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Biomedical subjects

S Adami

Publications and source records attributed to S Adami.

At least 145 records · Page 8Linked to original sources
PubMed1984

Hypomagnesaemia: studies of parathyroid hormone secretion and function.

Nine patients with hypomagnesaemia have been studied. Six had magnesium deficiency secondary to malabsorption or diarrhoea and three had excessive urinary losses of magnesium. Hypocalcaemia was also present in eight. Parathyroid hormone (PTH) was measured using amino-terminal and carboxy-terminal specific immunoradiometric assays and also, in one patient, using a cytochemical bioassay. Amino-terminal PTH (N-PTH) varied directly with the concentration of magnesium; carboxy-terminal PTH (C-PTH) was raised in all patients. When magnesium was injected, both N-PTH and C-PTH rose regardless of the initial concentration, indicating that hypomagnesaemia was limiting PTH secretion. The clearance of endogenous PTH was measured in one patient, after injection of magnesium. Seven minutes after reaching its peak, C-PTH had fallen to 69% and N-PTH fell to 22% of its maximum values; the initial half life of N-PTH was less than 2 min. In the same study biologically active PTH (bio-PTH) disappeared rapidly with a half-time of disappearance of 1.2 min. Responsiveness to PTH was measured by the rise in plasma cyclic 3'5'-adenosine monophosphate (cAMP) following PTH injection. The rise in plasma cAMP was inversely related to the concentrations of magnesium and PTH at the time. It is suggested that the concentration of PTH rather than the degree of hypomagnesaemia is the most important factor determining the responsiveness of target tissues to PTH in magnesium deficiency.

Adolescent↗
PubMed1983

Radioimmunoassay of 1,25-dihydroxy vitamin D2: studies on the metabolism of vitamin D2 in man.

A sensitive radioimmunoassay for 1,25-dihydroxy vitamin D2 was developed using a sheep antiserum which preferentially reacts with 1-hydroxylated forms of vitamin D. An improved isolation procedure was also developed using acetonitrile for the initial extraction of serum followed by chromatography on cartridges of C18 silica and high pressure liquid chromatography eluted with a ternary solvent system to separate 1,25-dihydroxy vitamin D2 and 1,25-dihydroxy vitamin D3. 25-hydroxy vitamin D2 and 25-hydroxy vitamin D3 were separated by further reverse phase high pressure liquid chromatography prior to competitive protein binding assay. The limits of detection were 4.3 pmol/1 (2.0 pg/ml) for the 1,25-dihydroxy metabolites and 1.25 nmol/1 (0.5 ng/ml) for both 25-hydroxy vitamin D2 and 25-hydroxy vitamin D3. 25-hydroxy vitamin D2 ranged from 2.0 to 11.3 nmol/1 (0.8-4.5 ng/ml) with a mean of 4.75 nmol/1 (1.9 ng/ml) in thirteen healthy British adults and this accounted for 9.0% of the mean total 25-hydroxy vitamin D. 1,25-dihydroxy vitamin D2 was detected in the sera of only one of these subjects whereas 1,25-dihydroxy vitamin D3 was present in all ranging from 48 to 163 pmol/1 (20-65 pg/ml) with a mean of 100 pmol/1 (42 pg/ml). Both 1,25-dihydroxy vitamin D2 and 1,25-dihydroxy vitamin D3 were detected in the sera of hypoparathyroid patients treated with vitamin D2 but the relationship between 25-hydroxy vitamin D and 1,25-dihydroxy vitamin D was complex. For example, when an excess of 25-hydroxy vitamin D2 was present the serum concentration of 1,25-dihydroxy vitamin D3 was disproportionately high. Conversely, in patients who had previously been treated with vitamin D2 but were receiving only vitamin D3 at the time of study, the major 25-hydroxy metabolite was in the vitamin D3 form and there was a disproportionately high amount of 1,25-dihydroxy vitamin D2. Total 1,25-dihydroxy vitamin D ranged from 110 to 400 pmol/1 (45-165 pg/ml) and was above the upper limit of normal for 1,25-dihydroxy vitamin D3 in half of these hypoparathyroid patients treated with pharmacological doses of vitamin D.

25-Hydroxyvitamin D 2↗
PubMed1983

Familial benign hypercalcaemia. Study of a large family.

