Incidental bile duct adenomas in a patient with obstructive jaundice.
Explore the source record for details and available documents.
Adenoma, Bile Duct↗
Biomedical subjects
T Diamond
Publications and source records attributed to T Diamond.
The effect of combined androgen blockade on bone turnover and bone mineral densities in men treated for prostate carcinoma: longitudinal evaluation and response to intermittent cyclic etidronate therapy.
BACKGROUND: Androgen receptor blocking agents have become an established form of therapy for men with disseminated prostate carcinoma. The purpose of this study was to evaluate markers of bone turnover and to measure bone mineral densities (BMD) in men with disseminated prostate carcinoma treated with combined androgen blockade prior to and after 6 months of intermittent cyclic etidronate therapy. METHODS: Twelve consecutive men with disseminated prostate carcinoma were evaluated at 0, 6, and 12 months after treatment with a long acting gonadotropin-releasing hormone agonist (goserelin acetate) and an androgen antagonist (flutamide). During the 6-12 month period, patients were treated with adjuvant intermittent cyclic etidronate therapy and calcium supplementation. Lumbar spine BMD was measured by spinal quantitative computed tomography (QCT) and femoral neck BMD by dual energy X-ray absorptiometry (DXA). RESULTS: Combined androgen blockade resulted in all men achieving serum free testosterone concentrations of <2.2 pmol/L (normal range, 38-114 pmol/ L). The mean serum prostate specific antigen activities decreased from 130.8+/-46 to 6.9+/-4.4 ng/mL (P < 0.05). Although serum calcium, parathyroid hormone, and 25-hydroxyvitamin D measurements remained unchanged, serum bone Gla-protein concentrations and urinary deoxypyridinolene excretion rates increased significantly (P < 0.01, respectively). Mean lumbar spine QCT decreased by 6.6+/-1.5% from 76.5 mg/cm3 (95% confidence interval [95% CI, 57-96 mg/cm3) to 73.9 mg/cm3 (95% CI, 55-93 mg/cm3) (P < 0.001) and mean femoral neck DXA decreased by 6.5+/-1.3% from 0.94 g/cm2 (95% CI, 0.81-1.07 g/cm2) to 0.91 g/cm2 (95% CI, 0.79-1.04 g/cm2) (P < 0.001). After treatment with adjuvant intermittent cyclic etidronate, mean lumbar spine QCT increased by 7.8+/-3.7% to a final value of 75 mg/cm3 (95% CI, 48.7-101 mg/cm3) (P=0.001 compared with the initial 6 months without intermittent cyclic etidronate therapy). Significant increases in BMD also were observed in the femoral neck and Ward's triangle. CONCLUSIONS: Androgen receptor blocking agents have an established role in the treatment of disseminated prostate carcinoma. However, combined androgen blockade in elderly men with disseminated prostate carcinoma results in high bone turnover with significant cancellous bone loss. The results of this study show that adjuvant therapy with intermittent cyclic etidronate may prevent these changes and decrease the risk of spinal fractures.
Absorptiometry, Photon↗
Hip fracture in elderly men: the importance of subclinical vitamin D deficiency and hypogonadism.
