Boy Frame
University of Michigan
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JAMA | 1979
Boy Frame
ABSTRACT The second volume of Metabolic Bone Disease contains seven additional essays on bone and mineral metabolism. Despite the books title, there is in many instances a scarcity of information on bone disease. Topics previously covered in the first volume do, however, make up for this deficit to some extent.The chapter on parathyroid physiology and primary hyperparathyroidism is a fine clinical contribution, but less than 10% of its content deals with the skeleton. The chapter on renal osteodystrophy is more closely centered about the bone. Hypoparathyroidism is covered exhaustively by Nagent de Deuxchaisnes and Krane, but again most of the 228 pages of the chapter is irrelevant to metabolic bone disease.Deftos essay on the thyroid gland might have contained additional information on the skeletal involvement in hyperthyroidism and less on medullary thyroid carcinoma in which the bones are hardly involved at all. While Pagets disease is not normally considered
JAMA | 1976
Boy Frame
When dealing with TSH-dependent thyroid cancer, it would appear wise to err on the side of maximal TSH suppression. Most would be willing to trade off a slight risk of thyroxine-induced osteopenia for adequate TSH suppression. I would not quibble with Dr Caplans suggestion of giving 0.3 mg/day of levothyroxine sodium in such a patient. The longterm deleterious effect on bone with the larger dose would appear to be minimal. The possibility of measuring maximal TSH suppression with TRH is interesting and is worthy of study.
Metabolism-clinical and Experimental | 1968
Richard A. Schacht; Wallace W. Tourtellotte; Boy Frame; Stewart N. Nickel
Abstract An analysis of the blood and CSF protein concentration and lipid profiles in 14 patients with clinical myxedema has been presented. In addition, the serum and CSF bromide concentrations were measured following the oral administration of sodium bromide during the pre- and post-treatment period. While the serum lipids and protein concentrations were noted to be elevated prior to treatment, the CSF constituents were elevated to a greater degree when compared to normal values than serum constituents, and treatment caused a return in concentration towards normal. Both serum and CSF bromide concentrations were elevated in the myxedematous state and returned toward normal following treatment, though a disproportionately greater rise in CSF than serum concentration was noted irrespective of treatment. That the evidence may reflect a breakdown in the “blood-CSF barrier” in myxedema, which is partially corrected by treatment, is discussed as a likely explanation for these observations.
JAMA Internal Medicine | 1964
Thomas N. James; Boy Frame; Irwin J. Schatz
JAMA Internal Medicine | 1965
Boy Frame
JAMA | 1963
Irwin J. Schatz; Stephen Podolsky; Boy Frame
The Cardiology | 1976
Irwin J. Schatz; Michael J Miller; Boy Frame
JAMA | 1983
Boy Frame
JAMA | 1967
Richard A. Schacht; Boy Frame
The Cardiology | 1976
Otto H. Gauer; R.J. Linden; Peter Sleight; Philip Hasleton; Donald Heath; Leonard Share; H. Rieckert; H. de Marées; Walter H Abelmann; Olav Thulesius; P. Chiche; A. Lellouch; J.P. Denizeau; J.L. Reid; C.T. Dollery; Fabio Magrini; Mohsen Ibrahim; Robert C. Tarazi; P. Weidinger; F. Kaindl; A Kroiss; K. Steinbach; F. Klimt; J. Rutenfranz; J.C. Demanet; E. Lang; H. Abelmann; J.L. McNay; Jürgen Stegemann; F. Loogen
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Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico
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