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It has been reported that the final outcome of laser resurfacing still depends to a large degree on the efficiency of the post laser resurfacing wound care in promoting wound healing and preventing early and late complications.The objective of this study was to evaluate and compare a new hydrocolloid dressing, H2460, with Flexzan(TM) for healing of an acute wound after laser skin resurfacing (LSR).Ten volunteers received LSR of the peri-orbital area with an erbium:YAG laser. Identical parameters were used on both sides: 2 J, 5 mm spot, 8 Hz, 300 micros pulse, two passes on the upper eyelids, four passes on the lower eyelids and six passes on the crow's feet area. Soon after the LSR, one side was covered with Flexzan dressing and the other side was covered with a new hydrocolloid dressing -- H2460. The side of the dressing was randomized by alternating both dressings. All volunteers were evaluated and digitally photographed every day for a week and at 1 month after LSR. The degree of erythema, swelling, bleeding, oozing, crusting, pigmentary changes, scarring, discomfort, itching, burning, ease of application of dressings, initial adhesion, overall adhesion, leakage of fluid, maceration of surrounding skin, ease of removal and adhesive residue upon removal were documented.In all volunteer and investigator's evaluations, the new dressing, H2460, achieved far better results than Flexzan in each category. After a 1-week follow-up all volunteers and the investigator evaluated the H2460 side as: healed better, simple to use, and caused less discomfort in 10 out of 10 volunteers. The blinded observer's assessment showed that the Flexzan side healed better in one volunteer.The new dressing, H2460, is a better and suitable alternative to Flexzan as a post LSR dressing.

We report on a 3-year-old boy with hair abnormalities and a generalized bone dysplasia. He had very short, sparse hair and craniosynotosis. His stature, growth, and limb lengths were normal, as was his neurological development. While this phenotype has some resemblance to cranioectodermal dysplasia, the radiographic and hair abnormalities are different. Histological studies showed abnormalities in the internal root sheath of the hair follicle and the hair shaft. These findings define a new ectodermal dysplasia syndrome of unknown cause. © 1993 Wiley-Liss, Inc.

Optical ranging using femtosecond laser pulses and nonlinear-optical cross correlation is demonstrated for the investigation of the microstructure of biological systems. By using pulses of 65-fsec duration generated by a colliding-pulse mode-locked ring dye laser, a spatial resolution of less than 15 μm is achieved with a detection sensitivity to remitted signals as small as 10−7 of the incident pulse energy. This technique is applied to measure the cornea in rabbit eyes in vivo as well as to investigate the epidermal structure of human skin in vitro.

Background and Design: Solar-induced cutaneous damage is mediated partly via oxidative pathways. Some evidence exists for a photoprotective role of antioxidants. In a double-blind, placebo-controlled study, we examined the effect of a long-term, orally administered antioxidant against UV-induced epidermal damage. Healthy human subjects supplemented their usual diet daily with either 400 IU of oral vitamin E (α-tocopherol acetate) or placebo over a 6-month period. Minimal erythema dose and histologic response to threefold minimal erythema dose exposure were determined at baseline, 1 month, and 6 months. Results: The minimal erythema dose did not vary substantially at the three time points within each treatment group or in the vitamin E—supplemented group vs the placebo group. The number of sunburn cells produced by a threefold minimal erythema dose exposure was also not significantly different between the two groups. Of note, however, vitamin E levels in plasma increased only modestly and in skin biopsy specimens were unchanged following 1 month and 6 months of supplementation. Conclusions: No clinical or histologic difference in the response to UVB could be detected between the placebo and vitamin E—supplemented groups. In this small study, daily ingestion of 400IU of oral α-tocopherol daily does not provide meaningful photoprotection. (Arch Dermatol. 1994;130:1257-1261)

