NailQoL represents a new concise, valid, reliable, and responsive instrument for measuring burden of skin disease for patients with onychomycosis.

Pancreatic panniculitis is an uncommon disorder with a distinctive histopathology. We report the youngest patient with pancreatic panniculitis caused by hypertriglyceridemia in association with nephrotic syndrome.

Eighty patients completed the study.Intervention: Patients were randomized by a computergenerated code to receive pads consisting of either moleskin with transparent duct tape (treatment group) or moleskin alone (control group). Patients were instructed to wear the pads for 7 consecutive days and leave the pad off on the seventh evening. This process was repeated for 2 months or until the wart resolved, whichever occurred first. Follow-up visits occurred at 1 and 2 months.Main Outcome Measure: Complete resolution of the target wart. Secondary outcomes included change in size of the target wart and recurrence rates at 6 months for warts with complete resolution.Results: There were no statistically significant differences in the proportions of patients with resolution of the target wart (8 [21%] of 39 patients in the treatment group vs 9 [22%] of 41 in the control group). Of patients with complete resolution, 6 (75%) in the treatment group and 3 (33%) in the control group had recurrence of the target wart by the sixth month. Conclusion:We found no statistically significant difference between duct tape and moleskin for the treatment of warts in an adult population.

WTP and annual income demonstrated moderate and strong test-retest reliability, respectively. Self-reported WTP can serve as a reliable measure for future health economics research on onychomycosis.

No abstract

No abstract

References1 Smith F. The molecular genetics of keratin disorders. Am J Clin Dermatol 2003; 4:347-64. 2 Lane EB, McLean WHI. Keratins and skin disorders. J Pathol 2004; 204:355-66. 3 Ishida-Yamamoto A, McGrath JA, Judge MR et al. Selective involvement of keratins K1 and K10 in the cytoskeletal abnormality of epidermolytic hyperkeratosis (bullous congenital ichthyosiform erythroderma). J Invest Dermatol 1992; 99:19-26. 4 Rothnagel JA, Traupe H, Wojcik S et al. Mutations in the rod domain of keratin 2e in patients with ichthyosis bullosa of Siemens. Nat Genet 1994; 7:485-90. 5 Kremer H, Zeeuwen P, McLean WHI et al. Ichthyosis bullosa of Siemens is caused by mutations in the keratin 2e gene. J Invest Dermatol 1994; 103:286-9. 6 McLean WHI, Morley SM, Lane EB et al. Ichthyosis bullosa of Siemens -a disease involving keratin 2e. J Invest Dermatol 1994; 103:277-81. 7 Akiyama M, Tsuji-Abe Y, Yanagihara M et al. Ichthyosis bullosa of Siemens: its correct diagnosis facilitated by molecular genetic testing. Br J Dermatol 2005; 152:1353-6. 8 Traupe H, Kolde G, Hamm H, Happle R. Ichthyosis bullosa of Siemens: a unique type of epidermolytic hyperkeratosis. J Am Acad Dermatol 1986; 14:1000-5. 9 Yang JM, Nam K, Kim HC et al. A novel glutamic acid to aspartic acid mutation of the 2B rod domain in the keratin 1 chain in epidermolytic hyperkeratosis. J Invest Dermatol 1999; 112:376-9. 10 Sun XK, Ma LL, Xie YQ et al. Keratin 1 and keratin 10 mutations causing epidermolytic hyperkeratosis in Chinese patient. J Dermatol Sci 2002; 29:195-200.Conflicts of interest: none declared. Fig 1. A well-demarcated, erythematous plaque with firm woody oedema involving the cheeks, chin and anterior neck.

No abstract