Clinics in Endocrinology and Metabolism (Clin Endocrinol Metabol )

Publisher: Elsevier

Description

Discontinued in 1986. Continued as Baillière's Clinical Endocrinology and Metabolism (0950-351X).

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  • Website
    Clinics in Endocrinology and Metabolism website
  • Other titles
    Clinics in endocrinology and metabolism
  • ISSN
    0300-595X
  • OCLC
    2446012
  • Material type
    Periodical
  • Document type
    Journal / Magazine / Newspaper

Publisher details

Elsevier

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Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: The diabetic foot can be classified into the neuropathic foot, characterized by the neuropathic ulcer, the Charcot joint and neuropathic oedema associated with a good circulation, in which neuropathy predominates, and the ischaemic foot in which atherosclerosis is the dominant factor leading to a reduction in blood flow with absent pulses. In the neuropathic foot, blood flow is increased, the vessels are still and dilated as a result of medial wall calcification and there is evidence for arteriovenous shunting. The neuropathic ulcer characteristically develops on the plantar surface following inflammatory autolysis and haematoma formation under neglected callosities. Chiropody is therefore the mainstay of treatment and recurrence is prevented by redistribution of weight bearing forces by moulded insoles in special footwear. Charcot osteoarthropathy is often preceded by fracture which is a further complication of diabetic neuropathy and which precipitates the rapid bone and joint destruction of the Charcot joint. Neuropathic oedema responds to ephedrine with a reduction in peripheral flow and an increase in urinary sodium excretion. The ischaemic foot is characterized by rest pain, ulceration and gangrene. Medical management can be successful in up to 72%, the remainder needing arteriography to assess suitability for arterial reconstruction or angioplasty. In the diabetic leg, atherosclerosis is predominant in the branches of the popliteal artery making arterial reconstruction difficult. Optimum care of the diabetic foot is provided in a diabetic foot clinic where the skills of chiropodist, shoe-fitter and nurse receive full support from physician and surgeon. Many lesions of the diabetic foot are avoidable and thus patient education is the cornerstone of prevention.
    Clinics in Endocrinology and Metabolism 12/1986; 15(4):889-916.
  • Clinics in Endocrinology and Metabolism 12/1986; 15(4):753-82.
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    ABSTRACT: Duration of disease is the major susceptibility factor for microangiopathy. Microangiopathy does not occur without the metabolic abnormality of diabetes and there is much circumstantial evidence to implicate poor diabetic control in its pathogenesis. The rate of development and severity of complications, however, are variable even in patients with apparently similar control and about 25% of diabetics will never develop clinical evidence of microangiopathy. Studies of identical twins suggest a genetic component in the pathogenesis of retinopathy in NIDDM, and less so in IDDM, but increased capillary basement membrane thickness does not occur in the non-diabetic identical co-twins of insulin dependent diabetics. There may also be genetic heterogeneity not only of diabetes, but also of its complications, although for a given type of diabetes the prevalence of microangiopathy is often very similar in different racial groups. Associations between several different HLA molecules (particularly DR4) and microangiopathy in IDDM have been reported but not consistently confirmed. Recently the finding of an increased frequency of the B3 allotype of the fourth component of complement C4B3 in subjects with retinopathy has suggested that there is an HLA linked association. Both complement and the immunoglobulins are concerned with humoral immunity and the report of an association between a phenotype of the IgG heavy chain markers on chromosome 14 and retinopathy is of particular interest. These associations appear to be additive but independent. These reports need confirmation but provide the best evidence we have for an immunogenetic component (HLA and non-HLA linked) of the aetiology of microangiopathy, at least in IDDM. The studies of identical twins, HLA and Gm associations provide good evidence that genetic factors are involved in susceptibility to microangiopathy, at least in some diabetics, although the most relevant genes may not have been identified. Searches for better genetic markers must continue in order to identify those patients at increased risk of developing microangiopathy.
    Clinics in Endocrinology and Metabolism 12/1986; 15(4):715-26.
