PubMed Health⌕ Search

Biomedical subjects

A M Pierides

Publications and source records attributed to A M Pierides.

53 records · Page 3Linked to original sources

Idiopathic membranous nephropathy.

The clinical and histopathological features of 37 patients with idiopathic membranous nephropathy are presented. Males were four times as commonly affected as females and the age at presentation ranged from nine to 70 years. The period of observation varied from three months to 23 years. Twenty-eight patients (76 percent) presented with the nephrotic syndrome and nine patients (24 per cent) presented with non-nephrotic proteinuria. At the end of the study, of the patients presenting with the nephrotic syndrome, seven (25 per cent) were in remission, seven (25 per cent) remained nephrotic, nine (32 per cent) showed only proteinuria and five (18 per cent) were dead or on dialysis. Altogether eight patients (28 per cent) developed renal failure. The nine patients who presented with non-nephrotic proteinuria appeared to do better, and none developed renal failure. The occurrence of spontaneous remission makes assessment of benefit from immunosuppressive therapy difficult. However, analysis of our data and a review of the literature suggest that in this condition oral prednisone, cyclophosphamide and azathioprine have no significant therapeutic properties. Histological assessment confirmed the occurrence of mild (Grade 1) changes in patients biopsied soon after presentation, and tubular atrophy increased with the duration of illness. Immunofluorescence confirmed deposition of mainly IgG and complement. Repeat biopsies in 14 patients showed no histological improvement and remission was not accompanied by resolution of histological abnormalities.

Adolescent↗

Quadriceps tendon ruptures in uremia. Treatment with surgery and 1alpha-hydroxycholecalciferol.

Three young patients with chronic renal failure, one on regular hemodialysis, suffered bilateral quadriceps tendon ruptures. All three had uncontrolled, severe osteitis fibrosa. In two, aluminium hydroxide failed to control secondary hyperparathyroidism, while 1alpha-hydroxycholecalciferol (1alphaOHD3) given after the injury resulted in rapid resolution of the hyperparathyroidism. Prevention of tendon ruptures in uremia depends on effective control of secondary hyperparathyroidism. Treatment should involve prompt surgical repair and reversal of the osteitis fibrosa with an effective vitamin D metabolite such as 1alphaOHD3.

Adolescent↗

Serum gamma glutamyl transferase and alkaline phosphatase activities in epileptics receiving anticonvulsant therapy.

1. Serum gamma glutamyl transferase (gammaGT) and alkaline phosphatase (ALP) activities have been estimated in 49 epileptic patients taking anticonvulsant drugs. 2. Serum gammaGT activity was clearly elevated in 12 of the patients and borderline in 8, giving a 40% frequency of abnormal values. 3. Total serum ALP activity was elevated in 7 out of 33 adult patients and 2 of 16 juveniles. 4. Electrophoresis on polyacrylamide gel showed that the bone isoenzyme was responsible for most of the increased serum ALP activity and that even when the total was not elevated, the contribution of the bone isoenzyme was greater than normal. 5. There was no correlation between total serum ALP and gammaGT activities but elevations of serum gammaGT were often accompanied by an increase in the proportion of the bone enzyme in the total serum ALP activity.

Adolescent↗

Variable response to long-term 1alpha-hydroxycholecalciferol in haemodialysis osteodystrophy.

Ten uraemic patients on regular haemodialysis were treated with 1alpha-hydroxycholecalciferol (1alpha-H.C.C.) for 5 to 14 months. Five patients who had histological osteitis fibrosa with or without osteomalacia responded well, with resolution of musculoskeletal pain, return of raised serum-alkaline-phosphatase concentrations to normal, resolution of radiological subperiosteal erosions, and improvement in histological signs of osteitis fibrosa and osteomalacia. In these patients 1alpha-H.C.C. proved a safe and effective drug. Five other patients did not improve. Characteristically these patients started with moderately severe histological osteomalacia and minimal, if any, osteitis fibrosa. Proximal myopathy was a prominent symptom and serum-alkaline-phosphatase was normal in four of them. Treatment with 1alpha-H.C.C. resulted in early troublesome hypercalcaemia, and repeat bone histology 5--11 months later showed no improvement. It is suggested that in these patients lack of 1,25-dihydroxycholecalciferol may not have been wholly responsible for the observed osteomalacia, hence 1alpha-H.C.C. alone was ineffective. Phosphate depeltion may have been an important contributing factor.

Alkaline Phosphatase↗

Barbiturate and anticonvulsant treatment in relation to osteomalacia with haemodialysis and renal transplantation.

Among 39 patients treated by regular haemodialysis for four years or more pathological fractures and histological evidence of osteomalacia were significantly more common in those taking barbiturates. Out of 58 transplant recipients surveyed after one year, seven had osteomalacia; four of these had been taking phenobarbitone and phenytoin and one had taken barbiturates alone. Sedatives and other drugs such as phenobarbitone and phenytoin that induce hepatic microsomal enzymes should probably be avoided when possible in patients with chronic renal failure and after transplantation.

Adult↗

Study on a family with anderson--Fabry's disease and associated familial spastic paraplegia.

A family in the north-east of England with Anderson--Fabry's disease is presented. Alpha-galactosidase activity in plasma and white cells was significantly reduced in three adult male members of the family. One of them had an abnormal chromosome karyotype pattern with an extra Y chromosome (47,XYY) and he was clinically less severely affected than his brothers. Coincidentally five other members of the family suffered from a form of familial spastic paraplegia.

Adult↗

1 alpha-hydroxycholecalciferol in hemodialysis renal osteodystrophy. Adverse effects of anticonvulsant therapy.

