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Sukdeb Mukherjee, MD; Robert M. Bilder, PhD; Harold A. Sackeim, PhD
College of Physicians and Surgeons of Columbia University 722 W 168th St Kolb Annex Room 422 New York, NY 10032

Arch Gen Psychiatry. 1986;43(2):193.

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

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Sandyk and Gillman have written a thoughtful comment on our proposal that TD may be associated with abnormal carbohydrate metabolism. We thank them for the additional information on glucose abnormalities in extrapyramidal disorders. They have suggested that the high FBS level noted by us in patients with TD could reflect a peripheral effect of neuroleptics on hepatic and pancreatic glucose and insulin metabolism. While this is pertinent, it remains of interest that the group with TD had a higher mean FBS level than the group without TD despite there being no difference between the groups with respect to medication status. If patients with TD were showing a greater glucogenic response to neuroleptics, could this response be predictive of TD development or is it an aftermath of TD? One problem with this explanation is the observation^1,2 that dopamine analogues may cause increased FBS levels by inhibiting pancreatic insulin . . . [Full Text PDF of this Article]

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