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561 patients with primary hyperparathyroidism were followed between 1961 and 1994. Relative survival was compared to that of the Australian population studied during the same time interval. Mortality was significantly greater in the hyperparathyroid population (P<0.001). Mortality was not greater in the patients with serum calcium levels >3.00 mmol/L compared to those with a serum calcium levels <3.00 mmol/L. 113 patients did not have parathyroid surgery. Their relative survival was not significantly different from those who had surgery but their mean serum calcium and parathyroid hormone (PTH) levels were significantly lower than those who had surgery. A re-analysis of the 453 patients followed between 1972 and 2011 was carried out and a 20-year survival analysis made of those diagnosed between 1972 and 1981 and those diagnosed between 1982 and 1991. The latter group had significantly worse relative mortality than the former group (P<0.001) but was significantly older at the time of diagnosis (56.94 ± 14.83 vs 52.01 ± 13.58, P<0.001). The serum calcium and serum PTH levels were not significantly different between these two groups.

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BACKGROUND: Potent oral bisphosphonates are the mainstay of therapy for osteoporosis. However, there are patients who cannot have oral bisphosphonates (e.g. because of gastrointestinal side-effects). Therefore, we wanted to examine the effects of intermittent i.v. pamidronate (APD) on bone mineral density (BMD) in patients who needed bisphosphonate therapy but could not have oral bisphosphonates. AIM: To assess BMD before and after intermittent i.v. APD in patients requiring a bisphosphonate either for the prevention of osteoporosis on concurrent steroid therapy or for the treatment of osteoporosis. METHODS: This was a retrospective audit of 84 consecutive patients at risk of fractures commencing APD between October 1997 and May 2000. Patients were treated with intermittent i.v. APD. BMD as measured by dual-energy X-ray absorptiometry before and after APD was the main outcome. RESULTS: The mean length of treatment and mean total APD dose were 16.8 +/- 7.0 months and 186.1 +/- 79.5 mg respectively. The reasons for using APD were failure to qualify for oral bisphosphonates on the pharmaceutical benefits scheme due to lack of documented minimal trauma fractures (58%), symptomatic gastro--oesophageal disease (20%), intolerance of oral bisphosphonates (18%) and lack of efficacy of calcitriol (4%). Mean baseline T-score at lumbar (L) 2-4 spine and femoral neck were -1.54 +/- 1.22 and - 2.87 +/- 1.19, respectively. From baseline to after APD treatment, there was a significant increase in L2-4 BMD (0.883 +/- 0.175 vs 0.912 +/- 0.176 g/cm(2), P < 0.001, mean increase +3.5%), in femoral neck BMD (0.667 +/- 0.137 vs 0.680 +/- 0.134 g/cm(2), P= 0.001, mean increase +2.1%) and in trochanteric BMD (0.549 +/- 0.129 vs 0.566 +/- 0.132 g/cm(2), P < 0.001, mean increase +3.1%). One-third of the patients were on oral glucocorticoids at the time of the present study and they had a similar increase in BMD compared to patients not on gluco-corticoids. Mild side-effects occurred in seven patients, none of whom discontinued treatment. CONCLUSION: Intermittent APD increases BMD and may be a suitable alternative for patients who cannot have oral bisphosphonates.

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The aim of this study was to determine the prevalence and extent of glycemic excursions (hypo- and hyperglycemic) in elderly patients with well-controlled type 2 diabetes using a Continuous Glucose Monitor System (CGMS) (Medtronic MiniMed). Elderly patients (>65 years old) with type 2 diabetes were recruited if their glycosylated hemoglobin (HbA1c) was <7.5% and if their oral hypoglycemic therapy included a sulfonylurea. Patients were asked to undergo two consecutive 72-h periods of continuous glucose monitoring at baseline and then again at 1 month (total 288 h). Patients were asked to record four self-monitored capillary blood glucose levels each day for calibration of the monitor and also to record meal times, exercise, and symptoms of hypoglycemia. The number of hyperglycemic (>144 mg/dL), hypoglycemic (<50 mg/dL), and borderline-hypoglycemic (50-65 mg/dL) events were determined (an event was defined as a glucose value that persisted for at least 15 min with or without symptoms). Twenty-five patients (21 men, four women) 73.9 +/- 4.4 years old with an HbA1c of 6.2 +/- 0.8% were each monitored for an average of 187.57 h. The mean glucose values were: fasting, 139 +/- 40 mg/dL; 2 h post-breakfast, 167 +/- 58 mg/dL; 2 h post-lunch, 157 +/- 53 mg/dL; and 2 h post-dinner, 149 +/- 49 mg/dL. Twenty patients (80%) experienced a total of 103 hypoglycemic events, and 14 of these patients experienced 54 events where the glucose levels were 144 mg/dL 2 h postprandial) were recorded after 57% of all meals (breakfast 60%, lunch 57.5%, dinner 55.2%). The CGMS was generally well tolerated, but 52% of patients could not be studied for the full 12 days of monitoring. Thus hypoglycemia and excessive postprandial glycemic excursions are common in well-controlled patients with type 2 diabetes treated with a sulfonylurea with or without metformin. The CGMS is a useful research and clinical tool to assess glycemia in patients with type 2 diabetes but is not tolerated by all subjects.

