Androgenetic alopecia (AGA) is a genetically determined progressive hair-loss condition which represents the most common cause of hair loss in men. The use of the medical term androgenetic alopecia reflects current knowledge about the important role of androgens and genetic factors in its etiology. In addition to androgen-dependent changes in the hair cycle, sustained microscopic follicular inflammation contributes to its onset. Furthermore, Prostaglandins have been demonstrated to have the ability in modulating hair follicle cycle; in particular, PGD2 inhibits hair growth while PGE2/F2a promote growth. Due to the progressive nature of AGA, the treatment should be started early and continued indefinitely, since the benefit will not be maintained upon ceasing therapy. To date, only two therapeutic agents have been approved by the Food and Drug Administration and European Medicines Agency for the treatment of AGA: topical minoxidil and oral finasteride. Considering the many pathogenetic mechanisms involved in AGA, various treatment options are available: topical and systemic drugs may be used and the choice depends on various factors including grading of AGA, patients' pathological conditions, practicability, costs and risks. So, the treatment for AGA should be based on personalized therapy and targeted at the different pathophysiological aspects of AGA.

Chemotherapy-induced alopecia (CIA) is probably one of the most shocking aspects for oncological patients and underestimated by physicians. Among hair loss risk factors there are treatment-related aspects such as drug dose, administration regimen and exposure to X-rays, but also patient-related characteristics. At the best of our knowledge no guidelines are available about CIA management. With this paper, based on literature background and our clinical experience, we would like to propose a list of actions in order to estimate the risk of hair loss before starting chemotherapy and to manage this condition before, during and after drug administration and to create a sort of practical guide for dermatologists and oncologist. There is an urgent need for prospective studies in order to clarify the mechanistic basis of alopecia associated to these drugs and consequently to design evidence-based management strategies.

Our results have shown that topical cetirizine 1% is responsible for a significant improvement of the initial framework of AGA.

Rosacea is a common chronic inflammatory disorder showing a wide range of clinical features such as telangiectasia, erythema, papules, and pustules primarily involving the central part of face (forehead, cheeks and nose) although extra facial manifestation have been described. We describe a case of rosacea with predominant scalp involvement successfully treated with a 8-week-course of doxycycline 40 mg once a day and probiotic therapy twice a day (Bifidobacterium breve BR03, Lactobacillus salivarius LS01 1 × 10(9) UFC/dose).

No abstract

Pitted keratolysis (PK) is a plantar skin disorder mainly caused by coryneform bacteria. A common treatment consists of the topical use of erythromycin. Hyperhidrosis is considered a predisposing factor for bacterial proliferation and, consequently, for the onset of PK. The aim of this study was to evaluate the relationship between PK erythromycin and hyperhidrosis. All patients with PK seen in Sant'Andrea Hospital, between January 2009 and December 2011, were collected. PK was clinically and microscopically diagnosed. All patients underwent only topical treatment with erythromycin 3% gel twice daily. At the beginning of the study and after 5 and 10 days of treatment, a clinical evaluation and a gravimetric measurement of plantar sweating were assessed. A total of 97 patients were diagnosed as PK and were included in the study. Gravimetric measurements showed that in 94 of 97 examined patients (96.90%) at the time of the diagnosis, there was a bilateral excessive sweating occurring specifically in the areas affected by PK. After 10 days of antibiotic therapy, hyperhidrosis regressed together with the clinical manifestations. According to these data, we hypothesize that hyperhidrosis is due to an eccrine sweat gland hyperfunction, probably secondary to bacterial infection.

Pseudomyogenic hemangioendothelioma (PMH) is a rare, mostly indolent, endothelial neoplasm of low‐grade malignancy, often mimicking myoid and epithelioid tumors histologically. It is more frequent in young adult males and it usually presents with multiple cutaneous nodules, mostly localized at the extremities. It traverses several tissue planes simultaneously and can involve dermis, subcutis, skeletal muscle, and bone. Histologically, it is characterized by plump spindle cells with eosinophilic cytoplasm, often arranged in fascicles and epithelioid cells with “pseudomyogenic” morphology. Immunohistochemically, PMH is positive for Factor VIII, FLI‐1, INI‐1, vimentin, MDM2, CDK4, CD31, AE1/AE3, EMA, and P63. The efficacy of treatments is only partially known. Because of the frequent multifocal aspect of PMH, which contraindicates surgery, systemic treatments, such as gemcitabine, sirolimus, and everolimus are used. Based on our observation of multifocal PMH of the foot in a 17‐year‐old male patient, treated with gemcitabine with complete cutaneous response in a 2‐year follow‐up, we decided to discuss this rare tumor and underline its progression and therapeutic approaches. Thanks to a correct diagnosis, it is possible to avoid aggressive therapeutic approaches, which would be necessary for nonindolent diseases, such as sarcoma, which often needs amputation.

Cutaneous larva migrans (CLM; also called creeping eruption) is a cutaneous ectoparasitosis commonly observed in tropical countries. It is characterized by an erythematous, pruritic, and raised lesion with linear or serpiginous distribution, typically localized at the lower extremities. Oral ivermectin represents the most recommended current treatment, with important adverse effects associated. We report the clinical case of a 52‐year old with CLM, successfully treated with topical ivermectin.