G. Fanghanel et al., METFORMINS EFFECTS ON GLUCOSE AND LIPID-METABOLISM IN PATIENTS WITH SECONDARY FAILURE TO SULFONYLUREAS, Diabetes care, 19(11), 1996, pp. 1185-1189
Citations number
38
Categorie Soggetti
Endocrynology & Metabolism","Medicine, General & Internal
OBJECTIVE - To compare results obtained with metformin versus those ob
tained with DNA-recombinant insulin in obese patients with NIDDM suffe
ring from secondary failure to sulfonylureas. RESEARCH DESIGN AND METH
ODS - We conducted an open, prospective, randomized, and comparative s
tudy comprising a total of 60 patients selected and placed in two para
llel groups. We had previously confirmed that the subjects had seconda
ry failure to high doses of sulfonylureas. The initial metformin dosag
e was a single 850 mg tablet, and the dosage was increased to two or t
hree tablets depending on the patient's metabolic changes. The initial
dosage of DNA-recombinant insulin was 24 U, subcutaneously administer
ed and divided into two portions: two-thirds at around 8:00 A.M., befo
re breakfast, and the remaining third at 8:00 P.M., before dinner. The
dosage was adjusted based on the patient's clinical and metabolic res
ponse. RESULTS - The initial average glucose value for the metformin g
roup was 269.1 +/- 32.2 mg/dl, decreasing by the end of the study to 1
59.7 +/- 30.5 mg/dl. For the insulin group, these figures went from 27
0.7 +/- 24.0 mg/dl at the beginning of the study to 134.8 +/- 26.7 mg/
dl. This decrease correlates with the reduction in glycosylated hemogl
obin from 12.8 to 8.9% for the first group and from 12.3 to 8.2% for t
he second, as well as with the reduction in triglyceride values from 2
30.3 to 183.1 mg/dl and from 218.4 to 186.3 mg/dl, respectively. The B
MI (27.5-26.4), blood pressure (systolic from 145.7-132.1 mmHg, diasto
lic from 90.3-84.8 mmHg), and total cholesterol levels (235-202 mg/dl)
decreased in only the metformin group. CONCLUSIONS - Metformin is an
effective, safe, and well-tolerated treatment that improves metabolic
control and favorably modifies secondary clinical alterations due to i
nsulin resistance, such as arterial hypertension, overweight, and hype
rlipidemia, in obese patients with NIDDM suffering from secondary fail
ure to sulfonylureas.