Presented by Henry Foong, Ipoh, Malaysia
Here is a patient I saw recently.
She is a 17-year-old girl who has a history
of severe alopecia since the age of 12 years.
It was abrupt and sudden with marked loss of scalp hair followed by eye
brows and other body hair.
Within a
month, she had developed alopecia universalis.
She was initially treated with intralesional triamcinolone and topical
minoxidil but did not help.
Subsequently
she had NB-UVB 3 times weekly in the local hospital but that also did not do
much good.
She was advised to go to
tertiary centres in KL but was disappointed with only one visit.
She could not go to NSC in Singapore because
of financial constraints.
As a Malay,
she always wears a tudong to cover her scalp.
There was no other systemic complaints.
She is the 4th in the family of 5 siblings.
No family history of alopecia.
She saw me yesterday.
Am trying out DPCP diphencyprone sensitisation for her.
She had a previous sensitisation done but
quit after one treatment.
She had total
alopecia affecting the scalp, eyebrow, eyelash, axillary and suprapubic area.
Used 0.1% DPCP concentration, left on the scalp for 24 hours and reviewed the
next day.
She does have good reaction
with small vesicles and plan to do it weekly till her hair grows.
The eyebrow hair loss was treated with
intralesional triamcinolone acetonide injection of 10 mg/ml strength.
According to literature, topical minoxidil 5% solution, topical clobetasol ointment and weekly methotrexate 25mg/wk do help too. Other novel therapy would include JAK inhibitors.
Comment: Who has had real success treating patients with AU? Are there any lab tests of real value?
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After DPCP sensitization
References:
1. Clinical Efficacy of Diphenylcyclopropenone in Alopecia
Areata: Retrospective Data Analysis of 50 Patients. Chiang KS, Mesinkovska NA, Piliang MP,
Bergfeld WF. J Investig Dermatol Symp Proc. 2015 Nov;17(2):50-5.
Abstract: Diphenylcyclopropenone (DPCP) is widely considered
the most effective topical immunotherapy for refractory or extensive alopecia
areata (AA), but questions regarding how long to try DPCP therapy before
terminating and what factors are prognostic of therapeutic success still remain
unanswered. In this retrospective study of 50 AA patients, we evaluated DPCP
efficacy and identified patient factors predictive of therapeutic
success/failure. The median duration of DPCP treatment was 3 years, with 47%
patients experiencing their first regrowth in the first 6 months of DPCP
therapy, 20% between 6 months-1 year, and 8% between 1-2 years. In our study,
treatment success, defined as ⩾50% terminal hair regrowth, was
reached in 71% of alopecia totalis patients and in 56% of alopecia universalis
patients. Three factors were statistically significant predictors of poor
treatment outcome-extent of hair loss before DPCP treatment, history of thyroid
disease, and extent of body hair involvement. Relapse was observed in 44% of
patients and significantly associated with history of thyroid disease. Common
side effects were itching, rash, and local lymphadenopathy. The results of this
study support our belief that DPCP therapy is a viable treatment option, can be
successfully accomplished at home, and should not be terminated before 2 years.
2. Pulse
corticosteroid therapy for alopecia areata: study of 139 patients.
Nakajima T1, Inui S, Itami S. Dermatology.
2007;215(4):320-4.
Author information
Abstract: Of the patients, 72.7% had hair loss on > 50%
of their scalp area. Among the recent-onset group (duration of AA < or = 6
months), 59.4% were good responders (> 75% regrowth of alopecia lesions),
while 15.8% with > 6 months duration showed a good response. Recent-onset AA
patients with less severe disease (< or = 50% hair loss) responded at a rate
of 88.0%, but only 21.4% of recent-onset patients with 100% hair loss
responded. No serious adverse effects were observed.
3. Association between vitamin D levels and alopecia areata.
Mahamid M, Abu-Elhija O, Samamra M, Mahamid A, Nseir W. Isr
Med Assoc J. 2014 Jun;16(6):367-70.
RESULTS: Mean CRP values were significantly higher in the AA
group than the control group (1.1 +/- 0.7 mg/dl vs. 0.4 +/- 0.8 mg/ dl, P <
0.05). Vitamin D levels were significantly decreased in the AA group (11.32 +/-
10.18 ng/ml vs. 21.55 +/- 13.62 ng/ml in the control group, P < 0.05).
Multivariate analysis showed that CRP (odds ratio 3.1, 95% confidence interval
2.6-4.2, P = 0.04) and serum vitamin D levels < 30 ng/ml (OR 2.3, 95% CI
2.2-3.1, P = 0.02) were associated with AA.
CONCLUSIONS: We found a significant correlation between AA
and vitamin D deficiency. Vitamin D deficiency can be a significant risk factor
for AA occurrence.
4. Pulse corticosteroid therapy with oral dexamethasone for the treatment of adult alopecia totalis and universalis JAAD, May 2016 Link.
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