  • [Show abstract] [Hide abstract]
    ABSTRACT: Many of the diabetic neuropathic syndromes are characterized by painful symptoms with a sensation of burning and associated with troublesome hyperaesthesia. It is important to distinguish between the acute and chronic forms of peripheral sensory neuropathy; while the former carries an excellent prognosis for symptomatic improvement within one year, the latter may cause persistent symptoms for many years. In contrast to the acute form, in which symptoms are particularly severe but abnormal neurological signs are minimal, patchy stocking and glove sensory loss together with peripheral small muscle wasting are often present in chronic sensorimotor neuropathy. Peripheral polyneuropathies are more common in patients with poor metabolic control, although recent evidence implicates blood glucose flux as a possible contributory factor to neuropathic pain. It is possible that blood glucose flux or altered peripheral blood flow leads to increased spontaneous activity in nociceptive afferent fibres which are present in the axonal sprouts that characterize small fibre neuropathy. In the diagnosis of the neuropathies, exclusion of other aetiological factors is of paramount importance as there is no specific diagnostic test for diabetic nerve damage. If there is no symptomatic improvement after a period of stable and optimal metabolic control together with simple analgesics, then the tricyclic drugs should be regarded as first line therapy. The rapid effect of these drugs suggests a peripheral rather than central mode of action.
    Clinics in Endocrinology and Metabolism 12/1986; 15(4):917-31.
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    ABSTRACT: Diabetic glomerulopathy is characterized by a very slow development of basement membrane (BM) accumulation, manifested as thickening of the peripheral BM and increased volume of the mesangial BM-like material (BMLM) with mesangial expansion. The initiation of the process is probably at the onset of diabetes since the BM thickening is detectable after a few years. The BM accumulations at the two sites (PBM and BMLM) in the glomerular tuft are considered as two different expressions of a fundamental BM abnormality. The two locations present different conditions for quantitation, may have a different biochemical make-up, and immediate functional implications of the abnormalities may differ as well. In the long run, however, the two in concert lead to the ultimate solidification of the glomerular tuft with loss of capillary surface. The end-stage is glomerular closure, with elimination of glomerular function. A very close correlation has been found between the total remnant surface area of the glomerular capillaries and the level of GFR. Along with the classical changes of the diabetic glomerulopathy, changes in glomerular size are detectable. In early diabetes during the stages of glomerular hyperfunction, hypertrophy develops acutely at the onset of diabetes, leading to an increase in capillary surface corresponding to the increase in filtration rate. In the advanced stages when glomerular closure involves a proportion of the nephrons compensatory hypertrophy develops, thereby probably helping to preserve capillary surface for a period of time. The exact mechanisms that may influence these developments are not known, but underlying them all are the metabolic abnormalities of diabetes.
    Clinics in Endocrinology and Metabolism 12/1986; 15(4):733-51.
  • [Show abstract] [Hide abstract]
    ABSTRACT: Diabetes causes cataract and certain physical changes in the lens. The diabetic lens is larger than the non-diabetic and shows greater light scatter and fluorescence. Both hyperglycaemia and lowering of blood glucose case refractive changes and hypermetropia is the most common. Classical 'snow-flake' juvenile cataract associated with hyperglycaemia is now rare. It has an osmotic mechanism. Diabetes is a risk factor for cataract in adults which is duration dependent, more frequent in women and leads to earlier surgery. It resembles non-diabetic senile cataract. Extracapsular cataract extraction is the method of choice for diabetic cataract with a better visual result and less risk of rubeosis iridis. A posterior chamber implant may still permit retinal photocoagulation if necessary. Diabetic retinopathy is still the leading cause of blindness in the working age group. The beneficial effect of photocoagulation has been shown by randomized controlled trials to be long-lasting for both proliferative retinopathy and maculopathy. Therefore there is a need for screening, especially for those with proliferative disease which may be present without symptoms. A knowledge of risk factors will enhance detection rate with duration as the strongest determinant for retinopathy. Any screening modality should be highly sensitive as well as specific. The role of different professionals as potential screeners should be considered. Adequate provisions include facilities for checking vision and for dimming ambient lighting. Mydriasis and a good ophthalmoscope light will increase detection rate. The use of a 45 degrees non-mydriatic camera is unlikely to supplant the use of an ophthalmoscope as a single field is likely to miss important lesions. A 60 degrees camera may confer a large enough field and the use of transparencies will provide magnification when films are projected but the camera is more difficult to use. A list of features chosen by a recent study to characterize sight-threatening retinopathy is included and their presence indicates the need for referral to an ophthalmic clinic for treatment or close observation.
