多点扇形皮下注射治疗胫前粘液性水肿的观察与护理

胫前粘液性水肿,又称甲状腺毒性粘液蛋白沉积症,是毒性弥漫性甲状腺肿(G raves病)的一种皮肤损害,约占G raves病的5%犤1犦,属于自身免疫病,是较少见的局限性皮肤病变。一般发生在胫骨前下1/3处,皮肤损害常呈对称性,早期皮肤呈广泛性红肿,之后出现皮肤的增厚、变粗,有广泛大小不等的棕褐色突起、不平的斑块或结节,边界清楚,后期可扩展到足背、踝关节等处,皮肤如橘皮样,皮损融合,毳毛增多、增长,毛干粗大,下肢粗大似橡皮腿,容易误诊,严重影响患者的自我形象和功能,降低其生活质量。目前,胫前粘液水肿临床上尚缺乏统一的治疗方法,除常规纠正甲状腺功能紊乱、部分病人全身使用糖皮质激素外,常用的治疗方法有:局部涂擦激素类软膏、单独皮质类固醇激素皮下注射犤2犦及手术植皮等,但疗效慢,易复发,且与局部注射的方法有密切关系。而我科自2004年底以来采用药物多点扇形皮下注射,共治疗了20例患者,疗效满意,受到患者的一致好评,现将方法、体会介绍如下。1临床资料1.1一般资料本组20例,男性13例,女性7例,其中12例为诊断甲亢后服放射性碘犤3犦治疗数月后出现胫前粘液性水肿,8例为诊断甲亢后行“甲状腺次全切除术”,术后1年左右甲亢...     

信息动态

胫前黏液性水肿(pretibial myxedema,PTM),又称局部性黏液性水肿、甲状腺相关皮肤病,是Grave's病很少出现的一种皮肤损害.皮损最常见的部位是小腿,特别是胫前或足背,但偶尔也可发生于肘部、手背部甚至面部.皮损形态不一,双侧出现,但不对称,可表现为圆形或卵圆形坚实水肿性斑块或结节,压之无凹陷,可呈正常皮色、淡红或棕色.根据皮损分3种类型:弥漫型、瘤样结节或红斑样皮疹型、象皮腿型.实验室检查有高滴度的甲状腺激素受体抗体.病理表现为表皮角化过度,真皮血管周围少量淋巴细胞,成纤维细胞增生,真皮中下部大量黏蛋白沉积,阿申蓝染色阳性.治疗上缺乏大样本随机双盲对照的临床试验,首选外用糖皮质激素,出现抵抗时可考虑口服糖皮质激素或免疫调节治疗,手术多不推荐.     

胫前黏液性水肿的研究进展

胫前黏液性水肿(pretibial myxedema,PTM),又称局部性黏液性水肿、甲状腺相关皮肤病,是Grave's病很少出现的一种皮肤损害.皮损最常见的部位是小腿,特别是胫前或足背,但偶尔也可发生于肘部、手背部甚至面部.皮损形态不一,双侧出现,但不对称,可表现为圆形或卵圆形坚实水肿性斑块或结节,压之无凹陷,可呈正常皮色、淡红或棕色.根据皮损分3种类型:弥漫型、瘤样结节或红斑样皮疹型、象皮腿型.实验室检查有高滴度的甲状腺激素受体抗体.病理表现为表皮角化过度,真皮血管周围少量淋巴细胞,成纤维细胞增生,真皮中下部大量黏蛋白沉积,阿申蓝染色阳性.治疗上缺乏大样本随机双盲对照的临床试验,首选外用糖皮质激素,出现抵抗时可考虑口服糖皮质激素或免疫调节治疗,手术多不推荐.     

