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  In this article
   Disseminated Hyp...
   Exogenous Ochronosis
   Hypomelanosis of Ito
   Idiopathic Gutta...
   Langerhans Cells...
   Longitudinal Mel...
   Penile Melanosis
   Repigmentation o...
   Repigmentation o...
   Riehl's Melanosis
   Surgical Treatme...
   Systemic 5-Fluor...
   Thiotepa-Induced...
   Tyrosinase Activ...
   References

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REVIEW
Year : 1992  |  Volume : 58  |  Issue : 5  |  Page : 305-309

What's new in pigmentary disorders?




Correspondence Address:
Sanjay Singh


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Source of Support: None, Conflict of Interest: None


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How to cite this article:
Singh S, Kaur V. What's new in pigmentary disorders?. Indian J Dermatol Venereol Leprol 1992;58:305-9

How to cite this URL:
Singh S, Kaur V. What's new in pigmentary disorders?. Indian J Dermatol Venereol Leprol [serial online] 1992 [cited 2019 Nov 20];58:305-9. Available from: http://www.ijdvl.com/text.asp?1992/58/5/305/3833


The selection of material for an article of this nature is always liable to be somewhat idiosyncratic, [1]sub partly tinted by the authors' likes and dislikes and partly by the availability of the material. There is no pretence of completeness, we have reviewed some interesting papers published in past couple of years. Various subtitles of this article are arranged in an alphabetical order.


  Disseminated Hypopigmented Keratosis Top


Morison et al [2] have reported 2 young female patients who had slowly progressive, benign eruption consisting of asymptomatic, well-demarcated, non follicular, hypo­pigmented, 1 to 2 mm flat-topped papules. Lesions were present on the trunk and extremities. Skin biopsy from - one patient showed hyperorthokeratosis, papillomatosis, telangiectasia, normal melanin content, and absence of inflammation. Such a condition has not been reported previously and the authors have named it disseminated hypopigmented keratosis. The differential diagnosis includes stucco keratoses, Darier's disease, verruca plana, and epidermodysplasia verruciformis.


  Exogenous Ochronosis Top


Hydroquinone-containing skin bleaching products are widely used by the black people, particularly in South Africa. In an epidemiological study conducted in South Africa [3] 69% of the users of such preparations had exogenous ochronosis. A surprising finding was that exogenous ochronosis developed even with the use of products in which concentration of hydroquinone was 2% or less, a concentration which has been considered safe until now.


  Hypomelanosis of Ito Top


In this neurocutaneous disorder patients have areas of hypopigmentation distributed over the body according to the  Lines of Blaschko More Details. A few reports of this condition have been published recently. [4],[5] Clover et al [6] have written an excellent summary of the condition. However, the most significant recent development has been the recognition that many patients of hypomelanosis of Ito have associated chromosomal mosaicism. An association between the pigmentary anomaly and chromosomal mosaicism, which is specific neither for a particular type of chromosomal aberration nor for hypomelanosis of Ito, has been suggested. This association lends support to the hypothesis that the pattern of hypopigmentation in hypomelanosis of Ito is the result of migration of 2 clones of primordial melanocytes, each with a different pigment potential. A pattern reminiscent of Blaschko lines is formed when these 2 cell lines alternate in their arrangement along the length of the embryo, while different patterns will appear when this alternating arrangement of neural crest cells is not established.


  Idiopathic Guttate Hypomelanosis Top


In a recent study using electron microscopy, [8] dopa-positive melanocytes and melanin content were found to be reduced in the lesions of idiopathic guttate hypomelanosis. The dopa-positive melanocytes had fragmented or absent dendrites and reduced numbers of melanosomes. Lesions in 10 patients were treated with application of liquid nitrogen for 10-second periods. Complete repigmentation occurred in 6-8 weeks and many active melanocytes were seen in the re- pigmented lesions. The authors hypothesized that destruction of epidermal melanin units by liquid nitrogen application might promote the migration of surrounding keratinocytes and melanocytes in the depigmented area, thus causing repigmentation.


  Langerhans Cells in Nonsegmental Vitiligo Top


In a recent study [9] Langerhans cells were studied in the lesions of active, stable, and re-pigmenting nonsegmental vitiligo. There was depletion of Langerhans cells in the active disease, while repopulation of the cells was seen in the stable disease. In patients who were re-pigmenting due to treatment with fluocinolone or PUVA, there was profound reduction in the number of Langerhans cells. The authors hypothesized that in the active disease Langerhans cells might be destroyed by cytotoxic factors or migrated to regional lymph nodes. The repopulated cells seen in stable vitiligo might have been derived from phenotypically transformed dermal dendritic cells. Both steroids and PUVA are known to deplete Langerhans cells and could have led to their profound reduction in re-pigmenting lesions of vitiligo. The exact role of Langerhans cells in the pathogenesis of vitiligo, however, remains to be understood.


