|Year : 2022 | Volume
| Issue : 3 | Page : 166-175
Frictional melanosis and macular amyloidosis – exploring the link
Ashwini Padubidri Kombettu MD , Chethana Gurumurthy, Vinutha Rangappa, Veeranna Shastry
Department of Dematology, JSS medical college, Mysore, India
|Date of Submission||29-Jan-2022|
|Date of Decision||27-Apr-2022|
|Date of Acceptance||19-May-2022|
|Date of Web Publication||30-Nov-2022|
Dr. Ashwini Padubidri Kombettu
Associate Professor, Department of Dematology, JSS medical college, Mysore
Source of Support: None, Conflict of Interest: None
Frictional melanosis is a condition that is often encountered in dermatology practice. The acquired pigmentary disorder has clinical similarity to the condition termed macular amyloidosis. These two entities have etiological-epidemiological and clinical overlap. Dermoscopy and histopathology can demonstrate subtle differences. The review is an attempt to understand the different etiological aspects proposed for these conditions. We discuss the clinical features of the two conditions, dermoscopic features and histopathological changes. It is imperative for dermatologists to be aware of the similarities and the differences between the two entities for their better management.
Keywords: Cutaneous amyloidosis, frictional melanosis, macular amyloidosis
|How to cite this article:|
Kombettu AP, Gurumurthy C, Rangappa V, Shastry V. Frictional melanosis and macular amyloidosis – exploring the link. Pigment Int 2022;9:166-75
| Introduction|| |
Frictional melanosis (FM) is a benign localized pigmentary skin disorder, commonly seen over forearms, arms, and shoulder. It presents as a mottled/rippled type of hyperpigmentation on bony prominences, more commonly in women with a history of chronic rubbing., Macular amyloidosis (MA) is a localized form of cutaneous amyloidosis. It clinically presents as dark brownish macules distributed on the back, upper, and lower extremities.,
There is considerable clinical and histological overlap between the two. When amyloid deposits are demonstrated, they are diagnosed as amyloidosis. The role of friction has been proposed to be the causative factor, though friction is not always noted in all cases.,
| Methodology|| |
An electronic search was conducted on google scholar using the terminologies frictional melanosis, macular amyloidosis (MA), cutaneous amyloidosis, dermoscopy in frictional melanosis, dermoscopy in cutaneous amyloidosis, histopathology in frictional melanosis, and Congo red staining. Articles written in the English language from 1970 to the present were considered.
Historical aspects, Etiology proposed, and terminologies
Hidano et al.’s report in 1984 on frictional melanosis was probably among the earliest description of this observation. They described cases of unusual brownish pigmentation occurring over the bony tissues such as clavicle, scapula, or vertebrae, occurring mainly in young women. The pigmentation usually showed rippled pattern on the upper back and clavicular region, a zebra-like pattern over the ribs, and a postage-stamp-like macule over the vertebral column.
A similar idiopathic pigmentation was described on the clavicular area, shin, and lateral aspect of arms in young Latin/Mexican and Japanese women. The condition was found to be related to the repeated friction by nylon towels, scrub pads, lifa, or brushes, widely used by young people. Sharquie and Al‐Dorky termed it Lifa disease. There was a history of chronic rubbing and friction with a lifa as a washing agent. The distribution of the rash was very characteristic as it was located only over bony prominences. The lesions were macular, symmetrically distributed, with a positive family history of similar pigmentation in 10% of patients.
A linear, vertical, midline, hyperpigmented patch distributed over the bony protuberances of the inferior thoracic and lumbar vertebrae was described in male students at the Orthodox Jewish Talmudic seminaries (Yeshivas). It was attributed to the friction from the rigid backrests against the skin of the lower back caused by the characteristic swaying activity that traditionally accompanies Torah study or “davening” (praying) and termed Davener’s dermatosis.,
Frictional asymptomatic darkening of the extensor surfaces was the terminology used to describe the uniform and bilateral darkening of the skin on extensor aspects of elbows and knees in middle-aged adults. Frictional melanosis of rubbing inner thighs was reported as a common problem among Iraqi females.
Since friction with clothing or any other such material was a common finding, the term frictional melanosis was proposed. Sharquie and Al‐Dorky speculated that the mechanism of pigmentation was due to repeated damage to the basal cell layer as a result of squeezing of the epidermis between the underlying bone and the offending wash brush (lifa). This would damage the melanocytes that would release their melanosomes into the dermis, which would be present as melanophages, leading to pigmentation in these cases. Wood’s light confirmed the dermal pigmentation in these cases.
