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By I. Aschnu. Berry College.

Her physical examination shows minimal proxi- mal weakness crestor 10mg line. Which of the following would be the best therapeutic intervention at this time? Continue steroids at the same dose for 3 more months and then pro- ceed with a slow taper B discount crestor 10 mg without prescription. Start tapering the steroids and start methotrexate or azathioprine C cheap crestor 5 mg mastercard. Discontinue the steroids and start cyclophosphamide D trusted 5 mg crestor. Order a muscle biopsy to see if the patient is in remission Key Concept/Objective: To understand the treatment of idiopathic inflammatory myopathies Corticosteroids are the mainstay of initial therapy for the inflammatory myopathies 5mg crestor with visa. Most patients with documented muscle inflammation should be started on these drugs at rela- tively high doses (1 mg/kg/day). A standard approach has been to maintain this dosage for up to 3 months or until clinical improvement occurs. After this initial period of high-dose therapy, the dose can be consolidated into a single morning dose and then tapered so that the total daily dose is reduced by 20% to 25% each month; a maintenance dose of 5 to 10 mg daily should be reached in about 6 to 8 months. The addition of second-line drugs to the prednisone regimen is now recommended within the first 3 months of initiating treat- ment. The most commonly used second-line agents for the treatment of inflammatory myopathy are methotrexate and azathioprine. Azathioprine and methotrexate have simi- lar efficacy in these disorders, and the choice of which to use may depend on tolerability 18 BOARD REVIEW or other comorbid conditions. Cyclophosphamide may be useful in the treatment of the antisynthetase syndrome with interstitial lung disease and in children with vasculitis- related complications of dermatomyositis. There is no indication in this case for the use of cyclophosphamide. After the diagnosis is made and the therapy is started, the response to therapy in patients with idiopathic inflammatory myopathies is followed clinically and with assessment of muscle enzyme levels; a muscle biopsy is usually not necessary in this setting. A 35-year-old woman comes to your office complaining of weakness and fatigue that has lasted for about 2 months. She has found it difficult to get up from a chair, and brushing her hair has become more prob- lematic. In addition, she has developed blanching of the hands with exposure to cold, as well as stiffness of the hands, wrists, and feet lasting for 1 to 2 hours in the morning. She can no longer wear her wed- ding ring because of finger swelling. She also notes that she gets out of breath easily after climbing just one flight of stairs. On examination, she has evidence of proximal muscle weakness; synovitis of the MCPs, PIPs, wrists, and MTPs; and rales at the lung bases. There is no evidence of rash or lower extrem- ity edema, and cardiac examination is normal. You suspect a connective tissue disease, and indeed, the screening ANA is positive at a titer of 1:640. What additional antinuclear test will be most useful diagnostically for this patient? Anti-Sm Key Concept/Objective: To know the extramuscular manifestations of polymyositis associated with Jo-1 antibodies Patients with polymyositis frequently have extramuscular manifestations. Almost 70% of patients with pulmonary fibrosis will have the autoantibody Jo-1 in their serum. Anti–Jo-1 is one of the antisynthetase antibodies cur- rently found only in patients with myositis. Besides pulmonary fibrosis, the antisynthetase syndrome includes Raynaud phenomenon, polyarthritis, and, in some cases, so-called mechanic’ s hands. The last condition causes cracked and fissured skin on the hands.

Broad reviews of the toxicology of these elements are available [57 discount 10 mg crestor otc,58] and are summarized below discount crestor 5 mg otc. In general terms discount crestor 5mg without a prescription, metal toxicity may be by virtue of (1) metabolic alterations quality 20mg crestor, (2) alterations in host–parasite interactions order 5 mg crestor with visa, (3) immunologic interactions of metal moieties by virtue of their ability to act as haptens (specific Corrosion and Biocompatibility of Implants 83 immunological activation) or antichemotactic agents (nonspecific immunological suppression) [59,60], and (4) by chemical carcinogenesis. Cobalt, chromium, nickel, and vanadium are all essential trace metals in that they are required for certain enzymatic reactions. In excessive amounts however, these elements are also toxic. Excessive cobalt may lead to polycythemia, hypothyroidism, cardiomy- opathy, and carcinogenesis [64,65]. Chromium can lead to nephropathy, hypersensitivity, and carcinogenesis [66,67]. Nickel can lead to eczematous dermatitis, hypersensitivity, and carcino- genesis. Vanadium can lead to cardiac and renal dysfunction, and has been associated with hypertension and depressive psychosis. The nonessential metallic elements also possess specific toxicities. Titanium, although generally regarded as inert, has been associated with pulmonary disease in patients with occupational exposure and in animal models. Aluminum toxicity is well documented in the setting of renal failure and can lead to anemia, osteomalacia, and neurological dysfunction, possibly including Alzheimer’s disease. However, considering the litany of documented toxicities of these elements, it is important to remember that the toxicities generally apply to soluble forms of these elements and may not apply to the chemical species that are the degradation products of prosthetic implants. Immunogenicity of Metallic Implants Some adverse responses to orthopedic biomaterial corrosion are subtle and continue to foster debate and investigation. One of these responses is ‘‘metal allergy,’’ or hypersensitivity to metallic biomaterial degradation. Dermal hypersensitivity to metal is common, affecting about 10–15% of the population [76–79]. Dermal contact and ingestion of metals have been reported to cause immune reactions, which most typically manifest as skin hives, eczema, redness, and itching [76,80,81]. As previously stated, all metals in contact with biological systems corrode [82,83 and the released soluble products, while not sensitizers on their own, can activate the immune system by forming complexes with native proteins [78,84,85]. These metal–protein complexes are considered to be candidate antigens (or, more loosely termed, allergens) for eliciting hypersensitivity responses. Metals known as sensitizers include beryllium, nickel [79–81,86], cobalt, and chromium, while occasional responses have been reported to tantalum, titanium [88,89], and vanadium. Nickel is the most common metal sensitizer in humans followed by cobalt and chromium [76,79–81]. The prevalence of metal sensitivity among the general population is approximately 10–15%, with nickel sensitivity the highest (approximately 14%). Cross-reactivity between nickel and cobalt is most common [76,78]. The amounts of these metals found in medical grade alloys were shown in Table 2. Hypersensitivity can be either an immediate (within minutes) humoral response (initiated by antibody or formation of antibody–antigen complexes of types I, II, and III reactions) or a delayed (hours to days) cell-mediated response [90,91]. It is the latter response with which implant related hypersensitivity reactions are generally associated, in particular type IV delayed type hypersensitivity (DTH). Cell-mediated delayed type hypersensitivity is characterized by antigen activation of sensi- tized TDTH lymphocytes releasing various cytokines, which result in the recruitment and activa- tion of macrophages. TDTH lymphocytes are subset populations of T helper (TH) lymphocytes purported to be of the CD4 TH-1 subtype (and in rare instances CD8 , cytotoxic T cells, TC). This TH-1 subpopulation of T cells is characterized by their cytokine release profile, e. TH-1 cells are generally associated with responses to intracellular pathogens and autoim- mune diseases. Although TH-1 cells mediate a DTH reaction, only 5% of the participating cells 84 Hallab et al. The majority of DTH participating cells are macrophages.

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