PubMed · 8375254
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S A Chmielewski, E E Miller. 1993. Micral-test sensitivity.. https://doi.org/10.2337/diacare.16.8.1210a
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BACKGROUND: Although guidelines recommend angiotensin-converting enzyme inhibitors for diabetic patients with microalbuminuria, this strategy requires that providers adhere to screening recommendations. In addition, the benefit of angiotensin-converting enzyme inhibitors in normoalbuminuric patients was recently demonstrated. OBJECTIVE: To evaluate the cost-effectiveness of treating all patients with type 2 diabetes. DESIGN: Markov model simulating the progression of diabetic nephropathy. DATA SOURCES: Randomized trials estimating the progression of diabetic nephropathy with and without angiotensin-converting enzyme inhibitors. TARGET POPULATION: Patients 50 years of age with newly diagnosed type 2 diabetes (fasting plasma glucose level > or = 7.8 mmol/L [140 mg/dL]). TIME HORIZON: Lifetime. PERSPECTIVE: Societal. INTERVENTIONS: Patients received angiotensin-converting enzyme inhibitors, screening for microalbuminuria, or screening for gross proteinuria. OUTCOME MEASURES: Lifetime cost, quality-adjusted life expectancy, and marginal cost-effectiveness. RESULTS OF BASE-CASE ANALYSIS: Screening for gross proteinuria had the highest cost and the lowest benefit. Compared with screening for microalbuminuria, treating all patients was more expensive ($15240 and $14940 per patient) but was associated with increased quality-adjusted life expectancy (11.82 and 11.78 quality-adjusted life-years). The marginal cost-effectiveness ratio was $7500 per quality-adjusted life-year gained. RESULTS OF SENSITIVITY ANALYSIS: Results were sensitive to the cost, effectiveness, and quality of life associated with angiotensin-converting enzyme inhibitor therapy, as well as age at diagnosis. The model was relatively insensitive to adherence with screening and costs of treating end-stage renal disease. CONCLUSIONS: Treating all middle-aged diabetic patients with angiotensin-converting enzyme inhibitors is a simple strategy that provides additional benefit at modest additional cost. The strategy assumes that patients meet the older diagnostic criteria for diabetes and makes sense only for those who are not bothered by treatment.
G-CSF not only functions as an endogenous hemopoietic growth factor for neutrophils, but also displays pro-Th2 and antiinflammatory properties that could be of therapeutic benefit in autoimmune settings. We evaluated the effect of treatment with G-CSF in a murine model of spontaneous systemic lupus erythematosus, a disease in which G-CSF is already administered to patients to alleviate neutropenia, a common complication. Chronic treatment of lupus-prone MRL-lpr/lpr mice with low doses (10 microg/kg) of recombinant human G-CSF, despite the induction of a shift toward the Th2 phenotype of the autoimmune response, increased glomerular deposition of Igs and accelerated lupus disease. Conversely, high-dose (200 microg/kg) treatment with G-CSF induced substantial protection, prolonging survival by >2 mo. In the animals treated with these high doses of G-CSF, neither the Th1/Th2 profile nor the serum levels of TNF-alpha and IL-10 were modified. Despite the presence of immune complexes in their kidney glomeruli, no inflammation ensued, and serum IL-12 and soluble TNF receptors remained at pre-disease levels. This uncoupling of immune complex deposition and kidney damage resulted from a local down-modulation of FcgammaRIII (CD16) expression within the glomeruli by G-CSF. Our results demonstrate a beneficial effect of high doses of G-CSF in the prevention of lupus nephritis that may hold promise for future clinical applications, provided caution is taken in dose adjustment.
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