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Dive into the research topics where Jerry M. Earll is active.

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Featured researches published by Jerry M. Earll.


The New England Journal of Medicine | 1977

Selective venous sampling to differentiate ectopic ACTH secretion from pituitary Cushing's syndrome.

Dominic F. Corrigan; Marcus Schaaf; Robert A. Whaley; Carol L. Czerwinski; Jerry M. Earll

Ectopic ACTH secretion may be indistinguishable from pituitary-dependent Cushings syndrome (Cushings disease) by current diagnostic tests.1 2 3 With increasing application of pituitary treatment ...


Annals of Internal Medicine | 1976

Ionized and Total Serum Calcium and Parathyroid Hormone in Hyperthyroidism

Kenneth D. Burman; John M. Monchik; Jerry M. Earll

Total and ionized calcium concentrations as well as parathyroid hormone levels were measured in a group of hyperthyroid persons. Ionized and total calcium levels were elevated in 21 of 45 (47%) and in 12 of 45 (27%) thyrotoxic patients, respectively. Mean ionized and total calcium levels were higher in these 45 patients than in normal persons. Using two different radioimmunoassay systems for a total of 44 determinations, mean parathyroid hormone levels were lower in thyrotoxic patients than in subjects with proved hyperparathyroidism. These data suggest that [1] elevations of both ionized and total calcium concentrations occur frequently in thyrotoxic patients; [2] ionized calcium concentrations may be elevated in a higher percentage of hyperthyroid subjects than are total calcium concentrations; and [3] the hypercalcemia associated with thyrotoxicosis is not associated with elevated parathyroid hormone levels.


Metabolism-clinical and Experimental | 1972

Serum ionized calcium during bed rest in fracture patients and normal men

Hunter Heath; Jerry M. Earll; Marcus Schaaf; Joseph T. Piechocki; Ting-Kai Li

Abstract Nine of ten patients immobilized for the treatment of tractures were found to have abnormal elevations of serum ionized calcium when determined with an ion-sensitive electrode, while only three of the ten had hypercalcemic values ( 10.2, 10.4, and 11.7 mg 100 ml ) by atomic absorption spectroscopy (normal range, 8.2–10.1 mg 100 ml ). Mean serum ionized calcium values were 5.3–7.2 mg 100 ml in seven of the patients ( normal range, 4.5–5.2 mg 100 ml ), and two others had normal mean values but some individual abnormal measurements. Because of these observations, daily measurements of serum total and ionized calcium, and urinary calcium were made on four normal volunteers before, during, and after a 12-day bed rest period. Abnormal elevations of serum ionized calcium occurred during bed rest in all four subjects (peaks, 5.7–5.9 mg 100 ml ), while serum total calcium remained normal. Elevations of urinary calcium occurred in all four, but no clear temporal relation with the serum ionized calcium was seen. It is concluded that bed rest produces early and significant elevations of the serum ionized calcium, while there are minimal changes in the serum total calcium. The pathogenesis of these changes remains obscure.


Metabolism-clinical and Experimental | 1967

“Disappearance” of cystinuria in a patient treated with prolonged low methionine diet

Felix O. Kolb; Jerry M. Earll; Harold A. Harper

Abstract A unique patient, in whom the use of a rigorously controlled low methionine diet for 10 years has been associated with the disappearance of his cystinuria, is reported. Ornithine, lysine and arginine continue to appear in the urine in large amounts and renal function remains excellent. Oral loading with methionine promptly resulted in reappearance of large amounts of cystine. Possible explanation for improvement of cystinuria while on a prolonged low methionine diet have been offered. This case confirms the effectiveness of a low methionine diet in selected adult patients and demonstrates that it is a safe long-term therapy for adults. Our experience with the use of low methionine diets in conjunction with d-penicillamine will be reported elsewhere. 1


Journal of Clinical Investigation | 1972

Alterations in thyroid iodine release and the peripheral metabolism of thyroxine during acute falciparum malaria in man

