Search PubMed⌕ Search

Biomedical subjects

J B Ferriss

Publications and source records attributed to J B Ferriss.

64 records · Page 4Linked to original sources
PubMedDate not supplied

Plasma angiotensin II concentrations in diabetic ketoacidosis and in hyperosmolar non-ketotic hyperglycemia.

Plasma angiotensin II concentrations were measured in 14 patients in diabetic ketoacidosis and in two patients with hyperosmolar non-ketotic hyperglycemia, before treatment and again when blood glucose control was restored. In the ketoacidosis group plasma angiotensin II before treatment was markedly raised in all patients with otherwise uncomplicated diabetes, but was within the normal range in some patients with long-term complications such as neuropathy, retinopathy and nephropathy. Mean angiotensin II before treatment was significantly higher in otherwise uncomplicated patients than in those with long-term complications. However, plasma angiotensin II decreased with improved control in all. Angiotensin II levels did not correlate with indices of rehydration such as changes in blood urea, packed cell volume and calculated changes in plasma volume. There was, however, a significant negative association between pre-treatment angiotensin II and pH. Two patients with hyperosmolar non-ketotic hyperglycemia were more dehydrated but less acidotic. Pre-treatment angiotensin II in each was well below the mean of the ketoacidosis group. These data are further evidence that the renin-angiotensin system may be imparied in diabetics with long-term complications. In addition, they suggest that factors other than fluid depletion are also important in activating the renin-angiotensin system in uncontrolled diabetes.

Adolescent↗
PubMedDate not supplied

Long-term outcomes of treatment of hyperthyroidism in Ireland.

We investigated the long-term outcome of treatment in 159 patients with hyperthyroidism first seen between 1979 and 1992. Median duration of follow-up was 10 1/2 years. We also inquired into current practice for the follow-up of hyperthyroidism by other endocrinologists in Ireland. Seven cases of unrecognised hyperthyroidism (4 per cent) and one of unrecognised hypothyroidism were identified. Among patients with Graves' disease, of those treated with an antithyroid drug, 28 per cent were in remission, 68 per cent had relapsed and 4 per cent had become hypothyroid. Of those treated by sub-total thyroidectomy, 31 per cent were in remission, 19 per cent had relapsed, 19 per cent were hypothyroid and 31 per cent were sub-clinically hypothyroid. Among patients treated with radioiodine, 19 per cent were euthyroid, 3 per cent were still hyperthyroid and three-quarters had become hypothyroid. In contrast, after radioiodine for toxic nodular goitre, 63 per cent were euthyroid and only 32 per cent had become hypothyroid (Chi Squared v. Graves' disease, P = 0.001). Of 73 patients receiving thyroxine replacement, plasma TSH was normal in only 41 per cent, although 82 per cent of patients had been seen by the family doctor within the previous 12 months. Seven of 17 other endocrinologists undertook long-term follow-up of hyperthyroid patients in their specialist clinics but none was using a computerised system to co-ordinate this. The findings confirm that careful follow-up is required for all hyperthyroid patients. The family doctor is well positioned to undertake this, but education and auditing are required.

Adolescent↗
PubMedDate not supplied

Premature hair greying may predict reduced bone mineral density in Graves' disease.

BACKGROUND: Premature hair greying has been associated with low bone mineral density (BMD), and it may be more frequent in Graves' disease. AIMS: To determine whether premature greying is associated with reduced BMD in women with Graves' disease and in control women, and to examine whether premature greying is more common in Graves' disease. METHODS: Premature greying (> 50% grey by 40 years) and BMD were determined in 44 women with a history of Graves' disease and 133 female controls referred for routine BMD measurement. Exclusion criteria included diseases or drugs known to affect BMD. RESULTS: Mean Z and T scores at the lumbar spine were significantly lower (P < 0.04) in subjects with premature greying than in those not prematurely grey among women with Graves' disease, but not among control women. Multiple regression confirmed this difference between Graves' and control women (P = 0.041). There were no differences at other measurement sites. Of Graves' patients, 36% were prematurely grey compared with 25% of control women (P = 0.14). CONCLUSION: Premature greying may be a weak marker for reduced BMD in women with a history of Graves' disease, but it is not a marker in normal women.

Adult↗
PubMedDate not supplied

Are the nutritional recommendations for insulin-dependent diabetic patients being achieved?

Dietary intake was assessed, using a 3-day recorded food diary, in 122 patients with insulin-dependent diabetes. Subjects were selected randomly from patients attending a diabetic clinic and stratified for age, sex, and duration of diabetes. The findings were compared to the dietary recommendations of the European Association for the Study of Diabetes (EASD) and to the findings in a recent Irish National Nutrition Survey. The average daily protein intake among diabetic patients was 18% of the total calories, significantly higher than recommended by EASD and significantly higher than in the age-matched general population. Dietary fat intake was on average 37% of total calorie intake, again significantly higher than recommended and greater than in the general population among older patients. Saturated fat intake was higher than recommended and polyunsaturated fat intake was low. The average carbohydrate intake was 42% of total calories, significantly lower than recommended and similar to that in the general population. Sugar intake was lower and starch intake was higher among patients than in the general population, however. Fibre intake was also lower than recommended, but was higher than in the general population. We conclude that the present dietary targets for diabetic patients are not being fully achieved.