    Clinics in Endocrinology and Metabolism 12/1986; 15(4):971-99.
  • Clinics in Endocrinology and Metabolism 12/1986; 15(4):807-21.
  • Clinics in Endocrinology and Metabolism 12/1986; 15(4):727-31.
  • [Show abstract] [Hide abstract]
    ABSTRACT: Diabetic retinopathy is a common, and potentially blinding or visually disabling complication of diabetes. Nearly all diabetic subjects will have some degree of retinopathy after 20 years of diabetes, and 50% of those with insulin dependent diabetes will have proliferative retinopathy after 15 years. Macular oedema frequently produces central vision loss and legal blindness, most commonly in non-insulin dependent diabetics. In recent years, several therapeutic modalities have been demonstrated to be effective on the basis of large-scale randomized, controlled clinical trials. These include panretinal photocoagulation (PRP), using the argon laser or xenon arc, for proliferative retinopathy, and focal photocoagulation for macular oedema. Vitrectomy surgery is effective for diabetic vitreous haemorrhage and traction retinal detachment, producing improved vision in most patients, but only a relatively small percentage of patients so treated recover good visual acuity (greater than or equal to 6/12). Other therapeutic modalities, such as hypophysectomy for severe retinopathy, remain controversial, while still others, such as rigorous blood glucose control and aldose reductase inhibitors, are currently under investigation. The primary care physician who deals with diabetic patients should be familiar with the lesions of diabetic retinopathy and with current therapeutic modalities. He should perform an examination of the posterior retina with the direct ophthalmoscope on each diabetic patient at each visit, and should institute prompt referral to an ophthalmologist at the first sign of change. Periodic examination of all diabetic patients by an ophthalmologist should be conducted at the intervals recommended in the previous section. Definitive evaluation and treatment of diabetic retinopathy should be carried out by the ophthalmologist.
    Clinics in Endocrinology and Metabolism 12/1986; 15(4):933-69.
  • Clinics in Endocrinology and Metabolism 12/1986; 15(4):837-53.
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    ABSTRACT: Diabetic nephropathy develops in about 45% of insulin dependent diabetics of whom two-thirds will develop renal failure, the rest dying from cardiovascular disease. Most of the excess mortality of insulin dependent diabetics occurs in those with proteinuria. Among non-insulin dependent diabetics nephropathy is also an important cause of increased mortality but this is mainly from cardiovascular disease. Once diabetic nephropathy is established it progresses relentlessly to end-stage renal failure over about seven years, but ranging from five to 20 years. The explanation for the different rates of progression in individual patients is not understood. Hypertension accompanies diabetic nephropathy and its treatment may retard the progression of renal failure. Other forms of intervention include glycaemic control which has not been shown to have any effect, and protein restriction for which no conclusions can be drawn at present. The diagnosis of diabetic nephropathy is straightforward in the presence of a typical history and clinical features. Non-diabetic renal disease is sometimes the cause of renal failure and may require specific treatment; prognosis for renal failure treatment may be better than for nephropathy patients with other diabetic complications. Other diabetic complications develop as diabetic nephropathy progresses, most notably cardiac and peripheral vascular disease. Proliferative retinopathy and neuropathy are considerable problems and their management needs attention both before and after renal failure treatment.
    Clinics in Endocrinology and Metabolism 12/1986; 15(4):783-805.
  • [Show abstract] [Hide abstract]
    ABSTRACT: Autonomic neuropathy is now well established as a relatively common and significant complication of diabetes mellitus. Its importance has been clarified in recent years during which the extent of autonomic control over all areas of body function has been defined. Using simple cardiovascular reflex tests, autonomic abnormalities can be demonstrated without any corresponding symptoms. The often stated concept of 'patchy' involvement in diabetic autonomic neuropathy should now be rejected as too should the view that autonomic neuropathy is either 'present' or 'absent' based on a single test result. When generalized and predominantly metabolic disturbances, as in diabetes, give rise to impaired nerve function, autonomic as well as somatic components of the nerve are affected. Where damage is severe this leads to the characteristic florid picture of symptomatic autonomic neuropathy with its particularly poor prognosis. For the physician in a busy clinic, much of the theoretical and experimental basis for autonomic neuropathy may not appear of direct relevance. However, he has now to be aware of the clinical implications of autonomic damage in the diabetic. This may have particular relevance in the care of the diabetic foot (see Chapter 10), the recognition of many of the vague symptoms associated with autonomic damage, the treatment of disabling features such as postural dizziness and nocturnal diarrhoea, and an awareness of the poor prognosis associated with symptomatic autonomic neuropathy. He will also need to be alert to the dangers of general anaesthesia in such patients, and the possibility of sudden unexpected deaths. Diabetic autonomic neuropathy causes widespread abnormalities, some of which are clinically apparent, some of which can be detected by sensitive tests, and others which have yet to be discovered. Inclusion of the neuropeptides and other hormones within the compass of autonomic control has opened up a whole new area of investigative interest, with many complex interrelationships which still need to be unravelled. This should lead to better understanding of the pathophysiological processes that cause damage to diabetic nerves. With so much research effort directed towards better glycaemic control and aldose reductase inhibitors (see Chapter 8), it may eventually be possible to reverse or prevent this potentially disabling and lethal complication of diabetes.
