Jörg Tittelbach

Successful Treatment of Necrobiotic Xanthogranuloma With Intravenous Immunoglobulin

Necrobiotic xanthogranuloma (NXG) is a rare systemic disease first described by Kossard and Winkelmann in 1980, and about 100 cases have been reported since then. It is clinically characterized by indurated yellowish to red-orange or brown papules or nodules that grow into larger and in some cases very extensive plaques covering the face (especially with periorbital distribution), trunk, and extremities. Lesions are nearly always asymptomatic, but secondarily they may become ulcerated. Moreover, pathologic changes in internal organs have been documented, including giant-cell myocardial disease. Because involvement of the heart seems to be relatively frequent, routine echocardiography and dynamic cardiac imaging are recommended in all patients. Necrobiotic xanthogranuloma also may involve other organs including the lung, larynx, pharynx, skeletal muscle, kidney, spleen, ovary, and intestine. Histopathologically, NXG is characterized by a granulomatous inflammation in the dermis extending into the subcutaneous fat. Dense infiltrates of macrophages with some foreign body–type giant cells and foamy macrophages are accompanied by areas of degenerated collagen and a moderate lymphocytic infiltrate in some cases with plasma cells. Mucin deposition or cholesterol clefts can be found. The underlying pathogenesis of the disease remains unknown, although in up to 80% of the patients, an association with paraproteinemia, especially monoclonal IgGproteinemia, can be found. Less often, bone marrow examination shows multiple myeloma. No first-line NXG therapy has been established. The recommended therapies of corticosteroids (intralesional and/or systemic), alkylating agents (such as cyclophosphamide, melphalan, or chlorambucil), interferon alfa, antimetabolites, antimicrobial treatment, and plasmapheresis have shown inconsistent success. To our knowledge, this is the first report of successful treatment of NXG with intravenous immunoglobulin (IVIg).

Update: Treatment of necrobiosis lipoidica

Necrobiosis lipoidica (NL) is a rare granulomatous disease of hitherto unclear etiology frequently seen in patients with diabetes. Characterized by its potential for ulcerations, it often presents a serious burden for those affected. There are currently neither German nor European guidelines for the treatment of NL. At the same time, standard treatment with topical or intralesional corticosteroids does not always show satisfactory results. We therefore set out to evaluate whether the various treatment regimens published since 2000 have actually expanded the therapeutic armamentarium in a relevant manner. Included were all publications that described more than one patient being treated with any given therapeutic modality. Overall, we analyzed data for 16 different treatment regimens reported in 49 publications.

Clinical efficacy of dressings for treatment of heavily exuding chronic wounds

The treatment of chronic ulcers is a complex issue and presents an increasing problem for caregivers everywhere. This is especially true in Germany, where more than 4 million chronic wounds are treated each year. Therapeutic decisions must be patient-centered and reflect wound etiology, localization, and healing status. The practice of using the same wound dressing during the entire healing period is no longer reasonable. Instead, multiple types of dressings may be needed for a single wound over its healing trajectory. Selection of the most appropriate dress- ing should be based on wound phase, depth, signs of infection, and level of exudate. Moisture balance is critical in wound care; dryness will hamper epithelial cell migration while excessive generation of fluid causes maceration at the wound margins. Hence, exudate management is a key issue in chronic wound therapy, particularly given that exudate from chronic wounds has a composition different from that of acute wound fluid. Several studies have shown that exudates from non-healing wounds contain significantly elevated levels of protease activity, increased formation of free radicals, and abundant amounts of proinflammatory cytokines, while concentra - tions of growth factors and protease inhibitors are markedly decreased. Application of dressings that remove and sequester excess amounts of wound fluid may not only help in restoring the correct balance of moisture, but also support the wound healing process by preventing tissue deterioration caused by abundant protease activity. Several types of dressings, such as hydrogels, hydrocolloids, alginates, hydrofibers, foams, and superabsorbent dressings, are reviewed here

Influence of the Galenic Form of a Skin-Protective Preparation on the Application Pattern Assessed by a Fluorescence Method

