Update on systemic therapies for atopic dermatitis.

PURPOSE OF REVIEW: Although many atopic dermatitis patients can be treated satisfactorily with topical medications and systemic anti-itch approaches, a smaller subset require more aggressive systemic therapies. Familiarity with the latest literature on the benefits and risks of these treatments will enable the clinician and patient to select the most appropriate therapy based on the patient's lifestyle, assessments of risks and comorbidities. RECENT FINDINGS: Additional data have come to light altering the risk and benefit ratio of certain systemic atopic dermatitis therapies. In 2011, we saw several head-to-head, randomized controlled trials of established systemic medications for the treatment of atopic dermatitis. A few new systemic atopic dermatitis treatments have highlighted how targeted therapies may inform us about disease pathogenesis. SUMMARY: In light of the risk of hepatosplenic T-cell lymphomas, a greater degree of caution is warranted in the use of azathioprine. NBUVB, mycophenolate, and methotrexate remain the reasonable first-line systemic treatment options for atopic dermatitis. A brief run-in with high-dose cyclosporine to clear atopic dermatitis followed by maintenance with low-dose cyclosporine or cellcept - both of which have better risk and benefit ratios is a reasonable approach. Interferon gamma and intravenous immunoglobulin, although expensive, are potential options, and possibly most ideal for atopic dermatitis patients plagued by significant viral skin infections such as eczema herpeticum. A better understanding of the immunopathogenesis of atopic dermatitis will come with the exploration of novel targeted therapies.

IMP3, NESP55, TTF-1 and CDX2 serve as an immunohistochemical panel in the distinction among small-cell carcinoma, gastrointestinal carcinoid, and pancreatic endocrine tumor metastasized to the liver.

Histopathologic distinction among small-cell carcinoma (SCC), pancreatic endocrine tumor (PET), and gastrointestinal carcinoids metastasized to the liver in needle core biopsies can be extremely challenging because of limited material, crush artifact, and lack of detailed clinical history. In this study, a total of 61 surgically resected or biopsied specimens, including 27 SCCs (lung, 17; colon, 1; gallbladder, 2; stomach, 1; and unknown primary, 6), 18 gastrointestinal carcinoid tumors (GICTs) (stomach, 2; small intestine, 14; colon, 2), and 16 PETs were immunohistochemically examined for the expression of IMP3, TTF-1, CDX2, and NESP55 to evaluate their diagnostic value. The results showed that 24 (89%) of 27 SCCs exhibited strong cytoplasmic staining for IMP3 in 60% to 100% of the tumor cells. Eighteen (67%) SCCs were strongly and diffusely positive for TTF-1. In the remaining 9 TTF-1-negative SCCs (including 4 extrapulmonary cases), 7 showed strong and diffuse IMP3 expression. All SCCs were negative for CDX2 except for 1 case of colonic origin that showed strong CDX2 immunoreactivity. All 16 metastatic PETs were positively stained for IMP3 with 12 cases (75%) showing a diffuse and moderate-to-strong staining pattern while they were negative for TTF-1. Six PETs exhibited moderate-to-strong positivity for CDX2 with nuclear staining in 5% to 40% of tumor cells, and 5 showed a varying degree of positivity for NESP55. Three (17%) of 18 metastatic GICTs showed moderate IMP3 staining in 50% to 90% of the tumor cells, whereas CDX2 was expressed in 17 (94%) cases with moderate-to-strong staining in 50% to 100% of tumor cells. No NESP55 immunoreactivity was detected in metastatic SCCs and GICTs. In conclusion, a panel of these 4 markers is useful in segregating among SCC, PET, and GICT to help determine the primary site of hepatic metastasis.