  Longitudinal Melanonychia Top


Longitudinal melanonychia is commonly seen in black persons. Most of these pigmented streaks are benign. Several causes of this condition have been recently reported. [10],[11],[12],[13] In a study of 6 cases, self-induced nail damage (manually or by chewing) was held responsible for the development of longitudinal melanonychia for the first time. [10] The author wrote that matrix melanocytes could be stimulated by trauma and the stimulation lasted long after the trauma ended. The melanin content of the nail matrix was increased without apparent melanocyte proliferation. The thumb was affected in all cases.

Another report [11] describes development of longitudinal melanonychia in a white woman during each of her 2 pregnancies. These lesions were associated with the development of 15-20 lentigines on her trunk and resolved after parturition Although the biopsies of affected nails were not performed, the authors wrote that the pigmented streaks could also be lentigines. Longitudinal melanonychia is association with pregnancy had not been described previously.

About 40% of patients of acquired immunodeficiency syndrome (AIDS) develop pigmented bands on the nails after zidovudine therapy. usually within 1­2 months. Recently 2 patients of AIDS have been described who developed longitudinal melanonychia. [12] In one case pigmentary changes appeared before zidovudine therapy and in another they appeared 2 weeks after discontinuation of short course of zidovudine and then continued to increase. Longitudinal melanonychia was associated with acral hyperpigmented macules of the fingers, palms and soles, buccal mucosa, and genitalia. Pigmentary changes induced by zidovudine are usually limited to the nails. It appeared that the pigmentary changes developed in these patients independent of zidovudine therapy.

Another report [13] described 4 patients with subungual intraepidermal (in situ) melanoma, 3 of them were children. The authors wrote that a rapidly growing pigmented nail streak which later caused dif fuse melanosis of the nail should be viewed with suspicion of subungual in situ melanoma. In such cases excision of the nail matrix, bed, and plate at the level of periosteum may be sufficient and digital amputation may be avoided.

A review on longitudinal melanonychia has been recently published. [14]


  Penile Melanosis Top


Five patients of this condition have been recently reported. [15] Patients had hyperpigmented macules on penile shaft and glans. Histology showed hyperpigmen­tation of the basal layer without melanocyte hyperplasia. During the follow-up of upto 13 years the lesions remained benign. The authors proposed that penile melanosis, Laugier-Hunziker syndrome of the buccal mucosa, and vulvovaginal melanosis should be together classified as essential melanotic hyperpigmentation of the mucosa.


  Repigmentation of Vitiligo and the Role of Hair Follicles Top


During repigmentation of vitiligo melanocytes migrate from the hair bulb to the basal cell layer of the perifollicular epidermis. In a recent study [16] it was found that in vitiligo, only melanin producing melanocytes were destroyed and in the vitiliginous skin dopa-negative melanocytes were present in the outer root sheath of hair follicle. During migration to the epidermis on treatment, these melanocytes matured from inactive to active form thus providing a source of melanocytes for lesions of vitiligo.


  Repigmentation of Achromic Hairs in Vitiligo Top


Hann et al [17] have described 3 patients of vitiligo with brow leukotrichia. After epidermal grafting and PUVA therapy, black hairs appeared at the area of leukotrichia.

Falabella [18] has also described repigmentation of the achromic hairs within the vitiliginous skin after transplantation of in vitro cultured epidermal autografts bearing melanocytes. It appears that melanocytes of skin form 2 subpopulations: epidermal and follicular, and that melanocytes from these compartments may interchange during repigmentation of depigmented lesions.


  Riehl's Melanosis Top


This condition has been regarded by the Japanese as pigmented cosmetic dermatitis. Riehl's melanosis occurring in a 27-year-old woman 2 months after starting the use of a compact face powder has been described from Spain. [19] Positive patch tests were obtained with a fragrance mix, hydroxy-citronellol, geraniol, and lemon oil. These fragrances were present in the face powder. The lesions healed 6 months after stopping the use of the powder.


