Therapeutic advances in alopecia areata
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Presented at the joint International Eczema Council and National Alopecia Areata Foundation Symposium, "Atopic Dermatitis and Alopecia Areata: Comparison and Contrast”, held during the 2019 Annual American Academy of Dermatology meeting in Washington, DC to explore the similarities and differences between these two common but complex skin diseases and the implications from bench to bedside.
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-History of hair loss is -
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Hamilton- Norwood type: recession of frontal hair line, latter followed by a vertex thinning with progression until top of the scalp is completely bald.
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signs of hyperandrogenism should be evaluated
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progesterone containing pills
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Thyroid disease,
Surgery, infection in last 6months to 1 year
Drug history
Iron deficiency
Smoking
UV exposure
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Androgenic alopecia is naturally progressive , so main strategy is to prevent progression and increase hair density.
1.Topical minoxidil:
2% for female and 5% spray for male 1 ml twice daily or half cup foam once daily.
There is transitory telogen shedding within first 8 weeks observed.
Response should be assessed after 6 months.
If response occurs, will be continued as main stay of treatment.
2.Finasteride oral ad Dutasteride oral
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0.5 mg daily dutasteride is alternative.
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Spironolactone 100-200 mg daily
Cyproterone acetate can be used
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College of Medicine, King Faisal University, AL Ahsa, Saudi Arabia.
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Prognosis: good for limited involvement. Poor for extensive hair loss.
Management: intralesional triamcinolone effective for limited number of lesions
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Multifactorial and polygenetic etiology.
Clinical features:
-History of hair loss is -
long standing
slowly progressing reduction of hair density, diameter
Miniaturization of hair
Diminished anagen hair and increased telogen hair
-Pattern of hair loss in male:
Hamilton- Norwood type: recession of frontal hair line, latter followed by a vertex thinning with progression until top of the scalp is completely bald.
-Pattern of hair loss in female:
Centrofrontal hair loss with preservation of frontal hair line
(Ludwig type) {figure - left}
Christmas tree pattern {figure- right}
-Family history of AGA often positive
In female
signs of hyperandrogenism should be evaluated
gynecological history
progesterone containing pills
-To exclude other causes history should be taken regarding-
Thyroid disease,
Surgery, infection in last 6months to 1 year
Drug history
Iron deficiency
Smoking
UV exposure
Hair color, cosmetics use.
Allergic contact dermatitis
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1.Topical minoxidil:
2% for female and 5% spray for male 1 ml twice daily or half cup foam once daily.
There is transitory telogen shedding within first 8 weeks observed.
Response should be assessed after 6 months.
If response occurs, will be continued as main stay of treatment.
2.Finasteride oral ad Dutasteride oral
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0.5 mg daily dutasteride is alternative.
Combination of topical minoxidil and finasteride is good option
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3.Antiandrogen and estrogenic drugs:
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A Rare International Dialogue (Sunday, May 12, 2019)
Theme One: Diagnosis and Beyond
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This document discusses integrase inhibitors for the treatment of HIV. It summarizes clinical trials comparing the integrase inhibitors raltegravir, elvitegravir, and dolutegravir to efavirenz and atazanavir/ritonavir in treatment-naive patients. The studies found integrase inhibitors were as effective as or better than comparators in suppressing HIV, with fewer side effects. Raltegravir given once daily was inferior to twice daily dosing. Elvitegravir/cobicistat was found to be noninferior to efavirenz and atazanavir/ritonavir through 144 weeks.
The role of integrase inhibitors in first line and later antiretroviral thera...
This document discusses integrase inhibitors for the treatment of HIV. It summarizes clinical trials comparing the integrase inhibitors raltegravir, elvitegravir, and dolutegravir to efavirenz and atazanavir/ritonavir in treatment-naive patients. The studies found integrase inhibitors were as effective as or better than comparators in suppressing HIV, with fewer side effects. Raltegravir given once daily was inferior to twice daily dosing. Elvitegravir/cobicistat was found to be noninferior to efavirenz and atazanavir/ritonavir through 144 weeks.
Day 2: Mark Lundie, Pfizer Canada, Slides (Nov 19) Access to Innovation Confe...
