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A gas–liquid chromatographic micromethod for quantitation of cholesterol in 20 μl of plasma was developed using 5α-cholestane as an internal standard, saponification with tetramethylammonium hydroxide–isopropanol, and extraction with tetrachloroethylene–methyl butyrate. Cholesterol levels in plasma samples were calculated by comparing cholesterol–cholestane peak height ratios with those of preassayed reference plasma. Over a plasma cholesterol range of 44 to 468 mg/100 ml, the gas–liquid chromatographic micromethod and the automated ferric chloride colorimetric method gave nearly identical results (r = 0.99) in duplicate aliquots of 131 plasma samples.

A micromethod for quantitation of α-lipoprotein cholesterol was devised for gas–liquid chromatography to minimize plasma sample size and facilitate lipid studies using capillary blood from children or small animals. α-Lipoprotein cholesterol was measured by gas–liquid chromatography in 20 μl of the centrifuged supernate obtained after addition of 5 μl of mixed heparin–manganese chloride solution 1:1 (v/v) to 50 μl of plasma. Comparison of venous α-lipoprotein cholesterol measured by gas–liquid chromatography with venous α-lipoprotein cholesterol measured by conventional heparin–manganese precipitation and ferric chloride (colorimetric) cholesterol determination gave a correlation coefficient of 0.98 for 80 plasma samples. Capillary α-lipoprotein cholesterol and venous α-lipoprotein cholesterol were closely correlated in 31 patients (r = 0.97).

BACKGROUND: We prospectively assessed growth and motor–social development during the first 18 months of life in 126 live births (122 pregnancies) to 109 women with polycystic ovary syndrome (PCOS) who conceived on and continued metformin (1.5–2.55 g/day) through pregnancy. METHODS: The lengths and weights of PCOS neonates were compared with gender‐specific Centers for Disease Control and Prevention (CDC) infant data. Gestational diabetes (GD) and pre‐eclampsia in women with PCOS were compared with 252 healthy women without PCOS who had ≥1 live birth (262 live births). RESULTS: There were 101 out of 126 (80%) term (≥37 gestational weeks) PCOS births, which was not significantly different (P = 0.7) from controls, 206 out of 252 (81.7%). There were two (1.6%) birth defects. GD occurred in nine out of 119 PCOS pregnancies (7.6%) versus 40 out of 251 (15.9%) controls, P = 0.027. The prevalence of pre‐eclampsia did not differ in PCOS versus control pregnancies (4.1 versus 3.6%, P = 0.8). The birth length and weight of the 52 male neonates did not differ (P > 0.05) from those of CDC males; the 74 female neonates were shorter than CDC females (48.9 ± 5.4 versus 50.6 ± 2.7 cm, P = 0.006) and weighed less (3.09 ± 0.85 versus 3.29 ± 0.52 kg, P = 0.04). There were no systematic differences in growth between PCOS and CDC infants over 18 months. At 3, 6, 9, 12 and 18 months, of a potential 100% motor–social development score, scores (±SD) were 95 ± 13, 98 ± 8%, 95 ± 10, 97 ± 8 and 94 ± 16%; no infants had motor–social developmental delays. CONCLUSIONS: Metformin reduced development of GD, was not teratogenic and did not adversely affect birth length and weight, growth or motor–social development in the first 18 months of life. [ABSTRACT FROM AUTHOR]

BACKGROUND: In an observational study of 13 women with polycystic ovary syndrome (PCOS) not optimally responsive to metformin diet, we assessed the efficacy and safety of addition of pioglitazone. We also compared these 13 women to 26 women with PCOS, who were responsive to metformin diet, matched by age and by pre- treatment menstrual history and not different by obesity categories. METHODS: Prospectively, as outpatients, with diet constant [1500-2000 calorie (depending on entry body mass index), 26% protein, 44% carbohydrate, 30% fat], metformin (2.55 g/day) was given for 12 months to 39 women, 13 not optimally responsive, 26 responsive to metformin diet, followed by addition of pioglitazone (45 mg/day) for 10 months in the 13 non-responders. Outcome measures included changes in sex hormones, insulin, insulin resistance (IR), insulin secretion, high density lipoprotein cholesterol, weight, and menstrual status. RESULTS: In 13 non-responders, on metformin diet, median serum insulin fell (21 to 16 µIU/ml, P < 0.05) and insulin secretion fell from 251 to 200 (P < 0.01); weight, dehydroepiandrosterone sulphate (DHEAS), testosterone and IR were unchanged (P ≥ 0.07). Compared with 14% pre- treatment, on metformin diet, expected menses occurred 46% of the time at 3 months (P = 0.05), 38% at 6 months (P = 0.07), 27% at 9 months, and 24% at 12 months. In 26 responders, on metformin diet, median weight fell (93 to 87 kg), testosterone fell (50 to 32 ng/dl), insulin fell (26 to 16 µIU/ml), IR fell (5.32 to 3.45) and insulin secretion fell (351 to 271) (P ≤ 0.017 for all). The occurrence of expected menses in the 26 responders was 2.5-fold higher than in the 13 non-responders (P < 0.0001). In 11 non-responders, on pioglitazone + metformin diet over 10 months versus antecedent metformin diet, DHEAS fell (211 to 171 µg/dl, P = 0.02), insulin fell (16 to 10 µIU/ml, P = 0.001), IR fell (3.37 to 1.73, P = 0.002), insulin secretion fell (217 to 124, P = 0.004), sex hormone-binding globulin rose (31 to 43 nmol/l, P = 0.006), and HDL cholesterol rose (38 to 42 mg/dl, P = 0.003). On pioglitazone + metformin diet, the occurrence of expected menses was 2-fold higher than on metformin diet (P < 0.0001). CONCLUSIONS: In women with PCOS who failed to respond optimally to metformin, when pioglitazone was added, insulin, glucose, IR, insulin secretion, and DHEAS fell, HDL cholesterol and sex hormone-binding globulin rose, and menstrual regularity improved, without adverse side-effects. [ABSTRACT FROM AUTHOR]