Macular amyloidosis (MA) represents a common variant of primary localized cutaneous amyloidosis. It was first described by Palitz and Peck in 1952. MA is seen more often in women with the age of onset ranging between 21 and 50 years.,,,,, Clinically, MA presents as hyperpigmented patches of grayish-brown macules with a rippled pattern, associated with the deposition of amyloid material in the papillary dermis., The sites most commonly involved are the interscapular area, extremities (shins and forearms), and clavicles, although pigmentation on the breast, face, neck, and axilla has also been reported.,, Various risk factors such as race, female gender, friction, atopy, genetic predisposition, and exposure to sunlight have been implicated in the etiopathogenesis of MA. Sun exposed areas may show more pigmentation than covered areas.
MA developing due to friction is reported.,, Typical cases exhibit moderately pruritic, brown, rippled macules, symmetrically distributed on thighs, shins, arms, upper back, breasts, and buttocks. MA presenting as poikiloderma is also reported.
But not all reports mentioned regarding association with friction. Eswaramoorthy et al.’s observation stated that there was no direct correlation between MA and atopy, sunlight, or friction to the skin. Frequent involvement of back and extensor aspects of upper limbs and clavicular areas compared to sun-protected sites such as lower back, legs, thighs, buttocks, and breast would point to exposure to ultraviolet rays as an etiological factor in MA.
MA was considered secondary to scratching motivated by pruriginous diseases and the term “scratch amyloidosis” was proposed for macular and lichenoid amyloidosis. They observed signs of scratching in most of the patients. The principal causes of pruritus are dermographism, photodermatitis, and dermatitis. Macular and also biphasic amyloidosis secondary to friction with nylon cloth is reported.,
Bernhard observed that MA on the back and nostalgia paresthetica would coexist considering the pruritus in these conditions. The so-called posterior pigmented pruritic patch and MA may be considered progressive evolutional stages of notalgia paresthetica.,
MA and lichen amyloidosis seem to be distinct clinical manifestations of the same disease and itching does not cause the transformation of Macular to Lichen amyloidosis.
Summary of the articles reviwed- [Table 1].
Clinical aspects: [Figure 1] and [Figure 2]
|Figure 1 Hyperpigmented patches with rippled pattern on arm , extending on to the extensor aspect of forearm in FM|
Click here to view
Frictional melanosis presents as brownish-black hyperpigmented patches, usually in a rippled pattern on forearms, arms, clavicular region, and back, mainly over bony prominences.,,, They are usually distributed symmetrically. MA has almost a similar presentation with hyperpigmented macules and patches on the extensor aspect of limbs and back. At times the pigmentation may have a greyish hue.,,,
Frictional melanosis over the face is described, though it is rare to find localized MA on the face. Mutalik et al. described six clinical patterns in facial frictional melanosis as zygomatico-supraorbitalis, meto-melanosis (involving forehead), pan facial, para nasal types, perioral type, and mixed type. Characteristic symmetric distribution with uniform black-brown pigmentation, without any textural change, was noted in these patterns. Other clinical differential diagnoses of facial frictional melanosis would include conditions such as melasma, facial acanthosis nigricans, lichen planus pigmentosus, pigmented contact dermatitis, sebomelanosis, pigmentary demarcation lines, and postinflammatory hyperpigmentation. Facial acanthosis nigricans shows pigmented patches usually over zygomatic, malar areas and forehead with a velvety skin textural change.
| Dermoscopic features of frictional melanosis|| |
Frictional melanosis on dermoscopy shows pseudoreticular brown pigment network, structureless brown areas, and prominent follicular openings.
The diffuse or reticular pattern is said to be based on the degree of epidermal pigmentation. It is reported that pigmentation is extensive in the former and focal in the latter.
There can be pockets of gray hue within the brownish background. Pigment globules, mainly distributed in the perifollicular areas, may be seen. Owing to repeated rubbing, broken hairs, dilated follicular openings, follicular pluggings are identified. Perifollicular white scales are noted due to follicular hyperkeratosis.
The brownish color, bluish-gray globules with follicular modifications are possibly explained on the ground by histopathological changes that consist of irregular acanthosis of epidermis, antler-like projection of rete ridges, hypermelanosis of the basal layer, and “patchy” pigment incontinence with follicular dilatation with plugs.