Adolescent↗
PubMedDate not supplied

Exchangeable sodium and renin in hypertensive diabetic patients with and without nephropathy.

The objective of this study was to examine total exchangeable sodium, plasma-blood volume, and the status of the renin-angiotensin system in hypertensive diabetic patients with established nephropathy. We also evaluated hypertensive patients with diabetes who were free of clinically apparent nephropathy or other diabetic complications. Total exchangeable sodium (by 24Na dilution) was expressed as percentage predicted. Subjects were studied as inpatients receiving unrestricted sodium intake and in stable metabolic control. Total exchangeable sodium was 100 +/- 2% in controls (n = 42), higher (p less than 0.01) at 108 +/- 2% in normotensive patients with diabetes (n = 30), and higher still (p less than 0.005) in hypertensive patients with diabetic nephropathy (n = 16) 118 +/- 4% (p less than 0.05 vs normotensive diabetics). The value correlated with blood pressure only in diabetics with nephropathy (r = 0.61, p less than 0.01). Plasma renin activity, and blood and plasma volumes were similar in nephropathic diabetics and controls. Hypertensive patients with maturity-onset (type II) diabetes free of nephropathy (n = 18) were compared with nondiabetic controls (n = 16) and normotensive patients with type II diabetes (n = 18) of similar age. Total exchangeable sodium in the controls was 100 +/- 3%, higher (p less than 0.01) in normotensive diabetics at 109 +/- 2%, but not significantly elevated in hypertensive diabetics at 106 +/- 2%. Again, blood and plasma volumes did not differ among the groups. Plasma renin activity was suppressed (p less than 0.01) to a comparable degree in both normotensive and hypertensive patients with type II diabetes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Diabetic control and the renin-angiotensin system, catecholamines, and blood pressure.

Diabetic ketoacidosis is usually associated with marked secondary hyperaldosteronism. Plasma levels of renin, angiotensin II, and aldosterone are markedly raised before treatment in most patients, with values falling rapidly toward normal as metabolic control is restored. In a few patients, mostly those with long-term complications of diabetes, plasma levels of renin, angiotensin II, and aldosterone before treatment remain within the normal range. In moderately hyperglycemic patients who have glycosuria but not ketonuria, plasma levels of all three substances are significantly higher than when control is improved. Occasionally, moderately hyperglycemic patients have mild secondary hyperaldosteronism. Improved metabolic control in such patients causes a rise in plasma volume and a rise in total exchangeable sodium, the latter to levels significantly above normal. Plasma catecholamine levels are markedly elevated in diabetic ketoacidosis, probably as a consequence of the ketoacidotic state. In nonketotic patients with moderate hyperglycemia, basal plasma norepinephrine levels are normal; catecholamine responses to exercise may be exaggerated, however. Epidemiological and animal studies suggest a relationship between blood pressure and blood glucose levels. There are few clinical studies of the effects of altering metabolic control of diabetes on blood pressure, and this is an important area for further study.

Aldosterone↗
PubMedDate not supplied

The pathogenesis of essential hypertension.

Essential hypertension is a quantitative abnormality, the pathological effects and risks increasing with the blood pressure level. In Western countries blood pressure rises with age in most individuals, so essential hypertension is more frequent in middle and older age groups. It is likely that an individual's blood pressure level is determined by many interacting factors. These include heredity, which probably acts multifactorially, and many environment influences, including psychological stress and obesity. Specific factors may be of varying importance in different individuals and in different populations. Several physiological mechanisms control the blood pressure level and may be altered in essential hypertension. In early hypertension sympathetic nervous activity is sometimes increased, although in long-standing hypertension this is less marked. Cardiac output may be increased in borderline hypertension but is normal in established hypertension, when total peripheral resistance is increased. Total exchangeable sodium is normal, while the renal pressure-natriuresis balance is altered, so that for a given pressure the hypertension kidney excretes less sodium. In some patients, plasma renin is low, probably as a result of renal adaption to prolonged hypertension. The pathogenic sequence in essential hypertension is uncertain. Increased autonomic activity may cause vasoconstriction in renal and other arterioles and increase cardiac output, leading to a rise in blood pressure. Elevated pressure itself produces structural changes in the resistance vessels, including those of the kidney, which eventually maintain the hypertension even when the initiating stimulus is removed. The way in which heredity and environment influence pathogenic mechanism is also uncertain. Heredity might, for example, influence the autonomic response to stress or the liability to irreversible changes in the resistance vessels or in the kidney. Environmental factors may also increase autonomic activity, enhance vascular reactivity or alter renal function.

Blood Pressure↗
PubMedDate not supplied

Concomitant Graves' disease and Hashimoto's thyroiditis, presenting as primary hypothyroidism.

Hypothyroidism in patients with Graves' disease is usually the result of ablative treatment. We describe a 58 year old man with Graves' ophthalmopathy and pre-tibial myxoedema, who presented with spontaneous primary hypothyroidism. Circulating TSH receptor antibody activity was increased, while thyroid microsomal antibody was detectable in titres greater than one in one hundred thousand. It is likely that the TSH receptor antibody of Graves' disease was ineffective in stimulating hyperthyroidism because of concomitant thyroid destruction due to Hashimoto's disease. Alternatively, primary hypothyroidism could have resulted from the effects of a circulating TSH receptor blocking antibody.

Graves Disease↗