OBJECTIVE: To determine the major risk factors for hip fracture in elderly men. DESIGN: Prospective recruitment, followed by analysis of clinical and biochemical variables. PATIENTS AND SETTING: Men aged 60 years and older who presented to St George Hospital (a 650-bed tertiary-care centre) in 1995, comprising all 41 men with hip fractures, as well as 41 hospital inpatient and 41 outpatient control subjects without hip fractures. MAIN OUTCOME MEASURES: Osteoporotic risk factors (including age, body weight, comorbid illnesses, alcohol intake, cigarettes smoked, and corticosteroid use) and serum concentrations of creatinine, urea, calcium, albumin, alkaline phosphatase, parathyroid hormone, 25-hydroxyvitamin D and free testosterone. RESULTS: There were no significant differences between the hip fracture and two control groups on any of the osteoporotic risk factors. Men with hip fracture had significantly lower mean serum 25-hydroxyvitamin D concentration (45.6 nmol/L; 95% confidence interval [CI], 36.9-52.3 nmol/L) than both inpatient (61.1 nmol/L; 95% CI, 50.0-72.2 nmol/L) and outpatient (65.9 nmol/L; 95% CI, 59.0-72.8 nmol/L) controls (P=0.007). Subclinical vitamin D deficiency (defined as <50 nmol/L serum 25-hydroxyvitamin D) was 63% in the fracture group, compared with 25% in the control groups combined (odds ratio, 3.9; 95% CI, 1.74-8.78; P=0.0007). Inpatients with and without hip fractures had significantly lower mean serum albumin, calcium and free testosterone concentrations than outpatients (P< 0.05). In a multiple regression analysis, subclinical vitamin D deficiency was the strongest predictor of hip fracture (beta [regression coefficient], 0.34+/-0.19; P=0.013). CONCLUSIONS: Subclinical vitamin D deficiency in Australian men may contribute significantly to the development of hip fracture through the effects of secondary hyperparathyroidism, resulting in increased bone loss.
Aged↗
Tumor expression studies indicate that HEM-1 is unlikely to be the active factor in oncogenic osteomalacia.
HEM-1 was isolated as a putative factor responsible for oncogenic osteomalacia by Kumar et al. (Proc Assoc Am Phys 107:296-305; 1995). The cDNA was identified on the basis of PTH-like immunoreactivity; however, no studies have been reported of the expression of HEM-1 mRNA in oncogenic osteomalacia tumors. In this study, expression of HEM-1 mRNA was investigated in two oncogenic osteomalacia tumors and in a series of normal tissues. An HEM-1 PCR product was amplified from a cDNA library from one of the tumors, with six base changes identified, as compared with the published sequence. No expression was detected, however, in the oncogenic osteomalacia tumors either by Northern blot analysis or by reverse transcriptase PCR. This indicates that, although a region of HEM-1 sequence is present in the tumor cell cDNA library, any HEM-1 expression must be at very low levels. It is unlikely, therefore, that the HEM-1 product is the active factor responsible for oncogenic osteomalacia. In the normal tissues examined, human placenta, fibroblasts, parathyroid gland, liver, fetal bone, and rat kidney cortex, HEM-1 mRNA was not detected, suggesting that it does not have a physiological role in these tissues.
Adenocarcinoma↗
Body mass and body composition after total thyroidectomy for benign goiters.
To date there are no data available as to whether postmenopausal women who undergo total thyroidectomy for benign euthyroid goiter demonstrate changes in body mass or body composition. We prospectively evaluated 8 postmenopausal women (mean age 57 +/- 7; range 48 to 70 years) who underwent total thyroidectomy for benign goiter. All patients were euthyroid preoperatively (serum free thyroxine [FT4] 12.7 +/- 0.6 pmol/L and serum thyrotropin [TSH] 0.98 +/- 0.2 mU/L) and were commenced on adequate thyroxine replacement immediately postoperatively in order to maintain a serum TSH within the normal range (0.5-4 mU/L). Body mass, body composition, and thyroid function were assessed preoperatively, and at 4 and 12 months postoperatively. Body composition was assessed by anthropometry and dual energy x-ray absorptiometry (Lunar DPX-L scanner). Eight healthy postmenopausal women without evidence of thyroid disease matched for age, weight, and estrogen therapy who were followed over the same period were used as controls. All patients were maintained in a euthyroid status throughout the study. No significant changes in body mass or any parameter of body composition were demonstrated at 4 and 12 months postoperatively. Similar findings were recorded in our control group. We conclude that total thyroidectomy in euthyroid postmenopausal women with benign goiter does not result in a significant change in either body mass or body composition if adequate thyroxine replacement is maintained.
Aged↗
Effects of glibenclamide on blood pressure and cardiovascular responsiveness in non-insulin dependent diabetes mellitus.
