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Ramon Medalle, MD; Robert Webb, MD; Christine Waterhouse, MD

Arch Intern Med. 1971;128(2):273-278.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Lactic acidosis has elicited considerable clinical interest since1961 when Huckabee^1,2 drew attention to it as a clinical entity. Waters et al³ listed the etiologies of excess lactic acid production as follows: no known cause (idiopathic, spontaneous), diabetes mellitus, phenformin hydrochloride, shock, acute anoxia, exercise, extracorporeal circulation, liver glycogen storage disease, and epinephrine injection. Only in the cases of glycogen storage disease^4-8 has the association of hyperlactacidemia with hypoglycemia been noted and the necessity of glucose administration been stressed. Among the reported cases of well documented lactic acidosis not associated with glycogen storage disease, four patients had concomitant hypoglycemia^9-12 but the authors failed to mention the role of hypoglycemia in those patients. Johnson and Waterhouse¹¹ did, however, point out the need of glucose and insulin in their report of lactic acidosis in a diabetic patient receiving phenfromin. This communication describes three patients with lactic acidosis and concomitant . . . [Full Text PDF of this Article]

Author Affiliations
Rochester, NY

From the Department of Medicine, University of Rochester (NY) School of Medicine and Dentistry.

Footnotes
Received for publication July 28, 1970; accepted Nov 25.

Reprint requests to 260 Crittenden Blvd, Rochester, NY 14620 (Dr. Waterhouse).

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