The efficacy of skin-protective preparations is still under debate. One aspect of efficient skin protection is dependent on the quality of application concerning the homogenous distribution of the skin-protective products. The periungual areas, the finger webs and tips are known to be frequently incompletely covered when a protective cream is applied. In a randomized study, a protective mousse and a standard commercially available protective cream were compared regarding their application adequacy and cosmetic acceptance. Thus, 2 groups of 50 subjects with healthy skin were recruited for a typical application of the cream or the mousse. Distribution was examined under long-wave UV light. Additionally, the cosmetic acceptance of both products was studied by means of a questionnaire. Results showed significant differences between the mousse and the cream. The mousse proved better coverage, particularly in the problem fields. Our results showed that a mousse can offer advantages in skin protection by virtue of its better distribution and acceptance.

Allergic contact dermatitis caused by methylchloroisothiazolinone/methylisothiazolinone in a medical device

Allergic contact dermatitis caused by methylchloroisothiazolinone/ methylisothiazolinone in a medical device Sibylle Schliemann1, Marléne Isaksson2, Christina Persson2, Magnus Bruze2, Jörg Tittelbach1 and Peter Elsner1 1Department of Dermatology, Universital Hospital Jena, Jena 07743, Germany and 2Department of Occupational and Environmental Dermatology, Skane University Hospital, Malmö, 205 02 Malmö, Sweden

Position paper: Telemedicine in occupational dermatology - current status and perspectives: Position paper: Telemedicine in occupational dermatology

Teledermatology is the use of telecommunication technologies to exchange medical information for diagnosis, consultation, treatment and teaching in dermatology. While its use has been evaluated in a wide range of dermatological diagnoses, only few studies exist on its validity, diagnostic precision, feasibility, and cost‐effectiveness in occupational dermatology. However, these studies show a considerable potential for diagnosis, prevention, treatment support and follow‐up of patients with occupational skin diseases. Asynchronous (store and forward; SAF) or synchronous dermatology teleconsults could assist occupational medicine specialists not only in occupational preventive care, but also in the context of skin cancer screening in outdoor workers. Thus, teledermatology might contribute to earlier prevention and notification of occupational skin diseases. Modern smartphone apps with artificial intelligence technologies may also facilitate self‐monitoring in employees working in high‐risk jobs.