  Surgical Treatment for Vitiligo Top


Several workers have reported success with the use of in vitro cultured epidermis for repigmentation of vitiligo. [20],[21],[22] All of them reported their results in 1989 working independently and using different methods. In a recent paper, [18] Falabella reported almost 100% repigmentation in 3 patients, 60% improvement in 2 patients, and 30% to 40% improvement in 3 patients. One patient did not respond at all. Patients were followed up between 1 and 2 years after grafting, and, with time, more pigment spread and coalescence of the re-pigmented spots occurred, along with a better colour matching with the surrounding skin. The results depended mainly on 2 factors i.e., stability of the depigmenting process and survival of the graft.

Lerner et al in 1987 cultured melanocytes and injected their suspension into a small suction blister area in a patient with piebaldism. [23] This technique is impractical for general use. Further, it has been observed that in guinea pig the spreading of pigmented spots was greater with non cultured melanocytes associated with keratinocytes, than melanocytes previously cultivated. [24] Taking note of these observations, Gautheir et a1 [25] have reported grafting of depigmented lesions with autologous non cultured melanocytes. Blisters were produced on the depigmented areas by freezing with liquid nitrogen and epidermal cell suspension (obtained from samples of skin from occipital area after trypsinization) was injected in each blister. The authors treated 2 women, one with vitiligo and another with naevus depigmentosus, with this method. Repigmentation appeared within 25 to 30 days and pigmented spots extended and coalesced within 3 months.


  Systemic 5-Fluorouracil­Induced Pigmented Macules Top


In a study [26] of cutaneous complications of systemic 5-fluorouracil therapy, 72 of 137 (52%) patients were found to have developed pigmented macules mainly on the palms and soles. Histology showed increase in melanin and no change in melanocyte count. This side effect of 5- fluorouracil therapy has not been described previously.


  Thiotepa-Induced Hyperpigmentation Top


Patterned hyperpigmentation may occur in women receiving thiotepa intravenously as treatment of metastatic adenocarcinoma of the breast. One recent report [27] describes 5 women who developed patterned hyperpigmentation confined to the skin occluded by adhesive materials. The authors measured concentration of thiotepa in occluded and nonoccluded skin, plasma, bandage with adhesive, and gauze containing sweat. They hypothesized that thiotepa might be excreted in sweat and accumulated beneath adhesive - containing bandages, where it exerted a local toxic effect causing pigmentation.


  Tyrosinase Activity and Skin Colour Top


Basically there are 3 types of normal skin colour i.e., white, black, and brown. The number of melanocytes is almost the same in these skin types and the biochemical basis for these 3 skin colours is not completely understood. In a study [28] foreskins from infants whose parents were either racially black or white were taken and tyrosinase activity measured. Tyrosinase activity in black foreskin samples was found to be 3 times that in the white samples.

