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Biomedical subjects

G S Spathis

Publications and source records attributed to G S Spathis.

At least 19 recordsLinked to original sources
PubMed1996

Mood disorder and chronic hypercalcemia.

Fifty-five patients with chronic hypercalcemia were compared with test norms, and two comparison groups of orthopedic patients and hypertensive patients on objective and subjective tests of mood. Sixteen percent of the hypercalcemic patients were found to score over the cut-off point for anxiety on the anxiety subsection of the Hospital Anxiety and Depression Scale, and 16% were diagnosed as suffering from depression on the Paykel Clinical Interview for Depression. There were, however, no significant differences between the comparison groups and those with hypercalcemia on the scales used. There has been debate about the management of individuals with hypercalcemia. This study supports a conservative rather than a surgical approach as far as psychological symptoms are concerned.

Adult↗
PubMed1993

DNR policy.

Explore the source record for details and available documents.

Humans↗
PubMed1990

Limited joint mobility in children and adolescents with insulin dependent diabetes mellitus.

Joint mobility was studied in 70 children with insulin dependent diabetes mellitus aged 8-17 years, and the prevalence of limited joint mobility (LJM) was found to be 31% (22/70). This figure fell to only 7% (5/70) when an alternative method of assessment was used. A high number of non-diabetic, non-sibling controls (6/51 (12%] were found to have LJM. There was a trend towards an increasing prevalence of LJM with increasing age and duration of diabetes, but it was also found in patients with recent onset diabetes. A large proportion of prepubertal patients were noted to have LJM. No correlation was found between LJM and either short stature or diabetic control. There is a need for standardisation of the methods used to define and stage LJM in diabetic patients, and the significance of this clinical finding remains unclear.

Adolescent↗
PubMed1990

Failure of thiazide diuretics to increase plasma calcium in mild primary hyperparathyroidism.

Thirteen patients with mild primary hyperparathyroidism who were taking thiazide diuretics intermittently for periods of up to 18 months were followed up for a mean of 5.3 years. No significant difference was found in either plasma total calcium corrected for albumin or whole blood ionized calcium in these patients between the periods on or off thiazides. We conclude that thiazide diuretics are not contraindicated in such patients.

Adult↗
PubMed1989

Pupillary size in children and adolescents with type 1 diabetes.

Pupillary adaptation to darkness was studied in 63 children and adolescents with Type 1 diabetes using a simple portable pupillometer. Results were compared with those in a group of age-related non-diabetic children and expressed as the ratio of the pupil diameter to the iris diameter (pupil diameter %). In the diabetic patients the pupil diameter % was 61.1 +/- 5.8 (44.4-71.9) % compared with 64.2 +/- 4.1 (53.2-72.6) % in the control subjects (p less than 0.001). Abnormal pupillary adaptation to darkness was found more commonly than abnormal heart rate variation in response to a variety of stimuli in the diabetic patients. Pupillary adaptation to darkness may be useful as an indicator of subclinical autonomic neuropathy in diabetic children.

Adolescent↗
PubMed1989

Hyponatraemia and Moduretic-grand mal seizures: a review.

Three cases are presented which emphasize the importance of hyponatraemia as a cause of grand mal seizures. The combination of hydrochlorothiazide and amiloride appears to increase the risk of hyponatraemia. We discuss the aetiology and treatment of hyponatraemia and review the necessity for such combination therapy. We recommend caution in prescribing diuretics and preparations such as Moduretic should be used only in those few patients shown to need potassium supplementation.

Aged↗
PubMed1987

Thyrotropin hyperresponsiveness to TRH despite hyperthyroxinemia in amiodarone-treated subjects.

Pituitary responsiveness to TRH was assessed prospectively over 24 weeks, in 15 patients receiving 300 mg amiodarone a day. All developed significant hyperthyroxinemia (both total and free), and marked elevations in reverse T3 compared to pretreatment levels. Although basal TSH levels were unchanged in all of them, TSH increased by greater than 50% when compared to pretreatment responses, in eight patients, while they remained unchanged (+/- 15%) in the remaining seven. All eight with exaggerated responses also showed significant reductions (P less than .001) in plasma levels of total and free T3, whereas in the seven who did not show any increase in TSH responses, T3 levels were unchanged. The increase in TSH response to TRH was strongly correlated (r = -.82, P less than .001) with T3 levels. Total and free T4 levels were equally elevated in both groups. These observations indicate that amiodarone effectively blocks the suppressive effect of hyperthyroxinemia on TSH secretion, and that T3 is the mediator of thyroid feedback control in amiodarone treated patients.

Amiodarone↗
PubMed1987

Intramuscular glucagon as a provocative stimulus for the assessment of pituitary function: growth hormone and cortisol responses.

The response of plasma growth hormone and cortisol to the intramuscular injection of 1 mg glucagon was used to assess anterior pituitary function in a group of 97 normal subjects (23 men, 74 women). Ninety-three subjects (96%) responded with a peak GH of at least 8 ng/mL, and 89 (92%) had either a peak cortisol of at least 500 nmol/L (18 micrograms/dL) or a maximal increment in plasma cortisol of at least 250 nmol/L (9 micrograms/dL) above the baseline. In 12 subjects, a second test showed that the responses were reproducible. A greater proportion of subjects over the age of 50 failed to achieve a peak GH of 10 ng/mL (7 of 20, 35%) compared to those who were either under 30 (1 of 37, 2.7%) or between 30 and 50 (4 of 40, 10%) (chi 2 = 12.85, P less than .005). GH responses were not affected by sex or elevation of the basal level of GH. In contrast, cortisol responses were smaller in men and in individuals with high basal cortisol levels but were not affected by age. Mild nausea in approximately 30% of subjects (29 of 97), and transient vomiting and retching in approximately 10% (10 of 97) were the only side effects that were noted. Glucagon is therefore a safe and reliable alternative to insulin-induced hypoglycemia for the assessment of both somatotrophic and corticotrophic function.