Epidermal cell-derived thymocyte activating factor (ETAF), a cytokine produced by keratinocytes, has previously been shown to be biochemically and functionally very similar, if not identical, to interleukin 1 (IL-1). Both ETAF and IL-1 have been demonstrated to be chemotactic for neutrophils and mononuclear cells in vitro. In order to demonstrate that this activity has physiological relevance we have used a simple in vivo model. The present study demonstrates that injection of high-titer ETAF or purified recombinant murine IL-1 into the mouse footpad results in an influx of neutrophils into the site with peak accumulation at 4 h. Footpad swelling also occurs with a time course roughly paralleling that of the neutrophil accumulation. Injection of control proteins failed to reproduce this phenomenon. Margination of neutrophils within blood vessels was seen within 1 h of injection of ETAF or IL-1, followed by entry into the stroma by 4 h. This suggests that chemotactic activity and not merely increased adherence or inhibition of migration is occurring. 5-10 d of daily, subcutaneous injection of ETAF on the mouse flank resulted in an infiltrate of neutrophils, and to a lesser degree, mononuclear cells in association with epidermal hyperplasia, subcutaneous fibrosis, and focal muscle necrosis in the panniculus carnosus. These findings were not seen in control sites injected with media. These findings provide direct in vivo experimental evidence suggesting a physiologic role for ETAF/IL-1 in local inflammation.

Subcutaneous implantation of osmotic pumps into CAF1 mice resulted in the formation of thick fibrous capsules around the pumps. When pumps were loaded with recombinant murine gamma-interferon (rMuIFN-gamma) to deliver 2 X 10(3) U/h for 14 d, there was a marked decrease in thickness and collagen content of the capsules from rMuIFN-gamma-treated animals compared with capsules from animals receiving diluent alone. The collagen content of the capsules was estimated by hydroxyproline analysis of the tissue and by quantitative electron microscopy of collagen bundles. Heat-inactivated rMuIFN-gamma failed to reduce the fibrotic response in this assay. These results provide compelling evidence that gamma-interferon can down-regulate collagen synthesis in vivo and suggest the possibility that this lymphokine may be useful in the treatment of disease states characterized by excessive fibrosis.

Four cases of neuroendocrine carcinomas (NECA) of the skin were studied by indirect immunofluorescence, using a monoclonal antikeratin antibody and a polyclonal antineurofilament antibody. Fifty to ninety percent and 80 to greater than 95% of the NECA cells stained with the antineurofilament antibody and the antikeratin antibody, respectively. Using double-labeling indirect immunofluorescence we could also demonstrate that, in 3 cases studied, some of the NECA cells, but not all, stained with both antikeratin and antineurofilament antibodies. These results, together with the recent knowledge of the intermediate filament protein type of normal Merkel cells (MC), tend to support the hypothesis that NECA cells do not originate from epithelial MC but from dermal neuroendocrine cells. A dual concept of intraepithelial MC and extraepithelial intradermal neuroendocrine cells, "from possible distinct origin," is proposed. Such a system has already been suggested for the neuroendocrine cells of the appendix and bronchial mucosae.

A peroxidase-antiperoxidase study using monoclonal antibodies directed against T and B lymphocytes and Langerhans cells/indeterminate cells (LC/IC) was undertaken in order to understand more clearly the changes observed in erythema multiforme. At the various stages of development, from normal skin to target lesions, the quantity of inflammatory cells differed, but in each case the number of T8+ (cytotoxic/suppressor) cells was greater than the number of T4+ (helper/inducer) cells in the epidermis, whereas the latter exceeded the former in the dermis. Concomitant with the initial epidermal changes, there was an increase in the number of T6+ (LC/IC) cells in the upper and lower epidermis. With slight to moderate basal unit destruction, the number of LC/IC in the upper epidermis exceeded those in the lower epidermis. With severe basal unit destruction, there was a loss of LC/IC in the lower epidermis as detected by T6 reactivity. In fully formed blisters, the LC/IC in the upper half of the epidermis were decreased in parallel with the degree of epidermal necrosis. The character of the lymphocytic inflammatory infiltrate and redistribution in LC/IC are similar to those findings described in allergic contact dermatitis. The clinical, histologic, and immunopathologic changes in erythema multiforme appear to be due in part to cellular immune mechanisms with the lymphocyte as the predominant effector cell, and our data suggest a possible role for LC/IC in this disorder.