OBJECTIVE: To compare the effects of chronic glibenclamide therapy and placebo on blood pressure and cardiovascular responsiveness in patients with non-insulin-dependent diabetes. DESIGN AND METHODS: Fourteen patients with non-insulin-dependent diabetes mellitus, seven of whom were receiving angiotensin converting enzyme inhibitor therapy, received glibenclamide or placebo for 1 month in a double-blind, randomized crossover study. At the end of each treatment period patients attended for studies of forearm vascular responsiveness to intra-brachial arterial infusions of angiotensin II, acetylcholine, sodium nitroprusside and noradrenaline, responses of blood pressure to intravenous infusions of noradrenaline and angiotensin II and 24 h ambulatory blood pressure monitoring. RESULTS: Administration of glibenclamide produced significantly better glycaemic control than placebo (fasting blood glucose level 8.5 +/- 2.4 versus 13.5 +/- 4.5 mmol/l, P < 0.001) and plasma insulin levels were significantly higher during glibenclamide treatment than they were with placebo (12.9 +/- 4.4 versus 9.2 +/- 4.1 mU/l, P < 0.05). Body weights at the ends of the glibenclamide treatment and placebo phases were similar (92.1 +/- 14.3 versus 91.1 +/- 14.3 kg, P = 0.085). Night-time systolic blood pressures were significantly higher during glibenclamide treatment than they were with placebo (128 +/- 17 versus 118 +/- 10 mmHg, P < 0.05) due to there being a smaller day-night difference in systolic blood pressure during glibenclamide treatment that appeared to occur mainly in patients receiving angiotensin converting enzyme inhibitors. Responses of diastolic blood pressure to intravenous infusion of angiotensin II and forearm vascular responses to intra-brachial arterial infusion of angiotensin II were significantly greater during glibenclamide treatment than they were with placebo (P < 0.05). However, the enhancement of forearm vascular responses during glibenclamide treatment appeared to be restricted to patients receiving angiotensin converting enzyme inhibitors. Responses of blood pressure to intravenous infusion of noradrenaline and forearm vascular responses to infusions of noradrenaline, acetylcholine and nitroprusside did not differ between glibenclamide treatment and placebo; neither did basal forearm vascular resistance. CONCLUSIONS: Glibenclamide therapy is associated with greater responses of blood pressure and forearm vascular responses to infusion of angiotensin and higher nocturnal blood pressures. This effect appears to be influenced by concomitant angiotensin converting enzyme inhibition.
Acetylcholine↗
Acute effects of oral glibenclamide on blood pressure and forearm vascular resistance in diabetics.
1. To determine the effects of an acute oral dose of glibenclamide on blood pressure (BP), basal forearm vascular resistance (FVR) and FVR responses to the K+(ATP) channel activating vasodilator diazoxide, a placebo-controlled, double-blind cross-over study was performed in eight male volunteers with non-insulin-dependent diabetes mellitus. 2. Changes in vascular responses to progressively increasing concentrations of diazoxide (3.75-30 mg/kg per min) and noradrenaline (25-100 ng/kg per min) were measured by venous occlusion plethysmography. 3. Glibenclamide significantly lowered plasma glucose levels compared with placebo (P < 0.02) and attenuated the decrease in FVR (P < 0.05) and the decrease in systolic BP (P < 0.05) that followed a meal. However, vasodilator responses to diazoxide were potentiated by the administration of oral glibenclamide (P < 0.01). 4. Acute administration of oral glibenclamide attenuates the normal decrease in FVR and systolic BP that follows a meal and potentiates rather than inhibits forearm vasodilator responses to intra-arterial diazoxide, probably via indirect humoral effects. These results suggest that glibenclamide has direct or indirect vasoconstrictor effects that antagonize the normal increase in forearm blood flow that follows a meal and that the inhibition of vascular K+(ATP) channels following acute oral glibenclamide administration is clinically insignificant compared with other indirect vascular effects of the drug.
Adult↗
Familial slipped capital femoral epiphysis: a report and considerations in management.
BACKGROUND: Familial inheritance of slipped capital femoral epiphysis (SCFE) is known. It has not been described in non-identical twins. A family where the mother and three of five siblings developed SCFE were investigated and managed. METHODS: Anthropometric measurement consisted of height-weight ratios. Serum sex hormone levels and bone Gla Protein was measured. Bone mineral densities were evaluated. RESULTS: The affected siblings had higher bodyweight percentiles. Other investigations were within normal limits. CONCLUSION: The unfavourable height-to-weight ratio was one of the mainstays in developing a management protocol for all siblings. The management protocol developed for the family is discussed.
