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Mark W J Strachan

Publications and source records attributed to Mark W J Strachan.

14 recordsLinked to original sources
PubMed2006

Second primary cancers in thyroid cancer patients: a multinational record linkage study.

CONTEXT: Increasing incidence and improved prognosis of thyroid cancer have led to concern about the development of second primary cancers, especially after radioiodine treatment. Thyroid cancer can also arise as a second primary neoplasm after other cancers. OBJECTIVE: The objective of the study was to assess the risk of second primary cancer after thyroid cancer and vice versa. DESIGN: This was a multinational record linkage study. SETTING: The study was conducted at 13 population-based cancer registries in Europe, Canada, Australia, and Singapore. PATIENTS OR OTHER PARTICIPANTS: A cohort of 39,002 people (356,035 person-yr of follow-up) with primary thyroid cancer were followed up for SPN for up to 25 yr, and 1,990 cases of thyroid cancer were diagnosed after another primary cancer. MAIN OUTCOME MEASURES: To assess any possible excess of second primary neoplasms after thyroid cancer, the observed numbers of neoplasms were compared with expected numbers derived from age-, sex-, and calendar period-specific cancer incidence rates from each of the cancer registries, yielding standardized incidence ratios (SIRs). The SIR of second primary thyroid cancer after various types of cancer was also calculated. RESULTS: During the observation period, there were 2821 second primary cancers (all sites combined) after initial diagnosis of thyroid cancer, SIR of 1.31 (95% confidence interval 1.26-1.36) with significantly elevated risks for many specific cancers. Significantly elevated risks of second primary thyroid cancer were also seen after many types of cancer. CONCLUSION: Pooled data from 13 cancer registries show a 30% increased risk of second primary cancer after thyroid cancer and increased risks of thyroid cancer after various primary cancers. Although bias (detection, surveillance, misclassification) and chance may contribute to some of these observations, it seems likely that shared risk factors and treatment effects are implicated in many. When following up patients who have been treated for primary thyroid cancer, clinicians should maintain a high index of suspicion for second primary cancers.

Aged↗
PubMed2006

Improving metabolic control leads to better working memory in adults with type 2 diabetes.

OBJECTIVE: The goals of this study were to determine whether improvements in metabolic control can ameliorate the cognitive dysfunction associated with type 2 diabetes and evaluate the possibility that such improvements are mediated by changes in circulating insulin or insulin resistance. RESEARCH DESIGN AND METHODS: This randomized double-blind trial enrolled 145 subjects at 18 centers in the U.S. Older adults with type 2 diabetes receiving metformin monotherapy received add-on therapy with either rosiglitazone, a thiazolidinedione insulin sensitizer, or glyburide. Cognitive function was assessed at baseline and week 24 using the Digit Symbol Substitution Test, the Rey Auditory Verbal Learning Test, and the Cambridge Neuropsychological Test Automated Battery. RESULTS: Pretreatment fasting plasma glucose (FPG) in both groups was similar, and after 24 weeks both treatment groups showed similar significant reductions in FPG (2.1-2.3 mmol/l). Working memory improved with both rosiglitazone (P < 0.001) and glyburide (P = 0.017). Improvement (25-31% reduction in errors) was most evident on the Paired Associates Learning Test and was significantly correlated (r = 0.30) with improved glycemic control as measured by FPG. CONCLUSIONS: Similar and statistically significant cognitive improvement was observed with both rosiglitazone and glyburide therapy, and the magnitude of this effect was correlated with the degree to which FPG improved. These results suggest that a cognitive benefit is achievable with pharmacological interventions targeting glycemic control.

Adult↗
PubMed2005

Changing trends in incidence and mortality of thyroid cancer in Scotland.

