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Dive into the research topics where Alexander B. Gutman is active.

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Featured researches published by Alexander B. Gutman.


The American Journal of Medicine | 1950

Effects of diet in essential hypertension: I. Baseline study: Effects in eighty-six cases of prolonged hospitalization on regular hospital diet

Donald M. Watkin; Herman F. Froeb; Frederick T. Hatch; Alexander B. Gutman

Abstract 1.1. To provide baseline points of reference for evaluation of the results of allegedly specific treatment of essential hypertension in a hospital environment, a study was made of the effects of hospitalization per se in eighty-six patients observed for a mean period of nine weeks on a standardized regular diet. 2.2. Observations on changes in symptomatology, basal blood pressure, heart size, electrocardiographic findings and retinopathy are recorded. 3.3. Precise data are afforded to support the general impression that the response of individual patients with essential hypertension to hospitalization per se is so variable and unpredictable that a prolonged period of observation is a prerequisite to valid appraisal of the specific effects of therapy.


The American Journal of Medicine | 1950

Effects of adrenocorticotropic hormone (ACTH) in gout

Alexander B. Gutman; Ts'ai-Fan Yü

Abstract 1.1. ACTH effected a very rapid and satisfactory response in the local and systemic manifestations of acute gout in seven of eleven cases treated, including one patient refractory to colchicine. ACTH therefore appears to be a useful agent in the therapy of acute gout. In many of these patients, however, ACTH was not convincingly superior to colchicine, and in four instances colchicine terminated attacks responding unsatisfactorily to ACTH. Unlike colchicine, ACTH is not suitable for prophylactic use in the prevention of acute gouty attacks. 2.2. Exacerbation of symptoms occurred in four patients following discontinuance of ACTH therapy after a satisfactory response. Such exacerbations usually suggested re-exhibition of the underlying disease upon termination of the suppressive effects of ACTH rather than initiation of a new attack of acute gout. The conjoint and continued prophylactic use of colchicine seems rational in patients subject to frequent recurrences. 3.3. Acute gouty arthritis developed only once in eight cases of interval gout when ACTH was given in full dosage and then abruptly discontinued. 4.4. In the prevention and treatment of chronic tophaceous gout, the use of ACTH is neither feasible nor desirable at present. Salicylates and carinamide are at least as effective uricosuric agents, are readily available and orally administered. 5.5. The available evidence does not appear to justify the view that the pituitary and/or adrenal glands play a central role in the pathogenesis of gout.


The American Journal of Medicine | 1952

Current principles of management in gout

Alexander B. Gutman; Ts'ai-Fan Yü

Abstract 1.1. Present knowledge concerning the fundamental nature of the gouty trait, the causes of acute gouty arthritis and the pathogenesis of chronic tophaceous gout, is reviewed. 2.2. The regulation of gout involves two more or less distinct problems: (1) prevention and suppression of attacks of acute gouty arthritis, which are not attributable to urate per se but to unknown causes; (2) prevention and mobilization of tophi, which represent excessive urate deposition in the tissues. Each problem requires specifically oriented management. Current principles of such management are outlined. 3.3. The three uses of colchicine, to terminate established attacks of acute gouty arthritis, to abort impending attacks, and as a prophylactic agent to prevent seizures in intercritical periods, are described and the results of each usage analyzed. The advantages of regular colchicine prophylaxis are stressed. 4.4. The use of corticotropin (ACTH) in acute gouty arthritis is described and the results in forty cases are presented. ACTH is usually effective if given in adequate dosage properly scheduled. 5.5. The use of phenylbutazone (butazolidine) in acute gouty arthritis is described and the results in twenty cases are presented. Administration is simple and relief is rapid and effective in most cases. Toxicity is low in short-term therapy. 6.6. The use of probenecid (benemid) as a uricosuric agent in chronic tophaceous gout is described. Experience with forty gouty subjects given daily dosage for six months to two years indicates that formation of new tophi and enlargement of old tophi can be prevented. Urate deposits in the tissues can be mobilized, with relief of chronic joint disability and shrinkage of visible tophi. 7.7. The conjoint use of restrictive diets to avoid precipitation of acute attacks and to minimize deposition of urate in the tissues is discussed.


Journal of Bone and Joint Surgery, American Volume | 1972

Views on the Pathogenesis and Management of Primary Gout-1971

Alexander B. Gutman

Prosthetic replacement is a good treatment option in osteoporotic patients with four-part fractures, fracture-dislocations, head-split fractures with more than 40% articular surface involvement, anatomic neck fractures, dislocations present for longer than 6 months, and selected three-part fractures. Early prosthetic replacement of proximal humeral fractures has a better outcome than late reconstructive prosthetic management. Prosthetic design features specific forfracture care have led to a reduction in complications. Techniques will continue to improve as prosthetic design features specific for fractures evolve.