瘢痕疙瘩组织及其周边正常皮肤成纤维细胞斑点粘合激酶表达差异的意义

目的:比较血小板源生长刺激因子刺激后瘢痕疙瘩组织(瘢痕疙瘩)和瘢痕疙瘩周边相对正常皮肤组织来源的成纤维细胞(周边)、正常人皮肤成纤维细胞(正常)斑点粘合激酶分子信号的表达及磷酸化差异,分析瘢痕特别是瘢痕发病过程中斑点粘合激酶的作用。方法:实验于2000-10/2002-10在日本国立神户大学医学部分子生物学实验室完成。5例瘢痕疙瘩成纤维细胞及瘢痕疙瘩周边相对正常皮肤成纤维细胞标本均来自日本国立神户大学附属医院形成外科及皮肤科瘢痕疙瘩切除患者,与患者说明目的并征得同意。以正常人皮肤成纤维细胞为标准对照组。应用免疫印迹方法检测瘢痕疙瘩及周边、正常皮肤成纤维细胞的斑点粘合激酶含量及其激酶蛋白磷酸化情况。结果:①无刺激条件下,瘢痕疙瘩成纤维细胞的斑点粘合激酶表达较瘢痕疙瘩周边及正常皮肤组织来源的成纤维细胞增强。②血小板源生长刺激因子-BB刺激后,瘢痕疙瘩及周边、正常皮肤来源的成纤维细胞斑点粘合激酶磷酸化均增强,但以瘢痕疙瘩成纤维细胞的斑点粘合激酶磷酸化更明显。③血小板源生长刺激因子-BB刺激后,瘢痕疙瘩成纤维细胞中斑点粘合激酶蛋白磷酸化明显高于瘢痕疙瘩周边及正常皮肤组织来源的成纤维细胞,但斑点粘合激酶含量无明显改变。结论:虽然瘢痕疙瘩成纤维细胞与瘢痕疙瘩周边相对正常皮肤成纤维细胞的斑点粘合激酶含量相同,但是斑点粘合激酶在瘢痕疙瘩成纤维细胞中高表达,表明斑点粘合激酶的磷酸化增强可能与瘢痕疙瘩的发生发展有关。     

脂多糖对增生性瘢痕患者正常皮肤成纤维细胞Ⅰ,Ⅲ型前胶原及胶原酶信使核糖核酸表达的调控及意义

目的:研究细菌脂多糖对增生性瘢痕患者正常皮肤成纤维细胞Ⅰ,Ⅲ型前胶原及胶原酶信使核糖核酸表达的影响,了解细菌脂多糖在增生性瘢痕形成中的生物学作用。方法:体外培养增生性瘢痕患者瘢痕组织及正常皮肤成纤维细胞,应用不同浓度(0.005~1.0μg/mL)的大肠杆菌细菌脂多糖(E.coli055:B5)对正常皮肤成纤维细胞进行刺激,并对刺激后细胞传代至表型稳定(第8代),采用逆转录-聚合酶链反应法检测细菌脂多糖对正常皮肤成纤维细胞Ⅰ,Ⅲ型前胶原及胶原酶信使核糖核酸表达的调控作用,观察剂量-效应关系。分别以同个体相同代数的瘢痕组织成纤维细胞和未经细菌脂多糖刺激的正常皮肤成纤维细胞做对照。结果:细菌脂多糖刺激浓度0.005~0.5μg/mL范围内促进正常皮肤成纤维细胞Ⅰ,Ⅲ型前胶原信使核糖核酸表达,抑制胶原酶信使核糖核酸表达(P<0.01),均在0.1μg/mL浓度点作用达高峰;当细菌脂多糖刺激浓度到达1.0μg/mL时,抑制正常皮肤成纤维细胞Ⅰ,Ⅲ型前胶原信使核糖核酸表达,促进胶原酶信使核糖核酸表达,且均显著低于阴性对照组(P<0.01);当浓度为0.1μg/mL时,正常皮肤成纤维细胞Ⅰ,Ⅲ型前胶原信使核糖核酸和胶原酶...     

