who received therapy. All seven patients noted the increased pigmen¬ tation that occurred in the treatment areas and rated this "tan" as pleasant and acceptable. By increasing the melanin content of pale skin, some of the erythematous papules, nodules, and cysts became somewhat less obvious. The laboratory studies were completed for the first three patients who entered the study; however, they were not performed in the remaining patients since no noteworthy differ¬ ences were observed between samples taken before treatments began and after treatments were completed. John A. Parrish, MD John S. Strauss, MD Thomas S. Fleming, Jr Thomas B. Fitzpatrick, MD Boston
Nonproprietary Name and Trademarks of Drug
papule with a 4-mm-wide border of depigmentation had recently appeared in the left supraclavicular area (Fig 1). Light microscopy of the plaque on the left flank showed benign nevus cells that
extended from the upper dermal aspect to the deep reticular dermis. The nevocytes were arranged in tight clusters, broad sheets, and single files and closely surrounded numerous hairs and other adnexal structures. There was no inflam¬ matory infiltrate within the nevus or the adjacent skin (Fig 2). Masson-Fontana silver stain showed melanin in only a few
nevocytes. Similarly, only scanty
amounts
of melanin were identified in the basal layer of the epidermis, overlying and surrounding the nevus. Sections of the papule in the left supraclavicular area showed an acanthotic type of pigmented seborrheic keratosis. Melanin was decreased on the basal layer of the adjacent epidermis. There was no evidence of inflammation in the area of the seborrheic keratosis or adjacent skin.
histological ap¬ typical halo nevus shows a dense infiltrate of lymphoid cells beneath the epidermis and intermin¬ gled with the nevus cells. There are also usually melanophages admixed with the lymphoid infiltrate. In later stages, the disappearance of nevus cells is followed by loss of the inflam¬ Comment.-The
pearance of
Methoxsalen—Maladinine, Meloxine, MOP, Oxsoralen.
8-
Maryanne Reese provided technical assistance project.
in this
Halo Congenital Nevus Without Histological Inflammation To the Editor.\p=m-\Brownstein
black
et
a
matory infiltrate.1
ever, there is
no
In this case, how¬
inflammation. Since
al
(Archives 113:1572-1575, 1977) described a congenital pigmented nevus
that was surrounded by a depigmented halo. There were also several hypopigmented areas on the face, neck, and back. They emphasized the lack of a histological inflammatory infiltrate in both the nevus and the depigmented halo zone. We report a similar observation in a congenital pigmented nevus that had become depigmented and that was surrounded by a halo. In addition, there were
multiple vitiliginous areas and a around a pigmented seborrheic
halo keratosis.
1 .—Brown-black papule with 4-mm border of depigmentation in left supracla¬ vicular area.
Fig
Fig 2.—Light microscopy of plaque on left original magnifi¬
flank (hematoxylin-eosin, cation x 100).
Report of a Case.\p=m-\A60-year-old man requested the removal of a 5.0 x 2.0-cm hypopigmented, slightly raised, elliptical plaque on his left flank. The plaque contained
number of coarse white hairs surrounded by a 5.0-cm-wide border of hypopigmentation. The plaque had been present since birth and had been dark brown in color. At the age of 14, a white halo began to develop around the lesion. At the same time, the lesion and the hairs within the lesion also became white. Since then, the size and color of the lesion had remained the same. Within the last 15 years, the patient noted the gradual appearance of depigmented, irregularly shaped patches on his trunk, lower legs, and left nipple. In addition, a 4-mm brown-
and
a
was
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the halo first
appeared approximately
earlier, it is possible that an inflammatory infiltrate was origi¬ nally present but has subsided. How¬ 45 years
ever, if this
the case, we would cells to have disap¬ peared also or to have greatly decreased in number. The persistence of the nevus cells and the lack of an inflammatory infiltrate around the
expect the
were
nevus
seborrheic keratosis, which recently
developed a halo, support the sugges¬ tion by Brownstein and co-workers that the depigmentation is not owing to autoimmune mechanisms.
Another unusual aspect of this case that should be mentioned is the curious clinical picture of the nevus. Most reports mentioned either total regression of the nevus or persistence of both configuration and pigmenta¬ tion of the nevus. Our patient's nevus, however, remained the same size but became depigmented. Laura A. King, MD Irvine, Calif Donald T. King, MD Torrance, Calif 1. Lever WF, Schaumburg-Lever G: Histopathology of the Skin, ed 5. Philadelphia, JB Lippincott Co, 1975, p 654.
Beta Carotene in
Porphyria
Congenital
To the Editor.\p=m-\Dr George Stretcher, in his article on erythropoietic porphyria, which appeared in the November Archives (113:1553-1557,1977), makes a reference to the lack of information about the long-term treatment with beta carotene. In 1973,I described a young woman, aged 18, with congenital porphyria at the Royal Society of Medicine (Proc R Soc Med 67:593-594,1974). The patient had usually suffered from intense blistering every summer and the typical sclerodermatous change of her face and hands had developed. In the summer of 1973, she had been given beta carotene, 25 mg three times a day, throughout the summer months and had been able to go out-of-doors in the sunshine without any skin blistering. Previously, she had never been able to expose her skin to sunshine without blistering and she would not venture out before dusk. Since then, she has taken beta carotene in the same dosage from April to October and has, for the first time in her life, been able to survive summer weather without apparent skin damage. In 1976, when in England there was a prolonged spell of sunny weather, the patient remained well on the betacarotene
regimen.