淋巴结结核并发丘疹坏死性结核疹一例

丘疹坏死性结核疹(PNT)是身体对其他部位(皮肤)结核分枝杆菌感染的一种免疫、过敏反应,其早期极易与变应性血管炎混淆,可依据病理活组织检查(活检)鉴别,也可行PCR检测明确诊断。该文报道1例淋巴结结核、药物性肝损害合并PNT患者,以双足皮疹为首发表现,予脱敏、对症治疗效果欠佳,追问患者既往病史并行病理活检后临床确诊。调整抗结核药及对症治疗,门诊随访未见新发皮疹。该例提示,对疑有结核分枝杆菌感染并发皮疹的患者,应警惕并发各型皮肤结核及其鉴别诊断,对无法耐受常规治疗的患者应合理调整药物配伍方案。     

An itchy vesiculobullous eruption in a patient with chronic lymphocytic leukaemia

Exaggerated reactions to insect bites are characteristic of patients with haemoproliferative disorders, particularly chronic lymphocytic leukaemia (CLL). Skin lesions usually appear after the diagnosis of leukaemia and seem unrelated to laboratory findings, disease course or therapy. Rarely, the eruption may precede the diagnosis of the haematologic malignancy. The patients usually do not recall of insect bites, and the diagnosis may require histological and laboratory investigations to exclude specific lesions or autoimmune bullous diseases. Lesions may run a chronic course and represent a therapeutic challenge. Here, we report an adult patient with CLL who developed itchy recurrent papulovesicular and bullous lesions. Differential diagnosis was made with cutaneous specific lesions of CLL, bullous pemphigoid and pemphigus vulgaris, but laboratory and histological investigations confirmed the diagnosis of an insect bite reaction. The patient was treated with oral H1 anti-histamines and topical corticosteroids under occlusion, with marked improvement after 10 days.     

Ichthyosiform eruption associated with lamivudine in a patient with chronic hepatitis-B infection

The side-effects of antiretroviral agents have been widely reported in the literature. Lamivudine is an antiretroviral agent, and skin eruption because of this agent has been rarely reported. Previous reports regarding these few side-effects of lamivudine include angioedema, urticaria, anaflactoid reactions, allergic contact dermatitis and alopecia. There is no report of an ichthyosiform eruption associated with lamivudine. The authors present a case of 43-year-old female patient presenting with an ichthyosiform eruption during lamivudine therapy for chronic hepatitis-B for the first time.     

CD44 in cancer

CD44 is a multistructural and multifunctional cell surface molecule involved in cell proliferation, cell differentiation, cell migration, angiogenesis, presentation of cytokines, chemokines, and growth factors to the corresponding receptors, and docking of proteases at the cell membrane, as well as in signaling for cell survival. All these biological properties are essential to the physiological activities of normal cells, but they are also associated with the pathologic activities of cancer cells. Experiments in animals have shown that targeting of CD44 by antibodies, antisense,and CD44-soluble proteins markedly reduces the malignant activities of various neoplasms, stressing the therapeutic potential of anti-CD44 agents. Furthermore, because alternative splicing and posttranslational modifications generate many different CD44 sequences, including, perhaps, tumor-specific sequences, the production of anti-CD44 tumor-specific agents may be a realistic therapeutic approach. However, in many cancers (renal cancer and non-Hodgkin's lymphomas are exceptions), a high level of CD44 expression is not always associated with an unfavorable outcome. On the contrary, in some neoplams CD44 upregulation is associated with a favorable outcome. Even worse, in many cases different research grows analyzing the same neoplastic disease reached contradictory conclusions regarding the correlation between CD44 expression and disease prognosis, possibly due to differences in methodology. These problems must be resolved before applying anti-CD44 therapy to human cancers.     

