Summary

Psoriasis vulgaris is a common and often chronic inflammatory skin disease. The incidence of psoriasis in Western industrialized countries ranges from 1.5% to 2%. Patients afflicted with severe psoriasis vulgaris may experience a significant reduction in quality of life. Despite the large variety of treatment options available, surveys have shown that patients still do not received optimal treatments. To optimize the treatment of psoriasis in Germany, the Deutsche Dermatologi sche Gesellschaft (DDG) and the Berufsverband Deutscher Dermatologen (BVDD) have initiated a project to develop evidence-based guidelines for the management of psoriasis. They were first published in 2006 and updated in 2011. The Guidelines focus on induction therapy in cases of mild, moderate and severe plaque-type psoriasis in adults including systemic therapy, UV therapy and topical therapies.

The therapeutic recommendations were developed based on the results of a systematic literature search and were finalized during a consensus meeting using structured consensus methods (nominal group process).

Human papillomavirus (HPV) is responsible for common condyloma acuminata and a number of premalignant and malignant anogenital lesions. These conditions are of particular concern in immunocompromised individuals who have higher risk of malignant transformation and are more difficult to treat. This is part I of a two-part review that will highlight the cutaneous features of condyloma acuminata and vaginal, vulvar, penile, and anal intraepithelial neoplasias, with an emphasis on presentation of these HPV-mediated diseases in the immunocompromised host. Counseling patients about these conditions requires a thorough understanding of the epidemiology, natural history of HPV, transmission and infectivity, risk of malignancy, and the role of the host immune response in clearing HPV lesions. Part II will provide an updated review of available treatments, with a focus on recent advances and the challenges faced in successfully treating HPV lesions in immunocompromised patients.

Human papillomavirus is responsible for common condyloma acuminata and a number of premalignant and malignant anogenital lesions. The immunocompromised population is at particular risk because of a higher incidence of malignant transformation. Lesions in this population may prove refractory to standard treatment. This is part II of a two-part review that will discuss the treatment of condyloma acuminata and vaginal, vulvar, penile, and anal intraepithelial neoplasias. This article will provide an updated review of available treatments, with a focus on recent advances and the challenges faced in successfully treating human papillomavirus lesions in the immunocompromised host.

A respected physician affiliated with an academic medical center is shopping at a local gift shop with his spouse. The physician is being helped by the owner of the shop, a fair-skinned woman that he estimates to be in her mid-forties. During this interaction, the physician cannot help but notice an asymmetric lesion with variable pigmentation on the woman’s left upper arm. Although this physician is not a dermatologist, he is a general surgeon with experience in excising malignant melanomas and performing sentinel lymph node biopsies. His experience and clinical acumen leads him to be clinically suspicious that this lesion might be a melanoma.

To the Editor: Reiter et al provide a comprehensive review of treatment options for calcinosis cutis (CC). However, they do not discuss the role of hematopoietic stem cell transplantation (HSCT), a treatment modality that has shown some promise in this condition and may have an increasing role as a potential treatment option as the evidence for this modality continues to evolve.

To the Editor: We thank Dr Velez and coauthors for their comments on our article, “Calcinosis cutis, part II: Treatment options.” Autologous stem cell transplantation (ASCT) exerts a positive effect on soft-tissue calcification. We agree with the author's suggestion that ASCT might be a reasonable choice for the treatment of extensive lifestyle-limiting and painful dystrophic calcinosis cutis that does not respond to traditional therapy. In ASCT, conditioning with high-dose cyclophosphamide, antithymocyte globulin, and/or total-body irradiation nullifies the majority of autoreactive effector cells involved in the adaptive and innate immune response, including B and T lymphocytes, monocytes, natural killer cells, and dendritic cells. Thus, the immunosuppressive effect of ASCT may be regarded as the key factor in autoimmune diseases. A favorable response of the underlying disease to ASCT will logically lead to the resolution of all accompanying symptoms, including skin calcification. Nevertheless, one should keep in mind the fact that the transplant-related mortality is approximately 7%, whereas transplant-related toxicity registered 2 years after ASCT was as high as 33%. Therefore, a careful risk-benefit evaluation must be performed for each patient. What we miss in the letter of Dr Velez and colleagues is the fact that not only dystrophic calcinosis cutis in connective tissue disease, but also calciphylaxis (in most cases a result of end-stage renal disease) may benefit from ASCT. In this context Mandelbrot et al described the resolution of extensive calciphylactic lesions in a young woman with systemic lupus erythematosus, undergoing hemodialysis for the treatment of lupus nephritis. It is not clear whether the calciphylaxis arose from systemic lupus erythematosus or was secondary to hemodialysis. However, the impressive fact was that the previously painful calciphylactic lesions had healed fully after ASCT treatment and the patient required no further medication for pain relief. In conclusion, ASCT may be regarded as a maximal variant of immunosuppressive therapy in autoimmune diseases and even reverses calcinosis cutis. We suggest ASCT as a therapy option for patients with severe therapy-refractory dystrophic calcinosis caused by autoimmune disease and in patients with extensive calciphylaxis.

