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。     

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.     

界线类偏瘤型麻风伴II型麻风反应误诊为结节性红斑一例

正临床资料患者,男,72岁。6个多月前患者无明显诱因出现皮疹及发热,最高体温达39.6℃,伴头昏、干咳、心悸、流涕,皮疹初发左侧腹部,表现为红色斑片、丘疹、结节,后逐渐增多并发展至躯干及四肢,皮疹及周围皮肤伴压痛,无瘙痒,可自行破溃,有红色粘稠物流出,期间未就诊、未行特殊处理后上述皮疹自行愈合并留下色素斑。2个多月前因再次出现发热及皮疹增多情况就诊于当地医院,经诊治(具体不详)后患者仍反复发热,皮疹不消退,遂为进一步诊治就诊于我院门诊,以发热原因和结节性红斑收住我院全科病房住院治疗。患者既往高血压病史,否认传染病史。患者生于贵州省荔波县,久居当地。     

皮肤结节病1例

<正>临床资料患者女,52岁。因全身散发红色丘疹3个月就诊。患者3个月前无明显诱因左乳房下出现较为密集的红色粟粒至绿豆大丘疹,后皮疹逐渐增多,泛发至面颈部、后背、四肢等处,伴有轻度瘙痒,无疼痛,无水疱、脓疱。曾于当地医院拟"湿疹"给予"雷公藤、糖皮质激素药膏"等治疗,皮疹部分消退,但停药后皮疹随之出现。发病以来无发热、咳嗽、咳痰、     

中间界线类麻风一例

患者男,58岁,2018年2月2日因躯干、四肢红色斑块3个月就诊。患者3个月前无明显诱因左胸出现乒乓球大小红色斑块,边界清楚。近1个月皮疹逐渐扩大增多,臀部、左大腿屈侧亦出现皮疹,伴局部感觉迟钝,无明显痛痒。曾外用铍药师软膏,皮疹未好转。诉左肩周围疼痛,无发热、腹泻,否认毛发脱落。患者自发病以来,精神食欲可,体重稍有下降,大小便正常。既往史无特殊。个人及家族史：久居于福建,4年前搬至北京。否认家族中有类似疾病史,否认麻风患者接触史……     

多发性丘疹、结节表现的瘤型麻风1例

患者男,63岁.因全身皮疹无痒痛3个月,至我院皮肤科门诊就诊.患者就诊前3个月于右上肢出现皮疹,逐渐增多,扩展至四肢、躯干,无自觉症状,曾经到外地多家医院就诊,拟诊“环状肉芽肿”、“皮肤淋巴瘤”、“组织细胞瘤”等,给予“泼尼松、维A酸”等治疗,治疗后皮疹仍逐渐增多.     

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。     

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     

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.