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Background The removal of unwanted hair with various laser systems and related procedures has been investigated for many years. All researchers have met difficulty when trying to achieve "permanent" hair removal. In addition, damage to the epidermis and other complications, including hyper- or hypopigmentation in pigmented skin, have occurred because the laser energy was applied indirectly to the hair bulb through the epidermis. Objective To achieve permanent hair removal with the use of a diode-pumped neodymium:yttrium-aluminum-garnet laser system with an insulated optical needle. Also, to establish laser treatment parameters that allow for quick and effective removal of hair with minimal pain and no long-term medical complications. Method The laser used in the study was capable of producing up to 500 mJ of energy per burst at a 1,064-nm wavelength. A pulse width of 200-500 μs and a burst frequency of 100-200 Hz could be selected, and both defined a subset of the treatment parameter space. An optical needle, typically 130 μm in diameter, was prepared before each new treatment was conducted. Three bursts of energy, 300 mJ each, with a 300-millisecond interval, were delivered through the optical needle into each hair follicle. Between 200 and 300 shin hairs, typically terminal hairs, on each of 5 volunteers were treated. These volunteers were observed over 18.5-30 months for the regrowth of hairs by hair count. Results At the end of the observation period (6-30 months after the last treatment), 3 of 5 volunteers showed permanent loss of 76%-94.3% of their unwanted hair. One volunteer lost 34.8% of the original hair, but regrown hair was much thinner than the original terminal hair. One volunteer lost only 22.8% of the original hair, and regrown hair was coarse terminal hair. Except for the loss of hair, no change in skin texture, sensation, or skin color was observed. Conclusion The direct insertion optical method (DIOM), delivering laser energy directly to the hair bulb through an optical needle, has proven to be effective and achieves permanent hair removal in 60% of volunteers without medical complications.

Linear focal elastosis and striae distensae coexisted in a 32-year-old black man in their typical distribution on the lower back. Many striae appeared when he lost 50 lb in 1991. Only some of them became hypertrophic and others remained atrophic; striae distensae of the shoulders and buttocks remained atrophic, whereas most in the lumbosacral region became indurated and cordlike. Histologically, the former lacked elastic fibers and the latter showed a marked increase in thick elastic fibers. Linear focal elastosis in some patients may represent hyperplasia of elastic fibers in response to their damage. This "elastic fiber keloid" seems to be equivalent to collagen keloid, i.e., ordinary keloid, in the lumbosacral region. (J Am Acad Dermatol 1998;39:309-13.)

We report the sixth case of linear focal elastosis. Our patient is a thin 29-year-old black man who was first seen with rows of papules with a yellow hue distributed symmetrically on the lumbar region of the back. The patient had been aware of these lesions since early childhood, and similar lesions reportedly had occurred in his late father. Light microscopic examination demonstrated dermal thickening but no change in the epidermis. The elastic tissue stain revealed fragmented elastic fibers throughout the dermis. This case meets previously defined diagnostic criteria for linear focal elastosis, which has been reported as isolated cases in elderly white or Japanese men. Our patient is the first young black man with a possible familial association.

Pemphigoid vegetans is a rare disease; only four cases have been reported. The relationship of pemphigoid vegetans to bullous pemphigoid is not completely defined. We describe a case in a 77-year-old woman who had multiple well-circumscribed, erythematous, erosive, and vegetating plaques in the axillae and inframammary areas and in the neck. Microscopic examination revealed epidermal hyperplasia, dermoepidermal junctional separation, and prominent dermal eosinophilia. In the perilesional skin IgG was deposited linearly at the basement membrane zone. In addition, our patient's IgG autoantibodies, primarily the IgG4 subclass, reacted with the epidermal side of salt-split normal human skin and with the 230 kd major bullous pemphigoid antigen. We conclude that pemphigoid vegetans is best classified as a bullous pemphigoid variant.

Four cases of benign Langerhans cell histiocytosis limited to the skin were studied. In all three self-healing cases (cases 2, 3, and 4) many dense bodies, myelin bodies, and worm bodies were found. In one chronic case (case 1) none of these was identified. In all four cases, in addition to CD1, HLA-DR, and S-100 stains, interferon-gamma and S-100 beta-subunit were positive in the dermal tumor cells. Both interferon-gamma and S-100 beta-subunits were negative in the normal epidermal Langerhans cells. A comprehensive literature review yielded 87 cases of skin-limited Langerhans cell histiocytosis. These cases could be subgrouped into three categories: (1) those that resolved spontaneously, (2) those that responded to therapy and had no recurrence, and (3) those with persistent or recurrent lesions, not responding to therapy but still limited to the skin.