Diabetic neuropathic pain in a leg amputated 44 years previously

The mechanism of neuropathic pain in the diabetic limb is far from clear. Phantom limb pain likewise is of obscure aetiology. The development of typical pain in an absent leg in a patient with diabetes many years after the amputation stimulates thought as to the mechanism, not only of neuropathic pain, but also of phantom limb pain. A 58-year-old man was diagnosed with type 2 diabetes 44 years after having undergone left below knee amputation for congenital AV malformation, at the age of 13. Eight months before the diagnosis of diabetes he began to complain of pain in the leg on the amputated side-pain very similar to that described in typical diabetic neuropathy. This was followed by similar pain in the right leg. MR scan of the spine revealed a small syringohydromyelia of the thoracic cord in addition to a prolapse of disc at L(5)/S(1) level on the left side, which was first noted 5 years previously. There were no other features of S(1) compression. The typical neuropathic character of the pain involving both the amputated and the intact limbs that developed with the diagnosis of type 2 diabetes suggest that the neuropathic pain may originate from centres higher than peripheral nerves.     

重症药疹的若干问题

重症多形红斑型、Steven—Johnson综合征及中毒性表皮坏死松解型药疹是药疹中的严重类型,近年来认为是一个逐渐加重的系谱性疾病。该文就其病因、分类、治疗及预测死亡率方面的研究进展作一综述。     

Psoriasiform eruption induced by infliximab

OBJECTIVE: To report a case of psoriasiform eruption induced by infliximab. CASE SUMMARY: A 46-year-old woman with enterocutaneous fistula secondary to Crohn's disease developed pruriginous, erythematous, desquamative plaques on her elbows, knees, hands, and buttocks after receiving the second and third doses of intravenous infliximab. Histologic examination showed a lichenoid pattern. No new cutaneous lesions appeared after cessation of infliximab therapy. DISCUSSION: Several cutaneous reactions secondary to infliximab, a monoclonal antibody against tumor necrosis factor-alfa, have been described. Psoriasiform dermatitis has not been reported as a cutaneous reaction to infliximab, but there have been several previous reports of psoriasiform dermatitis secondary to other drugs. An objective causality assessment revealed that the adverse event was probable. CONCLUSIONS: This is the first report of a clinico-pathologic dissociated pattern of cutaneous reaction showing a histopathologic picture of lichenoid dermatitis resulting from infliximab treatment.     

CD44 is a physiological E-selectin ligand on neutrophils

The selectin family of adhesion molecules and their glycoconjugated ligands are essential for blood polymorphonuclear neutrophil (PMN) extravasation into inflammatory and infectious sites. However, E-selectin ligands on PMNs are not well characterized. We show here that CD44 immunopurified from G-CSF-differentiated 32D cells or from peripheral blood PMNs binds specifically to E-selectin. In contrast, CD44 extracted from bone marrow stromal or brain endothelial cell lines does not interact with E-selectin, suggesting cell-specific posttranslational modifications of CD44. PMN-derived CD44 binding activity is mediated by sialylated, alpha(1,3) fucosylated, N-linked glycans. CD44 enables slow leukocyte rolling on E-selectin expressed on inflamed endothelium in vivo and cooperates with P-selectin glycoprotein ligand-1 to recruit neutrophils into thioglycollate-induced peritonitis and staphylococcal enterotoxin A-injected skin pouch. CD44 extracted from human PMNs also binds to E-selectin. Moreover, we demonstrate that CD44 is hypofucosylated in PMNs from a patient with leukocyte adhesion deficiency type II, suggesting that it contributes to the syndrome. These findings thus suggest broader roles for CD44 in the innate immune response and uncover a potential new target for diseases in which selectins play a prominent role.     

CD44 is a determinant of inflammatory bone loss

Chronic inflammation is a major trigger of local and systemic bone loss. Disintegration of cell-matrix interaction is a prerequisite for the invasion of inflammatory tissue into bone. CD44 is a type I transmembrane glycoprotein that connects a variety of extracellular matrix proteins to the cell surface. Tumor necrosis factor (TNF) is a major inducer of chronic inflammation and its overexpression leads to chronic inflammatory arthritis. By generating CD44(-/-) human TNF-transgenic (hTNFtg) mice, we show that destruction of joints and progressive crippling is far more severe in hTNFtg mice lacking CD44, which also develop severe generalized osteopenia. Mutant mice exhibit an increased bone resorption due to enhanced number, size, and resorptive capacity of osteoclasts, whereas bone formation and osteoblast differentiation are not affected. Responsiveness of CD44-deficient osteoclasts toward TNF is enhanced and associated with increased activation of the p38 mitogen-activated protein kinase. These data identify CD44 as a critical inhibitor of TNF-driven joint destruction and inflammatory bone loss.