October 30, 1975New England Journal of Medicine
Homozygous Familial Hypercholesterolemia
Why the study?
Do biochemical differences in LDL binding and enzyme suppression explain the variable response to therapy in homozygous familial hypercholesterolemia?
Population
Fibroblasts from 6 patients with homozygous familial hypercholesterolemia and normal controls.
Comparison
In vitro exposure to low-density lipoprotein vs Control and fibroblasts from normal controls
Design
Preclinical
Authors
Discussion
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Member takes
Implication
May aid stratification of therapy response in homozygous FH; leaves open whether fibroblast testing should guide clinical decisions.
Structured PICO
Do biochemical differences in LDL binding and enzyme suppression explain the variable response to therapy in homozygous familial hypercholesterolemia?
P
Population
Fibroblasts from 6 patients with homozygous familial hypercholesterolemia (4 therapy-responsive, 2 therapy-unresponsive) and normal controls.
I
Intervention
In vitro exposure to low-density lipoprotein (100 mug per milliliter)
C
Comparator
Control (without low-density lipoprotein) and fibroblasts from normal controls
O
Outcome
Suppression of 3-hydroxy-3-methylglutaryl coenzyme A reductase activity and low-density lipoprotein bindingsurrogate
Biochemical differences in LDL binding and HMG-CoA reductase suppression in fibroblasts correlate with clinical responsiveness to diet and drug therapy in homozygous familial hypercholesterolemia.
Cite This Study
Breslow et al. (1975) studied this question.