Chancroid is a venereal disease caused by the microorganism Haemophilus ducreyi . Herein we present two cases of chancroid, with a review of the diagnostic laboratory tests, the treatment of this disease, and the differential diagnosis of genital ulcers.

Despite steady improvement in the laser treatment of port wine stains (PWS), hypertrophic scarring remains a serious side-effect in approximately 10% of patients. The tunable dye laser (577 nm) has been shown to cause selective vascular destruction in normal and PWS skin. We have treated ten patients using a tunable dye laser (577 nm, 300 mu sec) resulting in clearing of the PWS without any evidence of hypertrophic scarring. Treatment requires no anesthesia or wound care, and there were no postoperative infections.

DNA damage repaired by the excision repair system and measured as unscheduled DNA synthesis (UDS) was assessed in freshly excised human skin after 193 and 248 nm ultraviolet (UV)-excimer laser ablative incisions. Laser irradiation at 248 nm induced DNA damage throughout a zone of cells surrounding the ablated and heat-damaged area. In contrast, with 193 nm irradiation UDS was not detected in cells adjacent to the ablated area, even though DNA strongly absorbs this wavelength. Our results suggest that the lack of UDS after 193 nm irradiation is due to: (1) "shielding" of DNA by the cellular interstitium, membrane, and cytoplasm, (2) DNA damage that is not repaired by excision repair, or (3) thermal effects that either temporarily or permanently inhibit the excision repair processes.

A retrospective study of 21 patients with the histopathologic diagnosis of minimal deviation melanoma (MDM; n = 18) and borderline melanoma (BM; n = 3) was undertaken to determine the prognosis for these patients compared with that for patients with other types of malignant melanoma. The findings indicate that the prognosis for these uncommon nevomelanocytic tumors is somewhat better than that for other malignant melanomas. Follow-up periods in this series ranged from 18 to 96 months (mean, 57 months). Primary lesions ranged in thickness from 1.6 to 10.4 mm. The histopathologic subtypes included the Spitz variant (nine patients), the spindle cell variant (six patients), the combined spindle and epithelioid cell type (three patients), and the small epithelioid cell type (three patients). Only two of the patients died of widespread metastatic disease. Comparison of the histologic and clinical prognostic indicators of mortality in patients who have malignant melanoma with the clinical and pathologic features seen in this series of 21 patients would appear to indicate a diminished tendency toward metastatic or recurrent disease in patients with MDM and BM.

Ablation of human atheromas with laser pulses that had only a small effect on normal artery tissue was shown in vitro in air and under saline using 1-mu sec pulses at 465 nm from a flashlamp-excited dye laser. At this wavelength, there is preferential absorption in atheromas due to carotenoids. The threshold fluence for ablation was 6.8 +/- 2.0 J/cm2 for atheromas and 15.9 +/- 2.2 J/cm2 for normal aorta tissue. At a fluence of 18 J/cm2 per pulse, the ablated mass per unit of energy ranged from 161 to 370 micrograms/J for atheromas and from 50 to 74 micrograms/J for normal aorta tissue. Ablation products consisted of cholesterol crystals, shredded collagen fibers, and small bits of calcific material. Most debris was less than 100 micron in diameter, but a few pieces were as large as 300 micron. High-speed photography of ablation in air suggested explosive ejection of debris, caused by vapor formation, at speeds on the scale of 300 m/sec. Histological analysis showed minimal thermal damage to residual tissue. These data indicate that selective laser ablation of atheromas is possible in vitro.

Presentation of Case A 25-year-old woman was admitted to the hospital because of syncope. She was well until five days earlier, when she began to experience orthostatic dizziness, nausea, and sweating, accompanied by the passage of tarry stools. Crampy pain in both lower abdominal quadrants prompted the removal of an intrauterine device, which had been inserted one month earlier; there was no improvement in the symptoms. On the day of admission she lost consciousness while walking to work and was brought to the Emergency Ward. Grand-mal seizures developed when the patient was 11 years of age and were controlled with . . .

