This is the first case series describing the successful application of imiquimod in the management of morphoea.

Our study suggests that the use of this fractionated radiofrequency device is a safe and effective method of skin rejuvenation for skin types V through VI.

Aging of the hands is a common problem that is often overlooked. The use of soft tissue fillers is a viable tool in hand rejuvenation. In this study hyaluronic acid proved to be superior in efficacy to collagen.

Fibrosis is characterized by the increased deposition of collagen and other matrix components by fibroblasts. This process occurs as a reaction to inflammation and is mediated by numerous cytokines including transforming growth factor beta (TGF-beta). Localized cutaneous scleroderma or morphea is characterized by fibrosis. Current treatment for morphea includes topical, intralesional, or systemic corticosteroids, vitamin D analog (calcitriol and calcipotriol), photochemotherapy, laser therapy, antimalarials, phenytoin, D-penicillamine, and colchicine, all with varying degrees of success. In this case report, imiquimod cream 5% (Aldara), which induces interferon and in turn inhibits TGF-beta, was employed to treat morphea.

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We have previously shown that inhibition of p38(MAPK) increases adrenergic-stimulated p42/44(MAPK) activation in rat pinealocytes. In this study we investigated whether p38(MAPK) played a role in the adrenergic regulation of arylalkylamine-N-acetyltransferase (AA-NAT) induction and melatonin (MT) synthesis. Treatment of pinealocytes with norepinephrine (NE) caused a time-dependent increase in the levels of AA-NAT mRNA, AA-NAT protein, and enzymatic activity as well as MT production. Cotreatment with SB202190, a selective p38(MAPK) inhibitor, although having no effect on AA-NAT activity or protein level 3 h after NE treatment, caused a sustained increase in AA-NAT activity and protein level after 6 h of NE treatment. The increases in NE-stimulated AA-NAT activity and protein level by SB202190 occurred in the absence of an increase in AA-NAT mRNA. Similar results were obtained when AA-NAT was induced by (Bu)(2)cAMP or when SB203580 was used to inhibit p38(MAPK). In comparison, SB202474, the inactive analog, had no effect on NE or (Bu)(2)cAMP-stimulated AA-NAT activity or protein level. SB202190 also increased cumulative NE-stimulated MT production, provided that the medium was supplemented with 5-methoxytryptamine. p38(MAPK) inhibitors had no effect on hydroxyindole-O-methyltransferase activity. These results show that inhibition of p38(MAPK), although having no effect on cAMP-mediated AA-NAT transcription, appears to increase AA-NAT activity either by increasing translation or by reducing degradation of the AA-NAT protein. The lack of effect on NE-stimulated MT accumulation by p38(MAPK) inhibitors in the absence of 5-methoxytryptamine could be secondary to a lack of substrate, or alternatively, hydroxyindole-O-methyltransferase may become limiting.

LTBI appears to be prevalent among psoriasis patients. Screening for LTBI in patients on biologics may reduce risk of active tuberculosis; however, current methods may not be fully effective. Clinicians may need to use other tools including risk factor assessment to fully evaluate risk.