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OBJECTIVE: Although it is accepted that elevated plasma homocysteine (tHcy) levels occur in end-stage renal disease and type 2 diabetes, the changes with milder renal dysfunction (e.g., microalbuminuria) are less clearly established. This study explores the relationship among tHcy, creatinine clearance (Ccr), and albumin excretion rate (AER) in a population with type 2 diabetes. RESEARCH DESIGN AND METHODS: A total of 260 patients with type 2 diabetes were screened in our outpatient clinic during 10 months. Fasting blood samples were collected, and AER was calculated from an overnight timed urine sample. Ccr was calculated using the Cockroft-Gault formula. RESULTS: A total of 198 subjects (76%) had normoalbuminuria (<20 microg/min), 50 subjects (19%) had microalbuminuria (20-200 microg/min), and 12 subjects (5%) had macroalbuminuria (>or=200 microg/min). Those with microalbuminuria had higher levels of tHcy than those with normoalbuminuria (13.2 +/- 7.8 vs. 11.3 +/- 4.6 micromol/l, P < 0.05). Patients were then subdivided based on low Ccr (<80 ml x min(-1) x 1.73 m(-2)) and normal Ccr (>or=80 x min(-1) x 1.73 m(-2)). None of the patients with macroalbuminuria had normal Ccr. In those with normoalbuminuria, tHcy levels were higher than in those with low Ccr than in those with normal Ccr (12.0 +/- 4.6 vs. 10.0 +/- 4.4 micromol/l, P < 0.01). The same was found for those with microalbuminuria (low Ccr versus normal Ccr: 14.6 +/- 9.0 vs. 10.2 +/- 2.8 micromol/l, P < 0.02). For normal Ccr, tHcy was similar irrespective of AER (normoalbuminuria versus microalbuminuria: 10.0 +/- 4.4 vs. 10.2 +/- 2.8 micromol/l, NS). For low Ccr, tHcy was higher in those with microalbuminuria versus normoalbuminuria (14.6 +/- 9.0 vs. 12.0 +/- 4.6 micromol/l, P = 0.01). Using multivariate regression, Ccr, but neither AER nor the presence of albuminuria, was an independent predictor of tHcy. CONCLUSIONS: These data strongly suggest that in patients with type 2 diabetes, the relationship between plasma tHcy and AER is largely due to associated changes in renal function, as defined by Ccr.

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UNLABELLED: The presence of recurrent medullary thyroid carcinoma (MTC) can be detected early by measurement of serum calcitonin levels, but the localization of recurrent tumors is often difficult. METHODS: We compared 99mTc-sestamibi scans with computed tomographic (CT) scans in 10 patients with recurrent MTC, who had basal serum calcitonin values ranging from 220-61800 ng/liter. Two patients additionally had bone scans performed because of the clinical suspicion of bone metastases. RESULTS: Seven of the 10 patients had at least one site of abnormal 99mTc-sestamibi uptake, and all of these patients had basal serum calcitonin values > 6000 ng/liter. Only five of the 10 patients had abnormal CT scans. Technetium-99m-sestamibi scans detected 22 abnormal sites in the soft tissues of the neck and chest, while CT scans detected only 11 lesions in the neck and chest. Five of these sestamibi positive sites (in the neck and mediastinum of one patient) were confirmed histologically to represent MTC. When imaging the liver, CT scans detected 47 lesions in three patients while 99mTc-sestamibi scans detected none. One of these liver lesions was confirmed as MTC histologically. When imaging bone in two of the patients, the bone scans detected 17 abnormal sites, while 99mTc-sestamibi scans detected six abnormal sites. CONCLUSION: Technetium-99m-sestamibi scans complement CT and bone scans in the localization of recurrent MTC in patients with extremely high calcitonin levels. Technetium-99m-sestamibi scans are more sensitive than CT scans in the assessment of the soft tissues of the neck and chest, but CT is more appropriate for imaging hepatic lesions and bone scans are better for imaging bone lesions. Technetium-99m-sestamibi scans are unlikely to be abnormal in patients with only mild elevation of calcitonin.

