Hyperkeratotic Plaques in the Axilla


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A 50-year-old woman presents with an intensely pruritic rash in her armpits first noted 2 months ago. She changed to a more “natural” deodorant 3 months earlier having read on the internet that some deodorants could potentially cause breast cancer. The rash persisted despite frequent washing and application of petroleum jelly. On examination, a brown to erythematous hyperkeratotic plaque was present in each axilla. Her dermatologic exam was otherwise unremarkable, and her past medical history was noncontributory. 

Histologic examination of the patient’s biopsy specimen revealed the characteristic features of granular parakeratosis (GP), a rare, benign dermatologic condition that typically develops over 1 to 12 months and classically affects intertriginous areas. Within the affected area(s), which may be...

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Histologic examination of the patient’s biopsy specimen revealed the characteristic features of granular parakeratosis (GP), a rare, benign dermatologic condition that typically develops over 1 to 12 months and classically affects intertriginous areas. Within the affected area(s), which may be unilateral or bilateral, one finds brown to erythematous hyperkeratotic papules that may be discrete, coalesced into plaques, or arranged in a reticular pattern.1 Lesions are usually pruritic and friable. At times they may become violaceous and lichenified as a result of persistent scratching.2 However, for some individuals the eruption is not bothersome beyond its appearance.

Some cases of GP are precipitated by an inciting topical agent, as was the case for this patient in whom the onset correlated with a recent change in deodorant; other cases, however, occur in the absence of aggravating factors. The axillae are most commonly affected, and GP was originally named “axillary granular parakeratosis” by Northcutt and colleagues, who first described the cutaneous condition in 1991.3   The name was subsequently truncated to granular parakeratosis once numerous cases affecting other intertriginous sites — such as the inframammary folds, popliteal fossa, and groin, as well as nonintertriginous areas including the lumbosacral area and face — were reported.4,5

All ages, genders, and ethnic groups are affected by GP, but the classical presentation of the condition involves the underarms of women in the 40- to 50-year-old range.5 Although GP is considered a rare condition, with an estimated incidence of 0.005%, it is speculated that it more often goes unrecognized and undiagnosed by clinicians.1

The etiology of GP has yet to be determined but several theories and associations exist. Northcutt et al hypothesized it to be a reaction induced by contact with topical antiperspirants and deodorants.3 Since then, GP has been linked to other topical irritants as well, such as zinc oxide and benzalkonium chloride, which are agents found in dermatologic products and common household items.5,6 Other associated conditions include warm occlusive environments, increased perspiration, skin maceration, and excessive washing in children.5

However, GP has also been reported to occur in the absence of recognized triggers as well as congenitally.  As such, an alternate hypothesis has been generated suggesting GP may represent an inherited or acquired disorder of cornification capable of occurring autonomously.5 Data from a mouse study comparing normal controls with those deficient in a factor essential for a functional epidermal barrier (caspase-14) support this hypothesis as mice deficient in this protease were more prone to develop parakeratosis than controls.7

Further complicating our understanding of GP is the fact that its histologic features have been noted as incidental findings in a wide range of other entities including dermatomyositis, molluscum contagiosum, dermatophyte infection, and a variety of keratinocytic neoplasms.5 In most of these reports there was no clinical evidence of GP.

Based on all of the available information, the current perception is that GP represents a reactive pattern rather than a distinct clinical entity that manifests in genetically predisposed patients in the presence of aggravating irritants, malignancies, or infections.5

The proposed mechanism in the pathogenesis of GP is the development of an abnormal sequence of keratinocyte maturation within the upper layers of the epidermis.

