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R Ewart

Publications and source records attributed to R Ewart.

6 recordsLinked to original sources
PubMed1993

C-peptide and the classification of diabetes mellitus patients in the Early Treatment Diabetic Retinopathy Study. Report number 6. The ETDRS Research Group.

The Early Treatment Diabetic Retinopathy Study (ETDRS), conducted at 22 clinical centers during the period 1980 to 1989, collected baseline data on C-peptide levels after ingestion of Sustacal in 582 patients with diabetes mellitus, prior to enrollment in the trial. Data on several clinical factors associated with diabetes were also collected from all 3711 enrolled patients. C-peptide data were used to develop sets of clinical criteria for the classification of ETDRS patients and to compare and contrast definitions of type of diabetes used in previous studies. The distribution of C-peptide levels was strikingly bimodal, suggesting a division of study participants into two groups--those with levels at 80 pmol/L or less and those with more than 80 pmol/L of C-peptide after Sustacal ingestion. Constellations of clinical characteristics that could serve as proxies for C-peptide level were ascertained. The result was two sets of clinically developed definitions for type of diabetes in the ETDRS. According to the more restrictive set of definitions, three groups were identified, compared to two groups using the "broad" set of definitions. Discriminant analysis was also used to classify ETDRS patients, yielding similar results. A comparison of definitions of type of diabetes used in the ETDRS and in previous studies revealed that even in the absence of C-peptide data, clinically derived definitions provided good discrimination between type I and type II diabetes.

Adult↗
PubMed1988

Inhibition of adenosine 3',5'-cyclic monophosphate phosphodiesterase by colchicine: implications for glucagon and corticosteroid secretion.

In the study reported, colchicine, often regarded as a specific inhibitor of microtubular function, was shown to exert a concentration-dependent inhibition of the low Km cyclic AMP phosphodiesterases of the pancreatic islet, adrenal cortex and various other tissues of the rat. The results indicated that colchicine is only slightly less active as an inhibitor of the enzyme than theophylline on a molar basis and kinetic analysis revealed that both inhibitors acted competitively in the case of the liver enzyme. Our results show that the inhibitory effect of colchicine upon cyclic AMP phosphodiesterase is a general property of the alkaloid at concentrations of 5 x 10(-5)M and above in both endocrine and non-endocrine tissues. Thus, results obtained employing colchicine at concentrations significantly greater than those which are known to lead to microtubular disaggregation must be viewed with great caution if incorrect implication of microtubular participation in biological processes is to be avoided. For example, we propose that the previously reported paradoxical stimulatory effects of colchicine on the secretion of glucagon from the rat pancreatic islet and on steroidogenesis in the rat adrenal may be due to cyclic AMP accumulation consequent upon phosphodiesterase inhibition in these endocrine tissues and not to microtubular disaggregation as has hitherto been assumed.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1981

Disordered breathing during sleep in hypothyroidism.

A 58-yr-old man with hypothyroidism and sleep apnea syndrome was studied to determine the cause of the nocturnal obstructive apnea and oxygen desaturation. Control studies showed free thyroxine (T4) concentration of 0.7 ng/dl (normal, 0.8 to 2.3 ng/dl), and thyroid-stimulating hormone of 32 microIU/ml (normal, less than 12 microIU/ml). Weight, pulmonary function, arterial blood gases, minute ventilation to carbon dioxide production ratio (VE/VCO2), and the ventilatory response to exercise (delta VE/delta VCO2) were normal. Episodes of obstructive apnea (4 per hour during non-REM (NREM) and 10 per hour during REM) and oxygen desaturation (9 per hour during NREM and 11 per hour during REM) were common during sleep. Oxygen saturation ranged between 72 and 99% and 70 and 97% during NREM and REM sleep, respectively. Medroxyprogesterone acetate (MPA) therapy for 4 wk caused a reduction in awake PaCO2 (38 to 33 mm Hg), and an increase in VE/VCO2 (17%), mouth occlusion pressure (50%), and AVE/VCO2 (23%). During sleep, apneas were completely eliminated and only one episode of oxygen desaturation occurred. L-thyroxine therapy for 2 months after a placebo period caused an awake isocapnic hyperpnea with no change in PaCO2 and VE/VCO2 despite a 23% increase in VE. Mouth occlusion pressure increased 37% but delta VE/delta VCO2 was unchanged. Obstructive apnea and oxygen desaturation during sleep were completely eliminated with L-thyroxine. The patient noted completed relief of symptoms with both MPA and L-thyroxine. We concluded that the sleep apnea syndrome was the presenting manifestation of hypothyroidism in this patient and was solely responsible for his symptoms and disability.

Carbon Dioxide↗
PubMedDate not supplied

Myasthenia gravis in conjunction with Graves' disease: a diagnostic challenge.

OBJECTIVE: To describe an association between Graves' disease and myasthenia gravis and discuss the clinical features and laboratory tests that may help distinguish these two diseases. METHODS: The clinical, laboratory, and electrophysiologic findings in a patient with Graves' disease and myasthenia gravis are presented. RESULTS: A 28-year-old African American man was admitted to the University of Louisville Hospital with generalized muscle weakness, exophthalmos, diplopia, weight loss, and mild dysphagia. The diagnosis of Graves' disease with ophthalmologic involvement was suspected clinically and confirmed by an undetectable thyrotropin level (<0.03 mIU/mL), high total thyroxine (20.5 mg/dL), and increased homogeneous 123I thyroid uptake. Because of the generalized muscle weakness and mild dysphagia, assessment was done by a neurology team, and severe thyrotoxic myopathy was diagnosed. He was treated with 131I and b-adrenergic blocking agents and scheduled for follow-up as an outpatient. Two weeks later, the patient presented in acute respiratory failure. The neurology team was reconsulted because of suspected myasthenic crisis. Anti-acetylcholine receptor antibodies were undetectable in the serum, and computed tomography of the chest showed no thymic enlargement. Repetitive nerve stimulation testing, however, showed findings consistent with an abnormality of the neuromuscular junction. The patient responded dramatically to an anticholinesterase agent and corticosteroids. CONCLUSION: The overlapping clinical features may cause diagnostic confusion when myasthenia gravis and Graves' disease coexist, and numerous tests may be needed to distinguish these two conditions, which have differing treatments and prognoses.

Acetylcholinesterase↗