Chronic skin ulcer following defibrillation

We would like to present the case of a patient whose condition, though unequivocal with regard to its cause, showed a unique clinical course previously undescribed. Five year prior to presentation at our department, the 57-year-old patient had required defi brillation during cardiac stent placement and subsequently sustained third-degree burns. Since then, there had been a chronic ulcer on the left lateral chest wall where the apical defi brillation electrode had been placed. The lesion had never healed and had recently increased in size. At presentation, the clinical exam showed a fi brin-coated ulcer with uninfl amed margins, measuring 3 cm in diameter (Figure 1 ). We decided to excise the entire ulcer, not least to rule out squamous cell carcinoma arising in a chronic ulcer associated with a burn scar. The differential diagnosis included scrofuloderma and chronic vegetating pyoderma. Histology showed focal sclerosis of collagen fi bers with calcifi cation (von Kossa stain, Figure 2 d) as well as a lymphohistiocytic infi ltrate with sparse plasma cells, neutrophils, and few eosinophils (Figure 2 a–c). Defi brillation is a treatment aimed at disrupting reentrant electric excitation of the myocardium by depolarizing at least 70 % of myocardial cells. The refractory period of approximately 250 ms thus created prevents propagation of the reentrant excitation wave, so that the natural conduction system can resume normal cardiac stimulation. The energy employed usually ranges from 200 to 360 joules, with a voltage of 2000–4000 volts delivered to the patient for approximately 3–40 ms. At a typical impedance between 50 and 100 ohms, this results in an electric current of up to 50 amperes. Compared to monophasic devices, modern defi brillators with their biphasic waveform shocks are more effective [ 1 ] , which results in lower energy transfer required and subsequently less myocardial damage. In addition, biphasic cardioversion less frequently causes pain and erythema [ 2 ] . In general, it should be pointed out that (low-grade) burns are a regular occurrence during defi brillation, their severity correlating with the number of electric shocks delivered and their energy [ 3 ] . Studies on whether such burn injuries might be positively affected by the application of betamethasone cream two hours prior to cardioversion showed no signifi cant difference compared to placebo, though [ 4 ] . As regards the mechanisms by which defi brillation may damage the skin, the focus used to be on thermal injury to tissues traversed by the electric current. Another mechanism of cell damage is electroporation due to the high current density applied. Animal studies have shown further alterations directly attributable to effects caused by the electric current, not by heat. For instance, changes in keratinocyte nuclei, sweat glands, and blood vessels as well as the deposition of calcium salts along collagen and elastic fi bers have all been observed around necrotic tissue [ 5, 6 ] . Other authors have described the same alterations – histologically also detected in our case – in humans following defi brillation [ 7 ] . In a pig study, calcifi cation of collagen fi bers was observed after only two days, in each case in the area of the cathode (usually placed in the apical region) but never in the anode region [ 5, 8 ] . A possible explanation might be an increase in pH (alkalinization) around the negatively charged cathode, subsequently resulting in dystrophic calcifi cation [ 9 ] . In the aforementioned study by Thomsen et al., histological changes similar to those caused by alkali exposure were found in the cathode area [ 5, 8 ] . With respect to the case described herein, it is therefore safe to assume that it was not the actual burn injury (direct thermal damage) that caused the nonhealing ulcer but rather electrolysis at the cathode, which ultimately led to the formation of calcium salts and thus dystrophic calcifi cation.

Contact allergy to mometasone furoate with cross‐reactivity to group B corticosteroids

Mometasone furoate is a synthetic 16 alpha-methyl analogue of beclomethasone and classified as a potent topical glucocorticoid with low risk of skin atrophy in spite of strong antiinflammatory activity (1). Contact allergies to mometasone furoate have only been recognized rarely (1–5). Mometasone furoate is not mentioned in the Coopman classification (Table 1), which divides corticoids into 4 cross-reactive chemical groups A–D (6–8).

Disseminated Mycobacterium marinum skin infection due to chronic lymphedema in an immunocompetent patient

A 64-year-old woman presented with a four-week history of unilateral erythematous, slightly pruritic papules and nodules on her right leg, which were unresponsive to broad-spectrum antibiotics. The patient denied any fever or other systemic symptoms, had no allergies and took no regular medication. Her medical history included endometrial carcinoma with pelvic lymphadenectomy seven years ago, resulting in chronic lymphedema of the right leg with two previous episodes of erysipelas. Dermatological investigation revealed disseminated, hair-follicle-associated reddish papules, plaques and nodules on the right leg in combination with lymphedema (Figures 1 a, b, 2 ). The results of routine laboratory tests were unremarkable, except for a positive interferon-gamma release assay (IGRA) for Mycobacterium (M.) tuberculosis . Pulmonary tuberculosis (TB) as well as sarcoidosis were ruled out by chest X-ray and sputum analysis. Soluble IL2 receptor (sIL2R) and angiotensin converting enzyme (ACE) were within the normal range. Histopathological examination of a skin biopsy from a nodule revealed a dense periadnexal, granulomatous infi ltrate

Blisters, ulcers, crusts, and atrophic scars on the back of the hands and the extensor aspects of the forearms

A 51-year-old secretary presented with a two-month history of skin lesions on the back of the hands as well as the extensor aspects of the fi ngers and forearms. She reported blisters that left poorly healing wounds covered with crusts. At the time of consultation, she was on adalimumab (40 mg every 14 days) and methotrexate (10 mg and 15 mg, alternating on a weekly basis) for rheumatoid arthritis. For the past four years, her regular antiinfl ammatory medication had also included naproxen. Topical treatment with zinc ointment had been without success.