Twenty-seven hypercalcaemic subjects were identified in three generations of a family. There were no clinical complications of chronic hypercalcaemia, but five had had parathyroid surgery which was unsuccessful in four. Twenty of the twenty-seven subjects were compared with twenty-four normocalcaemic controls from the same family and the findings were also compared with those from forty patients with surgically proven primary hyperparathyroidism. The relation between the serum and urinary calcium levels was studied by means of an oral calcium loading test. The ratio of calcium clearance to creatinine clearance was normal in this family (but elevated in the patients with primary hyperparathyroidism) and the concentration of parathyroid hormone was normal, as was the total urinary excretion of cyclic AMP. Thus, there was no evidence of either suppressed or increased parathyroid activity in this familial condition. Basal urinary calcium excretion was normal under steady-state conditions indicating that the hypercalcaemia could not be attributed to either increased bone resorption or increased calcium absorption from the gut. In accordance with this, the serum levels of 1,25-dihydroxycholecalciferol were normal. The hypercalcaemia in this condition can be accounted for in full by an increase in renal tubular reabsorption of calcium, and thus differs from that of primary hyperparathyroidism in which there is increased production of calcium from gut and/or bone as well as an increase in renal tubular reabsorption of calcium. Although the serum phosphate and renal tubular reabsorption of phosphate were both low in patients with familial benign hypercalcaemia, they were not as low as in patients with the same degree of hypercalcaemia due to primary hyperparathyroidism. The changes in phosphate transport in familial benign hypercalcaemia could be explained as a secondary effect of the increased filtered load of calcium in the kidney. The tendency towards hypermagnesaemia in our patients, which contrasts with a tendency towards hypomagnesaemia in primary hyperparathyroidism, could also be explained as a secondary effect of the abnormality of renal tubular reabsorption of calcium. Increased renal tubular calcium reabsorption and persistent normal functioning of the parathyroid glands in the face of hypercalcaemia remain the sole definite abnormalities of the syndrome.

Adolescent↗
PubMed1983

Controlled trial of calcitriol in the prevention of bone disease in haemodialysed patients.

Seventy-six patients receiving regular haemodialysis, without biochemical or radiological evidence of renal osteodystrophy, entered a five-year double-blind placebo-controlled trial of calcitriol (1,25-dihydroxycholecalciferol) in the prevention of bone disease. Significantly more patients on placebo developed bone disease as judged by a sustained elevation of plasma alkaline phosphatase or the development of sub-periosteal erosions on hand radiographs. Serum parathyroid hormone fell significantly in the patients receiving calcitriol and was significantly lower than in patients receiving placebo. It is concluded that calcitriol delays and may prevent the development of metabolic bone disease in patients receiving regular haemodialysis therapy.

Adolescent↗
PubMed1982

Regulation of calcium absorption by 1,25,dihydroxy-vitamin D--studies of the effects of a bisphosphonate treatment.

In 10 patients with Paget's disease of bone and 2 patients with osteoporosis, we studied the effects of hypocalcemia and hypophosphatemia induced by disodium-(3-amino-1-hydroxypropylidene)-1,-bisphosphonate (APD) treatment on the serum concentration of PTH and 1,25-dihydroxy-vitamin D [1,25(OH)2D3] and on calcium absorption and balance. The fall in serum calcium and phosphate was associated with a rise in the serum concentration of PTH and 1,25(OH)2D3, coupled with increases in net calcium absorption and calcium balance. The concentration of 1,25(OH)2D3 was significantly related (P less than 0.001) to the serum calcium (r = 0.66), the serum phosphate (r = 0.78), and the serum PTH (r = 0.71), confirming the interrelated control of these parameters on 1,25(OH)2D3 production. Moreover the rise in 1,25(OH)2D3 caused an appropriate rise in calcium absorption (r = 0.74) and calcium balance (r = 0.86), showing that this vitamin D metabolite contributes as a hormone to calcium homeostasis.

Aged↗
PubMed1982

Long-term effects of 1,25-dihydroxy vitamin D3 and 24,25-dihydroxy vitamin D3 in renal osteodystrophy.

