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Biomedical subjects

C A Pollock

Publications and source records attributed to C A Pollock.

65 records · Page 4Linked to original sources
PubMed1988

Lead intoxication in Sydney Harbour Bridge workers.

Thirty-eight Sydney Harbour Bridge workers were assessed for possible lead intoxication. Forty-seven per cent were found to have significant lead intoxication as assessed by calcium disodium edetate chelation (Ca EDTA) testing and were subsequently effectively and safely treated with Ca EDTA. The prevalence of neurological, constitutional, gastrointestinal and musculoskeletal symptoms was significantly greater in those with, than those without, lead toxicity. Although blood lead levels and, to a lesser extent, hematological parameters were of some use in diagnosis, they were not sufficiently sensitive and thus should not be used in screening workers at risk of lead intoxication. Ca EDTA testing remains the diagnostic method of choice. Patients exposed to lead dust and fumes, in whom symptoms of lead intoxication are present, should undergo such testing and if a positive result is obtained, then EDTA chelation therapy should be instituted.

Adult↗
PubMed1988

Acute renal failure due to focal necrotizing glomerulonephritis in a patient with non-Hodgkin's lymphoma. Resolution with treatment of lymphoma.

Renal disease in association with lymphoma is more prevalent than generally recognized. Glomerulonephritis may occur as a paraneoplastic phenomenon. We report a patient who presented with acute renal failure due to focal necrotizing glomerulonephritis in association with non-Hodgkin's lymphoma in whom the acute renal failure and glomerulonephritis resolved on clinical, biochemical and histological grounds with treatment of the lymphoma. Focal necrotizing glomerulonephritis is extremely uncommon in association with lymphoma and, to our knowledge, this association with follow-up and histological resolution of glomerulonephritis has not previously been reported.

Acute Kidney Injury↗
PubMed1987

Dialysis and transplantation in patients with renal failure due to systemic lupus erythematosus. The Australian and New Zealand experience.

Between 1977 and 1985, 5726 patients in Australia and New Zealand entered end stage renal failure programmes. Of these, 63 patients had renal failure due to systemic lupus erythematosus (a prevalence of 1.1% of patients entering renal replacement programmes). When compared with patients with other forms of glomerulonephritis, there was a female preponderance and a younger age distribution in patients with renal failure due to lupus nephritis. Integrated patient, dialysis, and transplant survival data showed that results in patients with renal failure due to lupus nephritis were comparable with those in patients with other forms of glomerulonephritis or in patients with renal failure due to any cause. Age at entry significantly affected survival, with significant differences being found in those patients under as opposed to over 50 years of age. Causes of death in patients with lupus nephritis were similar to those in patients with renal failure due to other causes. It is concluded that dialysis and transplantation are acceptable forms of treatment for patients with end stage renal failure due to systemic lupus erythematosus.

Adolescent↗
PubMedDate not supplied

Lead intoxication.

Lead intoxication was recognised as early as 2000 BC and the widespread use of lead has been a cause of endemic chronic plumbism in several societies throughout history. In the twentieth century, lead intoxication is still a common problem. In children it is largely due to ingestion of pica and environmental exposure, whereas adult groups at greatest risk are the industrially exposed: thus, screening of these workers should be undertaken at regular intervals. The clinical features of lead intoxication are nonspecific and often go unrecognised. The early manifestations are largely neuropsychiatric, followed by more significant disturbances of the central and peripheral nervous systems, symptomatic gastrointestinal, musculoskeletal, haematological and endocrine abnormalities. The association of lead poisoning with renal disease is well documented and must be considered, particularly if there is associated hypertension and/or gout. Blood lead concentrations are an unreliable predictor of body lead stores as they are indicative only of recent exposure. Haematological parameters have been used to assess those at risk of toxicity, but although more reliable than blood concentrations, they also fail to predict those patients at risk of toxicity. The recommended assessment for patients with suspected lead intoxication is a calcium disodium edetate chelation test, which is a sensitive marker for assessing body stores and subsequent intoxication. In children the dosage should be 50 mg/kg up to 1000 mg, and in adults 1000 mg administered intravenously or 2000 mg intramuscularly in divided doses 12 hours apart with subsequent 72 hour urinary lead estimations. Lead excretion levels greater than 350 micrograms/72 hours should be considered as suggestive of intoxication, particularly if supported by historical, clinical or biochemical evidence of lead exposure. Treatment of patients with positive chelation tests involves symptomatic treatment and a course of chelation therapy utilising calcium disodium edetate in doses similar to those used for testing, and in the more severely intoxicated patient, the addition of dimercaprol in doses of 75 mg/m2 every 4 hours to a total of 300 mg/m2/day. The safety of these treatment regimens is well documented.