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An homogeneous phase radioassay (HRA) for antithyroglobulin autoantibodies (TgAb) in serum was investigated. In this method TgAb is allowed to react with 125I-Tg in solution and the immune complexes formed are separated by precipitation with sheep anti-human gammaglobulin. HRA proved to be suitable for the screening of sera prior to thyroglobulin (Tg) radioimmunoassay; being both sensitive, and unaffected by high endogenous levels of Tg. HRA was more sensitive than either of two commercial TgAb kits; a hemagglutination assay (Wellcome Australia Ltd.) and a solid phase radioassay (CIS France). Positive responses were obtained with 4 out of 42 normal subjects (titers up to 1/10), 24 out of 31 with untreated Graves' disease (titers up to 1/10,000) and all out of 18 with Hashimoto's thyroiditis (titers up to 1/10,000). Binding of 125I-Tg was displaceable with added unlabelled Tg, but in no case could it be abolished with less than 1,000 micrograms/l. Some sera exhibited more than one class of binding site and variation in both affinity and capacity for Tg was observed. It was concluded that the use of an assay standard for the reporting of results in units of concentration is invalid, although units of TgAb activity may be used as long as the analytical method is specified. Serum levels of TgAb may also be reported in semi-quantitative terms, such as in this report where a binding titer is used, or alternatively, antigen binding capacity may be reported.

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Left ventricular mass (LV mass) and function were assessed in 16 acromegalic patients by echocardiography, and rest and exercise gated blood pool scanning (GBPS) respectively. At the time of study, five patients had active acromegaly, five were hypertensive and three had coexisting coronary artery disease. Increased LV mass was found in six (38%) patients, of whom four were hypertensive and two others had active acromegaly of long duration. One normotensive patient, who did not have coronary disease, had increased LV mass associated with persistently elevated growth hormone (GH) levels for the previous 11 years. Abnormal LV function, as detected by GBPS, occurred only in the three patients with coronary disease. Thus, acromegaly is associated with increased LV mass in hypertensive patients and normotensive patients who have prolonged elevation of GH levels prior to adequate treatment. We found no detectable impairment of LV function, at rest or exercise unless other cardiac disease was present.

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1 The effects of the beta 2-adrenoceptor stimulant, salbutamol, on cardiac metabolism have been studied in conscious mongrel dogs. The potential effects of anaesthesia on the study of cardiac metabolism have been avoided by prior implantation of arterial (A) and coronary sinus (CS) catheters for blood sampling and a central venous catheter for infusion. Extraction of substrates for myocardial energy metabolism (CA-CS) was assessed 3 to 24 days post-operatively. A 100 micrograms bolus of salbutamol was given followed by an infusion of 3 micrograms/min for 1 h. 2 Although heart rate increased significantly from 106 to 165 beats/min, fractional extraction of oxygen tended to fall from 84% to 77%. Thus an increase in coronary blood flow rather than in oxygen extraction must have maintained an oxygen supply commensurate with the salbutamol-induced tachycardia. 3 Neither CA-CS glucose nor fractional glucose extraction altered significantly during salbutamol infusion despite increases in arterial concentration (CA) of glucose and arterial insulin immunoreactivity and a decrease in CA of free fatty acids (FFA). This suggests that an insulin-antagonistic action accompanies the infusion of salbutamol. 4 The fractional extraction of lactate increased during salbutamol infusion. In part, this may have been a reflection of a decreased myocardial extraction of FFA with salbutamol in this model.

