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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of acromegaly with peripheral neuropathy characterized by acroparaesthesiae in the median nerve field of both sides is presented. Electrophysiological examination shows bilateral slowing of the motor conduction velocity of the median nerve through the carpal tunnel. The possible pathogenetic mechanisms of the peripheral neuropathy in acromegalic are discussed in the light of the most recent theories about the GH action. Suggestions are made that some associated hormonal disorders diabetes, hyperaldosteronism, hyperthyroidism) can play some part in the neuropathy pathogenesis.
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PMID:[A case of peripheral neuropathy in an acromegalic subject. Pathogenetic considerations]. 23 43

To our knowledge, the juvenile form of spongy degeneration of the CNS (SD-CNS); van Bogaert-Bertrand disease) has been described previously only three times. We report the case of 21 1/4-year-old Japanese woman who was first seen at the age of 11 with growth retardation, ptosis, and ophthalmoplegia. Her progressive neurodegenerative disease included retinitis pigmentosa, blindness, partial deafness, cerebellar dysfunction, hyporeflexia, and muscle wasting. Simultaneous endocrine defects were diabetes mellitus and probable hyperaldosteronism. Heart block developed later. She died of bronchopneumonia. Autopsy showed CNS stigmas typical of spongy degeneration. Additional findings included peripheral nerve demyelination, neurogenic muscle atrophy, pituitary and pancreatic atrophy, right adrenal agenesis, and a left adrenal coritcal lipid-cell adenoma. To our knowledge, our patient was the oldest survivor, the first patient of Japanese ancestry, and had a unique concurrence of certain oculoendocrine defects.
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PMID:Spongy degeneration of the CNS: an instance of the rare juvenile form. 50 59

The renin-angiotensin-aldosterone system was evaluated in two types of uncontrolled diabetes: a) diabetic ketoacidosis, and b) nonketotic hyperglycemia. In thirteen patients with ketoacidosis, mean plasma renin activity (PRA) was 58 plus or minus 12 (S.E.M.) ng. per milliliter per hour and in four patients, plasma aldosterone was 82 plus or minus 17 ng. per 100 ml. Corresponding values for upright salt-depleted subjects were 13 plus or minus 2 and 62 plus or minus 8. In eleven diabetics with nonketotic hyperglycemia (mean glucose 318 plus or minus 19 mg. per cent), mean blood volume was 4,660 ml. and PRA 2.1 plus or minus .7. After control of the diabetes (mean glucose 129 plus or minus 13) blood volume was 4,553 ml. and PRA 3.3 plus or minus 1 (NS). The results suggest that: 1) diabetic ketoacidosis is a state of severe secondary aldosteronism, 2) no significant change in blood volume or PRA occurs during short periods of hyperglycemia, and 3) insulin is not necessary for renin release.
Diabetes 1975 Feb
PMID:Plasma renin activity and blood volume in uncontrolled diabetes. Ketoacidosis, a state of secondary aldosteronism. 80 22

In non-renal (diabetic) glucosuria we did not find any statistically real relations between the concentration of glucose in the urine and cryoscopically measured osmolality in children with healthy kidneys. The close negative correlation of the conductance of the urine to the concentration of glucose is not only to be explained by changes of the viscosity, but is an expression of an increased re-absorption of sodium as a result of a compensatory hyperaldosteronism. In renal insufficiency the electrolytic conductibility of the urine is lower than the borderline area of the normal, even when under influence of the glucose excretion the osmolality of the urine is still to be found normal. Thus also on the conditions of a considerable glucosuria we can further judge the concentrating ability of the kidney in diabetes mellitus with the help of the measurement of the conductance of the urine.
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PMID:[Measurement of kidney concentrating ability in children with nonrenal glycosuria]. 96 Aug 53

Kearns-Sayre syndrome (KSS) is a form of mitochondrial myopathy in which specific clinical features, namely progressive external ophthalmoplegia, pigmentary retinal degeneration and cardiac conduction defects, occur. KSS has also been associated with a variety of endocrine and metabolic disorders, in particular short stature, gonadal failure, diabetes mellitus, thyroid disease, hyperaldosteronism, hypomagnesaemia, and bone, tooth and calcification abnormalities. A case is described exhibiting all of these features. A survey of the literature was conducted to determine the prevalence of these conditions among reported cases. Cases with hypoparathyroidism were considered separately to see if they constituted a distinct subgroup with multiple endocrine dysfunction. Short stature was common, being documented in 38% of cases. Gonadal dysfunction before or after puberty was also common (20% of cases) and affected both sexes equally. Diabetes mellitus was recorded in 13% of cases, half of which required insulin. Thyroid disease, hyperaldosteronism and hypomagnesaemia were uncommon but were probably not looked for in many cases. Bone or tooth abnormalities and calcification of the basal ganglia were found both in those with and without hypoparathyroidism. While endocrine and metabolic dysfunction was found more commonly in those with hypoparathyroidism this is likely to be due to increased recognition rather than increased prevalence. No evidence of an autoimmune polyendocrine syndrome including hypoparathyroidism was found.
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PMID:Endocrine dysfunction in Kearns-Sayre syndrome. 142 98