Two regular hemodialysis patients were assessed before, during and after therapy for 8 1/2 months with 1alpha-hydroxycholecalciferol (1alphaOHD3). The first patient (F.S.), treated with 2 mug daily, improved considerably with complete resolution of histological osteomalacia (O.M.), reduction in osteitis fibrosa (O.F.) and healing of Looser zones. The second patient (T.Y.), who was treated at the same time with a combination of phenobarbitone and phenytoin, showed no improvement while taking 3 mug of 1alphaOHD3 daily. It is suggested that hepatic microsomal enzyme inducing drugs antagonize the action of 1alphaOHD3 by interfering with its subsequent hepatic 25-hydroxylation.

Alkaline Phosphatase↗

Long term therapy with 1,25(OH)2D3 in dialysis bone disease.

Five patients with haemodialysis bone disease were treated with 1 to 1.5 mug of 1,25 (OH)2D3 daily for periods ranging from 6 -8 months. There was a significant improvement in calcium absorption but no troublesome hypercalcaemia was encountered. Secondary hyperparathyroidism improved, both histologically and radiologically, and there was a fall in serum PTH and return of serum alkaline phosphatase to within normal limits. There was also improvement in the patients' mineralisation status, but this change was slower and less marked. Muscle power improved significantly, both clinically and electromyographically.

Calcium↗

Serum lipids in uraemic patients on regular haemodialysis.

Measurement of serum lipids in 75 patients on regular haemodialysis showed that they had a higher mean serum triglyceride level than normal subjects. Cholesterol levels were not significantly different. Amongst haemodialysis patients men had higher serum triglycerides than women and women had higher cholesterol levels than men, a situation analogous to that found in normal subjects. In men, serum triglycerides correlated with percent body fat and treatment with Sustanon 250(R) intramuscularly weekly caused a significant rise.

Cholesterol↗

Central pontine myelinolysis. Two cases with associated electrolyte disturbance.

Two patients with central pontine myelinolysis are described. Both were middle aged women presenting with a history of protracted vomiting and drowsiness. Hyponatraemia (serum sodium 96 to 100 mmol/L) was a feature in both patients. No underlying malignancy, alcoholism, malnutrition or other serious disease was identified. Correction of electrolyte abnormalities was accompanied by deterioration in level of consciousness and development of a neurological syndrome characterized by quadriparesis, dysphasia and mutism. Death followed and histopathological examination confirmed classical myelinolysis in the central pons and extensive similar, though not identical, lesions in the cerebral hemispheres in both cases. The pathophysiological basis of the lesions is likely to be a special metabolic susceptibility of oligodendroglial cells in areas where neurones, glial cells and myelin sheaths lie in close proximity to one another.

Brain Diseases↗

Clofibrate-induced muscle damage in patients with chronic renal failure.

Muscle weakness and tenderness together with a rise in serum creatine kinase (C.K.) were noted in five uraemic patients treated with 1-2 g of clofibrate ('Atromid-S') daily. Excessive accumulation of both total and free serum chlorophenoxyisobutyric acid (C.P.I.B.), the active circulating metabolite after clofibrate therapy, was found in three patients in whom it was sought. It is suggested that chronic renal failure should be regarded as a contraindication to the use of clofibrate for the treatment of any coexisting hyperlipidaemia. If such therapy is contemplated it must be cautiously instituted at low dosage and the patient monitored by regular assessment of serum C.K. and levels of both total and free C.P.I.B.

Adult↗

Avascular necrosis of bone following renal transplantation.

Assessment of 78 successful renal transplants carried out in Newcastle upon Tyne between October 1967 and March 1973, revealed avascular necrosis of bone (A.N.) in 11 patients (14 percent). Pain and restriction of movement were the cardinal symptoms, while the onset was from five to 35 months after transplantation. In some patients one joint only was affected but in seven patients (64 per cent) A.N. developed in other joints too in an additive and progressive fashion. A time lag was usually noted between the onset of symptoms and radiological proof. These 11 patients with A.N. were compared with two control groups of unaffected renal transplant patients. Taking into account the patients' body weight, the cumulative dose of prednisone received by affected patients during the first three post-transplant months was found to be significantly higher than that for both control groups (P less than 0.05). Patients with A.N. were found to have had an unusually high incidence of early post-transplant surgical complications and the length of their initial stay in hospital was significantly prolonged (P less than 0.02) when compared to both control groups. It is possible that excessive corticosteroid therapy is more deleterious in transplant patients weakened by peri-renal haematomas, urinary extravasations and stormy prolonged post-operative periods. Having emphasized the detrimental effects of excessive anti-rejection corticosteroid therapy it must be mentioned that occasionally patients develop avascular necrosis even after low doses of steroid therapy, while others, receiving high doses of steroid therapy and undergoing a stormy post-operative course, do not develop this complaint. It is suggested that although excessive steroid therapy is positively harmful, avascular necrosis is not an invariable complication and that ofther factors including possibly a genetic predisposition operate to produce avascular necrosis of bone in renal transplant patients.

Adult↗

Assessment of renal osteodystrophy following renal transplantation.

Serial histological studies in patients after successful renal transplantation indicate that with restoration of adequate renal function osteomalacia invariably improves with symptomatic relief in bone pain. Histological changes of osteitis fibrosa resolve more slowly and radiological changes may persist longer, occasionally in the absence of confirmatory histological evidence of secondary hyperparathyroidism. For accurate and sensitive follow-up a combination of biochemistry, histology and radiology is desirable.

Alkaline Phosphatase↗