 
  References Top

1.Wilkinson JD. Recent advances in topical treatment. In: Recent advances in Dermatology (Champion RH, Pye RJ, eds), Edinburgh Churchill Livingstone, 1990; 231-40.  Back to cited text no. 1    
2.Morison WL, Kerker BJ, Tunnessen WW, Farmer ER. Disseminated hypopigmented Keratosis. Arch Dermatol 1991; 127: 848-50.  Back to cited text no. 2    
3.Hardwick N, Van Gelder LW, Van Der Merwe CA, Van Der Merwe MP. Exogenous ochronosis: an epidemiological study. Br J Dermatol 1989; 120: 229-38.  Back to cited text no. 3  [PUBMED]  
4.Griebel V, Krageloh - Mann I, Michaelis R. Hypomelanosis of Ito : report of four cases and survey of literature. Neuropediatrics 1989; 20: 234-7.  Back to cited text no. 4    
5.Singh S, Kaur V, Pandey SS: Hypomelanosis of Ito. Ind J Dermatol Venereol Leprol 1992; 58: 30-2.  Back to cited text no. 5    
6.Glover MT, Brett EM, Atherton DJ. Hypomelanosis of Ito: spectrum of the disease. J Pediatr 1989; 115: 75-80.  Back to cited text no. 6  [PUBMED]  
7.Thomas IT, Frias JL. (letter to the Editor), Lancet 1986; 2: 343.  Back to cited text no. 7    
8.Ploysangam T, Dee-Ananlops, Suvanprakorn P. Treatment of idiopathic guttate hypomelanosis with liquid nitrogen: light and electron microscopic study. J Am Acad Dermatol 1990; 23: 681-4.  Back to cited text no. 8    
9.Kao C-H, Yu H-S. Depletion and repopulation of Langerhans cells in nonsegmental type vitiligo. J Dermatol 1990; 17: 287-96.  Back to cited text no. 9    
10.Baran R. Nail biting and picking as.a possible cause of longitudinal melanonychia : a study of 6 cases. Dermatological 1990; 181: 126-8.  Back to cited text no. 10  [PUBMED]  
11.Fryer JM, Werth VP. Pregnancy -associated hyperpigmentation: longitudinal melanonychia. J Am Acad Dermatol 1992; 26: 493-4.  Back to cited text no. 11  [PUBMED]  
12.Gallais V, Lacour J Ph, Perrin C, Ghanem G, Bodokh I, Ortonne JP. Acral hyperpigmented macules and longitudinal melanonychia in AIDS patients. Br J Dermatol 1992; 126: 387-91.  Back to cited text no. 12    
13.Kato T, Usuba Y, Takematsu H, et al. A rapidly growing pigmented nail streak resulting in diffuse melanosis of the nail: a possible sign of subungual melanoma in situ. Cancer 1989; 64: 2191-7.  Back to cited text no. 13  [PUBMED]  
14.Baran R, Kechijian P. Longitudinal melanonychia (melanonychiastriata): diagnosis and management. J Am Acad Dermatol 1989; 21: 1165-75.  Back to cited text no. 14  [PUBMED]  
15.Revuz J, Clerici T. Penile Melanosis. J Am Acad Dermatol 1989, 20: 567-70.  Back to cited text no. 15  [PUBMED]  
16.Cui J, Shen L-Y, Wang G-C. Role of hair follicles in the repigmentation of vitiligo. J Invest Dermatol 1991; 97: 410-6.  Back to cited text no. 16    
17.Hann SK, Im S, Park YK, Hur W. Repigmentation of leukotrichia by epidermal grafting and systemic psoralen plus UVA. Arch Dermatol 1992; 128: 998-9.  Back to cited text no. 17  [PUBMED]  
18.Falabella R, Escobar C, Borrero I. Treatment of refractory and stable vitiligo by transplantation of in vitro cultured epidermal autografts bearing melanocytes. J Am Acad Dermatol 1992; 26: 230-6.  Back to cited text no. 18  [PUBMED]  
19.Serrano G, Pujol C, Cuadra J, Gallo S, Aliaga A. Riehl's Melanosis : pigmented contact dermatitis caused by fragrances. J Am Acad Dermatol 1989; 21: 1057-60.  Back to cited text no. 19  [PUBMED]  
20.Falabella R, Escobar C, Borrero I. Transplantation of in vitro cultured epidermis bearing melanocytes for repigmenting vitiligo. J Am Acad Dermatol 1989; 21: 257-64.  Back to cited text no. 20    
21.Brysk M M, Newton RM, Rajaraman S, etal. Repigmentation of vitiliginous skin by cultured cells. Pigment Cell Res 1989; 2: 202-7.  Back to cited text no. 21    
22.Plott R, Brysk M M, Newton R, et al, A surgical treatment for vitiligo : transplantation of autologous cultured epithelial grafts. J Dermatol Surg Oncol 1989; 15: 1161-6.  Back to cited text no. 22    
23.Lerner AB, Halaben R, Klaus SN, et al. Transplantation of human melanocytes. J Invest Dermatol 1987; 89: 219-24.  Back to cited text no. 23    
24.Gauthier Y, Surleve-Bazeille JE, Gauthier O, et al. Dimethyl benzanthracene (D M B A) and spreading of grafted melanocytes in guinea pigs (abstract). J Invest Dermatol 1989; 92: 141.  Back to cited text no. 24    
25.Gautheir Y, Surleve-Bazeille JE. Autologous grafting with noncultured melanocytes : a simplified method for treatment of depigmented lesions. J Am Acad Dermatol 1992; 26: 191-4.  Back to cited text no. 25    
26.Cho KH, Chung JH, Lee AY, Lee YS, Kim NK, Kim CW. Pigmented macules in patients treated with systemic 5- fluorourecil. J Dermatol 1988; 15: 342-6.  Back to cited text no. 26    
27.Horn TD, Beveridge RA, Egorin MJ, Abeloff MD, Hood AF. Observations and proposed mechanism of N, N', N"- triethylenethio­phosphor,amide (t hiotepa)- induced hyperpigmentation. Arch Dermatol 1989; 125: 524-7.  Back to cited text no. 27    
28.Iwata M, Corn T, Iwata S, Everett MA, Fuller BB. The relationship between tyrosinase activity and skin color in human foreskins. J Invest Dermatol 1990; 95: 9-15.  Back to cited text no. 28    




 

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