A patient with T4+ (helper-inducer) T cell chronic lymphocytic leukemia developed an erythema multiforme-like eruption, the diagnosis of which was supported by routine light microscopic findings. Immunopathologic studies using monoclonal antibodies demonstrate that despite an overwhelming majority of leukemic T4+ cells in the peripheral blood and dermal infiltrate, the predominant cells in the epidermal infiltrate are T8+ (cytotoxic-suppressor) cells. These findings are different from those seen in epidermotropic T cell leukemic infiltrates and are similar to those previously reported in erythema multiforme. Thus it is likely that the leukemic T4+ cells are participating in this cutaneous hypersensitivity reaction along with residual, normal T8+ cells.

The protective effect of a UVA (320-400 nm) induced tan against cutaneous injury by further UVA-irradiation was studied by evaluating the histopathologic changes in tanned and untanned normal human buttock skin 24 h after exposure to 2 and 4 minimal erythema doses of UVA. In each subject there were fewer polymorphonuclear leukocytes and less endothelial cell prominence and vessel wall necrosis in the UVA tanned skin than in the untanned UVA-irradiated skin. In the tanned control and tanned UVA-irradiated skin there was a prominent mononuclear cell inflammatory infiltrate that was much greater than in untanned skin. In immunoperoxidase stained tissue sections, the mononuclear cells were predominantly T cells, and in all of the specimens the number of phenotypic helper/inducer cells exceeded the phenotypic cytotoxic/suppressor cells. This demonstrates that a UVA tan provides photoprotection against acute UVA exposure. In addition, tanning, with or without further UVA-irradiation, was associated with a mononuclear cell inflammatory infiltrate.

Presentation of Case A 15-year-old boy was admitted to the hospital because of a progressive cutaneous disorder. He was born of an uneventful full-term third pregnancy and vaginal delivery and apparently developed normally as an infant. Soon after his first year of life hyperpigmented macules and hypopigmented papular lesions developed over the exposed areas of his skin and gradually spread to affect most of his body. At the age of three years he became blind in the right eye, and in more recent years vision was impaired in the left eye. He never attended school. Through the years his mother . . .

The ability of gamma interferon (IFN-gamma) to affect cutaneous collagen synthesis in vivo was examined in a murine wounding model. Reproducible areas of full-thickness skin necrosis were produced by argon laser radiation. Mice received recombinant murine IFN-gamma (rMuIFN-gamma) (8.7 X 10(3) units/hr) over 14 d via osmotic pumps implanted subcutaneously or intraperitoneally. At 14 and 21 d after wounding, there was less fibrous tissue in healing scars of treated animals as determined by light and transmission electron microscopy. Associated with the decrease in connective tissue was an increase in the acid mucopolysaccharide content of healing scars, which was largely hyaluronate. Quantitative image analysis of electron micrographs confirmed that less collagen was present in healing scars of animals receiving rMuIFN-gamma. The mean cross-sectional area of collagen fibers was smaller in specimens from treated mice, but no difference was seen in the size of collagen fibrils. The time required to obtain full skin closure was also delayed 23%-27% in treated animals. Using this injury model, we also found that rMuIFN-gamma significantly reduced the degree of perilesional erythema surrounding the laser injury sites and, in the first 6 d after wounding, the degree of polymorphonuclear infiltrate present histologically at lesional sites. Indeed, rMuIFN-gamma also decreased the cutaneous accumulation of neutrophils induced by known proinflammatory mediators, such as interleukin 1 and activated serum. Thus, systemically administered IFN-gamma not only down-regulates collagen synthesis in the skin but also modulates in a previously unrecognized manner: neutrophil accumulation at sites of tissue injury in vivo.

