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CASE REPORT |
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Year : 2018 | Volume
: 22
| Issue : 2 | Page : 90-92 |
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Follicular occlusion triad
Yugal Kishore Sharma, Shivanti Chauhan, Kirti Deo
Department of Dermatology, Dr. D. Y. Patil Medical College and Hospital, DPU, Pune, Maharashtra, India
Date of Web Publication | 21-Sep-2018 |
Correspondence Address: Dr. Shivanti Chauhan 172, New Mohanpuri, Meerut - 250 001, Uttar Pradesh India
 Source of Support: None, Conflict of Interest: None  | 2 |
DOI: 10.4103/jdds.jdds_22_18
Follicular occlusion triad is a complex comprising three conditions – hidradenitis suppurativa (HS), acne conglobata, and dissecting cellulitis of the scalp – which share the same underlying pathological process of follicular occlusion. Although these constituents are frequently occurring conditions, the triad per se is not commonly reported. We report the case of a 32-year-old male with Hurley Stage II HS, acne conglobata, and dissecting cellulitis of the scalp with mild anemia (hemoglobin: 10.2 g/dL) and raised C-reactive proteins (15 mg/dL). To the best of our knowledge, this appears to be the third case of follicular occlusion triad from India; also probably, only one case has earlier been reported from India with the additional condition of pilonidal cyst, i.e., a follicular occlusion tetrad.
Keywords: Acne conglobata, dissecting folliculitis, follicular occlusion, hidradenitis suppurativa
How to cite this article: Sharma YK, Chauhan S, Deo K. Follicular occlusion triad. J Dermatol Dermatol Surg 2018;22:90-2 |
Introduction | |  |
Follicular occlusion triad is a severely disabling symptom complex of three conditions, namely hidradenitis suppurativa (HS), acne conglobata, and dissecting cellulitis of the scalp;[1] concurrent pilonidal sinus with this triad constitutes follicular occlusion tetrad.[2] The exact pathogenesis of follicular occlusion remains obscure. Although constituted of frequently occurring conditions, the triad per se is not commonly reported; we report one such case.
Case Report | |  |
A 32-year-old male presented with a history of recurrent painful, pus-discharging eruptions developing sequentially over the face (and back for 13 years), axilla and groin for 3 years, and scalp for 2 months. Some of the lessions healed with scars (boxcar and pitted) along with scarring alopecia of the scalp, while fresh nodules, some discharging pus, erupted randomly despite numerous courses of antibiotics (azithromycin, doxycycline, and amoxicillin) over the years. There was no history of similar complaints in the family.
General physical and systemic examinations were normal. Dermatological examination revealed florid conglobate tender nodules as follows: few lessions with discharging sinuses and comedones, present over the axilla and groins > chest, back, buttocks, proximal limbs > head and neck with interspersed hyperpigmented patches, boxcar, and pitted scars. Cicatricial scalp alopecia was present [Figure 1]a, [Figure 1]b, [Figure 1]c, [Figure 1]d, [Figure 1]e, [Figure 1]f. Investigations revealed the following: hemoglobin, 10.2 g/dL; white blood cell count, 11,600/mm;[3] erythrocyte sedimentation rate, 41 mm/1st h; C-reactive proteins 15 mg/dL; and pus culture was positive for Staphylococcus aureus, whereas fungal cultures were negative. His Venereal Disease Research Laboratory, Mantoux and liver/renal function tests were normal. Consent for skin biopsy was refused. The above findings established the diagnosis of follicular occlusion triad, with Hurley Stage II HS, acne conglobata, and dissecting cellulitis of the scalp. He was administerted oral isotretinoin 0.5 mg/kg body weight (30 mg/day), clindamycin 0.1% lotion, and 2% benzoyl peroxide wash. Though he returned for collection of free samples of isotretinoin capsules from us after a fortnight motivated to continue further treatment, but failed to follow-up, as he was from a distinct outstation location. | Figure 1: (a and b) Hyperpigmented patches/papulonodules with boxcar and pitted scars. (c-e) Multiple intertriginous nodules and discharging sinuses in the axilla and groin. (f) Cicatricial alopecia and papules over the scalp
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To the best of our knowledge, only three cases of follicular occlusion, namely two, triad, and one tetrad have been reported hereto from India [Table 1]. These three and ours were from the fourth decade of life, were mild-to-moderate anemic, and were administered isotretinoin. | Table 1: Indian reports of follicular occlusion triad/tetrad including ours
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Discussion | |  |
Velpeau (1839) first reported recurrent painful abscesses in the axilla and groin; Verneuil (in 1854) named these as HS.[2] Spitzer (1901) first named acne conglobata to be severe nodulocystic truncal acne with discharging sinus tracts.[4] Spitzer (in 1903) first described the entity of follicular and perifollicular conglobate dermatitis of the scalp, while Barney (1931) first used the actual term dissecting cellulitis.[5] Also called perifolliculitis capitis abscedens et suffodiens, it manifests predominantly in African-American young adult males with chronic relapsing, recalcitrant perifollicular pustules, nodules, abscesses, and sinuses that evolve into scarring alopecia; musculoskeletal involvement may be associated.[6] A similar etiopathogenesis of acne conglobata, HS, and dissecting cellulitis of the scalp was first alluded to by Goeckerman (1940).[4] Brunsting (1952) pointed out their common features as follows: first, hyperplasia with hyperactivity of the pilosebaceous apparatus or apocrine gland; second, follicular orifice occlusion and double comedo formation; third, bacterial suppuration and undermined loose areolar tissue; and finally, cicatricial healing.[4]
In 1975, pilonidal cyst was added forming the tetrad. In 1989, Plewig and Steger substituted the term acne inversa for HS.[2]
Medical therapies for severe follicular occlusion disorders are systemic isotretinoin, antibiotics, and prednisone; infliximab may tide over recalcitrancy.[7] Destructive therapies include X-ray therapy, surgical excision, and laser ablation of hair follicles for dissecting cellulitis.[5]
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References | |  |
1. | Mittal RR, Gill SS, Jot T. Follicular occlusion triad. Indian J Dermatol Venereol Leprol 1993;59:88-9. [Full text] |
2. | Vasanth V, Chandrashekar BS. Follicular occlusion tetrad. Indian Dermatol Online J 2014;5:491-3. [Full text] |
3. | Gandhi V, Verma P, Yadav P. Follicular occlusion triad associated with reticulate pigmentary disorder: Is there a genetic linkage? Indian J Dermatol 2013;58:330.  [ PUBMED] [Full text] |
4. | Chicarilli ZN. Follicular occlusion triad: Hidradenitis suppurativa, acne conglobata, and dissecting cellulitis of the scalp. Ann Plast Surg 1987;18:230-7. |
5. | Scheinfeld N. Dissecting cellulitis (Perifolliculitis capitis abscedens et suffodiens): A comprehensive review focusing on new treatments and findings of the last decade with commentary comparing the therapies and causes of dissecting cellulitis to hidradenitis suppurativa. Dermatol Online J 2014;20:22692. |
6. | Gaopande VL, Kulkarni MM, Joshi AR, Dhande AN. Perifolliculitis capitis abscedens et suffodiens in a 7 years male: A case report with review of literature. Int J Trichology 2015;7:173-5. |
7. | Shirakawa M, Uramoto K, Harada FA. Treatment of acne conglobata with infliximab. J Am Acad Dermatol 2006;55:344-6. |
[Figure 1]
[Table 1]
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