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Biomedical subjects

H A Ellis

Publications and source records attributed to H A Ellis.

At least 55 records · Page 3Linked to original sources
PubMed1977

Effect of renal transplantation on marrow mast cell hyperplasia of chronic renal failure.

Marrow mast cells have been counted in iliac bone from patients with chronic renal failure treated by renal transplantation. Mast cell numbers were initially increased but returned to the normal range in many patients after renal transplantation. Improvement in osteitis fibrosa and osteomalacia after transplant was not clearly related to this diminution in the number of mast cells. The use of prednisone in renal transplant patients may have some effect in reducing the numbers of mast cells. There is no fully acceptable explanation for the increase in marrow mast cells which occurs in chronic renal failure.

Bone Marrow↗
PubMed1977

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↗
PubMed1976

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↗
PubMed1976

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↗
PubMed1976

Massive chronic feto-maternal bleeding associated with placental chorioangiomas.

After pregnancy complicated by polyhydramnios and the antenatal discovery of a very large placenta a newborn infant suffered from anemia, thrombocytopenia and hypoproteinemic edema, and was successfully treated by exchange transfusion. The placenta contained two chorioangiomas and there was diffuse placental hypertrophy with edema and patchy chorioangiomatosis. There was evidence of major chronic feto-maternal bleeding which could be the explanation for most of the hematological and biochemical problems which occurred. The child was developing normally at subsequent follow-up aged 15 weeks.

Anemia↗
PubMed1976

Achondrogenesis type I. A familial subvariant?

The clinical, pathological, and radiological features of 2 male sibs with a severe and lethal form of micromelic dwarfism are desribed. The family also includes 2 normal sibs. The histological and radiological appearances suggested a diagnosis of achondrogenesis type I, but the markedly deficient ossification of the skull and the presence of intrauterine rib fractures were atypical. These changes have been observed in two other families with 2 or more infants with suspected achondrogenesis, raising the possibility that these familial cases may be a subvariant of achondrogesis or even a distinct disease entity. The disease appears to be inherited as an autosomal recessive and death occurs shortly after birth because of severe pulmonary hypoplasia.

Achondroplasia↗
PubMed1976

Iliac bone marrow mast cells in relation to the renal osteodystrophy of patients treated by haemodialysis.

Mast cells have been counted in iliac bone biopsies from patients with chronic renal failure treated by haemodialysis, and attempts made to relate mast cells to the various features of azotaemic renal osteodystrophy. There was a significant increase in the number of marrow mast cells in comparison with controls, and haemodialysis has no favourable effect on the marrow mast cell hyperplasia which occurs in chronic renal failure. There was a general tendency towards greater numbers of mast cells in cases with most marked ostetis fibrosa but it was not possible consistently to relate hyperparathyroidism to mast cell numbers. Patients treated by parathyroidectomy, aluminium hydroxide, or the newer vitamin D metabolites failed to show any consistent fall in marrow mast cell numbers in spite of improvement in the ostetis fibrosa. The number of marrow mast cells was related to the duration of haemodialysis and to the amount of osteoid present and iversely to the percentage mineralization of bone. It was not possible to identify any causal relationship between the presence or severity of osteomalacia and the number of mast cells in the haemodialysed patients although mast cell hyperplasia was also observed in patients with osteomalacia unassociated with renal disease.

Adolescent↗
PubMed1976

Bone disease in long-term haemodialysis: the association of radiological with histological abnormalities.

The radiological findings in the skeletal surveys of 70 patients receiving long-term haemodialysis for chronic renal failure have been correlated with histological findings in a specimen obtained by biopsy of the iliac crest. Many significant associations were found, and the ones presented are those thought to be most useful in the interpretation of the radiological abnormalities. The main conclusions are that fractures and severe medullary rarefaction appear to be most commonly the result of osteomalacia; subperiosteal erosions are associated with the more severe grades of osteitis fibrosa; cortical striations and sclerosis are associated with an increased amount of osteoid, and sclerosis is diagnosed more frequently by radiological means than by iliac-crest biopsy.

Adult↗
PubMed1976

The influence of tumor volume and the degree of heating on the response of the solid Yoshida sarcoma to hyperthermia (40-42 degrees).

