1Westchester Health Associates, Dermatology and Mohs Surgery, Mount Kisco, New York 2Riverchase Dermatology and Cosmetic Surgery, Naples, Florida Address correspondence and reprint requests to: Daniel I. Wasserman, MD, Riverchase Dermatology and Cosmetic Surgery, 261 9th St S, Naples, FL 34102, or e-mail: [email protected] The authors have indicated no significant interest with commercial supporters.

Liposuction is currently the “gold standard” for fat reduction offered by physicians. The growing demand for less invasive procedures has led to a sudden growth of noninvasive alternatives during the past 5 years. Despite being readily available, many of these noninvasive technologies have not been thoroughly evaluated for their short-term and long-term efficacy. To review the varying mechanisms and literature of the commercially available noninvasive body sculpting technologies, specifically radiofrequency, ultrasound, lasers and light, and cryolipolysis. A literature search was performed and evaluated for relevant studies regarding radiofrequency, ultrasound, laser and light, and cryolipolysis technologies for the treatment of body shaping. Patients treated with radiofrequency usually receive 2 months of treatments, with improvements decreasing after 6 months. Multiple studies using ultrasound treatments showed a statistical significant decrease in waist circumference. However, these improvements diminished after 6-month follow-up. Previous studies analyzing laser treatment show mixed results. Studies involving cryolipolysis are limited but show decrease in fat thickness. Noninvasive body sculpting technologies are still early in their commercial development. Additional research is needed to assess efficacy and safety. Early results thus far are encouraging for some of these technologies, but their commercial acceptance appears to have outpaced their scientific scrutiny.

The introduction of the theory of selective photothermolysis has brought to medicine an entirely new therapeutic modality for treating cutaneous disorders. With ongoing research into existing therapies, cutaneous laser medicine is experiencing an expansion in application and safety profiles for many existing technologies. Additional trials and reports have also deepened our understanding and broadened our use for many existing cutaneous laser applications, such as for the treatment of pigment disorders, scarring, vascular disorders and noninvasive removal of fat. Recent data has demonstrated a valuable role of combined pharmacologic and laser modalities for the treatment of vascular malformations. This article will review recent developments of cutaneous laser science and technologies over the last several years, including such innovations as fractional photothermolysis and cryolipolysis.

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The introduction of the theory of selective photothermolysis has brought to medicine an entirely new therapeutic modality for treating cutaneous disorders. With ongoing research into existing therapies, cutaneous laser medicine is experiencing an expansion in application and safety profiles for many existing technologies. Additional trials and reports have also deepened our understanding and broadened our use for many existing cutaneous laser applications, such as for the treatment of pigment disorders, scarring, vascular disorders and noninvasive removal of fat. Recent data has demonstrated a valuable role of combined pharmacologic and laser modalities for the treatment of vascular malformations. This article will review recent developments of cutaneous laser science and technologies over the last several years, including such innovations as fractional photothermolysis and cryolipolysis.

DUSA Pharmaceuticals donated the Kerasticks and the light source for this study.

Controlled cold exposure has long been reported to be a cause of panniculitis in cases such as popsicle panniculitis. Cryolipolysis is a new technology that uses cold exposure, or energy extraction, to result in localized panniculitis and modulation of fat. Presently, the Zeltiq cryolipolysis device is FDA cleared for skin cooling, as well as various other indications, but not for lipolysis. There is, however, a pending premarket notification for noninvasive fat layer reduction. Initial animal and human studies have demonstrated significant reductions in the superficial fat layer thickness, ranging from 20% to 80%, following a single cryolipolysis treatment. The decrease in fat thickness occurs gradually over the first 3 months following treatment, and is most pronounced in patients with limited, discrete fat bulges. Erythema of the skin, bruising, and temporary numbness at the treatment site are commonly observed following treatment with the device, though these effects largely resolve in approximately 1 week. To date, there have been no reports of scarring, ulceration, or alterations in blood lipid or liver function profiles. Cryolipolysis is a new, noninvasive treatment option that may be of benefit in the treatment of excess adipose tissue.

