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Lesion multiple

HMR 1726, Terifluno-mide Dihydro-orotate dehydrogenase inhibitor Reduced number of active lesions Multiple Sclerosis... [Pg.161]

AVMs typically present as solitary lesion. Multiple brain AVMs occur in approximately 0.3%-3.2% of all cases. Surprisingly enough, Willinsky et al. (1990) reported 11 cases of multiple AVMs among 203 patients (6%). Although multiple AVMs may occur spontaneously, they are frequently associated with cutaneous or extracranial vascular anomalies (Salcman et al. 1992), such as Rendu-Osler-Weber disease and Wyburn-Mason syndrome. However, the clinical mode of presentation, age and sex of the patient, and anatomic distribution of the lesions are the same as those in patients with single arteriovenous malformations. [Pg.53]

Although, as with human disease, complement deposition is not conspicuous in the vasculitic lesions, multiple experimental observations indicate that complement activation has an important pathogenic role in this model (64,65). Depletion of complement with Cobra venom factor completely prevents the development of glomerulonephritis and vasculitis after injection of MPO-IgG or transfer of anti-MPO splenocytes (64). Injection of anti-MPO IgG into mice with knockout of various complement genes demonstrates that the alternative complement pathway, but not the classic pathway or the lectin pathway, is required for anti-MPO IgG mediated disease induction (64). Specifically, C4-/- mice with blockade of the classic pathway and the lectin pathway develop disease that is same as in wild type mice, whereas C5-/-mice with blockade of all pathways and factor B -/- mice with selective blockade of the alternative pathway are completely protected from disease induction. In accord with an important role for complement, the CS-inhibiting monoclonal antibody (BB5.1) prevents the induction of glomerulonephritis in mice after injection of anti-MPO IgG and LPS (65). Even when the anti-C5 antibody is administered a day after the anti-MPO, there is a marked reduction in disease induction. [Pg.598]

Histopathological examination shows the typical corelike lesions in a high proportion of muscle fibers in older patients this may amount to 100%. Most typically the cores are large and centrally-placed, but multiple cores may occur in the same fiber cross section. Most older patients show a striking predominance of type 1 (slow twitch oxidative) fibers and virtually all fibers with cores are type 1. Sometimes younger family members have more normal proportions of type 1 and type 2 fibers but, again, the cores are confined to the type 1 fibers. It is well established that muscle fiber types can interconvert due to altered physiological demands, and it is likely that fibers with cores convert to a basically slow twitch-oxidative metabolism to compensate for the fact that up to 50% of their cross sectional area may be devoid of mitochondria. [Pg.292]

Folliculitis caused by colonization with S. aureus or S. epidermidis on the face can be sometimes misdiagnosed as acne. The prominent lesions are superficial follicular pustules that are often distributed on the lateral cheeks, the chin and the temporal sites of the forehead. The rare folliculitis due to Candida may also present as multiple pustular eruptions. [Pg.122]

Actinic keratoses are the most common epithelial precancerous lesions which occur primarily on sun-exposed skin of middle-aged and elderly people as multiple erythematous macules or papules with a dry adherent scale (Figs. 12.1, 12.2 and 12.3). [Pg.133]

Solitary or multiple violaceous or brown flat-topped papules resembling lesions of lichen planus. [Pg.135]

Cheeran MC, Hu S, Sheng WS, Rashid A, Peterson PK, Lokensgard JR (2005) Differential responses of human brain cells to West Nile virus infection. J Neurovirol 11 512-524 Cudrici C, Ito T, Zafranskaia E, Niculescu F, Mullen KM, Vlaicu S, Judge SI, Calabresi PA, Rus H (2007) Dendritic cells are abundant in non-lesional gray matter in multiple sclerosis. Exp Mol Pathol 83 198-206... [Pg.137]

McManus C, Berman JW, Brett EM, Staunton H, FarreU M, Brosnan CE (1998) MCP-1, MCP-2 and MCP-3 expression in multiple sclerosis lesions an immunohistochemical and in situ hybridization study. J Neuroimmunol 86 20-29... [Pg.142]

