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)

Mucocutaneous lymph node syndrome, Kawasaki disease, is a potentially fatal pediatric disease characterized by prolonged high fever, conjunctivitis, stomatitis. myocarditis, aseptic meningitis and coronary artery vasculitis. We present peritonsillar abscess as a previously unreported otolaryngologic symptom and presentation of Kawasaki disease. A previously healthy 7-year-old boy required hospitalization for a peritonsillar abscess. Despite adequate surgical drainage and appropriate intravenous antibiotics, the patients' systemic symptoms persisted. After the week of hospitalization, the child was transferred to the intensive care unit with acute myocarditis, heart failure and severe arthritis. The diagnosis of Kawasaki disease was confirmed with echocardiographic evidence of coronary artery aneurysms and the development of the characteristic hand and foot desquamation. The patient's symptoms resolved with salicylates and intravenous gamma globulin therapy. He was discharged in good condition after 3 weeks of hospitalization. This is the first report of Kawasaki syndrome presenting with peritonsillar abscess. Although we discuss a unique presentation of this disease. Kawasaki syndrome often exhibits other otolaryngologic findings early in its course. A literature review of the clinical characteristics, pathogenesis and therapy of this disease is presented.
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PMID:Peritonsillar abscess in Kawasaki disease. 226 96

Systemic pathological alterations were studied in thirty-seven autopsied patients with Kawasaki disease. Systemic vasculitis was the most characteristic pathological finding and was present in all the patients. In addition to the vasculitis, there was a high incidence of inflammatory lesions in various organs and tissues: in the heart, endocarditis, myocarditis, and pericarditis; in the digestive system, stomatitis, sialoduct-adenitis, catarrhal enteritis, hepatitis, cholangitis, pancreatitis, and pancreas ductitis; in the respiratory system, bronchitis and segmental interstitial pneumonia; in the urinary system, focal interstitial nephritis, cystitis, and prostatitis; in the nervous system, aseptic leptomeningitis, choriomeningitis, gangliontis, and neuritis; in the hematopoietic system, lymphadenitis, splenitis, and thymitis. Dermatitis, panniculitis or myositis were also observed in some patients. Therefore, Kawasaki disease is a systemic inflammatory disease which mainly affects the cardiovascular system. These systemic inflammatory lesions are considered to correspond to the variegated clinical manifestaitions. The relationship between Kawasaki disease and infantile polyarteritis nodosa (IPN) were discussed, based on the clinicopathological characteristics.
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PMID:General pathology of Kawasaki disease. On the morphological alterations corresponding to the clinical manifestations. 744 9

Cardiac antigen-specific CD8(+) T cells are involved in the autoimmune component of human myocarditis. Here, we studied the differentiation and migration of pathogenic CD8(+) T cell effector cells in a new mouse model of autoimmune myocarditis. A transgenic mouse line was derived that expresses cardiac myocyte restricted membrane-bound ovalbumin (CMy-mOva). The endogenous adaptive immune system of CMy-mOva mice displays tolerance to ovalbumin. Adoptive transfer of naive CD8(+) T cells from the ovalbumin-specific T cell receptor-transgenic (TCR-transgenic) OT-I strain induces myocarditis in CMy-mOva mice only after subsequent inoculation with ovalbumin-expressing vesicular stomatitis virus (VSV-Ova). OT-I effector T cells derived in vitro in the presence or absence of IL-12 were adoptively transferred into CMy-mOva mice, and the consequences were compared. Although IL-12 was not required for the generation of cytolytic and IFN-gamma-producing effector T cells, only effectors primed in the presence of IL-12 infiltrated CMy-mOva hearts in significant numbers, causing lethal myocarditis. Furthermore, analysis of OT-I effectors collected from a mediastinal draining lymph node indicated that only effectors primed in vitro in the presence of IL-12 proliferated in vivo. These data demonstrate the importance of IL-12 in the differentiation of pathogenic CD8(+) T cells that can cause myocarditis.
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PMID:IL-12 is required for differentiation of pathogenic CD8+ T cell effectors that cause myocarditis. 1261 21