To the Editor: We read with great interest the article by Tziotzios and colleagues describing strategies to reduce cutaneous scarring, published in January 2012. This valuable review article very briefly touches on fractional laser therapy for scars, and comments that “there is a limited evidence base to support use of fractional laser therapy.”

To the Editor: We thank Dr Reddy et al for their comments and for suggesting a wider review of current evidence for the use of fractional lasers in the treatment of scars. The focus of our CME series was on the molecular pathobiology of hypertrophic and keloid scarring and on strategies to avoid or treat such scarring after dermatologic procedures, as conveyed by the titles of each part. We had therefore not evaluated treatments for atrophic scars nor those after burns or acne.

To the Editor: Sunscreens and sunblocks are significant means of protection from the cutaneous damages imparted by ultraviolet radiation (UVR). Chemical sunscreens, as opposed to physical sunblocks, typically consist of a combination of lipophilic organic compounds in order to absorb the broad UVR spectrum. These sunscreen oils are incorporated into the lipophilic phase of oil-in-water or water-in-oil emulsions to achieve an efficacious and esthetically acceptable product. Sunscreens are frequently exposed to temperature extremes. For example, depending on the ambient temperature, the interior temperature of an automobile can range from –3°C to 89°C. These extreme temperature exposures may have a profound effect on the chemical stability of sunscreens and induce irreversible emulsion instability via alteration of droplet-droplet interactions and phase transitions. These physical and chemical changes could reduce the ability of sunscreens to protect the skin by filtering and/or absorbing UVR.

To the Editor: Monitoring the severity of atopic dermatitis (AD) is crucial to disease management. Tools exist to assess disease severity for experimental studies; these tools are not practical in a high-volume clinical setting. Thus, a simple bedside marker of AD severity would be a useful addition to the armamentarium of AD management.

To the Editor: While the varicella-zoster virus (VZV; chickenpox) vaccine (Varivax) is widely utilized and has produced a dramatic decline in VZV-related morbidity and mortality, the herpes zoster virus (HZV) (shingles) vaccine (Zostavax) is used in only 2% to 7% of the target population over 50 years of age in the United States. Research has shown that the HZV vaccine is effective. A randomized, double-blind, placebo-controlled trial involving 38,546 patients 60 years of age or older demonstrated a reduction of 51.3% (P < .001) in the incidence of HZ. Furthermore, those who did develop HZ after receiving the vaccine benefited from a 66.5% (P < .001) decrease in the incidence of postherpetic neuralgia (PHN). Cost-effectiveness is more difficult to prove. Our society generally finds it acceptable to pay at least $100,000 per quality-adjusted life year (QALY). Utilizing the HZ vaccine, extending life by one QALY costs $44,000 for a 70-year-old woman and $191,000 for an 80-year-old man. The cost per QALY for a patient 80 years old falls by approximately 40% when PHN is considered. Finally, if the HZ vaccine were administered to 1,000,000 eligible recipients, it would prevent over 75,000 cases of HZ and over 20,000 cases of PHN, resulting in savings of $82 million to $103 million.

To the Editor: Psoriasis is an inflammatory skin disease that affects approximately 2% of the general population, and roughly 1% of children. Numerous large population-based studies have demonstrated the systemic effects of psoriatic disease in adults showing an increased risk of coronary artery disease, myocardial infarction, and stroke. Although the increased risk of cardiovascular disease in adults with psoriasis has been well documented, there are more limited data available on cardiovascular risk factors in children with psoriasis.

To the Editor: Lipodermatosclerosis (LDS) is believed to be associated with chronic venous insufficiency. Abnormal fibrinolysis, the excessive proteolytic activity by matrix metalloproteinase, and the up-regulation of inflammatory response by interleukin-8 are thought to be the causes for this condition. Treatment of LDS is difficult and therapeutic trials have shown variations in the response rate. Pentoxifylline has been shown to decrease platelet aggregation, fibrinogen levels, and production of cytokines, and to inhibit leukocyte/endothelial cell binding. Antimalarials may decrease the production of proinflammatory cytokines and affect matrix metalloprotein production. Jorizzo et al treated 6 patients with LDS using many systemic agents including hydroxychloroquine in one patient and pentoxifylline in two other patients, but no clinical benefit was observed. There was, however, no information about dosage and duration of the treatment for either agent. Because there is no universally accepted therapy for LDS, we have tried using a combination of hydroxychloroquine and pentoxifylline, based on the pharmacologic mechanisms described previously.

To the Editor: Dermatophytoma is a little-known microscopic manifestation of fungal nail infection only recently mentioned in the literature. It is characterized by abundant fungal filaments, large spores, or both, compacted and forming a fungal ball. Definitive diagnosis is made microscopically by observation of this fungal conglomerate via direct potassium hydroxide or chlorazol black E examination of nail samples from patients with suspected onychomycosis (). Clinically, it has been described as a linear band of white or yellowish color. Unfortunately, published clinical descriptions are scarce.