Leonard Wartofsky; Daniel Martin; Jerry M. Earll

Previous studies of thyroid function during various infections have yielded conflicting results, but most have suggested an acceleration of peripheral thyroxine (T(4)) turnover during the acute infectious illness. In the present studies, thyroid function was examined by a method allowing simultaneous analysis of both endogenous thyroidal release and peripheral T(4) disposal in normal volunteers after induction of acute falciparum malaria. Subjects received iodide-(125)I, followed in 5-7 days by (131)I-T(4) intravenously. 4 days later, infection was induced by the injection of parasitized red blood cells. Bidaily measurements of serum protein-bound (125)I and protein-bound (131)I, and urinary (125)I and (131)I, together with frequent estimates of serum (127)I-T(4) (Murphy-Pattee) and free T(4) (FT(4)), were made during a control period, during acute illness, and during convalescence. Alterations in the peripheral metabolism of (131)I-T(4) during infection included significant decreases in the fractional disappearance rate for T(4) [(k)], and in the clearance and daily disposal of T(4), all of which returned to control values during convalescence. Total serum (127)I-T(4) increased late in the infected period to become greater during convalescence than either before or during infection, while FT(4) did not increase significantly until convalescence. An analysis of serum (131)I-T(4)/(127)I-T(4) and (131)I-T(4)/PB(125)I ratios confirmed these observations. The slope with time of ratios for urinary (125)I/(131)I, a reflection of thyroidal iodine release, was decreased during infection, but rebounded to control values during the convalescent period. The observed increments in serum (127)I-T(4) concentration in the convalescent phase may reflect in part the slowing of (k), but together with the rising ratios of urine (125)I/(131)I suggests enhanced thyroidal T(4) secretion immediately after the acute illness. Thus, with malarial infection, there appears to be an initial depression followed by a rebound in rates of thyroidal iodine release. In contradistinction to other infections, fractional turnover and daily disposal of hormone is decreased in malaria, perhaps due to hepatic dysfunction and the consequent impairment in cellular deiodinative processes.


Annals of Internal Medicine | 1973

Transsphenoidal Microsurgery in the Treatment of Acromegaly.

Richard L. Atkinson; Donald P. Becker; A. M. Martins; Jerry M. Earll

Excerpt Application of modern technology to an old surgical approach has led to a treatment of acromegaly that promises a cure: eradication of the tumor with preservation of normal pituitary functi...


The Journal of Clinical Endocrinology and Metabolism | 1974

Studies of Prolactin and TSH Secretion by Continuous Infusion of Small Amounts of Thyrotropin-Releasing Hormone (TRH)

Gordon L. Noel; Richard C. Dimond; Jerry M. Earll; Andrew G. Frantz


JAMA | 1967

Glucose Suppression of Serum Growth Hormone in the Diagnosis of Acromegaly

Jerry M. Earll; Lowell L. Sparks; Peter H. Forsham


The Journal of Clinical Endocrinology and Metabolism | 1976

Effect of Acute Increases in Serum Triiodothyronine on TSH and Prolactin Responses to TRH, and Estimates of Pituitary Stores of TSH and Prolactin in Normal Subjects and in Patients with Primary Hypothyroidism

Richard C. Dimond; Gordon L. Noel; Andrew G. Frantz; Jerry M. Earll


JAMA | 1973

Ionic Calcium Determination in Primary Hyperparathyroidism

James C. Low; Marcus Schaaf; Jerry M. Earll; Joseph T. Piechocki; Ting-Kai Li

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Kenneth D. Burman

MedStar Washington Hospital Center

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Richard C. Dimond

Walter Reed Army Institute of Research

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Marcus Schaaf

Walter Reed Army Institute of Research

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Richard L. Atkinson

Virginia Commonwealth University

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Leonard Wartofsky

Walter Reed Army Institute of Research

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Frances D. Wright

Walter Reed Army Medical Center

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Hunter Heath

Walter Reed Army Institute of Research

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