OBJECTIVE: The incidence of thyroid cancer is increasing in several countries. The aim was to investigate trends in the incidence and mortality of thyroid cancer in Scotland, where thyroid cancer is relatively uncommon, between 1960 and 2002. DESIGN: Descriptive epidemiological study. METHODS: Thyroid cancer registrations between 1960 and 2000 were obtained from the Scottish Cancer Registry. Mortality data (1960-2002) and population estimates were supplied by the Registrar General for Scotland. Incidence and mortality data are expressed as age-specific rates and European age-standardized rates (EASRs). RESULTS: Thyroid cancer was three times more common in females than in males and was more common in older than younger age groups. Between 1960 and 2000, the annual EASR of thyroid cancer increased from 1.76 to 3.54 per 100,000 for females (P < 0.001) and from 0.83 to 1.25 per 100,000 in males (P < 0.001). The overall thyroid cancer increase between 1975 and 2000 was primarily caused by an increase in papillary thyroid cancer, particularly over the most recent decade. The incidence of follicular thyroid cancer also increased while the incidence of anaplastic and medullary thyroid cancer did not change significantly. Mortality from thyroid cancer fell progressively between 1960 and 2002. EASR for females decreased from 1.05 to 0.28 (P < 0.001) and in males from 0.73 to 0.34 (P < 0.001). For both sexes, in general, survival at 1-, 5- and 10-year follow-up intervals from diagnosis improved steadily over the study period. In both females and males, survival from thyroid cancer was better if the diagnosis was made under the age of 50 years. CONCLUSIONS: Thyroid cancer incidence has increased in Scotland over the past 40 years. This is accompanied by a change in the distribution of histological type with a particular increase in papillary carcinoma. The reasons for this may relate partly to changes in clinical practice and histological criteria. Falling mortality in the face of increasing incidence reflects improvements in survival, which should improve further with the introduction and implementation of standardized treatment protocols.

Adolescent↗
PubMed2005

Recurrent dizzy spells: all in the head!

Hypoglycaemia is an uncommon manifestation of hypopituitarism in non-diabetic adults. A 47-year-old woman with Cushing's disease was treated with bilateral adrenalectomy and pituitary radiotherapy following unsuccessful trans-sphenoidal surgery. Twenty years later, she presented with a tonic-clonic seizure and recurrent symptoms suggestive of spontaneous hypoglycaemia. Her symptoms continued despite manipulation of her glucocorticoid replacement therapy. Recurrent severe hypoglycaemia resolved after identification and treatment of her concomitant growth hormone deficiency. In patients with hypopituitarism, undiagnosed growth hormone deficiency can influence glucose metabolism and predispose to severe hypoglycaemia.

Disease Susceptibility↗
PubMed2004

The relationship between type 2 diabetes and cognitive dysfunction: longitudinal studies and their methodological limitations.

Type 2 diabetes and dementia in the elderly are major public health problems. Cross-sectional studies have suggested that these two conditions may be inter-related, but the nature of this association is uncertain. Causation can only be established through studies with a longitudinal design, taking into account the many potential confounding factors in any study of cognition. A literature search has identified 10 studies (nine population-based and one of case-controlled design) that included a definable diabetic population and assessments of cognitive function at baseline and at follow-up. These 10 studies utilised a combination of domain-specific cognitive assessments and a clinical diagnosis of dementia in the assessment of cognitive function. Diabetes was associated with either an accelerated cognitive decline or an increased incidence of dementia in eight of nine of the population-based studies. One study demonstrated a relationship between diabetes and vascular cognitive impairment, but not with other types of dementia. No association between type 2 diabetes and cognitive decline was demonstrated in the case-controlled study. These studies provide compelling evidence to support the view that people with type 2 diabetes are at increased risk of developing cognitive impairment in comparison with the general population.

Cognition Disorders↗
PubMed2004

Food cravings during acute hypoglycaemia in adults with Type 1 diabetes.

