Primary apocrine adenocarcinoma of the axilla.

Primary apocrine adenocarcinoma (AA) is a rare malignant cutaneous neoplasm that typically arises in areas of high apocrine gland density such as the axillae and the anogenital region. Due to the nonspecific clinical manifestation of AA, the differential diagnosis may be broad. The rarity of this neoplasm has led to a relative lack of well-established histologic and immunohistochemical diagnostic criteria, further complicating the diagnosis of AA. We report the case of a 49-year-old man with primary AA of the left axilla and provide a review of the clinical and histologic findings, epidemiology, and treatment modalities of this rare cutaneous neoplasm.

Bacterial infections following non-ablative fractional laser treatment: a case series and discussion.

Non-ablative fractional laser procedures have become increasingly popular since their introduction in 2004. The fractional 1,927 nm thulium laser is a non-ablative device that penetrates up to 300 µm in the skin and the 1,550 nm erbium:glass laser penetrates up to 1,400 µm. These procedures are considered minimally invasive with a high safety profile; therefore, infectious complications are exceedingly rare. However, we report five recent cases of bacterial infection with both gram-positive and gram-negative organisms following treatment with the fractional 1550/1927 nm laser approximately 1 day to 1 week post-procedure. One patient had a rapidly progressing pustular eruption with symptoms of sepsis. These patients were seen immediately, cultures were obtained and empiric antibiotic therapy was initiated. They recovered without long-term complications. Rapid-onset bacterial infections following non-ablative laser resurfacing with the 1550/1927 nm laser have not been previously reported in the literature. The infections can progress quickly and lead to serious sequelae, including systemic illness and severe scarring, if not identified and appropriately treated. We present these cases to highlight the importance of close surveillance and when appropriate, rapid intervention, following non-ablative fractional procedures, especially when patients present with atypical symptoms and signs.

Livedo reticularis from amantadine.

A 70-year-old Caucasian man with a medical history of Parkinson's disease presented with a 3-month history of violaceous reticulated patches on his upper and lower extremities. The lesions were asymptomatic. The patient did not have a history of cardioembolic events or autoimmune disorders. No new medications were started before the onset of the lesions. Review of systems was unremarkable. On examination, large erythematous to violaceous patches were present in a reticulated net-like pattern on the patient's upper and lower extremities (Figure 1 and Figure 2). No edema, erosions, or ulcerations were noted. An extensive workup for autoimmune, infectious, and hematologic causes of livedo reticularis was performed. Complete blood cell count, anti-nuclear antibodies (ANAs), anti-Ro and anti-La antibodies, antiphospholipid antibodies, protein C and S levels, cryoglobulin screen, rheumatoid factor, and hepatitis screen were all within normal limits. After these potential other causes were excluded, the patient was diagnosed with amantadine-induced livedo reticularis (LR), a medication he had been taking for 2 years for Parkinson's disease. The patient's dose of amantadine was decreased from 100 mg to 50 mg twice daily and over the next few months, his lesions gradually faded. Because his neurologic condition benefited from amantadine and his lesions were asymptomatic, his neurologist continued the medication.

Histopathologic study of hidradenitis suppurativa following long-pulsed 1064-nm Nd:YAG laser treatment.

OBJECTIVE: To assess clinical and histopathologic changes occurring after long-pulsed 1064-nm Nd:YAG laser treatment of hidradenitis suppurativa (HS). DESIGN: Prospective, controlled clinical and histologic study of patients with Hurley stage II HS disease. SETTING: Outpatient dermatology department at Henry Ford Hospital, Detroit, Michigan. PARTICIPANTS: Nineteen patients with Fitzpatrick skin types II to VI with Hurley stage II HS lesions of the axilla and groin. Interventions Two monthly laser sessions were performed using the long-pulsed 1064-nm Nd:YAG laser. Main Outcome Measure Clinical response was scored using the modified Sartorius scale for HS reflecting Lesion Area and Severity Index (LASI). Histologic changes were examined before treatment and 1 week, 1 month, and 2 months after treatment. RESULTS: The percentage change in HS severity after 2 sessions of laser treatment was -31.6 over all anatomic sites (P < .005), -24.4 for the axillary site (P = .008), and -36.8 for the inguinal site (P = .001). Histologic changes corresponded to clinical response. Findings from serial biopsy specimens showed increased inflammation at 1 week after treatment and decreased inflammation with resulting fibrosis and scarring at 1 month and 2 months after treatment. CONCLUSIONS: The long-pulsed 1064-nm Nd:YAG laser is a novel effective treatment option for HS. Our histopathologic data suggest that HS is primarily a follicular disorder. The Nd:YAG laser penetrates for selective photothermolysis of the follicular unit and destruction of organized inflammatory lesions in the superficial to mid dermis. Our study offers insight into the pathogenesis of HS and the mechanism of the Nd:YAG laser in treatment of patients with this chronic, debilitating disease.

Cutaneous manifestations of vasculitis.

OBJECTIVES: To discuss the clinical features, diagnostic evaluation, and treatment options for cutaneous vasculitis. METHODS: The literature in the PubMed database was reviewed regarding the presentation, pathophysiology, clinical workup, and treatment of cutaneous vasculitis. RESULTS: Available classification criteria of vasculitis are based on histopathologic criteria or clinicohistologic features. These have been designed more for research purposes than for clinical application. Skin findings such as palpable purpura, nodules, urticaria, ulcers, and infarction are clues to the presence of vasculitis. Pathologic findings of fibrinoid necrosis, infiltration by neutrophils or lymphocytes, and deposition of complement and immunoglobulin may be helpful in reaching a specific diagnosis. However, there is considerable overlap across different conditions. CONCLUSIONS: The correct diagnosis of cutaneous manifestations of vasculitis requires an understanding of vasculitis classification, recognition of specific clinical patterns, and the ability to interpret histopathologic data.

Annexin A1 reduces inflammatory reaction and tissue damage through inhibition of phospholipase A2 activation in adult rats following spinal cord injury.

Annexin A1 (ANXA1) has been suggested to be a mediator of the anti-inflammatory actions of glucocorticoids and more recently an endogenous neuroprotective agent. In the present study, we investigated the anti-inflammatory and neuroprotective effects of ANXA1 in a model of contusive spinal cord injury (SCI). Here we report that injections of ANXA1 (Ac 2-26) into the acutely injured spinal cord at 2 concentrations (5 and 20 microg) inhibited SCI-induced increases in phospholipase A2 and myeloperoxidase activities. In addition, ANXA1 administration reduced the expression of interleukin-1beta and activated caspase-3 at 24 hours, and glial fibrillary acidic protein at 4 weeks postinjury. Furthermore, ANXA1 administration significantly reversed phospholipase A2-induced spinal cord neuronal death in vitro and reduced tissue damage and increased white matter sparing in vivo, compared to the vehicle-treated controls. Fluorogold retrograde tracing showed that ANXA1 administration protected axons of long descending pathways at 6 weeks post-SCI. ANXA1 administration also significantly increased the number of animals that responded to transcranial magnetic motor-evoked potentials. However, no measurable behavioral improvement was found after these treatments. These results, particularly the improvements obtained in tissue sparing and electrophysiologic measures, suggest a neuroprotective effect of ANXA1.