Contact dermatitis is the most frequent occupational dermatosis and non-specific irritants in addition to specific Type IV sensitization are involved. We reviewed our database for data from 1994 to 1998 and selected 360 consecutive patients working in healthcare environments and experiencing contact dermatitis at their hands, wrists and forearms. We found that allergic contact dermatitis and irritant contact dermatitis were considered to be work-related in 16.5% (72/436) and 44.4% (194/436) of diagnoses, respectively. Occupational irritant contact dermatitis is due to exposure to a wide range of irritants in the workplace, such as soaps, solvents, cleansers and protective gloves, which conspire to remove the surface lipid layer and/or produce cellular damage. In this study the major relevant aetiological agents that induced occupational allergic contact dermatitis were: nickel sulphate (41 patch positivities), components of disinfectants [glutaraldehyde (5) and benzalkonium chloride (7)] and rubber chemicals [thiuram mix (15), carba mix (9) and tetramethylthiuram monosulphide (6)]. The best treatment for allergic contact dermatitis is to avoid those allergens causing the rash. Whenever this is not possible, contact with them needs to be reduced using properly selected protective gloves. Finally, subjects with atopic dermatitis should avoid 'wet work' and contact with irritants, because atopic dermatitis is significantly associated with irritant contact dermatitis.
The combination of desloratadine plus montelukast is effective in the treatment of CU. It may therefore be a valid alternative in patients with relatively mild CU, in view of its efficacy and the lack of adverse events.
Inhibition of multiple myeloma (MM) plasma cells in their permissive bone marrow microenvironment represents an attractive strategy for blocking the tumor/ vessel growth associated with the disease progression. However, target speci-ficity is an essential aim of this approach. Here, we identified platelet-derived growth factor (PDGF)-receptor beta (PDGFR) and pp60c-Src as shared constitutively activated tyrosine-kinases (TKs) in plasma cells and endothelial cells (ECs) isolated from MM patients (MMECs). Our cellular and molecular dissection showed that the PDGF-BB/PDGFR kinase axis promoted MM tumor growth and vessel sprouting by activating ERK1/2, AKT, and the transcription of MMEC-released proangio-genic factors, such as vascular endothe-lial growth factor (VEGF) and interleukin-8 (IL-8). Interestingly, pp60c-Src TK-activity was selectively induced by VEGF in MM tumor and ECs, and the use of small-interfering (si)RNAs validated pp60c-Src as a key signaling effector of VEGF loop required for MMEC survival, migration, and angiogenesis. We also assessed the antitumor/vessel activity of dasatinib, a novel orally bioactive PDGFR/Src TK-inhibitor that significantly delayed MM tumor growth and angiogenesis in vivo, showing a synergistic cytotoxicity with conventional and novel antimyeloma drugs (ie, melphalan, prednisone, bor-tezomib, and thalidomide). Overall data highlight the biologic and therapeutic relevance of the combined targeting of PDGFR/c-Src TKs in MM, providing a framework for future clinical trials. (Blood. 2008;112:1346-1356) Introduction Multiple myeloma (MM) is characterized by a clonal proliferation of immunoglobulin-secreting plasma cells in the bone marrow (BM), with clinical manifestations including lytic bone lesions, anemia, renal failure, immunodeficiency, and hypercalcemia. 1 For patients treated with conventional and high-dose chemotherapies, the median survival time from diagnosis is 3 to 4 years. 2 Approximately one-half of patients with newly diagnosed MM achieve remission from these therapies, but options are more limited for primary resistant or relapsing disease. Partial remission occurs in only 20% of resistant patients and in 45% of relapsing patients. Survival time improves in approximately 50% of those younger than 60 who are able to undergo high-dose chemotherapy followed by autologous stem cell transplantation, but approximately 30% of them are late in the graft intake or even develop myelodysplasia that prevents additional chemotherapy while relapse or resistant disease occurs. Induction of MM plasma cells is thought to involve genetic lesions (ie, translocations between immunoglobulin enhancers and oncogenes) and secondary events underlying the activation of bidirectional MM tumor-microenvironment interactions. 3-5 Indeed, homing and survival of MM plasma cells are sustained by overangiogenic sprouting of microvascular endothelial cells (ECs), 6,7 as well as by osteoclasts, fibroblasts, monocytes, macrophages, and mast cells, 4,8,9 thus resulting in a multiplicity of autocrine/...
Aseptic meningitis is a rare but well-recognized complication of drug therapy. The clinical presentation of drug-induced aseptic meningitis (DIAM) is distinct. Symptoms typically include fever, neck stiffness, headache, confusion, nausea and vomiting. The major categories of causative agents are non-steroidal anti-inflammatory drugs, antimicrobials and also intravenous immunoglobulins, monoclonal antibodies and vaccines. These drugs most commonly implicated as causes of aseptic meningitis act more likely through an immunological mechanisms. However, the exact pathogenetic mechanism of DIAM is still unknown. The diagnosis of drug-induced aseptic meningitis is difficult and infectious etiologies must be excluded. In some cases the diagnosis has been confirmed by rechallenging the patient with the suspected agent. In this case, informed written consent is necessary and rechallenge must be medically supervised both to document the response and to offer medical care and advice, if required. The outcome of DIAM is generally good, usually without long term sequelae.
A global assessment indicates that levocetirizine 5 mg once daily is an effective agent in patients with chronic idiopathic urticaria, as its action provides a rapid and satisfactory control of the symptoms and measures of subjective disease, although this is limited to the duration of treatment.
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