To summarize, in FM, the background color is brown, bluish-gray globules are seen, and follicular changes include patulous follicles with plugs. Vascular elements are not seen. Scales are white in the perifollicular area [Figure 3] and [Figure 4].
|Figure 3 Dark brown dots, brown pigment background, follicular scaling seen in frictional melanosis|
Click here to view
|Figure 4 Brown globules, streaks of scales and minimal follicular scaling seen in frictional melanosis|
Click here to view
| Dermoscopic features of macular amyloidosis|| |
Dermoscopy of MA shows a typical “hub and spoke” pattern that consists of the brown clod in the center (hub) and radiating brown lines (spokes) from the central clod.
Sometimes center pigment can be replaced by a scar-like or white area and in a few reports mixed pattern is observed. Alternate streaks of brown and white radiating from the central hub is another pattern appreciated in the condition (day lily appearance). Surrounding brown area takes many configurations such as streaks, leaf-like, or bulbous projections. It should be noted that melanin is present in the tip of papillae that forms the “hub” and the spokes are due to irregularly hyperplastic reactive epidermal basal pigmentation.
Other dermoscopic findings in MA are semicircular, hyperpigmented, lunar eclipse-shaped structures and hyperpigmented blotchy areas seen over a brown reticular pigment background.
To summarize, in MA, brown is the background color, and brown dots, clods, or streaks are the pigment pattern. No scales, no follicular changes, or no vascular elements are noted [Figure 5] and [Figure 6].
|Figure 5 Multiple dark brown dots seen on the brown pigment background in macular amyloidosis|
Click here to view
|Figure 6 Few hypopigmented to whitish structureless areas seen with multiple dark brown dots on a bluish brown background in the surrounding|
Click here to view
| Histopathology and ultrastructural studies|| |
Histology in most of the cases of frictional melanosis reveals marked diffuse hyperkeratosis and melanin deposit in the upper dermis. Acanthosis and papillomatosis can be noted in some. Exceptional detection of amyloid deposit in the papillary dermis was noted in a few reports.
Cutaneous MA on histopathology showed elongation of rete, widening of dermal papillae, and pigmentary incontinence. Mild to moderate deposits of amorphous, eosinophilic, Congo red positive substance in the papillary dermis was noted. Birefringence may not always be as noted under polarized microscopy probably due to scarcity of deposits.
Histochemical stains are not always conducive to the detection of amyloid. Mysore et al. studied 10 cases of frictional amyloidosis, where six patients showed positive amyloid on Congo red stain. In the remaining four cases, electron microscopy demonstrated amyloid material, which was not demonstrable by histopathology., It is postulated that frictional melanosis represents the early cases of frictional amyloidosis, where amyloid is either too small to be demonstrated by Congo red or not yet formed. Electron microscopy is the most sensitive tool for demonstrating amyloid.
It is further thought that friction not only leads to changes in the epidermis such as acanthosis and increased basal pigmentation but also damages keratinocytes and alters keratinization, which, in turn, entails the conversion of alpha-helical keratin into beta structured amyloid. This process is further aggravated in lichen amyloidosis, which also shows the effects of prolonged scratching and the formation of amyloidosis.
Studies have indicated an epidermal origin of the amyloid, where degenerating keratinocytes drop into the dermis and undergo transformation to amyloid. While this mechanism seems possible at least in MA, an alternative pathogenetic pathway is suggested in lichen amyloidosis, in which amyloid fibrils seem to form on the dermal surface of living basal keratinocytes.
There is no convincing explanation for the origin of the amyloid protein in the skin. Two theories, fibrillar body theory and secretory theory, have been proposed. The fibrillar body theory states that damaged keratinocytes undergo filamentous degeneration by apoptosis and transformation by dermal fibroblasts and histiocytes and are converted into amyloid that deposits in the papillary dermis. Secretion theory describes the deposition of amyloid from the degenerated basal keratinocytes at the dermoepidermal junction, which eventually drops into the papillary dermis through the damaged lamina densa of the basal layer.,,
Unusual patchy filamentous degeneration of collagen islands is described in MA. There are reports mentioning amyloid fibrils reacting to antihuman keratin antibodies, which indicates their epidermal origin.,,,
Ultrastructural studies revealed that a basal lamina-like substance with anchoring fibrils was present between and within amyloid deposits. By indirect immunofluorescence technique using an anti-basement membrane zone antiserum, linear fluorescence occurred at the dermoepidermal junction and in a reticular pattern in dermal papillae. It seemed that apoptotic keratinocytes brought down basal lamina and fine fibrous components attached to it when these cells dropped down to the papillary dermis and became the source of amyloid. These findings support the hypothesis that epidermal keratinocyte degeneration plays an important role in the histogenesis of cutaneous amyloidoses.