Simpson JE, Newcombe J, Cuzner ML, Woodroofe MN (1998) Expression of monocyte chemoattractant protein-1 and other beta-chemokines by resident glia and inflammatory cells in multiple sclerosis lesions. J Neuroimmunol 84 238-249 Simpson J, Rezaie P, Newcombe J, Cuzner ML, Male D, Woodroofe MN (2000) Expression of the beta-chemokine receptors CCR2, CCR3 and CCR5 in multiple sclerosis central nervous system tissue. J Neuroimmunol 108 192-200... [Pg.144]

The cultivation of viruses from material taken from lesions is an important step in the diagnosis of many viral diseases. Studies of the basic biology and multiplication processes of human viruses also require that they are grown in the laboratory under experimental conditions. Human pathogenic viruses can be propagated in three types of cell systems. [Pg.66]

O Multiple sclerosis symptoms are a function of the position of lesions within the central nervous system (CNS). [Pg.431]

Multiple sclerosis (MS) is a complex inflammatory disease of the central nervous system (CNS) that is variable in terms of symptoms and presentation. The name refers to two features of the disease multiple describes the number of CNS lesions and sclerosis refers to the demyelinated lesions. Today, these lesions are usually called plaques, rather than scleroses. Although scientific understanding of MS has progressed at a rapid pace, there are still many areas of evolving knowledge. [Pg.431]

Psoriasis is a T-lymphocyte-mediated inflammatory disease that results from a complex interplay between multiple genetic factors and environmental influences. Genetic predisposition coupled with some precipitating factor triggers an abnormal immune response, resulting in the initial psoriatic skin lesions. Keratinocyte proliferation is central to the clinical presentation of psoriasis. [Pg.949]

Abd Soft, nontender bowel sounds present Exts Within normal limits no joint pains Skin Multiple lesions on the scalp, chest, back, elbows, and knees evidence of excoriation on the chest. [Pg.952]

Tinea infections are superficial fungal infections in which the pathogen remains within the keratinous layers of the skin or nails. Typically these infections are named for the affected body part, such as tinea pedis (feet), tinea cruris (groin), and tinea corporis (body). Tinea infections are commonly referred to as ringworm due to the characteristic circular lesions. In actuality, tinea lesions can vary from rings to scales and single or multiple lesions. [Pg.1206]

Multiple myeloma is a malignancy of plasma cells that is characterized by an abnormal production of a monoclonal protein. Features of the disease include bone lesions, anemia, and... [Pg.1420]

The primary goal in the treatment of multiple myeloma is to decrease tumor burden and minimize complications associated with the disease. A watch and wait approach is an option for asymptomatic patients who have no lytic lesions in the bone. Once symptoms occur, treatment is required. Chemotherapy can be used to reduce tumor burden in patients with symptomatic disease, but increasingly, immunomodula-tors such as thalidomide and dexamethasone are initial therapy. Almost all patients will become refractory to initial treatment and will require the use of salvage therapies such as bortezomib. Autologous stem cell transplantation prolongs overall survival in patients who can tolerate high-dose chemotherapy and may be the treatment of choice for many patients. [Pg.1422]

Newly diagnosed, asymptomatic patients may be observed without treatment. This asymptomatic period may last for months to a couple years. All patients with multiple myeloma will become symptomatic, and once this occurs, treatment is required. First-line treatment may be one of several therapies, including VAD, thalidomide plus steroids, and autologous transplant. Nearly all patients will progress at some point, and second-line therapy usually will include bortezomib. All patients who have bone lesions should receive monthly bis-phosphonates, with the hope of reducing pain and fractures. [Pg.1423]

Bone disease is a common manifestation of multiple myeloma. Bisphosphonates should be initiated in symptomatic patients with bone lesions to slow osteopenia and reduce the fracture risk associated with the disease. Pamidronate and zolendronic acid have equivalent efficacy in the management of osteolytic lesions, but because of relative ease of administration, zolendronic acid is used most frequently.43 The use of zolendronic acid decreases pain and bone-related complications and improves quality of life. The suggestion that bisphosphonates have direct antimyeloma activity, based on the ability to inhibit NF-kB signaling, remains controversial. Recent cases of osteonecrosis of the jaw have been a major concern. Risk factors are unclear, but osteonecrosis of the jaw is more common in patients receiving intravenous administration of bisphosphonates and having dental procedures performed. It is recommended that patients... [Pg.1423]


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See also in sourсe #XX -- [ Pg.227 ]




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