BACKGROUND: Food craving is defined as an intense desire to eat a specific foodstuff. It may be distinguished from the sensation of hunger, which is relieved by nonspecific foodstuffs. No controlled studies have examined the effects of hypoglycaemia on food cravings. Thus, the aim of this study was to examine change in cravings for eight specified food types during euglycaemia and insulin-induced hypoglycaemia. METHODS: Thirteen adults with Type 1 diabetes attended two experimental sessions where acute hypoglycaemia was induced with either insulin aspart or human soluble insulin. Food cravings were assessed, using a questionnaire, at baseline and at the onset of the autonomic reaction to hypoglycaemia ("R"). RESULTS: The mean arterialised blood glucose concentration at baseline was 6.0+/-0.3 mmol l(-1) and at R was 1.9+/-0.4 mmol l(-1) (P<.01). Fifteen percent of subjects reported having a craving for food during euglycaemia. The prevalence increased to 65% during hypoglycaemia (P<.01). Cravings for seven of the eight food types increased during hypoglycaemia, but the greatest effect sizes (>1.0 standard deviations) were observed for three food types that had a high carbohydrate content. CONCLUSIONS: In people with Type 1 diabetes, acute hypoglycaemia produces a highly reliable generalised increase in cravings for food, particularly foodstuffs with a high content of carbohydrate. The mechanisms behind this response remain to be elicited.

Adult↗
PubMed2003

Clinical and radiological features of patients with macroprolactinaemia.

OBJECTIVES: Macroprolactin is a complex of prolactin (PRL) and IgG and may account for a significant proportion of cases of 'idiopathic hyperprolactinaemia'. In this study, we sought to determine the prevalence and clinical features of macroprolactinaemia in patients diagnosed with hyperprolactinaemia in our region, with a view to determining how patients with macroprolactinaemia should be investigated and managed. PATIENTS AND METHODS: An Immuno-1 automated immunoassay system with polyethylene glycol (PEG) precipitation was used to identify macroprolactin, with a recovery of </= 50% taken as indicating significant macroprolactinaemia. Macroprolactin was found in 58 (21%) of 273 patients with a total PRL > 700 mU/l. The clinical records of 51 (44 female) were available for retrospective review. RESULTS: The mean (range) age of patients was 39.5 (18-82) years. The median (range) concentrations for the various forms of PRL were: total PRL 1130 mU/l (728-5116), monomeric PRL 240 mU/l (50-656) and macroprolactin 895 mU/l (381-4854). Classical symptoms of hyperprolactinaemia were present in 39% of patients, although in many there were other possible explanations for their symptomatology. Pituitary adenomas were identified in six out of 36 people who underwent neuroimaging. Five of these patients had a microadenoma and one had a 10-mm macroadenoma (although, in this patient macroprolactin was identified after the discovery of the tumour). There was no relationship between macroprolactin concentrations and the presence of hyperprolactinaemic symptoms or neuroimaging abnormalities. CONCLUSIONS: Macroprolactinaemia is a common occurrence in patients with hyperprolactinaemia, but associated symptomatology may not necessarily be linked. The neuroimaging abnormalities were also probably incidental findings and it is questionable whether neuroimaging is necessary when significant macroprolactinaemia is identified and the concentration of monomeric PRL is not elevated (using the Immuno-1 assay system, following PEG precipitation).

Adenoma↗
PubMed2003

Severe hypercalcaemia secondary to isolated adrenocorticotrophic hormone deficiency and subacute thyroiditis.

Severe hypercalcaemia is usually due to either neoplastic disease or primary hyperparathyroidism. Rarer causes do exist, and exceptionally these may occur concomitantly. We describe the case of a 45-year-old man who presented in a debilitated state with severe hypercalcaemia (total serum calcium 3.56 mmol/L, albumin 35 g/L) and suppressed serum parathyroid hormone concentration. It was initially suspected that he had neoplastic disease, but routine thyroid function tests demonstrated evidence of thyrotoxicosis [thyroid-stimulating hormone <0.05 mU/L (0.15-3.5); free thyroxine 75 pmol/L (8-27); total tri-iodothyronine 7.0 nmol/L (1.0-2.6)], which was probably secondary to a silent or subacute thyroiditis. After extensive investigation, it was established that the patient also had isolated adrenocorticotrophic hormone deficiency, presumably secondary to lymphocytic hypophysitis. Glucocorticoid therapy resulted in a dramatic improvement in the patient's clinical state and 1 year later he remained euthyroid and normocalcaemic.

Adrenocorticotropic Hormone↗