Exposure of skin to nanosecond-domain laser pulses affects the pigmentary system by a process called selective photothermolysis, in which melanosomes and pigmented cells are preferentially altered. Due to the broad absorption spectrum of melanin, this effect may occur with wavelengths that penetrate to vastly different depths within tissue, potentially producing different biologic responses. The effects of single near-ultraviolet (355 nm), visible (532 nm), and near infrared (1064 nm) pulses of 10-12 nsec duration were determined in guinea pig skin using gross, histologic, and electron microscopic observations. Threshold response in pigmented skin was a transient immediate ash-white discoloration, requiring 0.11, 0.20, and 1.0 J/cm2, at 355, 532, and 1064 nm, respectively. At each wavelength, melanosomes were ruptured within keratinocytes and melanocytes, with cytoplasmic and nuclear alterations. Delayed epidermal depigmentation occurred, followed by gradual repigmentation. Deep follicular cells were altered only at 532 and 1064 nm, which produced permanent leukotrichia. The action spectrum for threshold response was consistent with mechanisms implied by selective photothermolysis. These data may be useful for consideration of treatment for cutaneous pigmentation abnormalities or unwanted follicular pigmentation, or both.

The preponderance of malignant melanomas that occur in the Japanese population affect the palmar and plantar areas, in contrast to those of whites, which occur predominantly on the head, neck, and trunk. Furthermore, a precursor lesion, the dysplastic nevus, has been well defined in nonacral white skin but not in the Japanese. In this paper, a similarity between benign and atypical acral nevomelanocytic proliferations in Japanese and whites is described. However, it appears that in the Japanese group the melanocytes in benign and atypical proliferations are less dendritic than those noted in whites, and, in both groups, extensive pigmentation was noted in both the epidermal and dermal components of benign and malignant lesions in this limited review. A practical approach to classifications of atypism is, likewise, offered, J Invest Dermatol 92:222S–226S, 1989

Local exposure of the sites of elicitation (ears) of contact hypersensitivity (CHS) in mice to relatively modest doses of ultraviolet radiation (FS40 sunlamps) daily for 4 days prior to challenge in previously immunized animals results in significant enhancement of the CHS response as measured by 24-h swelling. This effect was seen in both C3H/HeJ and A/J mice and with the use of both trinitrochlorobenzene and dinitrofluorobenzene as contact sensitizers. Doses of PUVA (parenteral administration of 8-methoxypsoralen followed by exposure to UVA, 320-400 nm, radiation) up to that which can systemically suppress the induction of CHS failed to affect the elicitation of CHS. Irritation of the sites of elicitation of CHS by applications of turpentine also failed to affect the CHS elicitation reaction. Enhancement of the CHS elicitation response by local ultraviolet radiation exposure prior to challenge appears to be a specific photobiologic event.

The ability of cachectin/tumor necrosis factor (TNF alpha) to induce acute dermal and subcutaneous inflammation was examined in a murine model. A number of other proteins, and diluent alone were examined as controls. After subcutaneous injection into the mouse footpad, recombinant human TNF alpha (rHuTNF alpha) induced acute inflammation with an initial marked dermal and subcutaneous neutrophil infiltrate by approximately 3 h, with a peak between 4 and 24 h and resolution by 79 h. Recombinant interleukin-2, cytochrome c, and heat-inactivated rHuTNF alpha induced negligible inflammation. Recombinant human lymphotoxin (TNF beta), another control protein, also induced acute inflammation in our system. Because TNF alpha and TFN beta are partially homologous, they may be acting through a similar mechanism. This pro-inflammatory effect of TNF alpha may result from chemotactic activity as well as by induction of secondary mediators. Inflammation induced by TNF alpha was partially suppressed by indomethacin treatment, suggesting that products of the cyclo-oxyganase pathway may mediate a portion of the inflammation involved. Five daily injections of rHuTNF alpha into the mouse footpad resulted in a predominantly mononuclear infiltrate and focal fibrosis. These results suggest that TNF alpha may be an important mediator of acute inflammation in vivo and might provide a signal for the production of collagen.

Minimal deviation melanomas are uncommon nevomelanocytic tumors of indeterminate risk that appear as pigmented or nonpigmented skin nodules and are clinically diagnosed as Spitz nevi, hemangiomas, or malignant melanomas. They are characterized histologically by expansile growth in the papillary dermis with reticular dermal infiltration (minimal deviation type) or without reticular dermal invasion (borderline type). The tumors exhibit lesser cytologic atypia in their vertical growth phase (histologic variance) than observed in common forms of melanoma. A retrospective study of outcome in 21 patients with minimal deviation melanoma (mean tumor thickness by Breslow's measurement = 3.6 mm) disclosed recurrent disease in only 3 patients after a mean observation period of 57 months, supporting the impression that these tumors are not as biologically aggressive as common malignant melanomas. The histologic subtypes of minimal deviation melanoma are reviewed along with a discussion of the concept of histologic variance.

