瘤型麻风1例

患者女,37岁。因躯干、四肢起红斑、丘疹、结节3年,加重伴眉毛脱落半年来诊。 患者3年前无明显诱因于左上臂出现两处红色丘疹,1年后躯干、四肢相继出现散在红斑、丘疹,无自觉症状。曾在当地医院就诊,诊断及治疗不详,皮疹无消退。半年前皮疹明显增多,躯干、四肢出现较多红色斑块及红色、紫红色结节,偶有破溃、出血,并出现眉毛脱落,无脱发。同时面部出现红斑、结节伴充血、肿胀。全身轻度乏力,无疼痛及瘙痒,偶有皮肤蚁行感。患者发病以来,精神、食欲及睡眠尚好,大小便正常。     

瘤型麻风1例

患者女,37岁.因躯干、四肢起红斑、丘疹、结节3年,加重伴眉毛脱落半年来诊. 患者3年前无明显诱因于左上臂出现两处红色丘疹,1年后躯干、四肢相继出现散在红斑、丘疹,无自觉症状.曾在当地医院就诊,诊断及治疗不详,皮疹无消退.半年前皮疹明显增多,躯干、四肢出现较多红色斑块及红色、紫红色结节,偶有破溃、出血,并出现眉毛脱落,无脱发.同时面部出现红斑、结节伴充血、肿胀.全身轻度乏力,无疼痛及瘙痒,偶有皮肤蚁行感.患者发病以来,精神、食欲及睡眠尚好,大小便正常.     

Ⅱ型麻风反应误诊1例

患者男,60岁。因全身皮肤反复起红斑、结节伴发热18个月来诊。患者18个月前无明显诱因,自左肘部起一红色结节,继之躯干、下肢亦发生多个红色斑块及结节,伴轻度瘙痒,未治疗。5个月前,患者觉双上肢皮肤麻木,去某综合医院皮肤科就诊,以“结节病”收住院,给予“泼尼松、利福平”等药物治疗（剂量不详）20天,皮疹全部消退出院。出院后9天,患者左侧面颊部发生一红色结节,疼痛,在村卫生室输液治疗10天无效,     

II型麻风反应误诊1例

患者男,60岁.因全身皮肤反复起红斑、结节伴发热18个月来诊.患者18个月前无明显诱因,自左肘部起一红色结节,继之躯干、下肢亦发生多个红色斑块及结节,伴轻度瘙痒,未治疗.5个月前,患者觉双上肢皮肤麻木,去某综合医院皮肤科就诊,以"结节病"收住院,给予"泼尼松、利福平"等药物治疗(剂量不详)20天,皮疹全部消退出院.     

中间界线类麻风伴Ⅰ型麻风反应1例

患者男,59岁,农民.面部反复出现红斑,颈部、躯干多处斑块2年,伴四肢远端麻木疼痛2月余. 患者2年前发现背部有两块约1 cm×1.5 cm、1.5 cm×2 cm白斑,不痛不痒,后逐渐增多,曾多次到医院检查,均认为是过敏引起,外用药膏(药名不详)无效.4个月前患者面、颈、背部突然多处出现红色、白色斑块,无自觉症状,私立医院拟"过敏性皮炎"治疗未见好转,3个月前自觉手足远端麻木、疼痛,到县综合医院就诊,拟诊"红斑狼疮伴痛风"收入院,并行实验室检查:类风湿因子、抗"O"均阴性.治疗(具体不详)1周未见好转.     

麻风图谱

患者女，26岁。双侧心毛脱落6年，全身反复起红包结节4年。 患者6年前出现双侧眉毛脱落。4年前开始于左踝外侧出现红色结节，伴疼痛。后皮损渐增多，累及面部和四肢。当地村卫生诊断不明，曾多次应用中药和消炎药物（具体药物不详）治疗，皮损反复发作。10余天前左上肢出现结市，疼痛明显。当地县医院诊断为结节性红斑，给予“地塞米松”等药物治疗6天，结节消退。     

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     

界线类偏瘤型麻风1例

<正>患者,女,61岁,农民。全身皮肤起丘疹、红斑、结节,双手、足麻木、肿胀、疼痛40余天。2013年3月1日患者面部、左上肢出现10余个丘疹,逐渐增大,伴轻微痒感。在村卫生室拟"过敏性皮炎"治疗3天(具体药物不详),无效。10天后,皮损累及双下肢,并出现双侧手、足麻木、肿胀及疼痛感,就诊于县人民医院风湿科,拟"风湿性关节炎"收入院治疗6天(药物不详),手、足肿胀消退,皮疹有所减轻。出院后第2天,又出现手、足肿胀,腰部亦发生数个结节并伴低热,2014年4月16日就诊于我院。     

Ⅱ型麻风反应1例

正1临床资料患者男,40岁,江西吉安人。面部反复暗红色丘疹和结节1年,泛发全身伴瘙痒并乏力1个月,伴寒战、发热和关节疼痛7d。1年前,无明显诱因额面部出现少量散在的暗红色丘疹和结节,无自觉症状。1个月前,皮损泛发至耳部、躯干及四肢,伴疼痛、瘙痒、乏力。外院以"血管炎"予静滴药物治疗(药名不详),乏力消失,丘疹、结节消退。7d前受凉后皮疹加重,全身再次发生丘疹、结节,伴寒战、发热、关节痛。既往史、个人史、家     

界线类偏瘤型麻风l例

患者,女,61岁,农民。全身皮肤起丘疹、红斑、结节,双手、足麻木、肿胀、疼痛40余天。2013年3月1日患者面部、左上肢出现10余个丘疹,逐渐增大,伴轻微痒感。在村卫生室拟“过敏性皮炎”治疗3天（具体药物不详）,无效。10天后,皮损累及双下肢,并出现双侧手、足麻木、肿胀及疼痛感,就诊于县人民医院风湿科,拟“风湿性关节炎”收入院治疗6天（药物不详）,     

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.     

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.     

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.     

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.