5-fluorouracil is an anti-cancer drug commonly used in oncology practice. Typical side effects are myelosupression, nausea, vomiting, diarrhea and stomatitis. Cardiotoxicity is the other toxicity. Cardiac side effects are ST segment changes, rhythm abnormalities, supraventricular and ventricular dysrhytmias. Pulseless ventricular tachycardia and ventricular fibrillation releated with bolus fluorouracil were not detected in the literature. Here we discussed a 46 year-old male patient that has no known cardiac history. After bolus fluorouracil administration, syncope and pulseless ventricular tachycardia developed in this patient. There are a few explanations about the cardiotoxicity of fluorouracil. One of these is the effect on nitric oxide. It causes a reduction in the levels of endothelial NO and this leads coronary vasospasm. Another explanation is protein kinase C mediated vasospasm. In animal studies toxic myocarditis like lesions were detected with fluorouracil infusions. Finally both myocardit and vasospasm may lead cardiac problems like sudden cardiac deaths. Bolus 5-fluorouracil is as cardiotoxic as 5-fluorouracil infusion and we must be careful about the arrhytmia after the bolus administration.
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PMID:Bolus fluorouracil induced syncope and pulseless ventricular tachycardia: a case report. 2160 46

Recombinant vesicular stomatitis virus (VSV) is widely used as a vaccine platform. However, the capacity of VSV-based vaccines to induce mucosal immunity has not been fully investigated. In the present study, a recombinant VSV expressing coxsackievirus B3 (CVB3) major immunogen VP1 has been generated and the immune protection elicited by VSV-VP1 was evaluated. We demonstrated that intranasal delivery of VSV-VP1 can induce a potent antigen-specific mucosal immune response as well as a systemic immune response, particularly the induction of polyfunctional T cells. Importantly, mice immunized with VSV-VP1 were better protected against CVB3-induced viral myocarditis than those receiving a chitosan-formulated DNA vaccine. Increased dendritic cell (DC) maturation in the mesenteric lymph node (MLN) was observed in the mice vaccinated with VSV-VP1, which could be a potential mechanism for the protective immune response. These findings support VSV as a viral delivery vector that can induce robust mucosal immunity that should be considered for further vaccine development.
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PMID:A vesicular stomatitis virus-based mucosal vaccine promotes dendritic cell maturation and elicits preferable immune response against coxsackievirus B3 induced viral myocarditis. 2487 23

We present a case of a patient with drug-induced hypersensitivity syndrome (DIHS) caused by salazosulfapyridine combined with syndrome of inappropriate secretion of antidiuretic hormone (SIADH) caused by interstitial pneumonia (IP). A 67-year-old man with a past history of rheumatism (RA) presented with right hemiparalysis and aphasia as the chief complaints. A diagnosis of left embolic cerebral infarction following trial therapy for RA based on computed tomography findings was made, and external decompression was performed. Salazosulfapyridine was newly started on day 7. Dabigatran was started on day 37. On day 41, the patient developed fever. On day 42, edema and erythema appeared on his face, and erythema and rash appeared on his trunk and extremities, with gradual transition to erythroderma. The drug eruption was initially attributed to the dabigatran. Various symptoms of organ dysfunction (enteritis, myocarditis, interstitial pneumonia, hepatic disorder, stomatitis, and others) then appeared and persisted; hence, a diagnosis of DIHS associated with human herpes virus 6 and cytomegalovirus infection induced by salazosulfapyridine was suggested, and the oral administration of salazosulfapyridine was discontinued on day 53. Hyponatremia was observed in association with exacerbation of IP. Due to low serum osmotic pressure and prompt improvement of the serum sodium level by fluid restriction, the SIADH was attributed to IP. In this case, steroid pulse therapy followed by gradual decrease therapy prevented worsening of the condition.
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PMID:A case of drug-induced hypersensitivity syndrome induced by salazosulfapyridine combined with SIADH caused by interstitial pneumonia. 3153 76