Filaggrin, a structural protein that binds keratin fibers, acts as an adhesion matrix for keratohyalin granules during the cornification/maturation process.2,3 Normally, keratohyalin granules are degraded in the deeper layers of the epidermis. Without functional filaggrin, keratohyalin granules are retained in the stratum granulosum and stratum corneum, causing disruption in keratinocyte maturation, leading to abnormal nuclei retention (ie, parakeratosis) and thickening of the stratum corneum.2

Northcutt et el proposed that GP could result from defective processing of filaggrin from profilaggrin.3 The absence of filaggrin in the cytoplasm of granular parakeratotic cells in GP, as evidenced using immunohistochemistry and electron microscopy techniques, supports this theory.5

Retention of the keratohyalin granules produces GP’s clinical picture of epidermal papules and plaques as well as the distinctive histologic features. Diffuse epidermal hyperplasia with or without associated papillomatosis is common.  Characteristic findings include marked compact parakeratosis, hyperkeratosis, and the hallmark finding of brightly staining basophilic keratohyalin granules throughout the stratum corneum.1 Focal vacuolization may be seen within the stratum granulosum.  A sparse lymphohistiocytic infiltrate, vascular proliferation, and capillary congestion may be observed in the papillary dermis. Cultures and periodic acid Schiff (PAS) stains are negative for bacteria and fungi.5

The differential diagnosis for GP is extensive and includes conditions that have a predilection for intertriginous areas. Common mimickers include contact dermatitis (irritant or allergic) and acanthosis nigricans. Various infectious and inflammatory conditions such as inverse psoriasis, intertrigo, erythrasma, and dermatophytosis should also be considered, as should the genodermatoses Hailey-Hailey and Darier diseases.5

Because the diaper area is most commonly affected in infants, the differential diagnosis in infants should also include seborrheic dermatitis, acrodermatitis enteropathica, and Langerhans cell histiocytosis.5 Fortunately, the distinct histologic features of GP, as well as other tests including cultures, can help confirm the specific diagnosis.

Multiple approaches may be considered in the treatment of GP; however, to date no approach has been proven superior and success rates are variable.5 Efficacy data outside of case reports are lacking.

Clearly, inciting triggers should be removed if recognized or suspected.  Reducing skin maceration and minimizing moisture may also lead to improvement; however, conservative management alone is not always effective.5

Reportedly effective medical interventions include topical and oral steroids, as well as various other topical agents such as retinoids, antifungals, calcineurin inhibitors, vitamin D analogues, and ammonium lactate.  Procedural and destructive approaches reported in the literature range from cryotherapy and botulinum toxin5 to yttrium aluminum garnet (YAG) and CO2 lasers and even mastopexy for a case of inframammary GP.8 However, one must remember that GP is considered a self-limited condition and may resolve spontaneously in the absence of any intervention.

The patient in the case described was instructed to discontinue the new deodorant and to keep the area clean and dry. She was also prescribed a low-potency topical steroid to reduce inflammation and pruritus. At her 1-month follow-up appointment, the rash had resolved and she had successfully restarted her old brand of deodorant with no recurrence.

Jessica Payne is a medical student and Julia R. Nunley, MD, is a professor of dermatology at the Medical College of Virginia Hospitals, Virginia Commonwealth University, Richmond, Virginia.


  1. Scheinfeld NS, Mones J. Granular parakeratosis: pathologic and clinical correlation of 18 cases of granular parakeratosis. J Am Acad Dermatol. 2005;52(5):863-867.
  2. Wallace CA, Pichardo RO, Yosipovitch G, et al. Granular parakeratosis: a case report and literature review. J Cutan Pathol. 2003;30(5):332-335.
  3. Northcutt AD, Nelson DM, Tschen JA. Axillary granular parakeratosis. J Am Acad Dermatol. 1991;24(4):541-544.
  4. Braun‐Falco M, Laaff H. Granular parakeratosis – a clinical‐pathological correlation of 10 cases. J Dtsch Dermatol Ges. 2009;7(4):340-344.
  5. Ding CY, Liu H, Khachemoune A. Granular parakeratosis: a comprehensive review and a critical reappraisal. Am J Clin Dermatol. 2015;16(6):495-500.
  6. Robinson AJ, Foster RS, Halbert AR, et al. Granular parakeratosis induced by benzalkonium chloride exposure from laundry rinse aids. Australas J Dermatol. 2017;58(3):e138-e140.
  7. Hoste E, Denecker G, Gilbert B, et al. Caspase-14-deficient mice are more prone to the development of parakeratosis. J Invest Dermatol. 2013;133(3):742-750.
  8. Nelson G, Lien MH, Messina JL, et al. Submammary granular parakeratosis treated with mastopexy. J Drugs Dermatol. 2017;16(8):810-812.
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