351 nm, 20-nsec XeF excimer laser irradiation has previously been shown to selectively target and damage melanosomes in human skin. In the following studies selective targeting with melanosomal photodisruption has been demonstrated in pigmented guinea pig skin with a Q-switched 40-nsec ruby laser, and a 750-nsec pulsed dye laser but not with a 400-usec pulsed dye laser. The pulse width dependence of melanosomal disruption, occurring only at pulsewidths shorter than the thermal relaxation time of the melanosome (0.5 - 1.0 usec), is in accordance with the theory of selective photothermolysis. Possible mechanisms of melanosomal photodisruption include development of sudden thermal gradients leading to cavitation or shock wave production.

Laser angioplasty, the in situ ablation of arterial obstructions with laser radiation, has been demonstrated in animal models and early clinical trials. A problem with this technique, however, is the possibility of thermal damage to adjacent or underlying normal tissues that also absorb the radiation. Using a spectrophotometer with an integrating sphere and a specially constructed tunable-dye laser-based spectrophotometer, we evaluated the transmittance and remittance of human cadaveric atheromas and adjacent normal aorta from 250 to 1,300 nm to identify wavebands where there is preferential light absorption by atheromas. Data were analyzed by both the Kubelka-Munk formalism and a Beer's law model. Both methods indicate that atheromas absorb more than normal aorta between 420 and 530 nm. At 470 nm the average Kubelka-Munk absorption coefficient of atheromas from 10 cadavers was 54 +/- 9 cm-1 compared with 26 +/- 6 cm-1 for normal aortic specimens from seven cadavers. Yellow chromophores responsible for the atheroma absorbance were extractable with xylenes. Thin-layer chromatography and absorption spectra identified the extracted chromophores as predominantly consisting of a mix of carotenoids, which are known constituents of atheromatous lesions. Preferential absorption of blue light by carotenoids in atheromas may permit selective ablation of atheromatous obstructions with appropriate pulses of laser radiation.

The skin of black and albino guinea pigs was irradiated with single, 750 nsec-long laser pulses at 435, 488, 530, and 560 nm in order to determine an action spectrum for the gross threshold response of immediate epidermal whitening. In addition, the immediate and delayed gross and histologic changes induced at, above, and below the threshold radiant exposures at all four wavelengths were studied. The action spectrum in the black guinea pigs was consistent with the reported absorption spectrum of DOPA-melanin. Histologically, there was epidermal damage immediately after radiant exposures at and above threshold at all four wavelengths. In addition, radiant exposures greater than threshold caused an immediate decrease in stainable epidermal pigment that was most marked at 435 and 488 nm. The healing response was also wavelength- and dose-dependent. Seven days after above-threshold exposures, there was little epidermal pigment in the 435 nm specimens. As wavelength increased, there was progressively more pigment, and in the 560 nm specimens, the epidermal pigment was equivalent to that seen in nonirradiated black guinea pig control specimens. Seven days after subthreshold radiant exposures, there was increased epidermal pigmentation and melanocytes at all four wavelengths. This was the most pronounced in the 435 nm specimens. There was no observable epidermal damage in albino guinea pig skin.

