone as initial therapy for acute graft-versus-host disease, 2008 by Department of peds in Michigan medical school
Showed that : Patients treated with etanercept plus steroids were significantly more likely to attain complete remission (CR) after 28 days than those treated with steroids alone (69 versus 33 percent)