The amyloid of lichen amyloidosis and MA is different from other known types of amyloid. By using an indirect immunofluorescence technique, it was proven that lichen amyloidosis and MA do not react with antibodies against amyloid fibril proteins that are previously characterized. Protein AP, which was demonstrated in amyloid of MA and lichen amyloidosis (LA), is known to be present in all forms of amyloid and is of unknown significance.
Electron microscopic studies revealed many of the cells that seemed to be macrophages by light microscopy were fibroblasts. The digesting action of fibroblasts was well developed and many melanosomes were taken into the cells making the cells resemble melanophages. The fibroblasts extended long, thin, and branched cytoplasmic processes to surround the amyloid mass, and the cells selectively extended these into the narrow spaces between collagen and amyloid. The fibroblast showed highly developed endocytotic activity and probable ingestion of amyloid by pinocytosis or phagocytosis.
Although amyloid can be suspected on routine hematoxylin and eosin stains as small, multifaceted, and amorphous globules within the papillae, it has to be confirmed by visualizing Congo red stained slides under polarized light for apple-green birefringence. The amyloid may be seen with several histochemical stains, including methyl violet, crystal violet, thioflavin T, and Congo red. Among them, Congo red and crystal violet seem more promising., Immunohistochemistry studies have shown intense staining of the amyloid with cytokeratin 5 (CK5) antibody and high molecular weight keratin (34betaE12).
The summary of the two conditions is given in [Table 2].
|Table 2 Summary of similarities and differences between frictional melanosis and macular amyloiosis|
Click here to view
Frictional melanosis is difficult to treat. Firstly, the patients should avoid rubbing the skin with nylon towels, sponges, brushes and back scratchers, and so on. Laser therapies like Q switched ND:YAG laser are found to be useful. Chemical peels such as trichloroacetic acid and glycolic acid are found to be effective agents in the treatment.,, Different treatment options for MA were reported including retinoids, corticosteroids, tacrolimus, vitamin D3 analogs cyclophosphamide, cyclosporine, amitriptyline, colchicine, capsaicin, menthol, surgical modalities like dermabrasion and laser treatment.
| Conclusion|| |
Frictional melanosis and MA are two terminologies with a clinical–epidemiological–etiological overlap. Both the conditions are seen more often in women, and both have a predilection for sites such as the upper back and extremities. Friction and sun exposure seem to play roles in the development. Friction is not associated in all of these cases, where multifactorial etiology is considered. Clinically, diffuse brownish-black hyperpigmentation with rippled pattern is reported in both. There are subtle differences in dermoscopy where both show pigmentary changes but frictional melanosis also shows follicular changes. Histopathological features have a similarity, though the occasional presence of amyloid prefers the diagnosis to be termed as MA. Frictional melanosis could represent the early cases of MA, where amyloid is either too small to be demonstrated by special stains or it is not yet formed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Siragusa M, Ferri R, Cavallari V, Schepis C. Friction melanosis, friction amyloidosis, macular amyloidosis, towel melanosis: many names for the same clinical entity. Eur J Dermatol 2001;11:545–8.
Al-Aboosi M. Frictional melanosis: a clinical, histologic, and ultrastructural study in Jordanian patients. Int J Dermatol 2004;43:261–4.
Hidano A, Mizuguchi M, Higaki Y. Friction melanosis. In Ann Dermatol Venereol 1984;111:1063–71.
Sharquie KE, Al‐Dorky MK. Frictional dermal melanosis (lifa disease) over bony prominences. J Dermatol 2001;28:12–5.
Magaña‐García M, Carrasco E, Herrera‐Goepfert R, Pueblitz‐Peredo S. Hyperpigmentation of the clavicular zone: a variant of friction melanosis. Int J Dermatol 1989;28:119–22.