Algorithms↗
Camurati-Engelmann disease: two case reports describing metadiaphyseal dysplasia associated with cerebellar ataxia.
This clinical report describes two patients presenting with progressive diaphyseal dysplasia (Camurati-Engelmann Disease) and cerebellar ataxia. The clinical and magnetic resonance imaging findings of the bony and cerebellar lesions are presented.
Aged↗
Renal function in jaundiced patients: a prospective analysis.
A prospective analysis was undertaken to assess renal function in patients with obstructive jaundice. A total of 59 jaundiced patients (serum bilirubin > 100 mumol/l) undergoing biliary decompression by surgical, endoscopic or radiological means received prophylactic fluid volume expansion (3 litres crystalloid fluid intravenously) during the 24 hours before intervention. Renal function (urea and electrolytes, creatinine, creatinine clearance, urinary output) was assessed preoperatively and on days 1-7 and on day 28 postoperatively. Two jaundiced patients (3.4%) developed renal failure (urinary output < 400 ml in 24 hours in the presence of an increased serum urea and/or creatinine) and subsequently died. The overall incidence of post-procedural renal impairment (urinary output < 800 ml in 24 hours) was 10.2%. It is concluded that, with vigilant control of fluid and electrolyte balance and pre-procedural intravenous volume expansion, the incidence of renal dysfunction in patients with obstructive jaundice is not as high as previously reported.
Aged↗
Outcome of palliative and gastric bypass surgery for pancreatic head carcinoma in 126 patients.
Explore the source record for details and available documents.
Drainage↗
Bronchobiliary fistula complicating open cholecystectomy.
Explore the source record for details and available documents.
Biliary Fistula↗
Possible adverse fetal effect of insulin lispro.
Explore the source record for details and available documents.
Abnormalities, Drug-Induced↗
Experimental study in bile duct-ligated rats of vasopressin and preoperative volume loading to prevent hypotensive crises.
Explore the source record for details and available documents.
Animals↗
Biochemical, histomorphometric and densitometric changes in patients with multiple myeloma: effects of glucocorticoid therapy and disease activity.
It is unknown whether bone changes which can occur in multiple myeloma (MM) are due to cytokine-induced osteoclastic bone resorption from a clone of abnormal plasma cells or high-dose glucocorticoid therapy. We studied 25 MM patients treated for 1-12 years with combination chemotherapy, subdivided into two groups. Group 1 consisted of 12 patients with stage I and II myeloma and group 2 consisted of 13 patients with stage III MM. Their serum biochemistry, tetracycline-labelled bone histomorphometry and bone densitometry were compared to age- and sex-matched controls. Patients with MM demonstrated increased indices of bone resorption (P < 0.001 versus controls) and, to a lesser extent, increased indices of bone formation (P < 0.01 versus controls). No patient had evidence of a mineralization defect. Lumbar spine, femoral neck and total body bone mineral density measurements (BMD) were significantly lower in group 2 compared with group 1 (P < 0.05). Following 12 months of therapy, lumbar spine BMD decreased by 6.6% (95% CI, 2.7% to -9.3%) and femoral neck BMD decreased by 9.5% (95% CI, -3.2% to -15.9%). In a stepwise regression analysis, cumulative prednisolone dosage (B Coef. = -0.39; P = 0.03) and plasma cell infiltrate (B Coef. = -0.08; P = 0.05) were the most important predictors of lumbar spine bone loss, whereas serum paraprotein (B Coef.= -0.35; P = 0.02) and plasma cell infiltrate (B Coef. = -0.20; P = 0.04) were the most important predictors of femoral neck bone loss. We conclude that MM is characterized by high bone turnover with osteoblast-osteoclast uncoupling. Both disease activity and high-dose glucocorticoid therapy may be responsible for the ongoing bone loss seen with MM.
