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http://projects.csail.mit.edu/courseware/?term=basketball-game-essay basketball game essay 23. Dong bj, hauck ww, gambertoglio jg, gee l, et al. Bioequivalence of generic and brand-name levothyroxine products in the treatment of hypothyroidism. Jama. 1997;277:1205–1213. 24. Mayor gh, orlando t, kurtz nm. Limitations of levothyroxine bioequivalence evaluation. An analysis of an attempted study. Am j ther. 1995;2:417–432. 25. Carr d, mcleod dt, parry g, thornes hm. Fine adjustment of thyroxine replacement dosage. Comparison of the thyrotrophin releasing hormone test using a sensitive thyrotrophin assay with measurement of free thyroid hormones and clinical assessment. Clin endocrinol. 1988;28:325–333. 26. Helfand m, crapo lm. Monitoring therapy in patients taking levothyroxine. Ann intern med. 1990;113:450–454. 27. Garg a, vanderpump mpj. Subclinical thyroid disease. Brit med bull. 2013;107:101–116. 28. Turner mr, camacho x, fischer hd, et al. Levothyroxine dose and risk of fractures in older adults.

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buy a custom essay 28 despite prophylaxis, 20% to 80% of patients will develop acute gvhd. 29 other factors that increase the risk of acute gvhd include increasing recipient or donor age (older than 20 years), female donor to a male recipient, and mismatches in minor histocompatibility antigens in hla-matched transplants. 28 t-cell depletion or receipt of an umbilical cord blood graft appears to lower the risk of acute gvhd. 1 clinical presentation and staging of acute gvhd acute gvhd targets the skin, liver and gi tract. It must be distinguished accurately from other causes of skin, liver, or gi toxicity in hsct patients. Other causes of toxicities affecting the skin, liver, or gi tract may include a drug reaction or an infectious process. A staging system based on clinical criteria is used to grade acute gvhd (figure 98–2). The severity of organ involvement is scored on an ordinal scale from 0 (no symptoms) to iv (severe symptoms), and then an overall grade is established based on the number and extent of involved organs. Immunosuppressive prophylaxis of acute gvhd  gvhd is a leading cause of morbidity and mortality after allogeneic hsct and thus, efforts have focused on preventing acute gvhd. The donor graft and preparative regimen influence the prophylactic regimen for acute gvhd, with two approaches having been taken by clinicians over time. One approach involves t-cell depletion, which was discussed more fully in the section on t-cell depletion earlier. The more common method is to use two-drug immunosuppressive therapy that typically consists of a calcineurin inhibitor (ie, cyclosporine or tacrolimus) with methotrexate after myeloablative hsct. Prophylaxis of acute gvhd for nonmyeloablative preparative regimens is varied, but a calcineurin inhibitor with either methotrexate or mycophenolate mofetil is used. 16 the calcineurin inhibitors (ie, cyclosporine and tacrolimus) should be initiated before donor cell infusion (eg, day –1) when used for gvhd prophylaxis. This schedule is recommended because of the known mechanism of action of calcineurin inhibitors, which entails blocking the proliferation of cytotoxic t cells by inhibiting production of t helper cell–derived interleukin-2 (il-2). Administering calcineurin inhibitors before the donor cell infusion allows inhibition of il-2 secretion to occur before a rejection response has been initiated. Studies comparing cyclosporine and tacrolimus in combination with methotrexate have shown that tacrolimus administration is associated with a lower incidence of grade ii to iv acute gvhd and a similar incidence of chronic gvhd but variable effects on overall survival. 30,31 adaptive dosing of the calcineurin inhibitors  most hsct centers have their own standardized approach to dose adjust the calcineurin inhibitors cyclosporine and tacrolimus to target concentration ranges. Cyclosporine and tacrolimus trough concentrations are associated with acute gvhd and nephrotoxicity. Cyclosporine trough concentrations usually are maintained between 150 and 400 ng/ml (125 and 333 nmol/l) in patients undergoing allogeneic hsct. Tacrolimus trough concentrations are targeted to a range of 10 to 20 ng/ml (10–20 mcg/l. 12. 4–24. 8 nmol/l). 32 dosage adjustments to either calcineurin inhibitor also should be made for elevated serum creatinine regardless of their serum concentrations. Nephrotoxicity can occur despite low or normal concentrations of the calcineurin overall clinical grade grading by organ system organ skin extent of involvement rash (% of body surface) desquamation liver intestine bilirubin (mg%) diarrhea (ml/day) pain/ileus < 25 25–50 > 50 code 1+ 2+ 3+ 4+ 2–3 3–6 6–15 > 15 1+ 2+ 3+ 4+ 500–1000 1000–1500 > 1500 1+ 2+ 3+ 4+ impairment of performance figure 98–2. Staging system for graft-versus-host disease. 1+ 2+ 3+ i ii iii iv 1454  section 16  |  oncologic disorders clinical presentation and diagnosis of acute graft-versus-host disease general •• patients may present with any or all of the following. Skin rash, gi complaints, or jaundice. •• signs and symptoms present after engraftment when donor lymphoid elements begin to proliferate. Symptoms •• patients may complain of nausea, vomiting, bloody diarrhea, or itching from skin rash. Signs •• skin. Maculopapular skin rash on the face, truck, extremities, palms, soles, and ears which may progress to generalized total-body erythroderma, bullous formation, and skin desquamation.

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http://cs.gmu.edu/~xzhou10/semester/sgs-thesis-template-toronto.html sgs thesis template toronto 46. Bouchard j, macedo e, soroko s, et al. Comparison of methods for estimating glomerular filtration rate in critically ill patients with acute kidney injury. Nephrol dial transplant. 2010;25:102–107. 47. Jelliffe r. Estimation of creatinine clearance in patients with unstable renal function, without a urine specimen. Am j nephrol. 2002;22:320–324. 48. Blot s, lipman j, roberts dm, roberts ja. The influence of acute kidney injury on antimicrobial dosing in critically ill patients. Are dose reductions always necessary?. Diagn microbiol. Infect dis 2014;79:77–84. 49. Susla gm. The impact of continuous renal replacement therapy on drug therapy. Clin pharmacol ther. 2009;86:562–565. 50. Pea f. Viale p, pavan f, furlanut m. Pharmacokinetic considerations for antimicrobial therapy in patients receiving replacement therapy. Clin pharmacokinet. 2007;46:997–1038. 26 chronic and end-stage renal disease kristine s. Schonder learning objectives upon completion of the chapter, the reader will be able to.

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