瘤型麻风伴II型麻风反应一例

临床资料患者,女,64岁。因眉毛脱落、全身皮肤红斑、丘疹6个月就诊。患者自述6个月前眉毛脱落,无明显诱因躯干和四肢出现暗红色丘疹、结节,表面皮肤干燥,无瘙痒和疼痛,无畏寒发热、胸闷腹痛等全身症状。1个月前于当地医院就诊,怀疑麻风,未予检查与治疗,转诊至我院。该患者既往体健,个人史无特殊,无子女。否认家族中类似病史。     

麻风5例误诊分析

<正>麻风临床表现复杂,容易误诊和漏诊。2010-2012年我们确诊5例麻风患者,报道如下。临床资料病例1,女,46岁。因全身皮肤泛发红斑3个月就诊。患者3个月前无明显诱因出现面部、四肢散发红斑,红斑渐增多、加重,面部、背部出现红色斑块,略痒,无发热、关节疼痛。多次在当地医院诊断"皮炎"、"湿疹"、"蕈样肉芽肿"、"红斑狼疮",治疗无好转。患者     

Sweet综合征样II型麻风反应一例

<正>麻风反应是由于免疫平衡紊乱所引起的一种对麻风杆菌抗原的急性超敏反应,根据超敏反应的性质不同,将麻风反应分为I型麻风反应[1]和II型麻风反应[2]。本院近日收治1例特殊类型的II型麻风反应,现报道如下。临床资料患者,男,49岁。全身反复丘疹、结节伴发热3年余,加重1个月。3年前无明显诱因胸背部出现浅红色丘疹,不疼不痒,自行购买消炎药服用,症状未见减轻。后皮疹扩大至四肢,伴发热,体温     

麻风误诊二例

<正>临床资料病例1:患者,女,24岁。2个月前双上肢丘疹、结节,微痒,外院诊断"湿疹、多形性日光疹",给予抗过敏抗炎治疗,无效。10天前面部、耳廓出现丘疹、结节,双手有肿胀感,不伴畏寒发热、麻木蚁行、关节肿痛等不适,为求进一步治疗来我院门诊就诊。患者平素健康,无家族史、传染病史,否认麻风接触史,未婚,未生育,月经史正常。体格检查:系统检查无异常。皮肤科检查:面部浸润,面部、耳廓、双上肢可见粟粒至黄豆大丘     

瘤型麻风伴II型麻风反应一例

正临床资料患者,女,26岁。因"全身丘疹、结节3+月"就诊。3个月前,患者无明显诱因头、面部、躯干、四肢出现散在浅红色丘疹,伴轻度瘙痒,无疼痛,就诊当地医院,诊断"银屑病",外涂卡泊三醇软膏,皮疹未好转。近1个月皮疹逐渐扩大增多,皮疹处出现痒痛,门诊以"皮疹原因待查"收入院。患者自发病以来,无发热、腹泻,无感觉麻木及感觉迟钝,否认毛发     

瘤型麻风一例

临床资料患者,男,47岁。因周身皮肤出现无痛痒性丘疹、结节1年来诊。患者1年前无明显诱因躯干、背部及双上肢出现丘疹、结节,无疼痛及瘙痒,于外院诊断为“过敏性皮炎”,给予口服及外用药物治疗(具体不详),病情未改善,结节逐渐增多,遍布全身,部分皮损自行破溃,不易愈合。1个月前于外院行皮肤病理活检及特殊染色检查后,怀疑麻风,为进一步诊疗转诊至我院。否认其它慢性疾病及传染病史,否认家族中有类似病史。     

瘤型麻风1例

正1临床资料患者男,42岁。躯干和四肢红色丘疹、结节伴轻微瘙痒2个月。2个月前无明显诱因患者四肢出现散在分布的米粒大红色丘疹,自觉轻微瘙痒,无疼痛等不适。后丘疹逐渐增大并增多,蔓延到躯干,部分皮损形成结节,表面无明显鳞屑。多家医院以"湿疹"或"结节性痒疹"治疗(具体不详),无效。患者自发病以来饮食、睡眠及精神可,大小便正常。患者既往体健,家族中无类似患者。体检:双侧颈部可触及粗大耳大神经,无明显压痛,皮损处痛觉、温觉及触觉等浅表感觉轻度减退,全身浅表淋巴结未触及,余系统检查未见异常。皮肤科情况:躯干及四肢散在分布黄豆大红色     

瘤型麻风一例

<正>第0106号临床资料患者,女,43岁,云南文山州人。因全身红斑、结节2月余就诊。患者2个月前无明显诱因躯干和四肢出现丘疹、结节,无瘙痒和疼痛,无畏寒发热、胸闷腹痛、关节疼痛等全身症状。曾在我院门诊拟"血管炎"治疗,应用甲泼尼龙片、非索非那定片,外用复方克霉唑乳膏(二丙酸倍他米松、克霉唑和硫酸庆大霉素复方制剂)治疗,一度好转,但停用糖皮质激素后皮疹反复。近一周来红斑、结节增多,皮疹有触痛,双踝关节处肿胀疼痛,门诊拟"血管炎?麻风?"收入院。患者既往体健,父亲体健,母亲因心脏病已故,二兄二姐均体健。     