Naimer SA, Trattner A, Biton A, Avinoach I, Vardy D. Davener’s dermatosis: a variant of friction hypermelanosis. J Am Acad Dermatol 2000;42:442–5.
Krishnamurthy S, Sigdel S, Brodell RT. Frictional asymptomatic darkening of the extensor surfaces. Cutis 2005;75:349–55.
Palitz LL, Peck S. Amyloidosis cutis: a macular variant. AMA Arch Derm Syphilol 1952;65:451–7.
Habermann MC, Montenegro MR. Primary cutaneous amyloidosis: clinical, laboratorial and histopathological study of 25 cases. Identification of gammaglobulins and C3 in the lesions by immunofluorescence. Dermatologica 1980;160:240–8.
Al-Ratrout JT, Satti MB. Primary localized cutaneous amyloidosis: a clinicopathologic study from Saudi Arabia. Int J Dermatol 1997;36:428–34.
Lines RR, Hansen RC. A hyperpigmented, rippled eruption in a Hispanic woman: macular amyloidosis. Arch Dermatol 1997;133:383–6.
Djuanda A, Wiryadi BE, Sularsito SA, Hidayat D. The epidemiology of cutaneous amyloidosis in Jakarta (Indonesia). Ann Acad Med Singap 1988;17:536–40.
Eswaramoorthy V, Kaur I, Das A, Kumar B. Macular amyloidosis: etiological factors. J Dermatol 1999;26:305–10.
Rasi A, Khatami A, Javaheri SM. Macular amyloidosis: an assessment of prevalence, sex, and age. Int J Dermatol 2004;43:898–9.
Kibbi AG, Rubeiz NG, Zaynoun ST, Kurban AK. Primary localized cutaneous amyloidosis. Int J Dermatol 1992;31:95–8.
Chang YT, Wong CK, Chow KC, Tsai CH. Apoptosis in primary cutaneous amyloidosis. Br J Dermatol 1999;140:210–5.
Shanon J, Sagher F. Interscapular cutaneous amyloidosis. Arch Dermatol 1970;102:195–8.
Tanigaki T, Hata S, Kitano Y et al.
Unusual pigmentation on the skin over trunk bones and extremities. Dermatologica 1985;170: 235–9.
Somani V, Shailaja H, Sita V, Razvi F. Nylon friction dermatitis: a venereol distinct subset of macular amyloidosis. Indian J Dermatol Venerol Leprol 1995;61:145–7.
Bandhlish A, Aggarwal A, Koranne RV. A clinico-epidemiological study of macular amyloidosis from north India. Ind J Dermatol 2012;57:269–74.
Wong CK, Lin CS. Friction amyloidosis. Int J Dermatol 1988;27:302–7.
Hashimoto K, Ito K, Kumakiri M, Headington J. Nylon brush macular amyloidosis. Arch Dermatol 1987;123:633–7.
Mysore V, Bhushnurmath SR, Muirhead DE, Al-Suwaid AR. Frictional amyloidosis in Oman--a study of ten cases. Indian J Dermatol Venereol Leprol 2002;68:28–32.
] [Full text]
Brownstein MH, Hashimoto K. Macular amyloidosis. Arch Dermatol 1972;106:50–7.
Kang HY, Kang WH. Macular amyloidosis presented as poikiloderma: a case report. J Korean Med Sci 2000;15:724–6.
Macsween RM, Saihan EM. Nylon cloth macular amyloidosis. Clin Exp Dermatol. 1997;22(1):28–9.
Iwasaki K, Mihara M, Nishiura S, Shimao S. Biphasic amyloidosis arising from friction melanosis. J Dermatol 1991;18:86–91.
Bernhard JD. Macular amyloidosis, notalgia paresthetica and pruritus: three sides of the same coin? Dermatologica 1991;183:53–4.
Cerroni L, Kopera D, Soyer HP, Kerl H. Notalgia paresthetica,” posterior pigmented pruritic patch” and macular amyloidosis. Three stages of a disease. Hautarzt 1993;44:777–80.
Mutalik SD, Pethe SV, Nikam BP, Rasal YD. Facial frictional melanosis in Indian patients: defining the entity. Clin Derm Rev 2019;3:78–83.
Errichetti E, Stinco G. Dermoscopy in general dermatology: a practical overview. Dermatol Ther 2016;6:471–507.
Errichetti E, Aimilios Lallas A. Hyperpigmented dermatoses. In: Lallas A, Errichetti E, Ioannides D, eds. Dermoscopy in General Dermatology. London: CRC Press; 2019. p. 106–21.