Twenty-three patients with end-stage renal failure on maintenance haemodialysis were treated with 1,25-dihydroxy vitamin D3 or 24-25-dihydroxy vitamin D3 for 3-32 months (total 232 patient months). Treatment with 1,25-dihydroxy vitamin D3 was marked by symptomatic, biochemical and histological improvements in the majority of patients. In contrast, treatment with 24,25-dihydroxy vitamin D3 produced no biochemical or histological improvements and such patients developed severe symptomatic bone disease. Successful renal transplantation resulted in rapid improvement in symptoms, biochemistry and bone histology in nine of 10 patients irrespective of whether prior treatment was with 1,25-dihydroxy vitamin D3, 24,25-dihydroxy vitamin D3 or both. During treatment with 1,25-dihydroxy vitamin D3 progressive reduction in dosage was required in the majority of patients because of hypercalcaemia, which was rapidly corrected by stopping treatment for a few days. Hypercalcaemia did not occur until serum alkaline phosphatase (AP) and amino terminal parathyroid hormone (N-PTH) had fallen towards normal. Treatment failure was uncommon in 1,25-dihydroxy vitamin D3-treated patients and was characterized by the early development of hypercalcaemia. Addition of 24,25-dihydroxy vitamin D3 in such patients rendered the hypercalcaemia more manageable but did not lead to any further improvement in biochemistry or bone histology. Treatment with 24,25-dihydroxy vitamin D3 was accompanied by the development of severe symptomatic bone disease in the majority of patients and a characteristic pattern of biochemical abnormalities with hypocalcaemia and rises in AP and N-PTH. Substitution of 1,25-dihydroxy vitamin D3 treatment for 24,25-dihydroxy vitamin D3 in these patients resulted in prompt improvement in clinical, biochemical and histological abnormalities. Successful renal transplantation was accompanied by rapid resolution of clinical, biochemical and histological features of renal osteodystrophy irrespective of whether previous treatment was with 1,25-dihydroxy vitamin D3 or 24,25-dihydroxy vitamin D3. Hypophosphataemia was common in the early months after renal transplantation without evidence of continuing hyperparathyroidism. The studies have confirmed that 1,25-dihydroxy vitamin D3 is effective in controlling clinical, biochemical and histological features of renal osteodystrophy while 24,25-dihydroxy vitamin D3 did not have a useful therapeutic effect in the dose used.

24,25-Dihydroxyvitamin D 3↗
PubMed1980

Comparison of 1,25(OH)2D3 and 24,25(OH)2D3 in the long-term treatment of renal osteodystrophy.

24,25(OH)2D3 has been compared with 1,25(OH)2D3 in the treatment of renal osteodystrophy. Treatment with 24, 25(OH)2D3 2 micrograms/day for 5-7 months was accompanied by deterioration in clinical, biochemical, radiological and histological features of osteodystrophy with no increase in Ca absorption. In contrast, treatment with 1,25(OH)2D3 0.25--1 microgram/day for 6-15 months resulted in rapid improvement in clinical, biochemical, radiological and histological features and a return of Ca absorption to normal. It is concluded that in the dose used 24,25(OH)2D3 alone is not an effective treatment for renal osteodystrophy.

24,25-Dihydroxyvitamin D 3↗
PubMed1979

[Incidence of thyroid diseases in primary hyperparathyroidism].

The incidence of thyroid diseases was evaluated in patients with primary hyperparathyroidism subjected to parathyroidectomy. Eleven patients (26.8%) were affected in this way: 2 with carcinoma, 5 with nodular goitre, and 4 with adenoma. The possible reasons for associations of this kind are discussed, and it is suggested that their high frequency points to a relationship of cause and affect.

Adenoma↗
PubMed1979

Fasting serum gastrin in primary hyperparathyroidism and in chronic hypercalcemia.

In order to investigate the frequency of fasting hypergastrinaemia in primary hyperparathyroidism (A) and in chronic hypercalcaemia (B), in 40 and 16 patients respectively gastrin, parathyroid hormone (PTH) and serum calcium levels were measured and compared with those of a control group (40 subjects) with similar distribution of sex and age. Moreover, possible linear relationships between these parameters were investigated. Notwithstanding significant differences in calcium and PTH levels between the three groups (A: high PTH, high Ca++; B: low PTH, high Ca++; C: normal PTH and Ca++ levels), no significant difference in gastrin levels were found. However, in the first group, a marked increase of gastrin was observed in one patient, very probably affected by a gastrin-secreting tumor (positive secretin test). While no linear relationship between PTH and gastrin values was present in all the three groups, a significant correlation between serum calcium and fasting gastrin was detectable in the group A, ruling-out the above mentioned patient. Present data suggest that PTH does not modify gastrin levels and that chronic moderate hypercalcaemia does not raise serum fasting gastrin, at least in clinical conditions. Moreover, the frequency of hypergastrinaemia in hyperparathyroidism is very low and it seems to be present only in patients with gastrin-secreting tumors.

Adult↗
PubMed1978

Failure of somatostatin to diagnose organic hyperinsulinism.

In four patients with organic hyperinsulinism (two with surgically proven beta-cell adenomas of the body of the pancreas) a standard tolbutamide test during continuous somatostatin infusion (5 microgram/min) was carried out. Tolbutamide induced insulin release was completely inhibited by somatostatin as in normal subjects. These results suggest that the inhibition test with somatostatin does not seem to be a better or safer way of diagnosing insulin producing tumours.

Adult↗