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PEARLS
 Supplementation
 Vitamin D
Chronic urticaria
AD
Vitiligo
Turmeric
 HS
Acne
 Acne
 HS
Chronic Urticaria
Vitamin D ↓ has been demonstrated in CU, and vitamin D replacement has been
shown to help symptoms of CU.
 Predominantly in allergy and immunology literature
 International studies, where reimbursement may differ from US
Can vitamin D supplementation ↓urticaria symptoms regardless of vitamin D
level?
Conclusion: “Add‐on therapy with high‐dose vitamin D3 (4000 IU/day) could be
considered a safe and potentially beneficial immunomodulator in patients with
chronic urticaria.”
Vitamin D – Chronic Urticaria
Mechanisms of benefit of Vitamin D in Urticaria?
• Anti‐inflammatory properties of vitamin D.
• Vitamin D shown to contribute to the conversion of CD4 + T cells to T regulatory cells,
which may help with suppression of pro‐inflammatory mechanisms.
• Inhibits production of numerous cytokines, such IL‐1, L‐6, IL‐12, IL‐23, and others.
• Enhances ICAM expression in mast cells →Modulate proliferation, apoptosis, cytokine
production of mast cells.
Conclusion?
• I check the level and replace as noted earlier, however….
•If the levels are normal, I still recommend taking 3000‐4000 IU/day of vitamin D 3
 Atopic dermatitis
Literature consistently shows low 25 (OH)D levels associated with
increased Fitzpatrick skin type
Mechanism of benefit of vitamin D in atopic dermatitis?
•Supplementation may increase antimicrobial peptides
•Cathelicidin, LL‐37, β‐defensin
• Vitamin D‐mediated activation of toll‐like receptors
• Anti‐inflammatory
Conclusion? When to consider vitamin D status in AD?
•Patient who is Skin Type IV or darker, regardless of age or severity of AD
•Adult patient with severe AD, regardless of phototype
•Replace to normalcy, then continue with maintenance dosing.
Vitiligo
 Pediatric patients:
• Recent study demonstrating benefit with vitamin D supplementation along with
topical tacrolimus treatment vs topical tacrolimus treatment alone*
• 1500 IU/day given if level < 20 and 3000 IU/day given if level < 10
•Re‐pigmentation more effective with combination treatment
 Adults:
•No clear evidence of association or benefit with supplementation at this time.
KaragüzelG, Sakarya NP, Bahadır S, Yaman S, ÖktenA. Vitamin D status and the effects of oral vitamin D treatment in children with
vitiligo: A prospective study. Clin Nutr ESPEN. 2016 Oct;15:28‐31.
Possible mechanism of how vitamin D may affect vitiligo:
• Immunomodulatory effects as described
• Vit D Receptor gene polymorphisms and relationship to autoimmunity. High doses
of D3 in patients with autoimmune disorders may compensate for resistance to its
effects based on gene polymorphisms
• Possible anti‐oxidant effect
Conclusion:
• Consider supplementation in children
• Consider checking 25(OH)D levels in adults, and supplementation if
deficient/insufficient
Hidradenitis Suppurativa
• 500 mg BID
Acne
• 500 mg QD‐BID
• Varies depending on age and motivation of patient
•study exploring P. acnes induced inflammatory mediators and the effect of certain
herbs on these mediators→
• P. acnes induced reactive oxygen species and pro‐inflammatory cytokines IL‐8
and TNF‐alpha ↓by curcuma longa*
Numerous studies showing following benefits :
•Alzheimer’s Disease and neuro‐protection
• Antibacterial, antiviral, anti‐larval, antifungal
• Cutaneous disease and skin health
• Anti‐neoplastic
• Anti‐inflammatory
•Cardiovascular health and cardio‐protection
• Anti‐oxidant
• Wound healing
• Diabetes control
• Numerous others…
Resistant” comedones, particularly if very itchy
• Think Malassezia
• Fluconazole 100‐200 mg QD for 2‐4 weeks, or longer as needed
 Consider Malassezia as well for:
• Extremely pruritic scalps with scattered non‐specific tiny papules
• Itchy scalp, chest and back
Dry lips from Isotretinoin
Make their own balm with 1% HC ointment in a lip pot container with
aquaphor
•Smoking cessation
• Weight loss, if patient is overweight or obese
• Turmeric at a dose of 500 mg BID
•Consider vitamin D and probiotics, depending on patient’s willingness,
financial constraints
•Consider bleach baths as inexpensive antisepsis. Alternatively, BPO wash
•If severe, TNF‐alpha inhibitors!
What is your diagnosis?
A.Scabies
B.Prurigo Nodularis
C.Dermatitis Herpetiformis
D.Bullous Pemphigoid
E.Lymphoma
DIF: Linear deposition of IgG along BMZ
I1:640 BMZ titer on monkey esophagus with
epidermal pattern on salt-split skin
Elevated BP180 (90) and BP230 (90)
Final diagnosis: Bullous pemphigoid (pemphigoid nodularis)
What is the most likely diagnosis?