Ankad BS, Drago NR, Koti VR, Nikam BP. Dermoscopic approach to hyperpigmented lesions in skin of color. Clin Dermatol Rev 2020;4:84–91. [Full text]
Sharquie KE, Noaimi AA, Hajji AA. Frictional melanosis of rubbing thighs in Iraqi patients. J Cosmet Dermatol Sci Appl 2014;4:203–11.
Kumar P, Neema S, Pathak N. Macular amyloidosis in a middle-aged woman. Pigment Int 2018;5:57–8. [Full text]
Sandhu S, Neema S, Radhakrishnan S. Dermoscopy of disorders of hyperpigmentation. Pigment Int. 2021;8:14–24.
Madarkar MS, Koti VR. FotoFinder dermoscopy analysis and histopathological correlation in primary localized cutaneous amyloidosis. Dermatol Practical Concept 2021;11:e2021057.
Matildes JO, e Silva LG. Macular amyloidosis. Acta Medica Portuguesa 1983;4:265–9.
Venkataram M, Shashikant M. Frictional melanosis and its clinical and histopathological features. Iran J Dermatol 2018;21:124–7.
Westermark P, Noren P. Two different pathogenetic pathways in lichen amyloidosus and macular amyloidosis. Arch Dermatol Res 1986;278:206–13.
Ishii M, Terao YI, Asai Y, Hamada T. Macular amyloidosis with patchy filamentous degeneration of collagen islands. J Cutan Pathol 1981;8:421–8.
Maeda HS, Ohta S, Saito Y, Nameki H, Ishikawa H. Epidermal origin of the amyloid in localized cutaneous amyloidosis. Br J Dermatol 1982;106:345–51.
Ito K, Hashimoto K. Antikeratin autoantibodies in the amyloid deposits of lichen amyloidosus and macular amyloidosis. Arch Dermatol Res 1989;281:377–82.
Kitano Y, Okada N, Kobayashi Y, Tanigaki T, Okano M, Yoshikawa K. A monoclonal anti‐keratin antibody reactive with amyloid deposit of primary cutaneous amyloidosis. J Dermatol 1987;14:427–9.
Kaoru IT. Anti-keratin autoantibodies and lichenoid and macular amyloidosis. Acta Med Biol 1989;37:13–8.
Kumakiri M, Hashimoto K, Tsukinaga I, Kimura T, Miura Y. Presence of basal lamina-like substance with anchoring fibrils within the amyloid deposits of primary localized cutaneous amyloidosis. J Invest Dermatol 1983;81:153–7.
Noren P, Westermark P. Immunofluorescence and histochemical studies of localized cutaneous amyloidosis. Br J Dermatol 1983;108:277–85.
Ishii M, Terao Y, Asai Y, Hamada T. High melanosome engulfing activity of cutaneous fibroblasts in macular amyloidosis: an electron microscopic study. J Cutan Pathol 1984;11:476–84.
Vijaya B, Dalal BS, Manjunath GV. Primary cutaneous amyloidosis: a clinico-pathological study with emphasis on polarized microscopy. Indian J Pathol Microbiol 2012;55:170–4. [Full text]
Aslani FS, Kargar H, Safaei A, Jowkar F, Hosseini M, Sepaskhah M. Comparison of immunostaining with hematoxylin-eosin and special stains in the diagnosis of cutaneous macular amyloidosis. Cureus 2020;12:e7606
Al-Dhalimi MA, Maluki AH, Tauma A. Efficacy and safety of 532-nm and 1,064-nm Q-switched Nd: YAG laser treatment of frictional dermal melanosis over bony prominences (Lifa disease). Dermatol Surg 2015;41:136–41.
Sacchidanand S, Shetty AB, Leelavathy B. Efficacy of 15% trichloroacetic acid and 50% glycolic acid peel in the treatment of frictional melanosis: a comparative study. J Cutan Aesthet Surg 2015;8:37–41.
Nandini AS, Kumar BS. TCA peel in the treatment of macular amyloidosis. J Evol Med Dent Sci 2014;3:11090– 95.
Weidner T, Illing T, Elsner P. Primary localized cutaneous amyloidosis: a systematic treatment review. Am J Clin Dermatol 2017;18:629–42.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]
[Table 1], [Table 2]