瘢痕疙瘩组织及其周边正常皮肤成纤维细胞斑点粘合激酶表达差异的意义

目的：比较血小板源生长刺激因子刺激后瘢痕疙瘩组织（瘢痕疙瘩）和瘢痕疙瘩周边相对正常皮肤组织来源的成纤维细胞（周边）、正常人皮肤成纤维细胞（正常）斑点粘合激酶分子信号的表达及磷酸化差异，分析瘢痕特别是瘢痕发病过程中斑点粘合激酶的作用。方法：实验于2000—10／2002—10在日本国立神户大学医学部分子生物学实验室完成。5例瘢痕疙瘩成纤维细胞及瘢痕疙瘩周边相对正常皮肤成纤维细胞标本均来自日本国立神户大学附属医院形成外科及皮肤科瘢痕疙瘩切除患者，与患者说明目的并征得同意。以正常人皮肤成纤维细胞为标准对照组。应用免疫印迹方法检测瘢痕疙瘩及周边、正常皮肤成纤维细胞的斑点粘合激酶含量及其激酶蛋白磷酸化情况。结果：①无刺激条件下，瘢痕疙瘩成纤维细胞的斑点粘合激酶表达较瘢痕疙瘩周边及正常皮肤组织来源的成纤维细胞增强。②血小板源生长刺激因子-BB刺激后，瘢痕疙瘩及周边、正常皮肤来源的成纤维细胞斑点粘合激酶磷酸化均增强，但以瘢痕疙瘩成纤维细胞的斑点粘合激酶磷酸化更明显。③血小板源生长刺激因子一BB刺激后，瘢痕疙瘩成纤维细胞中斑点粘合激酶蛋白磷酸化明显高于瘢痕疙瘩周边及正常皮肤组织来源的成纤维细胞，但斑点粘合激酶含量无明显改变。结论：虽然瘢痕疙瘩成纤维细胞与瘢痕疙瘩周边相对正常皮肤成纤维细胞的斑点粘合激酶含量相同，但是斑点粘合激酶在瘢痕疙瘩成纤维细胞中高表达，表明斑点粘合激酶的磷酸化增强可能与瘢痕疙瘩的发生发展有关。     

血小板源生长因子对瘢痕成纤维细胞胞外信号调节激酶的影响

目的:分析血小板源生长刺激因子(PDGF)刺激后各种成纤维细胞中胞外信号调节激酶(ERK)的表达及磷酸化情况,研究瘢痕特别是瘢痕疙瘩发病过程中ERK的作用。方法:应用免疫印迹(IB)方法检测5例瘢痕疙瘩成纤维细胞(KFB)、瘢痕疙瘩周边相对正常皮肤成纤维细胞(rNHDF)及正常人皮肤成纤维细胞(NHDF)的ERK表达及其蛋白磷酸化。结果:①无刺激条件下,ERK在KFB,rNHDF及NHDF中的表达及磷酸化无差异。②PDGF-BB刺激后,3组成纤维细胞ERK磷酸化增强,非磷酸化含量无明显改变。③DGF-BB刺激后,KFB中ERK蛋白磷酸化明显高于其他两组成纤维细胞。结论:瘢痕疙瘩细胞外基质的过度沉积可能与KFB内PDGF结合位点自身磷酸化和ERK的磷酸化增强有关。     

有关瘢痕形成机制研究:不同皮肤成纤维细胞对羊水的反应

目的:研究正常皮肤和胎儿皮肤成纤维细胞体外培养时对羊水的不同反应,探讨瘢痕形成的机制。方法:采用成纤维细胞体外培养技术,比较正常皮肤成纤维细胞与胎儿皮肤成纤维细胞对羊水的不同反应。结果:羊水对胎儿皮肤成纤维细胞无明显影响,刺激正常皮肤的成纤维细胞。结论:体外培养的正常皮肤成纤维细与胎儿皮肤成纤维细胞生长率相同,对羊水的反应不同。     

血小板源生长因子对瘢痕成纤维细胞胞外信号调节激酶的影响

目的：分析血小板源生长刺激因子(PDGF)刺激后各种成纤维细胞中胞外信号调节激酶(ERK)的表达及磷酸化情况，研究瘢痕特别是瘢痕疙瘩发病过程中ERK的作用。方法：应用免疫印迹(IB)方法检测5例瘢痕疙瘩成纤维细胞(KFB)、瘢痕疙瘩周边相对正常皮肤成纤维细胞(rNHDF)及正常人皮肤成纤维细胞(NHDF)的ERK表达及其蛋白磷酸化。结果：①无刺激条件下，ERK在KFB，rNHDF及NHDF中的表达及磷酸化无差异。②PDGF-BB刺激后，3组成纤维细胞ERK磷酸化增强，非磷酸化含量无明显改变。③DGF-BB刺激后，KFB中ERK蛋白磷酸化明显高于其他两组成纤维细胞。结论：瘢痕疙瘩细胞外基质的过度沉积可能与KFB内PDGF结合位点自身磷酸化和ERK的磷酸化增强有关。     

