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Authors: Dr Frank Po-Chao Chiu, Senior House Officer, Royal Brisbane Women’s Hospital, Brisbane, Queensland, Australia; Dr Jim Muir, Dermatologist, South East Dermatology, Brisbane, Queensland, Australia. DermNet NZ Editor in Chief: Adjunct A/Prof. Amanda Oakley, Dermatologist, Hamilton, New Zealand. Copy edited by Gus Mitchell. July 2019.
Colloid milium refers to a group of rare, degenerative, cutaneous deposition disorders.
The colloid degeneration disorders are characterised by amorphous, hyaline-like deposits in the dermis, which classically present as yellow-brown, semi-translucent papules and plaques over sun-exposed areas .
There are currently 5 different subtypes of colloid milium.
Since colloid milium was first described as “Das Colloid-Milium der Haut” by Wagner in 1866, it has also been known as colloid degeneration, colloid pseudomillium, milliary colloidoma, colloid infiltration hyaloma, and elastosis colloidalis conglomerata .
Adult colloid milium is the most commonly occurring subtype and typically develops in fair-skinned men aged 30–60 years with an outdoor occupation, such as farming . Men are four times more likely than women to develop adult colloid milium. Medical conditions occasionally associated with adult colloid milium include multiple myeloma and beta thalassaemia [1,2].
Juvenile colloid milium is exceedingly rare and tends to develop between 10–20 years of age, but has occurred in a child aged 4 years . Familial cases of juvenile colloid milium with an autosomal recessive inheritance have been reported .
Pigmented colloid milium usually follows the use of hydroquinone bleaching creams and extensive sun exposure. A case of pigmented colloid milium that was not associated with hydroquinone has also been reported in a Caucasian farmer with chronic exposure to fertilisers and sunlight .
There have been 13 reported cases of nodular colloid degeneration since it was first described in 1927; eight were males, and the mean age was 52 years (from a range of 25–76 years) [7,8].
A series of six elderly Caucasians were reported to have acral keratosis with eosinophilic dermal deposits; four were male and two were female, with a mean age of 74 years (from a range of 59–81 years).
Adult colloid milium is associated with exposure to excessive sunlight, petroleum, and chemical fertilisers, although its pathogenesis remains unclear.
It is suspected that sunlight ruptures elastin fibres resulting in an accumulation of proteins or fibroblast products in the dermis. Contributing factors may include trauma and photodynamic effects of phenols in gas oil .
Juvenile colloid milium is associated with chronic sun exposure and severe sunburn, resulting in keratinocyte degeneration .
The role of sun exposure in nodular colloid degeneration is uncertain, as a case has been described involving the penis . The colloid material is suspected to relate to actinic degeneration of elastic fibres (solar elastosis) .
The cause of acral keratosis with eosinophilic dermal deposits is unknown. It may involve sun exposure and the regression of viral warts, although evidence for active human papillomavirus infection was not observed [9,10].
Adult colloid milium typically presents with numerous flesh-coloured or yellow-brown, semi-translucent, dome-shaped papules, 1–4 mm in diameter.
Dermoscopy reveals yellow-brown clods.
Pigmented colloid milium is characterised by grey-black clustered papules on the face. Atrophy may occur among the milia .
Nodular colloid degeneration presents as an isolated nodule or plaque, approximately 5 cm in diameter, on chronically sun-exposed skin, particularly the face. The scalp, trunk, and extremities can also be affected .
Acral keratosis with eosinophilic dermal deposits presents as painless, slowly-progressive, hyperkeratotic papules on the top of the fingertips [2,10].
There are no systemic complications of adult colloid milium.
Juvenile colloid milium has been reported to induce ligneous conjunctivitis, a rare disease characterized by wood-like pseudomembranes developing on the mucous membrane of the eye (ocular and extraocular mucosae), and periodontitis, although the pathogenesis of these is unclear [1,14].
Colloid milium is confirmed by skin biopsy . See colloid milium pathology. It can be distinguished from amyloidosis and other conditions by using special stains, immunohistochemistry, and electron microscopy .
Histopathological features of adult colloid milium include:
In contrast to adult colloid milium, juvenile colloid milium lacks a Grenz zone and the colloid substance is found within the epidermis or superficial dermis .
In acral keratosis with eosinophilic dermal deposits, deposits of amorphous eosinophilic material are localised to the papillary dermis. This colloid milia subtype is not associated with elastotic degeneration (the breakdown of elastic tissue) or fissuring.
Under electron microscopy, the colloid ultrastructure appears as a medium electron-dense, amorphous, granular material with short, ill-defined, branching filaments that are much smaller than those seen in amyloid [1,2]. Desmosome remnants, active fibroblasts, binding proteins, and nuclear proteins have also been observed [2,12].
Adult colloid milium stains positive with crystal violet, congo red, and periodic acid-Schiff (PAS) stains [2,11] (see figure 3). Adult colloid milium stains a ‘robin’s egg blue’ with the Pinkus' acid orcein–Giemsa stain, and will fluoresce with thioflavin T .
Immunohistochemistry is often necessary to distinguish colloid milium from amyloidosis. Amyloid P protein is positive for adult colloid milium and amyloidosis. Unlike amyloidosis, adult colloid milium displays negative reactivity to cytokeratin (including MNF 116), laminin, type IV collagen, cotton dyes (including pagoda red), and light chain immunoglobulin [11,17]. Adult colloid milium stains positively for IgG, IgM, and NKH-1 (a stain for proteins related to elastic fibre microfibrils) .
Juvenile colloid milium does not stain positively for amyloid P protein but does stain positively with antikeratin and cytokeratin antibodies, including MNF116 and cytokeratin AE1/AE3 [2,13]. Juvenile colloid milium also stains positively for IgG within the colloid deposits . Positive pan-cytokeratin labelling and use of electron microscopy suggest that juvenile colloid milium deposits derive from degenerate, epidermal keratinocytes in contrast to adult colloid milium, where deposits are suspected to derive from degenerate elastic tissue in the dermis .
Colloid islands of both the pigmented and nodular colloid degeneration subtype are found in the upper dermis, with fissures and clefts that extend deep within the dermis [2,6,19]. Additional yellow-brown, banana-shaped ochronotic fibres are also seen between collagen and elastin bundles of the deep dermis in the pigmented colloid milium subtype .
Pigmented colloid milium and nodular colloid degeneration subtypes both stain positive with PAS and elastin stains, but are negative for congo red, in contrast to the adult colloid milium subtype [6,7].
In acral keratosis with eosinophilic dermal deposits, the deposits have stained positive with trichrome and PAS staining, while staining negative for congo red, amyloid protein P, type 4 collagen, and cytokeratin antibodies .
The differential diagnosis of colloid milium includes other conditions presenting with multiple papules [1,11,12]. This may include:
Treatment may include combinations of medical and physical therapies [1,11,12].
Excessive cautery, cryotherapy, and laser therapy may cause poor cosmetic results .
Colloid milium may become more extensive over time but tends to stabilise after three years . New lesions rarely develop after this period. If left untreated, colloid milium typically persists with no spontaneous resolution .
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