We observed a 40-year-old woman with necrobiotic xanthogranuloma from the inception of indurated eyelid and periorbital infiltrates and concurrent stage I multiple myeloma to resolution of infiltrates in skin and bone marrow after pulsed high-dose oral dexamethasone therapy. Ultrastructural studies revealed lipid vacuoles in epidermal keratinocytes, in dermal histiocytic macrophages, and in vascular and lymphatic endothelial cells. The presence of lipid vacuoles in epidermal keratinocytes has not been reported previously in xanthogranuloma.

The treatment of scleromyxedema has been largely ineffective. We report improvement of scleromyxedema with myopathy after treatment with isotretinoin, 40 mg twice a day. We review other therapeutic modalities used for this disorder and discuss properties of isotretinoin that may have contributed to the favorable response.

Peeling skin syndrome is a rare autosomal recessive disease characterized by widespread painless peeling of the skin in superficial sheets. We describe a 34-year-old man with a lifelong history of spontaneous asymptomatic peeling skin limited to the acral surfaces. This patient probably represents a localized variant of peeling skin syndrome, which has previously been described as a generalized condition. Light and electron microscopic studies of biopsy specimens taken before and after immersion in water were performed. It was concluded that this patient has abnormal keratohyalin granules and inadequate aggregation of keratin filaments that caused the separation of the epidermis in the stratum corneum through the clear zone. Alternatively, unknown keratin species expressed in the clear zone may also cause the abnormality. (J Am Acad Dermatol 2000;43:1112-9.).

We describe the second example of familial nevus sebaceus in a boy and his maternal half-brother .

Human T-lymphotropic virus type I (HTLV-I) is the etiologic agent of HTLV-I associated myelopathy (HAM)/tropical spastic paresis (TSP), and adult T-cell leukemia/lymphoma (ATLL). ATLL has been associated with HTLV-I in the southeastern United States. However, to our knowledge, no case reports of HAM/TSP in association with ATLL occurring in the United States have been described. We describe a 40-year-old black woman with a 10-year history of recalcitrant psoriasiform eruption and erythrodermic flares. Medical history is additionally significant for a 2-year history of HTLV-I-associated myelopathy and lower extremity spastic paresis. Polymerase chain reaction with Southern blot analysis was used to detect HTLV-I proviral genome from frozen skin biopsy specimens and peripheral blood mononuclear cells.

A 48-year-old white woman, skin type III, had a slate-gray discoloration of the face and dorsa of both hands after ingesting imipramine, 150 mg/day for 5 years. Her iris color was also darkened. One year after cessation of the therapy, the discoloration became lighter. Sun-protected skin showed no discoloration. Light microscopy revealed an accumulation of doubly refractile golden yellow granules in the papillary dermis, mostly scattered, with some concentration around the blood vessels but not in the endothelial cells. Electron micrographs showed numerous amorphous electron-dense inclusion bodies in histiocytes, phagocytes, fibroblasts, and dermal dendrocytes. Melanosomes were phagocytosed in the same cells but in separated locations. Imipramine is structurally related to ehlorprornazine and can cause slate-gray discoloration. However, the color of the granules deposited in the papillary dermis is golden-yellow and they are not deposited in endothelial cells.

Diffuse neonatal hemangiomatosis is a rare, frequently fatal disease characterized by multiple cutaneous and visceral hemangiomas. The skin, liver, lungs, intestines, and central nervous system are the most commonly affected organs. Death can result from high-output cardiac failure as a result of arteriovenous shunting. In this report we present a new constellation of findings in a patient with diffuse neonatal hemangiomatosis, namely, an absent corpus callosum, ectopia cordis (sternal agenesis) with median abdominal raphe, and tricuspid atresia.

A new case of congenital self-healing reticulohistiocytosis was studied with S-100 antibody and electron microscopy. Many tumor cells were 5-100-positive and contained Langerhans cell (LC) granules and concentrically laminated dense bodies. Octopus-like bodies and wormlike bodies were also found. The formation of LC granules at the cytomembrane was frequently found, not only between the cytomembrane and its own villi, but also between the cytomembranes of adjoining cells. These findings strongly support the cytomembrane origin of LC granules in general.