Chelating Agents↗
PubMedDate not supplied

Fibrogenic effects of cyclosporin A on the tubulointerstitium: role of cytokines and growth factors.

The clinical utility of cyclosporin A (CyA) as an immunosuppressive agent has been significantly limited by the frequent occurrence of chronic nephrotoxicity, characterised by tubular atrophy, interstitial fibrosis and progressive renal impairment. The pathogenesis of this condition remains poorly understood, but has been postulated to be due to either direct cytotoxicity or indirect injury secondary to chronic renal vasoconstriction. Using primary cultures of human proximal tubule cells (PTCs) and renal cortical fibroblasts (CFs) as an in vitro model of the tubulointerstitium, we have been able to demonstrate that clinically relevant concentrations of CyA are directly toxic to these cells and promote fibrogenesis by a combination of suppressed matrix metalloproteinase activity and augmented fibroblast collagen synthesis. The latter effect occurs secondary to the ability of CyA to stimulate autocrine secretion of insulin-like growth factor-I by CFs and paracrine secretion of transforming growth factor-beta(1) by PTCs. Many of these pro-fibrotic mechanisms are completely reversed by concurrent administration of the angiotensin-converting enzyme inhibitor, enalaprilat, which has proven efficacy in preventing chronic CyA nephropathy in vivo. These studies highlight the unique potential that human renal cell cultures offer for studying the role of local cytokine networks in tubulointerstitial disease and for developing more effective treatment strategies which specifically target fibrogenic growth factor activity following nephrotoxic injuries.

Animals↗
PubMedDate not supplied

Lead intoxication in paint removal workers on the Sydney Harbour Bridge.

Lead intoxication is far more prevalent than is recognized by those persons who are exposed to lead fumes and dust in industry, as the early symptoms of intoxication are subtle and non-specific. The levels of lead in blood are a poor reflection of lead stores in the body and their potential toxicity, but are used frequently as the only test for screening of lead intoxication. Chelation of lead with calcium-EDTA is a more sensitive test to detect those persons who are at risk of toxicity. Industrial workers who are exposed regularly to lead must be screened on a periodic basis and a diagnosis of lead poisoning must be considered if substantial morbidity is to be avoided. We report six cases of men with significant lead intoxication who were employed on the Sydney Harbour Bridge, all of whom have benefited symptomatically from calcium-EDTA chelation therapy.

Adult↗
PubMedDate not supplied

The influence of dialysis treatment modality on the decline of remaining renal function.

A retrospective investigation was undertaken in which the rate of decline of residual renal function (RRF), estimated from creatinine clearance, was compared in 55 continuous ambulatory peritoneal dialysis (CAPD) and 57 hemodialysis (HD) patients for whom a minimum of four (mean of 7.6) well-spaced historic measurements of residual clearance were available. Because of the intrinsic variability that attends such data, specialized nonlinear, growth curve statistical methods were employed. Residual function was found to decline exponentially after the onset of therapy in both cohorts. The rate of decline in the HD group was twice that of the CAPD group (5.8% +/- 0.4% per month for HD vs 2.9% +/- 0.3% per month for CAPD; difference significant at p less than 0.0001). This difference remained highly significant (p less than 0.01) when corrected for other potential risk factors such as age, gender, hypertensive status, and use of angiotensin converting enzyme inhibitors in patients with diabetic or other forms of glomerular nephropathy. Differences between cohorts were not significant for patients with other diagnoses (p greater than 0.1) although the size of some of these subsets was very small. The physiologic mechanism for the more rapid fall-off of RRF on HD remains speculative, but could be related to renal ischemia secondary to intratreatment hypovolemia and/or to nephrotoxic effects of the inflammatory mediators of extracorporeal circulation.

Female↗