Disorders of the adrenal cortex and medulla can result in glucose intolerance or overt diabetes mellitus. Cushing's syndrome, characterized by excessive secretion of glucocorticoids, impairs glucose tolerance primarily by causing insulin resistance at the post-receptor level. On the other hand, phaeochromocytoma and hyperaldosteronism, via the respective actions of catecholamines and hypokalaemia on the pancreatic beta-cell, impair glucose tolerance primarily by inhibiting insulin release. The glucose intolerance associated with these adrenal disorders is usually only mild to moderate in severity. Marked hyperglycaemia, glycosuria, and polyuria are uncommon and ketosis is rare. Moreover, the late complications of diabetes mellitus are distinctly uncommon in patients with these disorders, and the prognosis for morbidity and death is usually that of the underlying disease and not that of diabetes mellitus. The impaired glucose tolerance induced by all three of these adrenal disorders usually returns to normal once the underlying aetiology has been cured. These factors must guide the clinician in treatment of these secondary forms of diabetes, and suggest that tight (near normal) blood glucose control may not be an appropriate goal in patients with these disorders. The relationship between adrenal androgens and glucose tolerance is more uncertain. Several studies in humans have demonstrated an acute decline in serum concentrations of the adrenal steroids DHEA and DHEA-sulfate in response to experimentally-induced hyperinsulinaemia, but the regulatory role of insulin on adrenal androgen metabolism in normal physiology or disease remains speculative. In several animal models DHEA appears to exert potent anti-obesity and anti-diabetogenic actions, but such effects have yet to be demonstrated in humans. Human studies of DHEA are limited, and more research needs to be conducted to determine whether the observations made in animal models will prove applicable to man.
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PMID:Diabetes and adrenal disease. 144 72

To assess the cardiac characteristics and postoperative courses in patients with Cushing's syndrome, electrocardiography and echocardiography were performed to study 12 consecutive, unselected patients, and results were compared with those of essential hypertension and primary aldosteronism. Eleven patients had hypertension and 7 had diabetes mellitus. Before adrenalectomy, common electrocardiographic abnormalities consisted of high-voltage QRS complexes (10 patients) and negative T waves (7 patients). Echocardiograms showed left ventricular hypertrophy in 9 patients, and all the patients had evidence of asymmetric septal hypertrophy. In patients with left ventricular hypertrophy, the thickness of the interventricular septum ranged from 16 to 32 mm, whereas the ratio of the thickness of interventricular septum to that of the posterior wall ranged from 1.33 to 2.67. The interventricular septum in Cushing's syndrome was extremely thicker and asymmetric septal hypertrophy occurred more often than essential hypertension and primary aldosteronism. Nine patients could be followed up after operation. In these patients abnormal electrocardiographic findings had normalized, the thickness of interventricular septum had decreased and asymmetric septal hypertrophy had disappeared except in 1 patient. The reason why left ventricular hypertrophy in Cushing's syndrome is severe is still unknown. Because left ventricular hypertrophy is more severe and the frequency of asymmetric septal hypertrophy much greater in Cushing's syndrome than in essential and other secondary hypertension, it is thought that not only increased aortic pressure but excessive plasma cortisol may be etiologic factors in the progression of left ventricular hypertrophy in Cushing's syndrome.
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PMID:Cardiac characteristics and postoperative courses in Cushing's syndrome. 153 96