有关瘢痕形成机制研究：不同皮肤成纤维细胞对羊水的反应

目的：研究正常皮肤和胎儿皮肤成纤维细胞体外培养时对羊水的不同反应，探讨瘢痕形成的机制。方法：采用成纤维细胞体外培养技术，比较正常皮肤成纤维细胞与胎儿皮肤成纤维细胞对羊水的不同反应。结果：羊水对胎儿皮肤成纤维细胞无明显影响，刺激正常皮肤的成纤维细胞。结论：体外培养的正常皮肤成纤维细与胎儿皮肤成纤维细胞生长率相同，对羊水的反应不同。     

Pretibial myxedema

Pretibial myxedema is a localized dermopathy seen in patients with past or present hyperthyroidism. Massive intradermal deposition of mucin (acid mucopolysaccharide) produces the classic indurated nodules or plaques on the anterior lower legs. Most patients have elevated levels of LATS in their serum; however, this appears to be a marker for the disease, rather than a cause. Mild pretibial myxedema requires no treatment. Topical, intralesional or systemic steroids may be useful in severe cases.     

Myxedema coma: diagnosis and treatment

Myxedema coma, the extreme manifestation of hypothyroidism, is an uncommon but potentially lethal condition. Patients with hypothyroidism may exhibit a number of physiologic alterations to compensate for the lack of thyroid hormone. If these homeostatic mechanisms are overwhelmed by factors such as infection, the patient may decompensate into myxedema coma. Patients with hypothyroidism typically have a history of fatigue, weight gain, constipation and cold intolerance. Physicians should include hypothyroidism in the differential diagnosis of every patient with hyponatremia. Patients with suspected myxedema coma should be admitted to an intensive care unit for vigorous pulmonary and cardiovascular support. Most authorities recommend treatment with intravenous levothyroxine (T4) as opposed to intravenous liothyronine (T3). Hydrocortisone should be administered until coexisting adrenal insufficiency is ruled out. Family physicians are in an important position to prevent myxedema coma by maintaining a high level of suspicion for hypothyroidism.     

Idiopathic myxedema and blocking type antibodies to TSH receptor]

The pathogenetic role of thyrotropin-stimulation blocking antibodies (TSBab) in idiopathic myxedema has been described. Idiopathic myxedema is characterized as atrophic thyroid gland and positive autoantibodies to thyroid gland, including TSBab. TSBab is positive in 20-30% cases of idiopathic myxedema. TSBab is disappeared in some cases of TSBab positive idiopathic myxedema during treatment. In some of these cases, thyroid function recovered after the disappearance of TSBab. Transient neonatal hypothyroidism with TSBab positive was born in mothers of TSBab positive with autoimmune thyroid diseases. In these cases, thyroid function recovered with the disappearance of TSBab. Form these findings, it is suggested that TSBab may play a certain pathogenetic role in idiopathic myxedema.     

Intralesional and topical glucocorticoids for pretibial myxedema: A case report and review of literature

Pretibial myxedema (PTM), an uncommon manifestation of Graves’ disease (GD), is a local autoimmune reaction in the cutaneous tissue. The treatment of PTM is a clinical challenge. We herein report on a patient with PTM who achieved complete remission by multipoint subcutaneous injections of a long-acting glucocorticoid and topical glucocorticoid ointment application for a self-controlled study. A 53-year-old male presented with a history of GD for 3.5 years and a history of PTM for 1.5 years. Physical examination revealed slight exophthalmos, a diffusely enlarged thyroid gland, and PTM of both lower extremities. One milliliter of triamcinolone acetonide (40 mg) was mixed well with 9 mL of 2% lidocaine in a 10 mL syringe. Multipoint intralesional injections into the skin lesions of the right lower extremity were conducted with 0.5 mL of the premixed solution. A halometasone ointment was used once daily for PTM of the left lower extremity until the PTM had remitted completely. The patient’s PTM achieved complete remission in both legs after an approximately 5-mo period of therpy that included triamcinolone injections once a week for 8 wk and then once a month for 2 mo for the right lower extremity and halometasone ointment application once daily for 8 wk and then once 3-5 d for 2 mo for the left lower extremity. The total dosage of triamcinolone acetonide for the right leg was 200 mg. Our experience with this patient suggests that multipoint subcutaneous injections of a long-acting glucocorticoid and topical glucocorticoid ointment application are safe, effective, and convenient treatments. However, the topical application of a glucocorticoid ointment is a more convenient treatment for patients with PTM.     

