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W Jeffcoate

Publications and source records attributed to W Jeffcoate.

18 recordsLinked to original sources
PubMed2001

Why did the 5th Earl of Derby die?

The unexpected death of Ferdinando Stanley, 5th Earl of Derby, on April 16, 1594 was an event of major political importance in the later years of Queen Elizabeth I of England. When he had succeeded his father at the age of 38 he became head of one of the most influential families in the country. He also had a claim to the throne if Elizabeth died without naming a successor. Yet within seven months of entering into his inheritance, this previously fit man was suddenly taken ill and died a fortnight later. His death was so significant that the historian John Stow recorded his illness in great detail (Fig. 1).(1) Stow's remarkable account is compatible with a sinister interpretation of the cause.

Acute Kidney Injury↗
PubMed2000

The Charcot foot.

AIMS: To review the clinical manifestations of the Charcot foot in diabetes mellitus, with particular reference to theories concerning aetiology. METHODS: Systematic review of the published literature, searching for the keywords 'Charcot', 'foot and diabetes' and 'neuropathy' on Medline, as well as by examination of the references in recent published reviews. CONCLUSIONS: The Charcot foot of diabetes mellitus is a common problem, and yet is not widely recognized by non-specialists. The failure of professionals to identify the condition in its early phases is probably largely responsible for the gross deformity which follows continued weight-bearing. The condition is confined to those with severe peripheral neuropathy. It is thought to result from three factors: motor neuropathy leading to the development of abnormal forces within the foot, subsequent disorganization of the foot as a result of associated osteopenia and progressive destruction from continued weight-bearing, enabled by reduced pain sensation. The cause of the osteopenia is not known, but it is associated with increased bone blood flow, which may be mainly the result of loss of sympathetic innervation. The importance of increased limb blood flow in the pathogenesis of the Charcot foot has been recognized for over a century. Paradoxically, the increased flow is associated with evidence of macrovascular disease, in that the prevalence of vascular calcification of pedal vessels approaches 90%. After an interval of many months, the condition tends to evolve: the increased blood flow lessens, the osteopenia is reduced and the disorganized bones become sclerotic. This tendency for the condition to evolve remains unexplained, since it would not be expected if the condition was caused solely by progressive denervation. As a result, it is suggested that another factor may be involved in the pathogenesis of the Charcot foot: an abnormal vasomotor reflex, analogous to reflex sympathetic dystrophy, occurring against a background of severe peripheral neuropathy. The resolution of the condition occurs because it is the reflex component of the hyperaemia which proves self-limiting.

Diabetic Foot↗
PubMed1999

Assessment of corticosteroid replacement therapy in adults with adrenal insufficiency.

Recent work has taught us that our conventional approach to corticosteroid replacement therapy requires review. Specifically, the doses of hydrocortisone we have used are probably too high for the majority, and should ideally be administered in three or more doses through the day. Nevertheless, there is not much hard evidence that excessive glucocorticoid replacement per se will lead to adverse effects such as osteoporosis, even though it may exacerbate any tendency in those who are predisposed to it for other reasons. As such, there is no compelling need for using determinations of either UFC excretion or of the serum cortisol profile in the routine management of patients on replacement therapy. Nevertheless, such measures may be considered in those thought to be at particular risk of osteoporosis, and in whom it is felt that special effort should be made to ensure that they are receiving the minimum dose possible. In such circumstances, a cortisol day curve is likely to be of more value than measurement of UFC.

17-alpha-Hydroxyprogesterone↗
PubMed1996

Making sense.

Explore the source record for details and available documents.

Communication↗
PubMed1995

Endocrine investigation of gonadal dysfunction.

This article reviews the hormone assays available for the assessment of gonadal function and some pitfalls in their interpretation. Simple strategies are suggested for the investigation of disorders of gonadal function in males and females. Emphasis is placed on relating the indications for hormone assays to the appropriate clinical context.

Endocrine System Diseases↗
PubMed1994

Eighty-six cases of Addison's disease.

OBJECTIVES: Since there have been no recent reviews of Addison's disease, we have undertaken a retrospective case-notes review of all identifiable cases in Nottingham to define the prevalence, incidence and causes of Addison's disease. We have also reviewed the criteria for interpretation of the short Synacthen test in diagnosis. DESIGN: A retrospective study of all patients coded for the diagnosis and admitted to Nottingham's hospitals between 1 April 1987 and 31 March 1993, identified by the hospital Information Services. PATIENTS: A total of 86 cases were identifiable of whom 66 were still alive and living in the town. RESULTS AND CONCLUSIONS: The calculated prevalence was 110 per million population. The cause was attributed to autoimmune destruction of the adrenal cortex in 81 (93%). There were two cases of metastatic malignancy and three unrelated cases of late onset adrenoleukodystrophy, but none were attributable to tuberculosis. Twenty-one new cases were diagnosed between 1987 and 1993. The calculated incidence was 5.6 per million per annum. The biochemical basis of the diagnosis was reviewed in these 21 patients and as a result firm criteria are suggested for the interpretation of the short Synacthen test; criteria for normality being baseline cortisol >250 and 30 minute peak >600 nmol/l, taking into account clinical circumstances.

Addison Disease↗