    Clinics in Endocrinology and Metabolism 12/1986; 15(4):855-88.
  • Clinics in Endocrinology and Metabolism 12/1986; 15(4):823-36.
  • Clinics in Endocrinology and Metabolism 09/1986; 15(3):683-707.
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    ABSTRACT: The shape of the human growth curve is described and illustrated. Growth studies may be longitudinal, cross-sectional, mixed longitudinal or linked-longitudinal; each has advantages and disadvantages, and each requires appropriate statistical methods for handling the data. Standards for height and height velocity for use in a clinical setting wherein follow-up over several years is presumed are described and illustrated. Such standards have to take into account tempo of growth at ages over nine years. Cross-sectionally derived standards do not do this and are not suitable for clinical use. The techniques of measurement of height, sitting height and skinfolds are described and illustrated. Growth and development during puberty is described; there are changes in body composition as well as in body size and shape. Standards for pubertal stages of breasts, pubic hair and genitalia are given and emphasis is laid on the great variation in both the timing and the duration of these pubertal changes. Measurement of developmental age is discussed. The Greulich-Pyle and Tanner-Whitehouse methods for skeletal age are described. These methods can be used for predicting adult height which is useful both in diagnosis and in following the effects of treatment. In diagnosis the predicted adult height is compared to the range of expected heights in the children of the particular pair of parents concerned (the so-called 'target' range of heights) to see if smallness is simply due to delay. Change in Tanner-Whitehouse predicted height occurs on successful treatment of, for example, growth hormone deficient short stature, and is thus a guide to the success of treatment. Standards are also given for height of children from age two to nine inclusive, with allowance for height of their parents.
    Clinics in Endocrinology and Metabolism 09/1986; 15(3):411-51.
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    ABSTRACT: Since its clinical description in the last century, much progress has been made in our understanding of acromegaly. From an initial description of pituitary enlargement as just another manifestation of generalized visceromegaly, the pituitary abnormality has come to be recognized, in most instances, as the underlying aetiological factor. Gigantism and acromegaly are manifestations of disordered pituitary physiology, but the lesion responsible may be hypothalamic, adenohypophyseal or ectopic in location. The best known pathological hypothalamic basis for acromegaly is represented by a neuronal malformation or 'gangliocytoma'. It usually takes the form of an intrasellar gangliocytoma or, more rarely, a hypothalamic hamartoma. The neuronal elaboration of GHRH may play a role in the development of a growth hormone adenoma; the pituitary process may pass through an intermediate stage of somatotropic hyperplasia. When acromegaly has its basis in a pituitary abnormality, the lesion is almost exclusively an adenoma; the non-tumorous adenohypophysis shows no evidence of coexistent hyperplasia. Surprisingly, such tumours are more often engaged in the formation of multiple hormones rather than GH alone. They frequently produce not only GH and prolactin, the products characteristics of cells of the acidophil line, but also glycoprotein hormones, usually TSH. The spectrum of adenomas also varies in its degree of differentiation from a histogenetically primitive lesion, the acidophil stem cell adenoma, to well-differentiated tumours of varying cellular composition and hormone content. Each adenoma type has its clinicopathological, histochemical, immunocytological and ultrastructural characteristics. The isolation and characterization of GHRH has permitted the identification of neuroendocrine tumours, most of foregut origin, elaborating this releasing hormone. Such functional tumours induce hyperplasia of pituitary somatotrophs and may, on occasion, result in the formation of growth hormone adenomas. Resection of these GHRH-producing neoplasms results in reversal of endocrinological and sellar abnormalities. Future efforts should be directed toward the elucidation of the aetiology of pituitary adenomas, specifically whether they represent a proliferative process having its origin in endocrinological imbalance, presumably a hypothalamic abnormality, or whether it has a 'de novo' origin in the 'usual process of neoplastic transformation'.