The solid Yoshida sarcoma implanted on the feet of rats was subjected to local hyperthermia by water bath immersion. Tumor response was governed by the temperature and duration of heating (i.e., the degree of heating) and by tumor volume. With small tumors (1.0- to 1.5-ml volume) an intratumor temperature of 42 degrees maintained for 1 hr led to tumor regression in 11 to 13 days, and the tumor volume was halved every 2.6 days. Following 2 hr hyperthermia (42 degrees) the tumors disappeared in 6 to 7 days, and tumor volume was halved every 1.2 days. Tumors of 2 to 3-mol volume had left the exponential phase of the growth curve and required 2 hr at 42 degrees for cure. Following heating at 40 degrees for 1 hr, there was a 50% increase in O2 uptake and anaerobic CO2 production by the tumor, accompanied by enhanced dissemination by lymphatic, vascular, and direct routes, and tumor was found in organs not usually the site of metastases (e.g., testis and stomach). With large tumors (3.0 to 4.5 ml), the survival time of the rats was significantly reduced. These results occurred in the absence of a rise in body temperature of the animals. It is concluded that in this animal-tumor system, hyperthermia at a temperature inadequate for tumor destruction (40 degrees) can result in changes in the tumor that represent a hazard to the host.

Animals↗
PubMed1976

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↗
PubMed1976

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↗
PubMed1975

Quantitative observations on iliac bone marrow mast cells in chronic renal failure.

Mast cells have been counted in sections of iliac bone from 61 control subjects at necropsy. Mast cells were found in all but three, and the range was 0-33-7, median 1-95 per mm2 marrow. The majority (82%) had less than 4-99 mast cells per mm2 marrow; in 37-7% there was less than 1 mast cell per mm2 marrow. In a group of 45 patients with chronic renal failure there was a significant increase in the numbers of mast cells (P less than 0-001) with a range of 0-96-55-63, median 9-55 per mm2 marrow. Mast cells were common in the areas of marrow fibrosis associated with osteitis fibrosa but this was not the sole cause of the increase since there was also an excess of mast cells in the non-fibrous parts of the marrow. There was a tendency towards greater numbers of mast cells in those cases with most marked osteitis fibrosa in association with the prominent marrow fibrosis, but there was no significant relationship between mast cell numbers and other features of oesteitis fibrosa such as the number of osteoclasts and the amount of woven bone formation. There was no relationship between the numbers of mast cells and the amounts of total bone, ostoid, percentage mineralization of cancellous bone, or the presence of osteomalacia.

Adolescent↗
PubMed1975

Serum proteins as indicators of poor dietary intake in patients with chronic renal failure.

A study of serum proteins in patients on regular hemodialysis has shown that many have low serum transferrin levels but near normal serum albumin and normal or raised pre-albumin levels. Hemoglobin values were related to transferrin levels. Low transferrin levels also occurred in patients with advanced osteitis fibrosa. Deficient protein intake seems the likely explanation. Measurement of pre-albumin does not reflect low protein intake in chronic renal failure; reasons for this discussed.

Albumins↗
PubMed1975

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↗
PubMed1973

Azotaemic renal osteodystrophy: a quantitative study on iliac bone.

The histopathology of bone is described in 60 patients with chronic renal failure due to a variety of renal diseases. Changes of azotaemic renal osteodystrophy included osteitis fibrosa, osteomalacia, and osteosclerosis. Quantitative histology using a point-counting technique revealed a significant increase in total bone, mineralized bone, and osteoid in comparison with a control group of 68 individuals. Osteitis fibrosa due to secondary hyperparathyroidism occurred in 93%, osteomalacia in 40%, and osteosclerosis in 30% of patients. Woven bone formation was a characteristic feature and was related to the severity of osteitis fibrosa. There were significant correlations between the weights of parathyroid glands and the number of osteoclasts, amounts of woven bone, and marrow fibrosis in the ilium. Hyperparathyroidism caused degradation of mineralized bone but the loss was balanced or exceeded by the aggradation of woven mineralized bone. Woven bone formation together with excess osteoid gave rise to osteosclerosis. The histological findings indicate that hyperparathyroidism and osteitis fibrosa usually occur early in chronic renal failure and that osteomalacia develops subsequently.

Adult↗