Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038362 (stomatitis)
 8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 39-year-old woman was admitted to our hospital with an eight-month history of dyspnea on exertion, weakness and increasing fatigue. She reported repeated episodes of menometrorrhagia and underwent a myomectomy. She is not a vegetarian. Her menstrual bleeding: 3-5 days per month. Two months ago, she complained of burning sensation of the tongue upon swallowing food and noted brittle nails. She tolerated soft foods. On physical examination, she was pale; her nails were very thin, fragile and somewhat concave. Her oral examination showed angular stomatitis, depapillated tongue and glossitis. The clinical diagnosis was anemia and dysphagia. Laboratory tests were: Hb: 7.0g/dL, MCV: 57.42fL, MCH: 15.82 pg; leukocytes: 4,980; reticulocytes: 2.18%, reticulocyte index: 0.1%, serum iron: 21ug/dl, total iron binding capacity (TIBC): 286, transferrin saturation: 7% and serum ferritin: 27ng/ml. The peripheral blood smear showed anisocytosis and hypochromic microcytic cells. Thevenon test was negative. Abdominal ultrasound: uterine myoma. A barium swallow X-ray showed a 2-mm linear filling defect between the 4th and 5th cervical vertebrae in the anteroposterior and lateral view; it protruded from the anterior wall and reduced esophageal lumen by 60%. In the endoscopy, we found a fibrous web in the cricopharyngeal area. Serial dilatations were performed over a guidewire using Savary-Gilliard dilators with diameter up to 14 mm, improving dysphagia. She was treated with transfusional therapy and parenteral iron. She was discharged with ferrous sulfate and folic acid. The Plummer-Vinson syndrome, Paterson-Brown-Kelly or sideropenic dysphagia is characterized by dysphagia, irondeficiency anemia and upper esophageal web. The syndrome is described as very rare.
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PMID:[Plummer-Vinson syndrome: report of a case and review of literature]. 2302 85

Targeted therapies and immunotherapies are associated with a wide range of dermatologic adverse events (dAEs) resulting from common signaling pathways involved in malignant behavior and normal homeostatic functions of the epidermis and dermis. Dermatologic toxicities include damage to the skin, oral mucosa, hair, and nails. Acneiform rash is the most common dAE, observed in 25-85% of patients treated by epidermal growth factor receptor and mitogen-activated protein kinase kinase inhibitors. BRAF inhibitors mostly induce secondary skin tumors, squamous cell carcinoma and keratoacanthomas, changes in pre-existing pigmented lesions, as well as hand-foot skin reactions and maculopapular hypersensitivity-like rash. Immune checkpoint inhibitors (ICIs) most frequently induce nonspecific maculopapular rash, but also eczema-like or psoriatic lesions, lichenoid dermatitis, xerosis, and pruritus. Of the oral mucosal toxicities observed with targeted therapies, oral mucositis is the most frequent with mammalian target of rapamycin (mTOR) inhibitors, followed by stomatitis associated to multikinase angiogenesis and HER inhibitors, geographic tongue, oral hyperkeratotic lesions, lichenoid reactions, and hyperpigmentation. ICIs typically induce oral lichenoid reactions and xerostomia. Targeted therapies and endocrine therapy also commonly induce alopecia, although this is still underreported with the latter. Finally, targeted therapies may damage nail folds, with paronychia and periungual pyogenic granuloma distinct from chemotherapy-induced lesions. Mild onycholysis, brittle nails, and a slower nail growth rate may also be observed. Targeted therapies and immunotherapies often profoundly diminish patients' quality of life, which impacts treatment outcomes. Close collaboration between dermatologists and oncologists is therefore essential.
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PMID:Toxic Side Effects of Targeted Therapies and Immunotherapies Affecting the Skin, Oral Mucosa, Hair, and Nails. 3037 1