Metástasis en glándula parótida por tumoraciones cutáneas melanoma y no melanoma de cabeza y cuello. Pronóstico y tratamiento / Parotid metastatic from cutaneous melanoma y no melanoma of head and neck. Prognostic and treatment

Introducción y objetivo: El melanoma y las tumoraciones cutáneas no melanomas (TCNM) situadas en cabeza y cuello pueden extenderse a la glándula parótida (GP), bien por continuidad o por diseminación a través del sistema linfático. Cuando esto ocurre, el tratamiento a seguir es preferentemente quirúrgico, siempre y cuando la evolución tumoral, el estado general del paciente y la no diseminación del tumor a otras zonas del organismo lo permitan. Nuestro objetivo es analizar el tratamiento seguido, el número de recidivas y la mortalidad en nuestra serie de las citadas tumoraciones, con invasión de la GP. Material y método: Presentamos una serie de 26 pacientes (24 varones y 2 mujeres) con afectación tumoral parotídea consecuencia de metástasis de melanoma o de TCNM. A todos se les realizó tratamiento quirúrgico, parotidectomía del lóbulo superficial en 5 casos y parotidectomía total en 21. La disección cervical radical modificada tipo III se efectuó en 19 pacientes. Posteriormente siguieron tratamiento radio y/o quimio o inmunoterápico. Resultados: Desarrollamos el estudio desde 2012 a 2018, con un seguimiento de los pacientes de 0 a 114 meses, encontrando un grado de recidiva del 15.38% y una mortalidad del 34.6%. La complicación más frecuente como consecuencia de la cirugía ablativa realizada fue la parálisis facial en los 3 casos en que no se preservó el nervio facial y la neuropraxia del nervio facial, principalmente de sus ramas bucal y marginal, que cedió con el tiempo. Conclusiones: El tratamiento de las tumoraciones metastásicas de la GP consecuencia de este tipo de tumoraciones cutáneas, es preferentemente quirúrgico con exéresis de la glándula y respetando el nervio facial siempre que la invasión tumoral no lo afecte. La radioterapia postoperatoria será también útil como complemento del tratamiento. Los resultados con el tratamiento combinado son actualmente poco esperanzadores, pero se espera una mejoría de las expectativas principalmente por los tratamientos inmunoterápicos en el caso de los melanomas y radioterápicos en las invasiones por carcinomas espinocelulares. Seguramente todo ello permitirá que el tratamiento quirúrgico sea menos radical y con secuelas escasas

Background and objective: When developed on head and neck, both melanoma and non-melanoma skin cancer (NMSC) can be spread to the parotid gland (PG) because of its permanence or due to the lymphatic spreading. In this case, the most appropriate option is the surgical procedure, provided that the progression of the tumor, the general condition of the patient and the non-dissemination of the tumor allow it. Our aim is to analyze the treatment followed and the number of recurrences, as well as mortality of our series in which the tumors cited invades the GP. Methods: The study includes a selection of 26 patients (22 male and 2 female) with a parotid gland tumor diagnosis as a consequence of a melanoma/ NMSC metastasis. All of them had undergone surgical procedure, 5 with a superficial lobe parotidectomy, and the remaining 19 with a total parotidectomy. Modified radical neck dissection Type III was applied to 19 patients. After that, they continued receiving radiotherapy and/or chemo o inmunotherapy. Results: This study was conducted between 2012 and 2018, with a patient’s follow-up from 0 to 114 months. Patients had a recurrence rate of 15.38% a mortality of 34.6%. The most frequent complications as a result of the surgical ablation were the facial paralysis in all 3 cases where the facial nerve was not preserved, and the neurapraxia in the facial nerve, specifically the marginal mandibular branches and the buccal branches, which decreased over time. Conclusions: The preferred treatment of metastasis of PG tumors as a consequence of this kind of skin cancer is the surgical procedure with gland exeresis and keeping the facial nerve, as long as the tumor invasion does not affect it. Postoperative radiotherapy will also be an essentially useful resource as a treatment complement. For the moment, the results of the combinated therapy are not encouraging. However, thanks to the immunotherapies applied in melanoma cases and to the radiotherapy applied in squamous cell carcinoma invasions, best prospects are expected. Probably, this will result in less radical surgical procedures with few sequelae

Solanidine and tomatidine trigger scar pruritus.

Scar pruritus is frequently encountered in clinical practice (particularly in burn patients) owing to its poorly known pathogenesis and difficult treatment. In previous work, we demonstrated the usefulness of a diet excluding edible solanaceae (viz., potatoes, tomatoes, peppers and aubergines) in patients with antihistamine-resistant scar pruritus. We hypothesized that alkaloids in solanaceae (particularly their secondary metabolites or aglycones) might be the actual pruritogens. In order to test this hypothesis, we conducted a single-blind prospective study on patients responding favourably to a solanaceae-free diet whose scar pruritus could be ascribed to one of the four foods. The study involved applying the aglycones solanidine and tomatidine to each scar and checking whether, and which, had a pruritogenic effect. A total of 18 patients (90%) responded by developing pruritus; also, the triggering aglycone coincided with that prevailing in the pruritogenic food. We concluded that solanaceae aglycones are directly involved in the pathogenesis of scar pruritus.

Keloids: A viral hypothesis.

The triggering cause of keloid formation on a healing wound remains an enigma. In fact, the hypotheses put forward so far to explain this phenomenon seem inconsistent with some clinical features of the disease. The recently established bonds between infectious agents and some pathologies of unknown origin such as peptic ulcer disease, Kaposi's sarcoma or cervical cancer among others led us to consider a potential infectious origin for keloids. This paper presents an infection-based hypothesis (specifically, a viral hypothesis) intended to account for most of their clinical features. Essentially, we hypothesize that healthy individuals carrying a virus, whether known or unknown, associated to some adjuvant, and having some genetic susceptibility, may develop keloids during the scar maturation process in the following manner: the virus would make the bone marrow or lymphatic system its reservoir, residing there in a silent state, and reach the wound via two different mechanisms. The primary mechanism might use an internal circuit through which the viral genome would be transported from its myeloid reservoir to the wound via bone marrow or circulating fibrocytes chemotactically attracted to the damaged skin region. The secondary mechanism might involve an external circuit by which infecting virions via saliva would be shed in the wound directly (preferentially in the sternal or deltoid region) or indirectly (other satellite regions) via the hands or some fomites. A combination of both mechanisms might also be possible. Once in the wound, the virus would switch from a silent state to a latent state by effect of some chemical stimulus probably generated during the tissue repair process; in the new state, the transcription of some of the powerful viral proteins might cause thorough derailment of the normal repair process. As a result, keloid growth might depend both on individual susceptibility and on the viral load deposited into the wound; the greater the susceptibility and viral load were, the more markedly the keloid would develop and the more aggressive it would be.