Glucose tolerance studies in lichen planus

A study of glucose tolerance and insulin response to oral glucose was carried out in 56 consecutive histologically confirmed cases of lichen planus. 30.3% patients showed abnormal glucose tolerance. The pattern of insulin response was similar to that seen in type II diabetes. Insulin/glucose ratio showed the same relationship as seen in type II diabetes. These results reinforce the possibility of glucose intolerance in lichen planus patients. However, no correlation between glucose tolerance abnormalities and duration and distribution of lesions was observed.     

Abnormal glucose tolerance associated with lichen planus.

A study was made of 52 patients with lichen planus. Abnormal oral glucose tolerance was found in 19 (36%), including 5 with overt diabetes. The criteria for abnormality were based on an age-related score method. A family history of diabetes was found to be present in 14 (26%). The most common abnormality observed in the glucose tolerance test was an elevation of the blood glucose level 2 hours after administration of the glucose. These results further support the supposition of a disorder in carbohydrate metabolism associated with lichen planus.     

Bullous lichen planus and lichen planus pemphigoides-clinico-pathological comparisons

Two patients with lichen planus pemphigoides and two with bullous lichen planus were compared. Lichen planus pemphigoides was clinically distinguished by a more generalized lichen planus, more extensive blistering, the need for systemic corticosteroids and by a longer course. The blister of bullous lichen planus was a subepidermal bulla showing degeneration of the epidermal basal layer and other features of lichen planus, whereas in lichen planus pemphigoides the bulla was similar to that of bullous pemphigoid albeit with rather more neutrophils than are usually seen. Direct immunofluorescence was positive in lichen planus pemphigoides and negative in bullous lichen planus. Lichen planus pemphigoides and bullous lichen planus are separate entities: the former is an auto-immune disease precipitated by lichen planus and not related to bullous pemphigoid, the latter is probably not auto-immune but represents the extreme consequence of the lymphoid infiltrate at the dermo-epidermal junction.     

Apoptosis in lichen planus

A study of the degeneration of basal epidermal cells in lichen planus has confirmed the role of apoptosis. Lymphocytes were present in close proximity to all epidermal cells showing the early morphological features of apoptosis. This is further evidence implicating a cell-mediated immune reaction in the pathogenesis of lichen planus.     

肥厚性扁平苔藓

报告8例肥厚性扁平苔藓.8例患者中6例年龄>75岁,平均病程6.6年.皮损多位于小腿外侧或胫前.表现为暗红色或紫红色肥厚性斑块.皮损组织病理检查:表皮角化过度,颗粒层楔形增厚,棘层肥厚,表皮细胞多增大,可见胶样小体;真皮浅层胶原纤维及扩张的血管与表皮呈垂直方向排列,真皮乳头层淋巴细胞、组织细胞呈带状浸润.     

Oral lichen planus

Oral lichen planus (OLP) is a relatively common mucosal disease that can present isolated or associated with cutaneous lichen planus. Contrarily to its cutaneous counterpart, though, OLP tends to be chronic, relapsing, and difficult to treat. Severe morbidity is related to erosive forms, and more aggressive presentations have been described, such as the "gingivo-vulvar syndrome". This article reviews the current knowledge about the pathogenesis, clinical picture, differential and laboratorial diagnosis, prognosis, and treatment of OLP.     

Oral lichen planus

A 42-year-old woman presented with a 2-year history of persistent, gray-white lip discoloration and discomfort that had not improved after empiric treatment with topical 5-fluorouracil cream. Histopathologic examination demonstrated interface dermatitis with epidermal atrophy. A diagnosis of oral lichen planus was made based on clinicopathologic correlation, and treatment with topical tacrolimus ointment was initiated.     

Familial lichen planus

We observed the simultaneous occurrence of generalized lichen planus in a woman and her mother. Both patients improved after therapy with topical steroid and salicylic acid ointment. Of the eighty-one cases of familial lichen planus previously reported, the vast majority (89 percent) occurred in blood relatives. The intervals of onset between familial cases were long, ranging from six weeks to thirty years (mean 73.4 months). These observations suggest that familial lichen planus may result from genetic predisposition, rather than from an infectious cause.     

Oesophageal lichen planus

A 50-year-old woman with severe oral lichen planus complained of painful dysphagia. Fiberoptic endoscopy revealed erosive lichen planus of the oesophagus which responded to treatment with systemic corticosteroids.     

Oral lichen planus

Oral lichen planus is a common multifactorial disease. This article is not a complete review of the disease, but instead a discussion of selected aspects such as clinical features, possible vascular influences, and the relation of stress and drugs and metals to the disease. Immunologic theories and cancerous potentials are discussed critically. Finally, a detailed treatment plan of the inflammatory disease is presented, including avoidance of stimulating factors and the use of corticosteroids and retinoids.     

Oesophageal lichen planus

We present a case of lichen planus affecting the oesophagus of an 80-year-old woman. Symptomatically, the lesions manifested themselves as dysphagia requiring repeated oesophageal dilatations. The patient was unable to tolerate several conventional treatments and so pulsed methylprednisolone was given with some beneficial short-term effects. Due to potential for malignant change in lichen planus of the mucous membranes it is important to remember this complication and investigate patients with oesophageal symptoms.