Absorptiometry, Photon↗
Acute effects of oral glibenclamide on blood pressure and forearm vascular resistance in diabetics.
1. To determine the effects of an acute oral dose of glibenclamide on blood pressure (BP), basal forearm vascular resistance (FVR) and FVR responses to the K+ATP channel activating vasodilator diazoxide, a placebo-controlled, double-blind cross-over study was performed in eight male volunteers with non-insulin-dependent diabetes mellitus. 2. Changes in vascular responses to progressively increasing concentrations of diazoxide (3.75-30 mg/kg per min) and noradrenaline (25-100 ng/kg per min) were measured by venous occlusion plethysmography. 3. Glibenclamide significantly lowered plasma glucose levels compared with placebo (P < 0.02) and attenuated the decrease in FVR (P < 0.05) and the decrease in systolic BP (P < 0.05) that followed a meal. However, vasodilator responses to diazoxide were potentiated by the administration of oral glibenclamide (P < 0.01). 4. Acute administration of oral glibenclamide attenuates the normal decrease in FVR and systolic BP that follows a meal and potentiates rather than inhibits forearm vasodilator responses to intra-arterial diazoxide, probably via indirect humoral effects. These results suggest that glibenclamide has direct or indirect vasoconstrictor effects that antagonize the normal increase in forearm blood flow that follows a meal and that the inhibition of vascular K+ATP channels following acute oral glibenclamide administration is clinically insignificant compared with other indirect vascular effects of the drug.
Adenosine Triphosphate↗
Delayed presentation of porta hepatis injury following blunt abdominal trauma.
A 73 year old lady developed abdominal pain, anaemia and obstructive jaundice 18 days after a road traffic accident. The jaundice was due to compression of the biliary confluence by a haematoma which was caused by a laceration of the left portal vein. The portal vein was repaired (lateral venorrhaphy) and post-operative recovery was uncomplicated. Porta hepatis injuries are difficult to diagnose and delayed presentation is not uncommon. Significant morbidity and mortality may ensue if aggressive management is not adopted.
Abdominal Injuries↗
Comparative effects of glibenclamide and metformin on ambulatory blood pressure and cardiovascular reactivity in NIDDM.
OBJECTIVE: To compare the effects of chronic glibenclamide and metformin therapy on blood pressure (BP) and cardiovascular responsiveness in patients with NIDDM. RESEARCH DESIGN AND METHODS: Fourteen patients with NIDDM received metformin or glibenclamide for 1 month in a double-blind, randomized crossover study. At the end of each treatment period, patients were tested for forearm vascular responsiveness to intrabrachial arterial infusion of diazoxide (an ATP-sensitive potassium channel opener), acetylcholine, sodium nitroprusside, and norepinephrine, BP responses to intravenous infusions of NE and angiotensin II, BP responses to cold pressor testing and isometric exercise, and 24-h ambulatory BP monitoring. RESULTS: Metformin and glibenclamide produced similar glycemic control. Mean 24-h BPs did not differ between the two groups, but mean 24-h heart rates were significantly lower (75 +/- 6 bpm vs. 80 +/- 6 bpm) on glibenclamide therapy than on metformin. Plasma norepinephrine levels were significantly higher on glibenclamide (6.41 +/- 1.77 vs. 4.26 +/- 1.54 mmol/l, P < 0.01), and systolic BP responses to intravenous norepinephrine and angiotensin II were significantly higher on glibenclamide than on metformin (P < 0.02 and P < 0.05, respectively). Systolic BP responses to cold pressor testing appeared higher on glibenclamide than on metformin, but the difference did not quite achieve statistical significance (P = 0.052). Baseline forearm vascular resistance did not differ between the two drugs, nor did forearm vascular resistance responses to diazoxide, acetylcholine, sodium nitroprusside, and norepinephrine differ. CONCLUSIONS: Glibenclamide therapy is accompanied by greater systolic BP responses to norepinephrine and angiotensin II and higher plasma norepinephrine levels than those that occur on metformin therapy. Lower heart rates on glibenclamide therapy despite evidence of greater sympathetic activity suggests that glibenclamide may have negative chronotropic effects.
Acetylcholine↗