瘤型麻风1例

正1临床资料患者男,31岁,贵州籍。躯干及四肢红色丘疹、斑块伴瘙痒半年。半年前,无明显诱因四肢出现散在分布的红色丘疹、斑块和结节,两个月前,患者前胸及后背出现红色丘疹,双侧眉毛外1/3处脱落,外院以"湿疹",予抗过敏药物口服加外用激素软膏治疗,皮损无明显改善。发病以来,精神食欲可,体质量正常,大小便也正常,否认麻风、结核、肝炎等传染病史和接触史,也无药物过敏史。体检:系统检查     

麻风2例并文献复习

报道2例麻风。例1女,23岁。面部、双上肢反复红斑、结节伴眉毛脱落2个月。例2男,53岁。全身红斑、结节、丘疹伴疼痛、发热20天。皮损组织病理均示:表皮轻度萎缩,真皮内见由泡沫样组织细胞构成的结节状浸润,与表皮间有无浸润带。诊断:麻风。     

Mast cells in leprosy and leprosy reaction

BACKGROUND: Mast cells can be visualized in routine, acid-fast-staining, paraffin tissue section as metachromatic staining cells, and can be activated to release inflammatory mediators which play a role in the cell-mediated immune response. METHODS: Skin biopsy tissues were taken from the most active skin lesion of each leprosy patient at the time of diagnosis (nonreactional group) and at the time of reaction (reactional group) during the years 1994-1997 in the leprosy clinic at the Department of Dermatology, Faculty of Medicine, Siriraj Hospital, Mahidol University, Thailand. Mast cells were identified by metachromatic staining (purple) in Fite's stain sections and reported as the average number of cells per high power field in three compartments: at the center and periphery of the granuloma and in the interstitium. The data were analyzed in three groups: nonreactional group, type I, and type II leprosy reactions. The mast cell count of each group and each compartment of the section, expressed as the mean +/- standard error, was compared. RESULTS: A total of 95 persons were included in the study, but 108 tissue sections were obtained due to nine cases having more than one section. Of these patients, 63 cases (66.32%) had no reaction, 19 cases (20%) had type I reaction, and 13 cases had type II reaction. There was no difference in age and sex among these groups. The mast cell count in the interstitium was higher than that within the granuloma, both at the center and at the periphery, in every type, and the count in this area reduced significantly in leprosy reactions, both type I and type II, compared with the nonreactional group. CONCLUSIONS: The change in the average mast cell number in nonreactional leprosy and leprosy reactions may indicate the important role of mast cells in dynamic changes in the cell-mediated immune response in leprosy and leprosy reactions.     

Prevalence of leprosy in children of leprosy parents

A cross sectional clinical study was done in slums and adjoining village of Raipur town. All the children in 100 families, in which at least one patient of proved leprosy was present were examined. Children of 100 non-leprosy families served as control. In leprous families prevalence was 14.2 times higher in comparison to children in control group. Also prevalence was higher in children of those families in which number of patients were more than one, or there was lepromatous leprosy. In children the common type of lesion were tuberculoid, indeterminate, borderline and pure neural type in that order, while no case of lepromatous leprosy was seen.     

Dimorphous leprosy

In 1981 we observed two cases of leprosy in Salzburg. The two Vietnamese refugees already had advanced borderline disease. Treatment with dapsone resulted in clearing of the skin in both cases. One of the patients developed a leprosy reaction during treatment.     

Lepromatous leprosy

A 51-year-old woman presented with a 2-month history of pruritic, erythematous papules and plaques on her arms that were treated as chronic urticaria. Histopathologic examination demonstrated acid-fast bacilli, and a diagnosis of lepromatous leprosy was made. Presentation and treatment of leprosy are reviewed.     

Lesional T-cell subset in leprosy and leprosy reaction

BACKGROUND: The T-cell-mediated immune response plays an important role in leprosy. The in situ proportion and pattern of distribution of T-cell subsets in leprosy skin lesions have been studied, but no conclusion could be drawn. METHODS: We used monoclonal antibodies for T-helper and T-suppressor surface antigen to define the nature of dermal infiltration in 17 cases of nonreactional leprosy and 20 cases of reactional leprosy. RESULTS: We found T helper admixed with T suppressor in an aggregated pattern in the granulomas of most cases of nonreactional leprosy and in type I reactional leprosy, but a diffuse infiltrate throughout the dermis of type II reactional leprosy. The T-helper/suppressor ratio was 1.68 in tuberculoid and 1.5 in lepromatous cases. The T-helper/ suppressor ratios of borderline tuberculoid (3.11) and type I reactional leprosy (2.54) were not statistically different. The T-helper/suppressor ratio of type II reactional leprosy (5.83) was statistically higher than nonreactional lepromatous cases. CONCLUSIONS: The alteration of the T-helper/suppressor ratio in our study is mainly due to the reduction of T-suppressor cells in the dermal infiltrates, especially in type II reactional leprosy. Further studies of T-suppressor functions may be important in the pathogenesis of leprosy.