This case describes an unusual presentation of dermatomyositis in a patient with ovarian carcinoma. The eruption appeared as a venous stasislike dermatitis. The temporal sequence of onset after chemotherapy administration suggested a possible drug-induced process. However, in the context of underlying ovarian carcinoma, a paraneoplastic process offered an alternative explanation for the dermatomyositis.

To the Editor: Hypopigmented mycosis fungoides (MF) is a rare variant of MF, described mostly in patients of Asian or African descent.1Qari M.S. Li N. Demierre M.F. Hypopigmented mycosis fungoides and literature review.J Cut Med Surg. 2000; 4: 142-148PubMed Google Scholar The pathogenesis of hypopigmented MF remains to be elucidated. The hypopigmentation is thought to be caused by the cytotoxic effect of T-suppressor lymphocytes on the surrounding melanocytes. The condition is easily misdiagnosed.1Qari M.S. Li N. Demierre M.F. Hypopigmented mycosis fungoides and literature review.J Cut Med Surg. 2000; 4: 142-148PubMed Google Scholar, 2Sezer E. Sezer T. Senavli A. Koseoglu D. Filiz N. Hypopigmented mycosis fungoides in a Caucasian child.Eur J Dermatol. 2006; 16: 584PubMed Google Scholar The exact incidence of hypopigmented MF is still unknown, likely because of under- or misdiagnosis. Biopsy of early hypopigmented MF may initially suggest T-cell dyscrasia, later progressing into MF. Because of the risk of lymphoma, tumor necrosis factor-alfa (TNF-α) inhibitors, such as infliximab, adalimumab, and etanercept, are typically avoided in patients with history of systemic lymphoma. There are a few reports of infliximab and adalimumab treatment associated with the onset or exacerbation of cutaneous T-cell lymphoma.3Dalle S. Balme B. Berger F. Hayett S. Thomas L. Mycosis fungoides–associated follicular mucinosis under adalimumab.Br J Dermatol. 2005; 153: 207-208Crossref PubMed Scopus (34) Google Scholar, 4Sanli H. Ataman S. Akay B.N. Yilmaz A. Yildizlar D. Gurgey E. Mycosis fungoides in a patient with ankylosing spondylitis during infliximab therapy.J Drugs Dermatol. 2007; 6: 834-836PubMed Google ScholarHere we report a case of hypopigmented T-cell dyscrasia on the skin that progressed to hypopigmented MF after etanercept treatment over a 6-month period. The patient is a 61-year-old African American female with a history of seronegative rheumatoid arthritis who presented to the dermatology department with a 20-year history of a few pruritic hypopigmented patches on her face, trunk, and extremities (Fig 1). Although T-cell dyscrasia was suspected 7 years before the initiation of etanercept, multiple skin biopsies were nondiagnostic. For the arthopathy, the patient was treated initially with methotrexate and later switched to etanercept for 6 months. After initiating etanercept, the patient reported an increasing number of hypopigmented patches with a worsening of pruritus. After 6 months of twice-weekly etanercept injections, physical examination of the chest, back, arms, and legs revealed multiple 1- to 10-cm hypopigmented patches with no scale. No ectropion, alopecia, or lymphadenopathy was noted.A punch biopsy taken from the left back revealed atypical lymphoid epidermotropism consistent with cutaneous T-cell lymphoma (Fig 2, A). The specimen was noted to exhibit mild to moderate superficial perivascular atypical lymphocyte infiltrate with alignment along the basement membrane zone with vacuolization and epidermotropism with focal Pautrier microabscess, coarse papillary dermal fibrosis, and occasional plasma cell and numerous melanophages, consistent with the diagnosis of MF (Fig 2, B).Fig 2A, Subtle alignment of lymphocytes with halos along the dermoepidermal junction. B, Focal intraepidermal aggregate of atypical lymphocytes (Pautrier microabscess). (Hematoxylin–eosin stain; original magnification: A, ×20; B, ×40.)View Large Image Figure ViewerDownload Hi-res image Download (PPT)A follow-up T-cell flow cytometry panel supported the diagnosis of MF. Etanercept was discontinued. The patient was placed back on methotrexate and ultraviolet phototherapy with reduction of pruritus and number of lesions.In hypopigmented MF, the predominant location of the persistent hypopigmented lesions on nonphotodistributed areas of the body is a clue to diagnosis. Pruritus is a commonly associated symptom. In this case, the patient was started on etanercept, a TNF-α inhibitor, for rheumatoid arthritis, which worsened her pruritus and increased the number of hypopigmented lesions. A worsening of systemic lymphoma is a well known risk of TNF-α blockers. There have been few reports of onset or worsening MF variants associated with treatment with other TNF-α blockers including infliximab and adalimumab.3Dalle S. Balme B. Berger F. Hayett S. Thomas L. Mycosis fungoides–associated follicular mucinosis under adalimumab.Br J Dermatol. 