A.Lichen planus
B. Lichenoid drug reaction
C. Secondary syphilis
D. Keratosis lichenoides chronica
E. Pityriasis lichenoides
This disorder may be associated with which of the following
conditions:
A. Hyperthyroidism
B. Lymphoproliferative disorders
C. Hepatitis C infection
D. Inflammatory bowel disease
E. Connective tissue disease
What is the most likely diagnosis?
A) Sarcoidosis
B) Disseminated cryptococosis
C) Lepromatous leprosy
D) Granulomatous mycosis fungoides
E) Granulomatous secondary syphilis
Which special stain would be useful to confirm the diagnosis?
A) Ziehl-Neelsen stain
B) Fite stain
C) PAS stain
D) GMS stain
E) IHC using Anti – Treponema antibody
• Superficial and deep
lymphocytic infiltrate
•Perivascular and periadnexal
The pathologist says it looks like lupus erythematosus. What is
your next step?
A. Ask about work and hobbies
B. Ask about exposure to ticks
C. Check renal function
D. Check CPK/aldolase
E. Ask about rash in others at home
Besides equestrians, what other patient population might
have a similar problem? Patients with
A.Chronic migraines
B.Chronic low back pain
C.Diabetes
D.Inflammatory bowel disease
E.Metastatic melanoma on nivolumab
What is the diagnosis?
A. Infection
B. Sweet’s syndrome
C. Pyoderma gangrenosum
D. Acute halogenoderma
E. Still’s disease
↓Oxadative stress
↓Aberrant immune response
↑Melanocytes regrowth/ proliferation
*Neclear erthroid 2-related factor 2- antioxidant response
element (Nrf2-Are): critical pathway in protecting cells from
oxidative stress
• Afamelanotide
• A synthetic analog of naturally occurring alpha- MSH
• Best outcome in darker racial ethnic group
• Max. improv. Combination with NBUVB
•Prostaglandin f2α analogues:
Latanoprost
Bimatoprost
• Nrf2 activators:
• Dimethyl fumarate ( Tecfidera): protected normal and
vitiligoo melanocytes against monobenzone induced
toxicity.
• JAK1/JAK2 inhibitir:
• Ruxolitinib 1.5% cream BD
• 20 week study → 23% improvement in VASI score.
Aad pearls
Aad pearls
Aad pearls
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  • 4. PEARLS  Supplementation  Vitamin D Chronic urticaria AD Vitiligo Turmeric  HS Acne  Acne  HS
  • 5. Chronic Urticaria Vitamin D ↓ has been demonstrated in CU, and vitamin D replacement has been shown to help symptoms of CU.  Predominantly in allergy and immunology literature  International studies, where reimbursement may differ from US Can vitamin D supplementation ↓urticaria symptoms regardless of vitamin D level? Conclusion: “Add‐on therapy with high‐dose vitamin D3 (4000 IU/day) could be considered a safe and potentially beneficial immunomodulator in patients with chronic urticaria.”
  • 6. Vitamin D – Chronic Urticaria Mechanisms of benefit of Vitamin D in Urticaria? • Anti‐inflammatory properties of vitamin D. • Vitamin D shown to contribute to the conversion of CD4 + T cells to T regulatory cells, which may help with suppression of pro‐inflammatory mechanisms. • Inhibits production of numerous cytokines, such IL‐1, L‐6, IL‐12, IL‐23, and others. • Enhances ICAM expression in mast cells →Modulate proliferation, apoptosis, cytokine production of mast cells.
  • 7. Conclusion? • I check the level and replace as noted earlier, however…. •If the levels are normal, I still recommend taking 3000‐4000 IU/day of vitamin D 3
  • 8.  Atopic dermatitis Literature consistently shows low 25 (OH)D levels associated with increased Fitzpatrick skin type Mechanism of benefit of vitamin D in atopic dermatitis? •Supplementation may increase antimicrobial peptides •Cathelicidin, LL‐37, β‐defensin • Vitamin D‐mediated activation of toll‐like receptors • Anti‐inflammatory
  • 9. Conclusion? When to consider vitamin D status in AD? •Patient who is Skin Type IV or darker, regardless of age or severity of AD •Adult patient with severe AD, regardless of phototype •Replace to normalcy, then continue with maintenance dosing.
  • 10. Vitiligo  Pediatric patients: • Recent study demonstrating benefit with vitamin D supplementation along with topical tacrolimus treatment vs topical tacrolimus treatment alone* • 1500 IU/day given if level < 20 and 3000 IU/day given if level < 10 •Re‐pigmentation more effective with combination treatment  Adults: •No clear evidence of association or benefit with supplementation at this time. KaragüzelG, Sakarya NP, Bahadır S, Yaman S, ÖktenA. Vitamin D status and the effects of oral vitamin D treatment in children with vitiligo: A prospective study. Clin Nutr ESPEN. 2016 Oct;15:28‐31.