Adolescent↗
PubMed1986

Strict nocturnal diabetic control diminishes subsequent glycemic escape during acute insulin withdrawal.

Five Type 1 (insulin dependent) diabetic patients with no endogenous insulin secretion and very low antiinsulin antibody levels (IBC less than 4%) were studied twice. Nocturnal plasma glucose was maintained by intravenous insulin just beyond each extreme of the normal range, either "hypoglycemic," at 2.71 +/- 0.03 mmol/L, or "hyperglycemic," 8.59 +/- 0.13 mmol/L. Glucose turnover measurements were performed before and after insulin was discontinued the following morning. The steady state plasma glucose concentration achieved during subsequent glycemic escape was significantly lower following nocturnal hypoglycemia, (16.1 +/- 0.3 v 20.2 +/- 0.03 mmol/L; P less than 0.01). The initial rate of rise of plasma glucose was identical in both groups. Free insulin levels, although significantly higher in the hypoglycemic study, before withdrawal, 24.3 +/- 6.0 v 13.3 +/- 0.8 mU/L, (P less than 0.01), fell to similarly low levels 1 hour after insulin withdrawal. Free fatty acid and total ketone concentrations were normalized during hypoglycemia, but remained elevated in the hyperglycemic group. Lactate concentrations were not different in the two studies. During glycemic escape glucose appearance rate (Ra) rose faster following hypoglycemia, but similar final rates were achieved in each group. When related to plasma glucose concentration glucose uptake (Rd) was normal following hypoglycemia and remained persistently greater than the hyperglycemic group throughout the 5 hours following insulin withdrawal. Plasma cortisol, pancreatic glucagon, and growth hormone levels were not significantly different in the two groups following withdrawal. It is suggested that the persistent normal glucose uptake, following glycemic control that has been sufficient to normalize plasma metabolites, will limit glycemic excursions caused by acute reductions in plasma-free insulin concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

Iodine kinetic studies during amiodarone treatment.

Iodine kinetic studies were performed serially in 15 patients taking 300 mg amiodarone/day for 6 months to assess the biological significance of the high iodine content of the drug. Urinary inorganic iodide excretion increased from 0.25 +/- 0.03 (+/- SE) mumol/mmol creatinine before treatment to over 7 mumol/mmol during therapy. Thyroid iodide clearance fell from 5.93 +/- 0.82 ml/min to less than 0.5 ml/min, while plasma inorganic iodide rose from 0.05 +/- 0.01 mumol/liter to approximately 2.2 mumol/liter during treatment. Thyroid absolute iodide uptake rose from 16.3 +/- 2.7 to 54.6 +/- 5.7 nmol/h after 6 weeks of therapy (P less than 0.001). Thereafter, it progressively declined, but it was still significantly elevated (32.0 +/- 4.3 nmol/h) after 24 weeks (P less than 0.01). The calculated daily excretion of inorganic iodide rose to over 80 mumol during the study, accounting for about 10% of amiodarone iodine. During this time, the patients all had the characteristic plasma thyroid hormone changes associated with amiodarone therapy, i.e. increased T4, free T4, and rT3 and decreased T3, while remaining clinically euthyroid. The massive increase in available inorganic iodide during amiodarone treatment is probably responsible for the induction of both the hypothyroidism and the thyrotoxicosis that can occur in patients receiving the drug.

Adult↗
PubMed1985

Low-dose 131I in treatment of Graves' disease.

One hundred and sixty-four patients with Graves' disease were treated with low-dose radioiodine (2 mCi), with a mean follow up of 4 1/2 years. At this time 74 (45%) were euthyroid having had a single dose, with a total of 131 (80%) being controlled with one or more doses. Three (2%) were still toxic but their mean follow up was only 3 years. Thirty (18%) were rendered hypothyroid, two-thirds of these after a single dose of 2 mCi 131I. The one-year incidence of hypothyroidism was 6%, with an incidence at 6 years of 20%. Previous surgery, medical treatment and thyroid antibody status appeared to have no influence on the outcome.

Adult↗
PubMed1985

Low-dose radioiodine given six-monthly in Graves' disease.

Experience using low-dose radioiodine given six-monthly instead of yearly in hyperthyroid patients with Graves' disease is reported. One hundred and thirty-five patients have been treated over a three-year period with 74 MBq (2 mCi) doses of 131I. Thirty-eight percent were controlled with a single dose. Those patients requiring more than one dose were treated with a further 74 MBq (2 mCi) 131I at six-monthly intervals until euthyroid. Using this approach, 46% were euthyroid one year after starting treatment, and 75% were euthyroid at two years. The incidence of hypothyroidism following treatment was 2.2% at one year, with a yearly incidence thereafter of 4-6%. Six-monthly scheduling of low-dose radioiodine in Graves' disease can reduce the time taken to become euthyroid, compared with conventional yearly low-dose treatments. Further follow up is required to confirm the present low incidence of hypothyroidism following treatment.

Aged↗