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This document discusses gene therapy, including its history, mechanisms, approaches, challenges, and future directions. Some key points:
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Cancer Webinar+May7
An Integrative Choice for Cancer Support in Small Animals
FREE Live Webinar on May 7th, 10am Pacific / 1pm Eastern
Register at: www.naturalpetrx.com
Guest: Dr. Nancy Scalan, DVM
Host: Geoff D\'Arcy D.O.M
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Audio and slides for this presentation are available on YouTube: http://youtu.be/6W_xoH4s-Yk
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This document discusses targeted gene therapy and provides an overview of the topic. It begins with an introduction and then covers the history of gene therapy. The main types of gene therapy are described as germline therapy, ex vivo somatic gene therapy, and in vivo somatic gene therapy. The key steps in gene therapy are outlined, including identification of the affected gene, cloning the healthy gene, loading the vector, delivering the gene into target cells, and integration into the DNA. Various vector agents and routes of administration are discussed. Applications of gene therapy for cancer are summarized, including tumor suppressor genes, suicide genes, and anti-angiogenic therapy. The conclusion states that gene therapy has the potential to revolutionize medicine in the future.
Gene Therapy
Gene therapy involves introducing new genes into cells to treat disease. Researchers are testing approaches like replacing mutated genes, inactivating genes, or introducing new therapeutic genes. Genes can be transferred into somatic or germ cells using vectors like adeno-associated viral or lentiviral vectors. Examples discussed include successful gene therapy trials for sickle cell disease and hemophilia that showed therapeutic levels of proteins and correction of disease symptoms for over a year. However, challenges remain regarding safe and targeted delivery of genes, immune responses, and ethical issues surrounding gene editing and enhancement.
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This study examined the effects of vitamin D treatment on thyroid autoimmunity. 82 participants diagnosed with autoimmune thyroid disease and vitamin D deficiency were randomly assigned to a treatment group that received 1000 IU of vitamin D daily for 1 month or a control group. Laboratory tests were performed at baseline and after 1 month. The results showed that vitamin D supplementation decreased antibody levels in the treatment group, but did not affect thyroid function. The study suggests vitamin D may be part of future autoimmune thyroid disease treatment, but larger and longer studies are still needed.
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This document summarizes research on scaling up antiretroviral therapy (ART) in resource-limited countries. It discusses using cost-effectiveness analysis to evaluate the value of ART programs in Côte d'Ivoire, India, and South Africa. The research finds that providing both first-line and second-line ART is cost-effective in these countries. It also finds that earlier initiation of ART in South Africa increases survival and is cost-effective. Faster scale-up of ART programs can significantly reduce AIDS-related deaths.
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Dr. Angela Christiano presented an update on genetic and immunological studies in alopecia areata. Her research is focused on defining the genetic basis of alopecia areata to clarify how the disease develops—a key initial step toward creating novel therapies. Dr. Christiano is the Richard and Mildred Rhodebeck Professor of Dermatology, Genetics and Development, Vice Chair for Basic Science Research in Dermatology, and Director of the Center for Human Genetics at Columbia University.Treatment of Alopecia Areata: Overview
Dr. Maria Hordinsky presented an overview of key things adults need to know about alopecia areata, including the risks and benefits of current and evolving off-label treatment options. Dr. Hordinsky is Professor and Head of the Department of Dermatology at the University of Minnesota. She is recognized for her clinical expertise in alopecia areata and hair diseases.
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Dr. Natasha Mesinkovska, NAAF’s Chief Scientific Officer, presented the latest progress of NAAF’s Treatment Development Program and how your involvement is critical to developing treatments for alopecia areata. In addition to overseeing NAAF’s research efforts, Dr. Mesinkovska is Director of Clinical Research in Dermatology at the University of California Irvine.
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Presented at the joint International Eczema Council and National Alopecia Areata Foundation Symposium, "Atopic Dermatitis and Alopecia Areata: Comparison and Contrast”, held during the 2019 Annual American Academy of Dermatology meeting in Washington, DC to explore the similarities and differences between these two common but complex skin diseases and the implications from bench to bedside.
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AA is not necessarily a single disease entity, but rather a stereotypic hair follicle damage response pattern that can be triggered by various pathogenic mechanisms. In some patients with autoreactive T cells, AA represents an autoimmune disease (AAA), while in others it may occur in response to stress, infection, or dysbiosis without specific autoimmunity. The classic AA clinical presentation arises when hair follicle immune privilege collapses during the growth (anagen) phase, attracting inflammatory cells that secrete IFNγ and induce premature regression (catagen). While causal therapy targeting autoreactive T cells may be possible for AAA, symptomatic therapies aiming to protect immune privilege and repair follicle damage are generally beneficial across AA variants.The atopic dermatitis pathogenesis and implications for alopecia areata
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This document summarizes the key discussion points from a breakout group at a genetics, immunology, and therapeutic targets conference. The group discussed that while some new targets have been identified for alopecia areata, more exploration is needed into other potential targets, cell types, and signaling pathways. Questions remain about how to better stratify and select patients for current and new treatments. Additional resources are needed, including more funding for immunological and genetic studies, as well as research into the hair follicle biology and environmental factors. The North American Alopecia Areata Foundation can help by continuing to support exploratory research ideas, driving drug development, and convening research summits to define research priorities.