  • 11. Possible mechanism of how vitamin D may affect vitiligo: • Immunomodulatory effects as described • Vit D Receptor gene polymorphisms and relationship to autoimmunity. High doses of D3 in patients with autoimmune disorders may compensate for resistance to its effects based on gene polymorphisms • Possible anti‐oxidant effect
  • 12. Conclusion: • Consider supplementation in children • Consider checking 25(OH)D levels in adults, and supplementation if deficient/insufficient
  • 13. Hidradenitis Suppurativa • 500 mg BID Acne • 500 mg QD‐BID • Varies depending on age and motivation of patient •study exploring P. acnes induced inflammatory mediators and the effect of certain herbs on these mediators→ • P. acnes induced reactive oxygen species and pro‐inflammatory cytokines IL‐8 and TNF‐alpha ↓by curcuma longa*
  • 14. Numerous studies showing following benefits : •Alzheimer’s Disease and neuro‐protection • Antibacterial, antiviral, anti‐larval, antifungal • Cutaneous disease and skin health • Anti‐neoplastic • Anti‐inflammatory •Cardiovascular health and cardio‐protection • Anti‐oxidant • Wound healing • Diabetes control • Numerous others…
  • 15. Resistant” comedones, particularly if very itchy • Think Malassezia • Fluconazole 100‐200 mg QD for 2‐4 weeks, or longer as needed  Consider Malassezia as well for: • Extremely pruritic scalps with scattered non‐specific tiny papules • Itchy scalp, chest and back Dry lips from Isotretinoin Make their own balm with 1% HC ointment in a lip pot container with aquaphor
  • 16. •Smoking cessation • Weight loss, if patient is overweight or obese • Turmeric at a dose of 500 mg BID •Consider vitamin D and probiotics, depending on patient’s willingness, financial constraints •Consider bleach baths as inexpensive antisepsis. Alternatively, BPO wash •If severe, TNF‐alpha inhibitors!
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  • 21. What is your diagnosis? A.Scabies B.Prurigo Nodularis C.Dermatitis Herpetiformis D.Bullous Pemphigoid E.Lymphoma
  • 22. DIF: Linear deposition of IgG along BMZ I1:640 BMZ titer on monkey esophagus with epidermal pattern on salt-split skin Elevated BP180 (90) and BP230 (90) Final diagnosis: Bullous pemphigoid (pemphigoid nodularis)
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  • 26. What is the most likely diagnosis? A.Lichen planus B. Lichenoid drug reaction C. Secondary syphilis D. Keratosis lichenoides chronica E. Pityriasis lichenoides
  • 27. This disorder may be associated with which of the following conditions: A. Hyperthyroidism B. Lymphoproliferative disorders C. Hepatitis C infection D. Inflammatory bowel disease E. Connective tissue disease
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  • 31. What is the most likely diagnosis? A) Sarcoidosis B) Disseminated cryptococosis C) Lepromatous leprosy D) Granulomatous mycosis fungoides E) Granulomatous secondary syphilis
  • 32. Which special stain would be useful to confirm the diagnosis? A) Ziehl-Neelsen stain B) Fite stain C) PAS stain D) GMS stain E) IHC using Anti – Treponema antibody
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  • 35. • Superficial and deep lymphocytic infiltrate •Perivascular and periadnexal
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  • 37. The pathologist says it looks like lupus erythematosus. What is your next step? A. Ask about work and hobbies B. Ask about exposure to ticks C. Check renal function D. Check CPK/aldolase E. Ask about rash in others at home
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  • 39. Besides equestrians, what other patient population might have a similar problem? Patients with A.Chronic migraines B.Chronic low back pain C.Diabetes D.Inflammatory bowel disease E.Metastatic melanoma on nivolumab
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  • 43. What is the diagnosis? A. Infection B. Sweet’s syndrome C. Pyoderma gangrenosum D. Acute halogenoderma E. Still’s disease
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  • 47. ↓Oxadative stress ↓Aberrant immune response ↑Melanocytes regrowth/ proliferation
  • 48. *Neclear erthroid 2-related factor 2- antioxidant response element (Nrf2-Are): critical pathway in protecting cells from oxidative stress
  • 49. • Afamelanotide • A synthetic analog of naturally occurring alpha- MSH • Best outcome in darker racial ethnic group • Max. improv. Combination with NBUVB •Prostaglandin f2α analogues: Latanoprost Bimatoprost
  • 50. • Nrf2 activators: • Dimethyl fumarate ( Tecfidera): protected normal and vitiligoo melanocytes against monobenzone induced toxicity. • JAK1/JAK2 inhibitir: • Ruxolitinib 1.5% cream BD • 20 week study → 23% improvement in VASI score.