Diagnosis and treatment of autoimmune thyroid disease (ATD) complicated by pregnancy]

During pregnancy, distinguishing TBII-negative Graves' disease from HCG-related thyrotoxicosis is important. There has been no convincing evidence for any adverse effects of maternal hyper- or hypothyroidism, or thionamides transferred from the mother on fetal organogenesis. In Graves' disease, maintaining maternal free T4 within normal range with thionamides may be preferable to fetal euthyroidism when toxemia of pregnancy or glucose intolerance develops, since there is little evidence indicating fetal hypothyroidism due to maternal ingestion of thionamides can cause intellectual retardation. TBII and/or TSAb levels should be determined by the 3rd trimester in patients with a history of ablative therapy for Graves' disease, and in patients with primary myxedema, in order to predict or treat fetal hyper- and hypothyroidism.     

Myxedema coma and normal serum thyroxine

A 76-year-old man who developed the clinical syndrome of myxedema coma was found to have a normal serum thyroxine concentration. Further investigation revealed the presence of a low serum T3 level before and after sodium levothyroxine therapy when the serum T4 value was in the hyperthyroid range. In addition, he demonstrated an inability to release TSH after intravenous administration of TRH and was found to have an enlarged sella turcica. A partial defect in peripheral conversion of T4 to T3 is postulated.     

Management options for patients with pretibial lacerations

Pretibial lacerations are a common injury, particularly in older adults. Patients may present to the emergency department for treatment, be treated in GP surgeries by community nurses or they may self-treat. This article reviews the treatment options available to enable healthcare professionals to make informed decisions regarding the management of patients with such injuries.     

Evaluation of a new free-thyroxin assay

The Amerlex Free Thyroxin (T4) Radioimmunoassay Kit (Amersham International Ltd.) is a new direct equilibrium radioimmunoassay for free T4 based on an antiserum with very high affinity for T4, and a unique 125I-labeled T4 analog as tracer. It is a very simple single-tube radioimmunoassay, making use of Amerlex particles to separate antibody-bound from free species. Interassay precision (CV) is 3.7% at 13 pmol/L and 2.3% at 30 pmol/L; within-assay precision is 4.2% at 21 pmol/L. The reference interval is 11-22 pmol/L. The assay did not misclassify any patients tested who had untreated myxedema or untreated thyrotoxicosis. The free T4 assay excelled both the free T4 index and the T4/T4-binding globulin ratio in correcting for increased thyroxin-binding globulin from pregnancy, and it was better than the index but not better than the ratio in correcting for increased thyroxin-binding globulin in users of oral contraceptives.     

Hypothyroidism in elderly people

Abnormal thyroid function tests are common for older adults, but the clinical significance of abnormal results and the need for treatment vary. Nonthyroidal illness (eg, low T3 and T4 syndromes) needs to be ruled out before making the diagnosis of hypothyroidism. Overt hypothyroidism and myxedema coma always require treatment, but treatment of subclinical hypothyroidism is not as clear. The purpose of this review article is to summarize existing data in the elderly population on the etiology, diagnosis, and management of overt hypothyroidism and subclinical hypothyroidism.     

Cardiac enzyme changes in myxedema coma

A 74-year-old man with myxedema and hypothermia had increased activities in plasma of creatine kinase (CK; EC 2.7.3.2), aspartate aminotransferase (AST; EC 2.6.1.1), and lactate dehydrogenase (LD; EC 1.1.1.27) and increased proportions of CK-MB (up to 20% of total CK) and LD1 isoenzymes, but no clinical or investigational evidence of associated myocardial infarction. This case illustrates that plasma enzyme activity and isoenzyme profiles in such clinical settings should be interpreted with caution, because increases in CK-MB and LD1 may relate to myxedema coma or hypothermia (or both) rather than to myocardial infarction.