The American Journal of Medicine | 1951

Mobilization of gouty tophi by protracted use of uricosuric agents

Ts'ai-Fan Yü; Alexander B. Gutman

Abstract A case of advanced tophaceous gout exhibiting unequivocal reduction in size of many tophi in the course of protracted uricosuric therapy is described. It may be possible by proper use of uricosuric agents not only to minimize new tophus formation but also to cause the disappearance of old established tophi.


Seminars in Arthritis and Rheumatism | 1972

Renal mechanisms for regulation of uric acid excretion, with special reference to normal and gouty man☆

Alexander B. Gutman; Ts'ai Fan Yü

T HIS REVIEW BEGINS with a brief description of the historical development of the long sequence of hypotheses relating to the disposition of uric acid by the kidneys. Of course these evolved in conjunction with more general concepts intended to explain how the kidney so precisely performs all its diverse and intricate functions. Pitts’ has recently given an incisive and illuminating account of these broader endeavors; the successive hypotheses relating specifically to uric acid have been previously reviewed by Br


The American Journal of Medicine | 1973

Hyperglutamatemia in primary gout

Alexander B. Gutman; Ts’ai-Fan Yü

chnerMortensen2 and Smith.3 Recognized as a characteristic component of the urine since its discovery there by Scheele in 1776, uric acid figured prominently in the initial speculations concerning the mechanisms of renal function, notably the controversies over the Bowman-Heidenhain-Marshall concept of tubular secretion vs. the LudwigCushny-Richards view of filtration-reabsorption. In fact, in the early morphological studies of renal function, uric acid was widely employed experimentally as a marker because of its insolubility and ready detection in kidney tissue sections after uric acid loading. For many years such morphological investigation was all that was possible since suitably refined methods of chemical identification of uric acid were not yet available. The development of more sensitive colorimetric procedures by Folin, and concomitantly of renal clearance techniques, opened the way to further progress. Soon a dichotomy developed. Tubular secretion was incontrovertibly established as the major mechanism of uric acid excretion in the uricotelic bird and reptile, whereas the accumulated evidence in ureotelic mammals supported the filtration-reabsorption hypothesis in the pattern well established for glucose,


Postgraduate Medicine | 1972

Medical management of gout

Alexander B. Gutman

Abstract The mean plasma glutamate concentration, determined by column chromatography, was found to be 80 ± 27 μmol/liter in 62 gouty subjects with distinct hyperuricemia, and 79 ± 14 μmol/liter in 12 distinctly hyperuricemic but asymptomatic young sons of gouty subjects, as compared to 53 ± 16 μmol/ liter and 56 ± 15 μmol/liter in their normouricemic counterparts (p p > ?0.02). The data support the view that catabolism of glutamate is somewhat impaired in many patients with primary gout. Whether this is due to a deficiency in glutamate dehydrogenase activity, as postulated by Pagliara and Goodman, remains to be determined. The abnormalities in glutamine metabolism previously described in many patients with primary gout could be secondary to the abnormalities in glutamate metabolism and, for reasons discussed, both appear to be compatible with a polygenic and multifactorial origin in most cases of primary gout.


Archive | 1974

Reduced Renal Ammoniagenesis in Primary Gout

Alexander B. Gutman; Ts’ai-Fan Yü

Hyperuricemia predisposes to gout, but it is not possible to determine whether gout will occur in the asymptomatic hyperuricemic individual. Hence, hyperuricemia, unless very marked, is managed conservatively until overt signs of gout appear. Prognosis in most cases of primary gout has improved dramatically with earlier diagnosis and the introduction of potent and relatively safe uricosuric drugs and allo-purinol. The incidence of acute attacks can be reduced, and joint disability and deformity are no longer inevitable.


The American Journal of Medicine | 1950

Effects of diet in essential hypertension: II. Results with unmodified kempner rice diet in fifty hospitalized patients

Donald M. Watkin; Herman F. Froeb; Frederick T. Hatch; Alexander B. Gutman

The rate of NH3 diffusion is influenced by (1) the transtubular pH gradient, (2) the availability of titratable acid precursors, and (3) the urine flow rates. In our subjects for the present study of urinary excretion of titratable acid, NH+ 4, and uric acid, urine samples were collected as a rule from 6:30 A. M. to 8:30 A. M. after an overnight fast, both the gouty and the non-gouty subjects alike. the urine flow rates were more or less in the same range, approximately 1.0 ± 0.3 ml/min.

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Ts'ai-Fan Yü

Icahn School of Medicine at Mount Sinai

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Ts’ai-Fan Yü

City University of New York

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Ts'ai Fan Yü

City University of New York

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