    Clinics in Endocrinology and Metabolism 09/1986; 15(3):655-81.
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    ABSTRACT: Short stature may complicate the treatment during childhood of brain tumours and, to a lesser extent, ALL. A number of factors may be responsible, including spinal irradiation, malnutrition, recurrent tumour, chemotherapy, precocious puberty and radiation-induced GH deficiency. GH is always the first pituitary hormone to be affected by radiation damage to the hypothalamic-pituitary axis but larger radiation doses may result in panhypopituitarism. Some children retain normal GH responses to certain provocative stimuli, although physiological GH secretion is reduced. Nonetheless, in children suspected of radiation-induced GH deficiency, pharmacological tests of GH secretion remain useful, the ITT being the test of choice because of the marked radiation sensitivity of the GH response to hypoglycaemia. The hypothalamus is more radiosensitive than the pituitary. In many patients with radiation-induced GH deficiency, the damage appears to be at the hypothalamic level resulting in a deficiency of endogenous GRF. Treatment with synthetic GRF may provide an alternative to GH therapy in such children. Finally, there is no evidence to suggest that GH therapy given to a child with radiation-induced GH deficiency might induce a brain tumour recurrence or a relapse of ALL.
    Clinics in Endocrinology and Metabolism 09/1986; 15(3):591-606.
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    ABSTRACT: The basis for understanding clinical disorders in the neuroregulation of GH secretion is derived from the complexity of the CNS-hypothalamic-pituitary axis. Studies in animals and humans demonstrate an anatomic, physiological and pharmacological evidence for neurosecretory control over GH secretion including neurohormones (GRH, somatostatin), neurotransmitters (dopaminergic, adrenergic, cholinergic, serotonergic, histaminergic, GABAergic), and neuropeptides (gut hormones, opioids, CRH, TRH, etc). The observation of a defect in the neuroregulatory control of GH secretion in CNS-irradiated humans and animals led to the hypothesis of a disorder in neurosecretion, GHND, as a cause for short stature. We speculate that in this heterogeneous group of children a disruption in the neurotransmitter-neurohormonal functional pathway could modify secretion ultimately expressed as poor growth velocity and short stature.
    Clinics in Endocrinology and Metabolism 09/1986; 15(3):537-90.
  • Clinics in Endocrinology and Metabolism 09/1986; 15(3):629-53.
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    ABSTRACT: According to the results reported in the literature and from our own experience, the following recommendations for the treatment of children with GHD can be given: In order to start GH replacement therapy in early childhood the diagnosis of GHD should be made as early as possible. The growth hormone dose during prepubertal age should not fall short of 12 IU/m2 per week. During spontaneous or induced puberty, the dose needs to be increased, possibly by a factor of two. Daily subcutaneous injections appear most suitable. Treatment with growth hormone releasing factors in cases with hypothalamic GHD, although a promising alternative to the treatment with hGH (Thorner et al, 1985), must be considered experimental at this point. Thyroxine replacement at a daily dose of 75-100 micrograms/m2 should be given in cases of secondary hypothyroidism. Glucocorticoid replacement, if required, should be given at low doses (e.g. hydrocortisone 10 (to 15) mg/m2 per day in divided doses). In cases with additional gonadotropin deficiency, sex steroids (or anabolic steroids) should be given with frequent monitoring of bone maturity not before the age of 13 in girls or 15 years in boys. In boys depot testosterone starting at low doses (e.g. 50-100 mg/month i.m.) will induce a puberty-like increment in height velocity. Since the effect of oestrogens--even in low doses--on growth is uncertain, their administration before achievement of near-normal adult height should be avoided. With the advancement of diagnostic techniques and with the experience in treatment accumulated over the past 25 years, patients with GHD need no longer become dwarfs.
    Clinics in Endocrinology and Metabolism 09/1986; 15(3):495-510.