The specific targeting of melanosomes may allow for laser therapy of pigmented cutaneous lesions. The mechanism of selective destruction of pigmented cells by various lasers, however, has not been fully clarified. Black, brown, and albino guinea pigs were exposed to optical pulses at various radiant exposure doses from a Q-switched, 40 nsec, 694 rim ruby laser. Biopsies were analyzed by light and electron microscopy (EM). Albino animals failed to develop clinical or microscopic evidence of cutaneous injury after irradiation. In both black and brown animals, the clinical thresh- old for gross change was 0.4 J/cm2, which produced an ash-white spot. By light microscopy, alterations appeared at 0.3J/cm2 and included separation at the dermoepidermal junction, and the formation of vacuolated epidermal cells with a peripheral cytoplasmic condensation of pigment. By EM, enlarged melanosomes with a central lucent zone were observed within affected epidermal cells at 0.3J/cm2. At 0.8 and 1.2J/cm2, individual melanosomes were more intensely damaged and disruption of melanosomes deep in the hair papillae was observed. Dermal-epidermal blisters were formed precisely at the lamina lucida, leaving basal cell membranes and hemidesmosomes intact. Possible mechanisms for melanosomal injury are discussed. These observations show that the effects of the Q-switched ruby laser are melanin-specific and melanin-dependent, and may be useful in the selective destruction of pigmented as well as superficial cutaneous lesions.

• Q-switched ruby laser pulses cause selective damage to cutaneous pigmented cells. Repair of this selective damage has not been well described. Therefore, using epilated pigmented and albino guinea pig skin, we studied the acute injury and tissue repair caused by 40-ns, Q-switched ruby laser pulses. Gross observation and light and electron microscopy were performed. No specific changes were evident in the albino guinea pigs. In pigmented animals, with radiant exposures of 0.4 J/cm 2 or greater, white spots confined to the 2.5-mm exposure sites developed immediately and faded over 20 minutes. Delayed depigmentation occurred at seven to ten days, followed by full repigmentation by four to eight weeks. Regrowing hairs in sites irradiated at and above 0.4 J/cm 2 remained white for at least four months. Histologically, vacuolation of pigment-laden cells was seen immediately in the epidermis and the follicular epithelium at exposures of 0.3 J/cm 2 and greater. Melanosomal disruption was seen immediately by electron microscopy at and above 0.3 J/cm 2 . Over the next seven days, epidermal necrosis was followed by regeneration of a depigmented epidermis. By four months, melanosomes and melanin pigmentation had returned; however, hair follicles remained depigmented and devoid of melanocytes. This study demonstrates that selective melanosomal disruption caused by Q-switched ruby laser pulses leads to transient cutaneous depigmentation and persistent follicular depigmentation. Potential exists for selective treatment of pigmented epidermal and dermal lesions with this modality. ( Arch Dermatol 1989;125:43-49)

• Although the blue-green argon laser light has been used successfully to treat port-wine stains (PWSs) for many years, it produces substantial epidermal damage. We have previously shown in normal human skin that pulsed yellow tunable dye lasers (577-nm wavelength) can cause highly selective damage to cutaneous microvessels with minimal injury to the overlying epidermis. Pulsed tunable dye lasers also produce selective vascular injury in the abnormal vessels of PWSs, with clinically apparent lightening of the lesions. Both epidermal injury and fibrosis are less severe with this laser treatment than with argon and carbon dioxide laser treatments. Clinical and histologic responses of PWSs treated by argon, CO 2 , and pulsed yellow dye lasers were compared and followed up for one month in three patients. Although larger and longer-term clinical trials are necessary to fully evaluate this new treatment modality, it appears that pulsed yellow laser radiation offers a more selective, less traumatic, and probably superior form of treatment for PWSs. ( Arch Dermatol 1986;122:1016-1022)

To the Editor.— Erythropoietic protoporphyria (EPP) is an inherited disorder of porphyrin metabolism resulting in the elevation of red blood cell, plasma, and fecal protoporphyrin levels, plus cutaneous photosensitivity. The most common symptoms are painful burning and pruritus of exposed skin, often arising within minutes of exposure to ultraviolet light. Acute skin findings may include erythema or edema. However, skin lesions following attacks may be subtle or absent.1,2 The onset of symptoms in EPP is normally in infancy or in early childhood on first exposure to sunlight; it is rare for initial symptoms to occur late in life.3The most common of the porphyrias to present in adulthood is porphyria cutanea tarda. This porphyria typically presents in middle age, and is commonly associated with alcohol abuse or diabetes mellitus. Skin manifestations include vesicles, bullae, and milia, and scarring in sun-exposed skin, as well as increased skin fragility, sclerotic