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This document summarizes the discussions from a health economics and burden of disease breakout group on alopecia areata. The group discussed questions that still need answers around how alopecia areata impacts work, income, mental health, and patients' life courses. They also identified the need for partnerships to measure clinically relevant outcomes, better database access, and connections between stakeholders. The group suggested the North American Alopecia Areata Foundation could help fund research to address practice gaps, identify patients for research, and coordinate among pharmaceutical companies and payers.
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Recomendamos muito.
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Esta publicação só está disponível em inglês até o momento.
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1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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Therapeutic advances in alopecia areata
- 1. Therapeutic Advances in Alopecia Areata Brett King, MD, PhD Associate Professor of Dermatology Yale University School of Medicine
- 2. Disclosures • Off-label use of medications will be discussed • I have received honoraria and/or consulting fees from: Aclaris Therapeutics, Concert Pharmaceuticals, Dermavant Sciences, Eli Lilly, Pfizer • I am a clinical trial investigator for: Concert Pharmaceuticals, Eli Lilly, Pfizer • I am on a speaker bureau for: Pfizer, Regeneron, Sanofi Genzyme
- 3. Alopecia Areata: Treatment • Intralesional corticosteroids • Topical corticosteroids • Topical immunotherapy (e.g. diphenylcyclopropenone, squaric acid) • Topical minoxidil • Oral corticosteroids • Methotrexate • Cyclosporine * No reliably effective therapies, especially for severe disease Strazzulla LC, et al. Alopecia areata: An appraisal of new treatment approaches and overview of current therapies. J Am Acad Dermatol. 2018;78(1):15-24.
- 4. Baseline 2 months tofacitinib 5 mg BID 5 months tofa 10 + 5 mg daily 8 months tofa 10 + 5 mg daily
- 5. Ruxolitinib 20 mg BID Nat Med. 2014;20(9):1043-9.
- 6. Alopecia Areata: Pathogenesis Divito SJ, Kupper TS. Nat Med. 2014;20(9):989–90. Based on Xing L, et al. Nat Med. 2014;20(9):1043-9.
- 7. CytokineSignalingisMediated byJAK-STATPathway Janus kinase (JAK) family consists of JAK 1, JAK 2, JAK 3, and Tyrosine Kinase 2 Vitiligo cytokine: IFN-g JAK 1/2 AA cytokines: IL-15, IFN-g JAK 1/2/3 JAK inhibitorJAK inhibitor Damsky W, King BA. J Am Acad Dermatol. 2017;76(4):736-744. AD cytokines: IL-4, IL-13 JAK 1/3
- 8. JAmAcadDermatol. 2017;76(1):22-28. JAmAcad Dermatol. 2017;76(1):29-32. JAmAcadDermatol. 2019;80(2):568-9. Brittany G. Craiglow, MD, and Brett A. King, MD, PhD New Haven, Connecticut JAmAcad Dermatol. 2019;80(2):566-8. Lucy Y. Liu, MD, and Brett A. King, MD, PhD New Haven, Connecticut JAmAcad Dermatol. 2018;78(2):403-4.
- 9. JAKi in AA: Clinical Trials JAK INHIBITOR TARGET ROUTE OF ADMINISTRATION PHASE STATUS IDENTIFIER ATI-501 JAK1/3 oral 2 active, not recruiting NCT03594227 ATI-502 JAK1/3 topical 2 not yet recruiting NCT03759340 baricitinib JAK1/3 oral 2/3 recruiting NCT03570749 CTP-543 JAK1/2 oral 2b/3 not yet recruiting NCT03811912 PF-06651600 JAK3 oral 2b/3 recruiting NCT03732807
- 10. Other Therapeutic Possibilities? • Apremilast • Ustekinumab • Dupilumab • Fecal transplant
- 11. Other Therapeutic Possibilities : Apremilast
- 12. Other Therapeutic Possibilities: Ustekinumab
- 13. Other Therapeutic Possibilities: Dupilumab
- 14. Other Therapeutic Possibilities: Fecal Transplant
- 15. The Future of AA Treatment • JAK inhibitors • Apremilast • Ustekinumab • Dupilumab • Fecal transplant • Other?
- 16. Thank you