• Title/Summary/Keyword: Focal inflammatory lesions

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Chemical burns of the oral mucosa caused by Policresulen: report of a case (Policresulen 오용에 의한 구강 궤양의 발병 증례 및 화학화상에 대한 고찰)

  • Jung, Jung-Woo;Byun, Jin-Seok;Jung, Jae-Kwang;Choi, Jae-Kap
    • Journal of Oral Medicine and Pain
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    • v.38 no.2
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    • pp.109-114
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    • 2013
  • Chemical burn on the oral mucosa is caused by contact with various chemical products and manifests with localized mucositis, keratotic white lesions, bleeding, and painful tissue surface due to the coagulation of the tissue. Policresulen ($Albothyl^{(R)}$) is a topical antiseptic, commonly used over-the-counter drug for vaginitis, thrush and stomatitis. This drug is highly acidic with pH 0.6, and can act as a strong corrosive agent to oral mucosa. When inadvertently used in oral cavity, it may cause chemical burns of oral mucosa, resulting necrosis and bleeding surface resembling to erythema multifome. A 56 years old female patient presented with the chief complaints of painful ulcerations on the tongue, the upper and lower lips. On intraoral examination, an erythromatous, erosive or ulcerative surface covered with inflammatory exudates or bleeding crust is observed on the anterior half of the tongue and the upper and lower lips. She has occasionally applied the policresulen solution topically on the tongue to relieve pain from recurrent focal glossitis for about 10 years. In this time she applied it broadly and repeatedly to the tongue, the upper and lower lips for the purpose of pain relief by herself without instruction by physician or dentist. After cessation of policresulen application, the oral mucosa was rapidly recovered with use of topical steroids. In 2 weeks the lesions subsided completely. In summary, inadvertent use of $Albothyl^{(R)}$ on oral mucosa may result in chemical burn, causing mucosal erosion, ulceration and inflammation. It can be recovered by topical use of corticosteroid for 2 weeks after cessation of using $Albothyl^{(R)}$.

Chunghyul-dan for the Prevention of Stroke Progression in Silent Brain Infarction (무증후성 뇌경색 환자에 대한 청혈단(淸血丹)의 중풍예방효과)

  • Cho Ki-Ho;Ji Nam-Gue;Jung Woo-Sang;Park Seong-Uk;Moon Sang-Kwan;Ko Chang-Nam;Kim Young-Suk;Bae Hyung-Sup
    • The Journal of Korean Medicine
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    • v.26 no.2 s.62
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    • pp.77-84
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    • 2005
  • Objectives: Chunghyul-dan is a combinatorial herbal medicine, and previous studies reported it had therapeutic effects for microangiopathy, which is a major part. in the progression of stroke, as well as having anti-hypertensive, anti-hyperlipidemic, anti-apoptotic, anti-oxidative, and anti-inflammatory activities, Therefore, we examined the inhibitory effect of Chunghyul-dan on stroke occurrence in patients with silent brain infarction. Methods: We prescribed Chunghyul-dan at 600 mg a day to patients with silent brain infarction confirmed by brain MRI, and monitored stroke occurrence, drug compliances, and adverse effects for 1 year, We then performed follow-up brain MRI to detect new vascular lesions after 1 year of Chunghyul-dan medication. As for the subjects lost to follow-up, we assessed their prognosis after 1 year by telephone. Results: There were twenty-one subjects who were treated with Chunghyul-dan for more than 1 year, None of them experienced new clinical syndromes characterized by rapidly developing clinical symptoms and signs of focal and at times global loss of brain function, which could be accompanied with evidence of stroke occurrence, or any adverse effects during the Chunghyul-dan medication period. These results might be explained by various biochemical effects of Chunghyul-dan on microangiopathy, which is closely related with cell cycle progression, hypertension, hyperlipidemia, vascular inflammation, and oxidative damage. Of the 10 subjects lost to follow-up, six were reached; two of them had stroke occurrence. Conclusions: We suggest Chunghyul-dan could be useful for prevention of stroke occurrence in patients with silent brain infarction by preventing the progression of microangiopathy. Further study with a randomized controlled trial is needed to confirm this suggestion.

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Expressions of Matrix Metalloproteinase-9 and Tissue Inhibitor of Metalloproteinase-2 with Changes of Interleukin-6 and Interleukin-18 in Atherosclerotic Lesions of Hypercholesterolemic Rabbits (고콜레스테롤혈증 가토의 죽상경화성 병변에서 Interleukin-6와 Interleukin-18의 변화 및 Matrix Metalloproteinase-9과 Tissue Inhibitor of Metalloproteinase-2의 발현)

  • 권영무;김성숙;장봉현
    • Journal of Chest Surgery
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    • v.35 no.6
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    • pp.407-419
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    • 2002
  • Atherosclerosis is a chronic inflammatory disease of the arterial wall characterized by progressive accumulation of lipids, cells, and extracellular matrix. Matrix metalloproteinases(MMPs) and tissue inhibitor of metalloproteinases(TIMPS) contribute to vascular matrix remodeling in atherosclerosis, and some cytokines may play role in the synthesis or activation of MMPs or TIMPs. Material and Method: We produced experimental atherosclerotic plaques in 9 rabbits by atherogenic hypercholesterol diet for 12 weeks, and 10 other rabbits were used as control group with standard laboratory chow, At that time, 19 rabbits were sacrificed and aorta, coronary arteries and blood specimens were prepared. The expressions of MMP-9, TIMP-2 and interleukin(IL)-18, and the bioactivity of IL-6 were investigated with H&E stain, immunohistochemical stain, immunoblotting(Western blot analysis), and bioassay. Result: Serum cholesterol in the experimental group increased up to 1258$\pm$262 mg/dL(control group: 41$\pm$7 mg/dL). All experimental group showed well-developed atherosclerotic plaques in aorta and coronary artery. The expression of MMP-9 in aorta and coronary artery of the experimental group showed significant increase than that of the control group by immunohistochemistry. Among the experimental group, complicated lesions with intimal rupture or complete luminal occlusion, demonstrated stronger expression of MMP-9. Interestingly, there was no difference in expression of TIMP-2 between the experimental and the control group. These findings were confirmed by Western blot analysis. The bioassay revealed significant up-regulation of serum bioactivity of IL-6 in the experimental group(4819.60$\pm$2021.25 IU/$m\ell$) compared to that of IL-6 in the control group(27.20 $\pm$ 12.19 IU/$m\ell$). IL-18 was expressed in all atherosclerotic plaques, whereas little or no expression was detected in the control group. Conclusion: The increased MMP-9 expression along with the unchanged TIMP-2 expression seem to be contributory factors in extracellular matrix degradation in atherosclerosis. Focal overexpression of MMP-9 may promote plaque destabilization and cause complications of atherosclerotic plaques such as thrombosis with/without acute coronary syndrome. Elevation of IL-6 and IL-18 may be more than just markers of atherosclerosis but actual participants in lesion development. Identification of critical regulatory pathway is important to improve the understanding of the cellular and molecular basis of atherosclerosis and may open the way for novel therapeutic strategies.