Concomitant Cutaneous Langerhans Cell Hystiocytosis and Leukemia Cutis.

Leukemia cutis develops in <4% of all acute leukemias. Concurrent acute myeloid leukemia (AML) and Langerhans cell histiocytosis (LCH) is rare, with most cases involving lymph nodes or spleen, and no cutaneous involvement. We report the case of a 59-year-old man who presented with fever, malaise, and fatigue. The CBC showed leukocytosis (30.4 × 10/L, 9% blasts), anemia, and thrombocytopenia. Bone marrow biopsy was diagnosed with AML, not otherwise specified, with mutations of FLT3 and IDH2 (R140Q). The patient developed skin rash on the right flank with the clinical differential diagnosis of herpes simplex virus or varicella-zoster virus infection/reactivation versus leukemia cutis. A skin biopsy showed leukemia cutis in mid and deep dermis. Immunohistochemistry positive for CD4, CD33, CD117, and myeloperoxidase (MPO) supported myeloid and monocytic differentiation. Clusters of Langerhans cells positive for S100, CD1a, CD4, langerin and aberrant CD33 and MPO were found admixed with the AML cells. Langerhans cells were negative for BRAF V600E by immunohistochemistry. The diagnosis of leukemia cutis and concomitant LCH was established. The aberrant expression of CD33 and MPO shared by AML and LCH suggests a possible relationship among these 2 lesions. No LCH or Langerhans cell differentiation was found in the bone marrow. The patient achieved complete remission 4 months after chemotherapy and the skin lesions resolved. To our knowledge, we present for the first time a case of concomitant cutaneous LCH and leukemia cutis.

Paradoxical adipose hyperplasia secondary to cryolipolysis: An underreported entity?

BACKGROUND AND OBJECTIVE: Cryolipolysis is a non-invasive, safe, and effective treatment for localized fat reduction. Paradoxical adipose hyperplasia (PAH) is a rare adverse effect in which patients develop painless, firm, and well-demarcated tissue masses in the treatment areas approximately 3-6 months following cryolipolysis. The incidence of PAH has been estimated at 0.0051% or 1 in 20,000 treated patients. We report two cases of PAH seen in our practice, which may suggest the incidence is greater than previously reported. STUDY DESIGN/PATIENTS AND METHODS: A 44-year-old man underwent cryolipolysis for unwanted fat in the pectoral region. At 4 month follow-up, the patient had well-demarcated tissue growth in the treatment areas. He elected to undergo additional cryolipolysis treatment to the areas. Two months later, he was found to have further tissue growth in the treatment areas. The patient then underwent corrective treatment with liposuction. A 52-year-old man underwent cryolipolysis for unwanted lower abdominal fat. At one year follow-up, he had a well-demarcated, subcutaneous mass on the lower abdomen corresponding to the treatment site. The patient elected to undergo corrective treatment with liposuction. Adipose tissue samples from the treated and non-treated areas, for control, were collected, processed, and stained to evaluate cellularity and tissue structure. RESULTS: In our practice, the incidence of PAH is 0.47% or 2 in 422 cryolipolysis treatments. This is 100 times greater than the device manufacturer's reported incidence. Histopathologic examination of the subcutaneous tissue mass showed an increased number of adipocytes, fibrosis, and scar tissue in the treated areas when compared to controls. No lipoblasts, a marker of malignant neoplastic proliferation, were identified on the histopathologic examination of the affected tissues. CONCLUSION: The incidence of PAH is likely underreported. Further investigation is necessary to elucidate its mechanism of action. By understanding the pathogenesis, this rare adverse effect may be avoided, or even utilized as a therapeutic alternative for the treatment of congenital or acquired lipodystrophy.

Antibiotic overuse and resistance in dermatology.

Antibiotics have a significant role in dermatology, treating a wide range of diseases, including acne, rosacea, inflammatory skin conditions and skin structure infections, such as cellulitis, folliculitis, carbuncles, and furuncles. Because of their consistent use, utility, and availability, antibiotics are susceptible to overuse within the medical practice, and, specific to this discussion, in the dermatologic setting. The issue of continuously increasing risk of antibiotic resistance remains an important concern to the dermatologist. The scope of this review will be to provide an overview of the common antibiotics used in the dermatologic setting with an emphasis on identifying areas of overuse, reported bacterial resistance, and discussion of clinical management aimed at decreasing antibiotic resistance.

A model of TH17-associated ileal hyperplasia that requires both IL-17A and IFNγ to generate self-tolerance and prevent colitis.

Homeostasis in the ileum, which is commonly disrupted in patients with Crohn's disease, involves ongoing immune responses. To study how homeostatic processes of the ileum impact CD4+T cell responses, we used TCR transgenic tools to breed mice that spontaneously produced CD4+T cells reactive to an antigen expressed in the ileum. At an early age, the ilea of these mice exhibit crypt hyperplasia and accumulate increased numbers of TH17 cells bearing non-transgenic clonotypes. Half of these mice subsequently developed colitis linked to broad mucosal infiltration by TH17 and TH1 cells expressing non-transgenic clonotypes, chronic wasting disease and loss of ileal crypt hyperplasia. By contrast, adult mice with normal growth continued to exhibit TH17-associated ileal crypt hyperplasia and additionally accumulated ileal-reactive Treg cells. Both IL-17A and IFNγ were protective, as their deficiency precluded ileal-reactive Treg accumulation and exacerbated colitic disease. IL-23R blockade prevented progression to colitis, whereas nTreg cell transfers prevented colitic disease, ileal crypt hyperplasia and ileal-reactive Treg accumulation. Thus, our studies identify an IL-17A and IFNγ-dependent homeostatic process that mobilizes ileal-reactive Treg cells and is disrupted by IL-23.