2005; 153: 207-208Crossref PubMed Scopus (34) Google Scholar, 4Sanli H. Ataman S. Akay B.N. Yilmaz A. Yildizlar D. Gurgey E. Mycosis fungoides in a patient with ankylosing spondylitis during infliximab therapy.J Drugs Dermatol. 2007; 6: 834-836PubMed Google Scholar The hypopigmented variant joins the list of subtypes of MF unmasked by the initiation of etanercept treatment. To the Editor: Hypopigmented mycosis fungoides (MF) is a rare variant of MF, described mostly in patients of Asian or African descent.1Qari M.S. Li N. Demierre M.F. Hypopigmented mycosis fungoides and literature review.J Cut Med Surg. 2000; 4: 142-148PubMed Google Scholar The pathogenesis of hypopigmented MF remains to be elucidated. The hypopigmentation is thought to be caused by the cytotoxic effect of T-suppressor lymphocytes on the surrounding melanocytes. The condition is easily misdiagnosed.1Qari M.S. Li N. Demierre M.F. Hypopigmented mycosis fungoides and literature review.J Cut Med Surg. 2000; 4: 142-148PubMed Google Scholar, 2Sezer E. Sezer T. Senavli A. Koseoglu D. Filiz N. Hypopigmented mycosis fungoides in a Caucasian child.Eur J Dermatol. 2006; 16: 584PubMed Google Scholar The exact incidence of hypopigmented MF is still unknown, likely because of under- or misdiagnosis. Biopsy of early hypopigmented MF may initially suggest T-cell dyscrasia, later progressing into MF. Because of the risk of lymphoma, tumor necrosis factor-alfa (TNF-α) inhibitors, such as infliximab, adalimumab, and etanercept, are typically avoided in patients with history of systemic lymphoma. There are a few reports of infliximab and adalimumab treatment associated with the onset or exacerbation of cutaneous T-cell lymphoma.3Dalle S. Balme B. Berger F. Hayett S. Thomas L. Mycosis fungoides–associated follicular mucinosis under adalimumab.Br J Dermatol. 2005; 153: 207-208Crossref PubMed Scopus (34) Google Scholar, 4Sanli H. Ataman S. Akay B.N. Yilmaz A. Yildizlar D. Gurgey E. Mycosis fungoides in a patient with ankylosing spondylitis during infliximab therapy.J Drugs Dermatol. 2007; 6: 834-836PubMed Google Scholar Here we report a case of hypopigmented T-cell dyscrasia on the skin that progressed to hypopigmented MF after etanercept treatment over a 6-month period. The patient is a 61-year-old African American female with a history of seronegative rheumatoid arthritis who presented to the dermatology department with a 20-year history of a few pruritic hypopigmented patches on her face, trunk, and extremities (Fig 1). Although T-cell dyscrasia was suspected 7 years before the initiation of etanercept, multiple skin biopsies were nondiagnostic. For the arthopathy, the patient was treated initially with methotrexate and later switched to etanercept for 6 months. After initiating etanercept, the patient reported an increasing number of hypopigmented patches with a worsening of pruritus. After 6 months of twice-weekly etanercept injections, physical examination of the chest, back, arms, and legs revealed multiple 1- to 10-cm hypopigmented patches with no scale. No ectropion, alopecia, or lymphadenopathy was noted. A punch biopsy taken from the left back revealed atypical lymphoid epidermotropism consistent with cutaneous T-cell lymphoma (Fig 2, A). The specimen was noted to exhibit mild to moderate superficial perivascular atypical lymphocyte infiltrate with alignment along the basement membrane zone with vacuolization and epidermotropism with focal Pautrier microabscess, coarse papillary dermal fibrosis, and occasional plasma cell and numerous melanophages, consistent with the diagnosis of MF (Fig 2, B). A follow-up T-cell flow cytometry panel supported the diagnosis of MF. Etanercept was discontinued. The patient was placed back on methotrexate and ultraviolet phototherapy with reduction of pruritus and number of lesions. In hypopigmented MF, the predominant location of the persistent hypopigmented lesions on nonphotodistributed areas of the body is a clue to diagnosis. Pruritus is a commonly associated symptom. In this case, the patient was started on etanercept, a TNF-α inhibitor, for rheumatoid arthritis, which worsened her pruritus and increased the number of hypopigmented lesions. A worsening of systemic lymphoma is a well known risk of TNF-α blockers. There have been few reports of onset or worsening MF variants associated with treatment with other TNF-α blockers including infliximab and adalimumab.3Dalle S. Balme B. Berger F. Hayett S. Thomas L. Mycosis fungoides–associated follicular mucinosis under adalimumab.Br J Dermatol. 2005; 153: 207-208Crossref PubMed Scopus (34) Google Scholar, 4Sanli H. Ataman S. Akay B.N. Yilmaz A. Yildizlar D. Gurgey E. Mycosis fungoides in a patient with ankylosing spondylitis during infliximab therapy.J Drugs Dermatol. 2007; 6: 834-836PubMed Google Scholar The hypopigmented variant joins the list of subtypes of MF unmasked by the initiation of etanercept treatment.

