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"Source: Hanefeld el al. (1990).

"Source: Hanefeld el al. (1990).

markedly reduced, making acarbose the drug of choice for treating the metabolic syndrome after dietary failure (Hanefeld et al., 1990). In long-term trials, acarbose also lowered serum triglycerides and VLDL significantly, while cholesterol levels were not affected (Leonhardt et al., 1991).

The therapeutic effects of acarbose and biguanides have been compared in Type-II diabetics (Pagano and Cavallo-Perin, 1990) and found to be nearly equally effective. The same was true in studies (by Schwedes et al. (1982), who compared acarbose and metformin in poorly controlled NIDDM, while Schoffling et al. (1982) reported that acarbose was even more effective than metformin. Drost et al. (1982) concluded from their studies, however, that there was no basic difference between the hypoglycaemic effects of acarbose and metformin. Petersen (1982) tested the efficacy of acarbose versus buformin in NIDDM. Acarbose was found to reduce postprandial but not fasting blood glucose levels and to be slightly less effective than buformin.

In most countries of the Western world, sulphonylureas are the most widely used oral antidiabetic agents. With the recognition of the metabolic syndrome in many Type-II diabetics, however, it became clear that insulinotropic drugs such as sulphonylureas should no longer be the first choice in the initial treatment of hyperinsulinaemic insulin-resistant diabetics, if other equally effective drugs are available to lower blood glucose levels. For that purpose, several studies were conducted to compare the effect of acarbose and glibenclamide on blood glucose and HbA] (Folsch et al., 1990; Spengler et al., 1992). It was found that 3 x 100mg of acarbose was nearly as effective as 3 x 3.5 mg glibenclamide (Fig. 28). Fasting blood glucose decreased from 8.6 to 6.7 mM following acarbose and from 8.6 to 6.7 mM following glibenclamide. Postprandial blood glucose was lowered from 11.3 to 8.7 versus 11.1 to 8.2 mM. The incidence of hypoglycaemia in sulphonylurea-treated patients was 0.22 per 1000 patient-years, while no hypoglycaemic episodes were reported in acarbose-treated patients (Wiholm and Wester-holm, 1984).

geometric means, 1 s-fange

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Fig. 28. HbA( levels during 6 months of treatment with acarbose or glibenclamide. (Source: Folsch el al1990.)

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Fig. 28. HbA( levels during 6 months of treatment with acarbose or glibenclamide. (Source: Folsch el al1990.)

The combination of acarbose and sulphonylureas is mainly used in patients with secondary sulphonylurea failure. Rosak (1990) reported a lowering of fasting blood glucose by 42 mg per 100 ml in diabetics treated with acarbose and sulphonylureas versus 14 mg per 100 ml with only sulphonylureas. Postprandial blood glucose was decreased by 57 mg per 100 ml, while sulphonylureas alone produced an increase of 4 mg per 100 ml in secondary sulphonylurea failure.

The combination of sulphonylureas and acarbose (3 x 100 mg) versus sulphonylureas and phenformin (75 mg) was tested for 3 months by Pagano and Cavallo-Perin (1990), who could not find any significant difference between the two treatments as far as blood glucose, plasma insulin and HbA] were concerned. However, there was a 20% increase in plasma lactate in the biguanide group and no variation in the acarbose patients.

The treatment with acarbose of Type-II diabetics who had already been transferred to insulin, revealed an insulin-saving effect. The total daily insulin dosage was reduced by 10IU per patient with acarbose, while insulin and placebo increased the daily insulin dosage by 0.7 IU. Blood glucose levels in the acarbose group was lowered (Rosak, 1990) and HbA! was decreased from 9.1 to 7.5% in 29 Type-Il diabetics. Fasting blood glucose was lowered by 0.3 mM, while with insulin only blood glucose increased by 1.1 mM.

In patients with diabetes plus liver cirrhosis, acarbose treatment appears to be favourable because it improves the detoxification of ammonia (Muting, 1984). Acarbose induces an increased growth of lactobacteria, lowers intestinal pH and hyperammonaemia, inducing a beneficial effect on portosystemic encephalopathy. It also reduces lipolysis and ketogenesis in cirrhotic patients (Zillikens et al., 1989), following a late evening meal with 100 mg acarbose.

In conclusion, the best indication for acarbose is in the early stages of NIDDM and in overweight diabetic patients who do not respond well to diet therapy. Acarbose can be used as monotherapy and also in association with sulphonylureas and insulin. It lowers postprandial and fasting blood glucose, decreases hypertriglyceridaemia and hyperinsulinaemia, and improves HbAj. It is therefore justified to expect also a beneficial effect of acarbose on the development of long-term diabetic complications.

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