Summary
Severe hyperlactemia of 8.7, 8.6 and 7.9 mmol/l, respectively, developed in three patients with hyperosmolar syndromes (two hypernatremic, 417 and 415 mosmol/kg H2O; one hyperglycemic 437 mosmol/kg H2O) during rehydration treatment with 5% fructose in water (fructose dosage 0.5 g/kg body wt. per hour). After resolution of the electrolyte disturbances, the infusion of fructose at the same dosage increased the plasma lactate concentration in two of the patients to 4.9 and 4.0 mmol/l, indicating near normalization of hepatic lactate utilization. Thus, in addition to peripheral insulin resistance and decreased muscular glucose utilization, the hyperosmolar state is associated with a reduced tolerance to fructose. This is most likely due to an osmolality-dependent impairment of hepatic gluconeogenesis. In rehydration therapy for hyperosmolar syndromes, fructose-containing infusion solutions should no longer be used.
This is a preview of subscription content, log in via an institution to check access.
Abbreviations
- DSW:
-
infusion solution of 5% dextrose in water
- FSW:
-
infusion solution of 5% fructose in water
- Lac:
-
plasma lactate concentration
- RR:
-
blood pressure
References
Berg G, Matzkies F, Bickel H (1974) Dosierungsgrenzen bei der Infusion von Glucose, Sorbit, Fructose und Xylit und deren Mischungen. Dtsch med Wochenschr 99:663–638
Bergström J, Fürst P, Gallyas F, Hultman E, Vinnars E (1976) Lactate production during fructose infusion with or without amino acids. Acta Med Scand 200:99–105
Björkman O, Gunnarsson R, Wahren J, Felig P (1984) Renal-hepatic interaction in the hyperglycemic and gluconeogenetic response to fructose. 6th ESPEN Congress, Milan 1984, Abstract 0.50
Bratusch-Marrain P, De Fronzo R (1983) Impairment of insulin-mediated glucose metabolism in man. Diabetes 32:1028–1034
Bratusch-Marrain P, Kleinberger G, Pichler P (1981) Das hypernatriamisch-hyperosmolare Syndrom. Dtsch Med Wochenschr 106:210–214
Cohen RD, Woods HF (1976) Clinical and biochemical aspects of lactic acidosis. Blackwell, Oxford
Dietze G, Wicklmayr M, Hepp KD, Grunst J, Stiegler G, Mehnert H (1974) Der Stoffwechsel des Splanchnicusgebiets unter dem Einfluß von Fructose. Infusionsth Klin Ernahr 1:552–555
Frösch ER, Wolf HP, Baitsch H, Prader H, Labhart A (1963) Hereditary fructose intolerance. An inborn defect of hepatic fructose-1-phosphate splitting aldolase. Am J Med 34:151–153
Graig GM, Crane CW (1971) Lactic acidosis complicating liver failure after intravenous fructose. Br Med J 4:211–212
Kleinberger G (1980) Einfluß der insulinfreien Rehydratation auf die diabetische Stoffwechselentgleisungen. Wien Klin Wochenschr 92:616–629
Kleinberger G, Bauer K, Gassner A, Pichler M, Waldhäusel W, Westphal G (1980) Treatment of electrolyte derangements in severely uncontrolled diabetes. In: Waldhausel W (ed) Diabetes 1979. International Congress Series 500, Excerpta Medica, pp 693–699
Komjati M, Waldhäusel W, Kastner G, Bratusch-Marrain P (1981) Effect of hyperosmolality on glucose uptake and ketogenesis in isolated rat hepatocytes. Diabetes 30 [Suppl]:35 A
Rosenthal NR, Barrett EJ (1985) An assessment of insulin action in hyperosmolar hyperglycemic nonketotic diabetic patients. J Clin Endocrinol Metabol 60:607–610
Waldhäusel W, Kleinberger G, Korn A, Dudczak R, Bratusch-Marrain P, Novotny P (1979) Severe hyperglycemia: effects of rehydration on endocrine derangements and blood glucose concentration. Diabetes 28:577–584
Woods HF, Alberti KGMM (1972) Dangers of intravenous fructose. Lancet II:1354–1357
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Druml, W., Kleinberger, G., Lenz, K. et al. Fructose-induced hyperlactemia in hyperosmolar syndromes. Klin Wochenschr 64, 615–618 (1986). https://doi.org/10.1007/BF01735263
Received:
Revised:
Accepted:
Issue Date:
DOI: https://doi.org/10.1007/BF01735263