Keratitis-ichthyosis-deafness syndrome is a rare congenital ectodermal disorder, characterized by presence of skin lesions, neurosensory hearing loss, and vascularizing keratitis. Several autosomal dominant mutations in the Connexin 26 gene (GJB2) have been discovered as a cause of this syndrome. We report two patients who presented with a combination of clinical features of keratitis-ichthyosis-deafness syndrome (e.g., congenital bilateral neurosensory hearing loss and erythrokeratoderma), however, lacking other characteristics typical of this condition. In addition, they both demonstrated striking mucocutaneous findings (e.g., chronic lip fissuring, gingival hyperemia), resulting in diagnostic difficulties. In both patients, a GJB2 mutation (N14K) was identified, which shares the same gene with classic Keratitis-ichthyosis-deafness syndrome but has never been described in patients with this condition. We propose that the findings observed in our patients are a distinct subtype of Keratitis-ichthyosis-deafness syndrome, thus expanding the spectrum of connexin-associated keratodermias.

The authors have indicated no significant interest with commercial supporters.

WASSERMAN, DANIEL I. MD*1; SACK, JASON MD*1; GONZALEZ-SERVA, ALDO MD†; KONNIKOV, NELLIE MD‡; BOHAC, GERRY MD§; DEMIERRE, MARIE-FRANCE MD, FRCPC* Author Information

Objective: The objective of this study was to characterize the temporal bone phenotype associated with a mutation of GJB2 (encoding connexin 26). Study Design: The authors conducted correlative clinical, molecular genetic, and postmortem histopathologic analysis. Methods: The study subject was a male infant with keratitis-ichthyosis-deafness (KID) syndrome. We performed a nucleotide sequence analysis of GJB2 and a histopathologic analysis of the temporal bones. Results: The subject was heterozygous for G45E, a previously reported KID syndrome mutation of GJB2. The primary inner ear abnormality was dysplasia of the cochlear and saccular neuroepithelium. Conclusions: GJB2 mutations can cause deafness in KID syndrome, and possibly in other GJB2 mutant phenotypes, by disrupting cochlear differentiation.