piperidines and Radiodermatitis

Radiation recall dermatitis is an uncommon inflammatory reaction of the skin appearing after several days to several years at the site of previous irradiation; it is precipitated by the use of triggering drugs, although rarely by BRAF or MEK inhibitors.. We report an unusual case of recall dermatitis induced 3 months after initiation of vemurafenib and cobimetinib therapy.. Radiation recall dermatitis is a cutaneous reaction that must be known and which in rare cases such as ours may occur a long time after the end of radiotherapy.

Topics: Adrenal Gland Neoplasms; Antineoplastic Agents; Azetidines; Ear Auricle; Ear Neoplasms; Facial Dermatoses; Humans; Male; MAP Kinase Kinase 1; Melanoma; Middle Aged; Piperidines; Radiodermatitis; Skin Neoplasms; Vemurafenib

The radiation recall reaction (RRR) is an inflammatory reaction that occurs in previously irradiated areas. The phenomenon is probably due to an idiosyncratic hypersensitivity reaction, in which a second agent can recall the inflammatory reaction.. This case report documents a cold-weather-induced radiation recall dermatitis (RRD). We observed a severe RRD in a patient after chemoradiotherapy treatment with cisplatin for a nasopharyngeal carcinoma, precipitated by cold temperatures, which developed 9 days after completion of therapy. In the medical literature, RRD following extreme cold temperatures seems to be a peculiar event.. Until further information on the interaction is available, future studies on combined chemotherapy with cisplatin should be carefully monitored and any side effects clearly documented. This case suggests that environmental conditions may play a contributing role in the development of RRD. This case also implies that neither fraction size nor total radiation dose is a determining factor in the development of the dermatologic reaction.

Topics: Aged; Antineoplastic Agents; Butyrophenones; Carcinoma, Squamous Cell; Chemoradiotherapy; Cisplatin; Cold Temperature; Drug Therapy, Combination; Female; Humans; Methylprednisolone; Nasopharyngeal Neoplasms; Neoplasm Staging; Piperidines; Radiodermatitis

Topics: Carcinoma; Chemotherapy, Adjuvant; Drug Eruptions; Histamine H2 Antagonists; Humans; Lymph Node Excision; Lymphatic Metastasis; Male; Middle Aged; Piperidines; Psoriasis; Radiodermatitis; Radiotherapy, Adjuvant; Tongue Neoplasms

A possible involvement of histamine in acute radiation dermatitis in mice was investigated. The dose of 40 Gy of gamma irradiation induced erythema and edema in C57BL/6 mice treated with vehicle. However, in C57BL/6 mice treated with chlorpheniramine and WBB6F1-W/Wv mice, erythema and edema were not observed. In all of these mice, epilation and dry desquamation were induced, but bepotastine significantly reduced the extent of these areas. These results suggest that gamma irradiation-induced erythema and edema were caused by histamine released from mast cells via histamine H1 receptor, and epilation was induced by other inflammatory mediators.

Topics: Acute Disease; Animals; Chlorpheniramine; Dose-Response Relationship, Drug; Edema; Erythema; Hair Removal; Histamine; Histamine H1 Antagonists; Histamine Release; Male; Mast Cells; Mice; Mice, Inbred C57BL; Piperidines; Pyridines; Radiodermatitis; Receptors, Histamine H1

The ultraviolet (UV) components of sunlight induce damage to the DNA in skin cells, which is considered to be the initiating step in the harmful biological effects of UV radiation. Repair of DNA damage results in the formation of single-strand DNA breaks, which activate the nuclear poly(ADP-ribose) polymerase (PARP). Overactivation of PARP worsens the oxidative cell damage and impairs the energy metabolism, raising the possibility that moderation of PARP activation following DNA damage may protect skin cells from UV radiation. The topical effects of the novel PARP inhibitor O-(3-pyperidino-2-hydroxy-1-propyl) pyridine-3-carboxylic acid amidoxime monohydrochloride (BGP-15M) were investigated on UV-induced skin damage in a hairless mouse model. For evaluation of the UV-induced acute photodamage to the skin and the potential protective effect of BGP-15M, DNA injury was detected by measuring the formation of single-strand DNA breaks and counting the resulting sunburn (apoptotic) cells. The ADP-ribosylation of PARP was assessed by Western blot analysis and then quantified. In addition, the UV-induced immunosuppression was investigated by the immunostaining of tumor necrosis factor alpha and interleukin-10 expressions in epidermal cells. The signs of inflammation were examined clinically and histochemically. Besides its primary effect in decreasing the activity of nuclear PARP, topically applied BGP-15M proved to be protective against solar and artificial UV radiation-induced acute skin damage. The DNA injury was decreased (P<0.01). An inhibition of immunosuppression was observed by down-regulation of the epidermal production of cytokines IL-10 and TNFalpha. In the mouse skin, clinical or histological signs of UV-induced inflammation could not be observed. These data suggest that BGP-15M directly interferes with UV-induced cellular processes and modifies the activity of PARP. The effects provided by topical application of the new PARP-regulator BGP-15M indicate that it may be a novel type of agent in photoprotection of the skin.

Topics: Adenosine Diphosphate; Administration, Topical; Animals; DNA Damage; DNA, Single-Stranded; Epidermis; Interleukin-10; Mice; Mice, Nude; Oximes; Piperidines; Poly(ADP-ribose) Polymerase Inhibitors; Protective Agents; Radiodermatitis; Sunburn; Tumor Necrosis Factor-alpha; Ultraviolet Rays