This paper attempts to define the theory and practice of a modern approach to the initial workup of the patient with hypertension. The process includes a complete general medical evaluation along with special measures to enable the fullest characterization and clinical differentiation of the disease. The initial workup aims to (a) establish that the hypertension is sustained and should be treated; (b) identify all definable and curable causes for the hypertension; (c) identify the presence and degree of attendant risk factors such as smoking, alcohol use, obesity, diabetes, and abnormal lipid metabolism; (d) characterize the hypertension in terms of its pathophysiology; and (e) assess the presence and degree of target organ damage to the heart, brain, and kidneys. Because all diastolic hypertension is due to arteriolar vasoconstriction, a fundamental strategy of this process is to distinguish between renin-mediated and sodium-related vasoconstrictive forces and to evaluate which is preponderant. The chief instruments of this strategy are the renin-sodium profile and the response of plasma renin activity and blood pressure to specific antirenin system drugs. The captopril test, an important protocol in making this distinction, is primarily a powerful screening tool for confirming the possible presence or absence of curable renovascular disease or curable primary aldosteronism. That renin profiling cannot accurately discriminate between the contributions of either the renin or sodium-volume factors in that large fraction of medium-renin patients is not a viable reason for not performing the test. The test has its greatest strength for identifying sizable numbers of otherwise unrecognizable patients with very high or very low renin concentrations who might have curable disorders and who likely reflect different pathophysiologic vasoconstrictive mechanisms for which entirely different drug therapies are appropriate. However, the baseline renin test is also useful for assessing prognosis and the likelihood of a heart attack and it is valuable for deciding whether to use an anti-renin system drug (for medium and high renin concentrations) as opposed to natriuretic agents (low-renin patients) such as a diuretic or calcium antagonists as the primary step. In our present state of knowledge, the basic diagnostic biochemical workup includes the renin-sodium profile and the 24-h urinary sodium, potassium, and microalbumin excretion rates. This package is further enriched by baseline electrocardiography and echocardiography and the evaluation of glucose and lipid patterns.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical evaluation and differential diagnosis of the individual hypertensive patient. 191 3

During an 8-year-period from 1981, a total of 6 of 45 patients with pheochromocytoma developed severe hypoglycemia (plasma glucose, 12-50 mg/dl) 2-4 1/2 hours after removal of the tumor. In order to elucidate the pathogenesis of the hypoglycemic attack, the levels of plasma immunoreactive insulin (IRI) and glucose were sequentially measured at surgery in 10 patients with pheochromocytoma, from the beginning of the operation until usually 5 hours after tumor resection. The same examinations were carried out in 4 patients with primary aldosteronism and 1 patient with Cushing's syndrome as controls. The highest plasma IRI levels observed in the 2 patients with postexcisional hypoglycemia were 174 and 2,081 microU/ml and those in the 8 patients without hypoglycemia were 13-222 microU/ml (mean, 77), but they were only 14-33 microU/ml (mean, 22) in the 5 control patients. The mean of the highest plasma IRI/glucose ratios in the immediate postoperative phase was 1.37 +/- 0.87 in the 10 patients with pheochromocytoma but only 0.16 +/- 0.04 in the 5 control patients (p less than 0.01). Review of the clinical data in our series disclosed that patients with higher levels of preoperative urinary epinephrine excretion and those with either diabetes mellitus or impaired glucose tolerance tended to develop postoperative hypoglycemia. These observations suggest that endogenous insulin secretion is suppressed by increase plasma catecholamines, and that excessive rebound secretion of insulin after removal of a pheochromocytoma is a rather common phenomenon. Intravenous infusion of glucose is necessary and plasma glucose levels should be monitored after resection of a pheochromocytoma.
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PMID:Hypoglycemia induced by excessive rebound secretion of insulin after removal of pheochromocytoma. 219 84

Since the mechanisms responsible for stimulation of kidney Na-K-ATPase during streptozotocin-induced diabetes are unknown, we studied the possible role(s) of kidney hyperfiltration and hypertrophy and of hyperaldosteronism on Na-K-ATPase induction. For this purpose, we studied the relationship between Na-K-ATPase activity in individual nephron segments and alterations of glomerular filtration rate during the early phase of diabetes. Within 2 days after streptozotocin administration, Na-K-ATPase activity markedly increased in the proximal convoluted tubule, medullary thick ascending limb and cortical and outer medullary collecting tubule, but not in the proximal straight tubule, cortical thick ascending limb and distal convoluted tubule. Streptozotocin administration also markedly enhanced the glomerular filtration rate but only after 4 days following initiation of treatment. Changes in Na-K-ATPase were specific since the activity of adenylate cyclase, another marker of basolateral membranes, was not altered. Finally, when animals were adrenalectomized prior to streptozotocin treatment, Na-K-ATPase stimulation was curtailed in the collecting tubule but not in more proximal segments. These results suggest that diabetes alters Na-K-ATPase activity in specific nephron segments independent of alterations of glomerular filtration rate and of kidney hypertrophy, and that the stimulation of collecting tubule Na-K-ATPase is secondary to hyperaldosteronism.
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PMID:Mechanism of increased tubular Na-K-ATPase during streptozotocin-induced diabetes. 281 17


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