Two cases of transient bullous dermolysis of the newborn are reported. The first patient, a white boy, had normal skin at birth, but multiple blisters soon developed. The oral mucous membranes were not affected. All lesions healed within 4 months without scars but with many milia. At the age of 17 months the boy was reexamined and was found to have no blisters or milia. The second patient, a Japanese baby girl, had extensive denudation of her hands at birth. Generalized blisters and involvement of the oral mucous membrane developed. Blistering stopped within 1 1/4 months, and all lesions healed without scars. Histologically the blisters were subepidermal in both cases. Some lesional basal cells contained periodic acid-Schiff-positive inclusions. Electron microscopy revealed collagenolysis, diminution or loss of anchoring fibrils, and stellate inclusions in dilated rough endoplasmic reticulum in the keratinocytes of the lower epidermis. These stellate inclusions consisted of filamentous bundles with 25 to 33 nm cross-striations.

A lupuslike disease with cutaneous manifestations secondary to the use of chlorpromazine (Thorazine) is presented. Skin biopsy specimens demonstrated classic findings consistent with lupus erythematosus and abundant mucin deposition in the cutaneous lesions—a finding not previously reported to occur in drug-induced lupuslike disease. Laboratory and serologic examinations included a positive antinuclear antibody titer, presence of single-stranded deoxyribonucleic acid (DNA), absence of double-stranded DNA, presence of antihistone antibodies, normal complement level, increased IgM level, and prolongation of partial thromboplastin time. These data confirmed our clinical and histologic diagnosis. Cessation of the medication (chlorpromazine) led to resolution of the skin abnormalities. Electron microscopy revealed electrondense drug metabolites in vascular endothelial cells, as well as tubuloreticular inclusion bodies. This is only the second reported case of chlorpromazineinduced lupuslike disease with cutaneous manifestations.

Milia developed in two patients with different chronic dermatoses after 2 weeks of treatment with clobetasol propionate ointment. Routine histologic and immunohistochem-ical analysis showed the cysts to be of eccrine gland origin.

Several skin diseases and tumors were immunohistochemically studied with the use of monoclonal antibodies against myelin proteins and neurofilament proteins. In prurigo nodularis, many nerve fibers were found embedded in dense inflammatory cell infiltration. Abnormal innervation was observed in piloleiomyoma. The axons were demonstrated within the cytoplasm of granular cells of granular cell schwannoma. In neurofibroma, tumor cells had myelin proteins in their cytoplasms. Many cells and fibers that contained myelin proteins were demonstrated in nevus cell nevus, especially in compound nevus and intradermal nevus, and it was suggested that schwannian cells may be the origin of some nevus cells.

A 30-year-old patient had a linear lesion involving the forearm and hand for 30 years. Histologic examination of this lesion revealed hyperkeratosis, hypergranulosis, and acanthosis. There also were funnel-shaped areas of epidermal depression containing parakeratotic columns which penetrated hair follicles and sweat ducts. The differential diagnosis of this lesion is discussed.

Three cases of d-penicillamine-induced skin lesions, two hemorrhagic and one elastosis perforans serpiginosa (EPS)—like, were examined with the electron microscope. In hemorrhagic lesions elastic fibers were diminished. In EPS lesions elastic fibers were remarkably increased in the papillary and reticular dermis. These appeared bramble bush—like with elastic fiber stains as described by Lund. Ultrastructurally, the bramble bush fibers consisted of near-normal core and abnormal coat which is medium electron—dense and lacks the alternating pattern of dense and light layers of the normal dermal elastic fibers. The "thorns" were formed as regular swellings of this coating material at regular intervals and at a right angle to the long axis of these fibers. In some fibers the coating material did not encircle the entire circumference of the core, suggesting that it was added upon the normal elastic fiber after the disease process began. Elastic fibers in the perforation canal through the epidermis were either intact bramble bush fiber or degeneration of it. Collagen fibers in both hemorrhagic and EPS lesions were poorly stained with routine electron microscopic stains. The most striking abnormality was an extreme variation of thickness of individual fibers ranging from 0.01 μm to 0.05 μm. Banding patterns and periodicity were normal. Subendothelial separation of vascular endothelial cells in small vessels and actual degeneration of subendothelial elastic fibers (internal elastic membrane) in larger vessels seem to be the basic defect in hemorrhagic lesions. Elastosis perforans serpiginosa seems to be a phenomenon caused by a variety of abnormal elastic fibers. Clearly, the ones in our case are completely different from idiopathic ones. It is assumed that any abnormal elastic fibers which elicit foreign body recognition by the host are commonly eliminated through this phenomenon.