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The relative absorption of saccharides on different chain length has been reexamined. Whether glucose is administered as a monosaccharide, a disaccharide (maltose), an intermediate polysaccharide mixture with a mean chain length of five glucose units (Caloreen), or a polysaccharide (starch), the rate of rise and fall in blood glucose concentration is similar in healthy subjects. In a maturity onset diabetic, peak blood glucose is similar whether monosaccharide or Caloreen is ingested. Plasma insulin and plasma free fatty acid responses to glucose saccharide ingestion do not appear to be affected by chain length. The dietary form in which starch is administered, rather than chain length, is probably important.

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1. Infusion of salbutamol (3.0 microgram/min after a bolus injection of 100 microgram) produced hypokalaemia in conscious dogs. 2. Measurement of arterial and coronary sinus potassium differences revealed no significant potassium loss from the heart with established hypokalaemia. 3. Shortly after the initial salbutamol bolus and before steady-state hypokalaemia had been achieved during salbutamol infusion, a prolongation of QTc occurred; this corresponded to a significant myocardial potassium of -0.12 mmol/l plasma. 4. Urinary electrolyte excretions indicated that the hypokalaemia was not due to urinary potassium loss. 5. It was deduced that potassium had moved intracellularly. No change in hydrogen ion status occurred to account for this. Pronounced rises in plasma insulin immunoreactivities during salbutamol infusions suggested this as one mechanism for potassium shifts.

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Significant uptake and release of immunoreactive insulin by the heart have been observed in man, and this is related to plasma insulin levels. Exercise and the fed state appear to affect the myocardial handling of insulin. The findings could not be related to myocardial carbohydrate metabolism, but could, during exercise, be related to myocardial lipid metabolism.

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Plasma lipids, blood glucose, and urinary glucose excretion were measured in 270 juvenile diabetic children upon admission to and throughout periods of summer camping during which the effect of a usual and a modified diabetic diet was assessed. The usual diabetic diet contained 700-1,500 mg. cholesterol daily with a polyunsaturated/saturated (P/S) ratio of 0.1, while the modified diet limited cholesterol to 300 mg. daily with a P/S ratio of 1.0. Both diets maintained calories with 40 per cent as fat, 40 per cent as carbohydrate, and 20 per cent as protein. Analysis of fasting blood glucose, qualitative and quantitative glucose excretion, and body weight indicated that groups were comparable except for the diet used. Elevated mean levels of cholesterol and triglycerides were approximately equally distributed in diabetic children of both sexes upon admission to camp, with 24 per cent demonstrating hyperlipoproteinemia. Eleven per cent had type II, 10 per cent type IV, and 3 per cent type V hyperlipoproteinemia upon admission. After following the usual diet, 21 per cent were type II, 1 per cent type IV, and none type V, with no reduction in the over-all incidence of hyperlipoproteinemia despite lower triglyceride and glucose levels. After consumption of the modified diet, hyperlipoproteinemia was reduced to 5 per cent, with 4 per cent type II and 1 per cent type IV. Results of this study indicated that plasma lipids in juvenile diabetics were elevated when first observed and that the control of blood sugar levels along with a diabetic diet with lower cholesterol and increased polyunsaturated fat significantly reduced the incidence of hyperlipoproteinemia more effectively than control of blood sugar levels alone.

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Eight male patients with cystic fibrosis, normal nutrition, normal physical activity, relatively mild pulmonary disease, no evidence of liver disease and no family history of diabetes mellitus underwent a series of carbohydrate tolerance tests in comparison with a group of 18 normal male subjects matched for age and body weight. Compared with the normal group, the patients with cystic fibrosis had significantly impaired glucose tolerance and significantly lower serum immunoreactive insulin levels during oral and intravenous glucose tolerance tests; serum insulin levels were also significantly lower after intravenous administration of tolbutamide in the patients with cystic fibrosis, but the reduction in blood glucose concentration in each group was not significantly different. During an intravenous insulin test, the decrease in blood glucose concentration was the same for both groups, in spite of significantly lower serum insulin levels in the patients with cystic fibrosis .The percentage fall in plasma free fatty acids was at least as great in the patients with cystic fibrosis as in normals during the test procedures; while a significant decrease in plasma alpha-amino nitrogen after intravenously administered insulin was seen only in the patients with cystic fibrosis. These studies suggest that the carbohydrate intolerance of cystic fibrosis is consequent upon an impaired insulin response to glucose, but that this insulin deficiency is partly compensated for by increased peripheral tissue sensitivity to insulin.

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