Salicylate use: a negative predictive factor for finding pathology explanatory for iron deficiency anaemia.

PURPOSE: To determine whether the use of salicylates is a predictive factor for detecting explanatory pathology during gastroscopy or colonoscopy procedures in patients with iron deficiency anaemia (IDA). METHODS: This retrospective study included patients who underwent a gastroscopy and/or a colonoscopyto determine the cause of IDA at Treant Healthcare, hospital location Scheper in Emmen, the Netherlands, between 2010 and 2016. The study compared two groups. The first group consisted of patients who were not taking antithrombotics at the time of, and during the last six months prior to, the endoscopy. The second group consisted of patients who used salicylates at the time of, and during the last six months prior, to the endoscopy. Data were collected on whether and which explanatory pathology was found in the endoscopic evaluation. RESULTS: In total, 464 patients were included, of whom, 174 were using a salicylate and 290 were not. In 41.2% of the patients, explanatory pathology was found, which was not significantly different between the two groups with univariate analysis (p = 0.207). However, the patients in the group of salicylate users were significantly older and more often male. When correcting for these differences in group characteristics during multivariate analysis, the use of salicylates was found to be a negative predictive factor for finding explanatory pathology (p < 0.001; OR 2.307). CONCLUSION: When determining the chance of finding explanatory pathology during endoscopic evaluation in patients with IDA, the use of salicylates should be taken into account as a negative predictive factor for finding explanatory pathology during endoscopic evaluation.

Transient thyroiditis after parathyroidectomy for tertiary hyperparathyroidism.

Thyrotoxicosis due to thyroiditis is predominantly caused by infection or autoimmune disease of the thyroid. Parathyroid surgery however, is a lesser known cause of thyroiditis, due to thyroid manipulation. We treated a patient who developed transient symptomatic thyroiditis following parathyroid surgery for tertiary hyperparathyroidism. Therefore, the differential diagnosis for patients with symptoms after parathyroid surgery should include transient thyroiditis.

Hypocitraturia: a common but not well-known cause of nephrolithiasis.

Nephrolithiasis is a frequent problem that can cause serious morbidity. When associated with an underlying metabolic disorder the recurrence rate is higher. Hypocitraturia is estimated to be present in 20-60% of cases. Several secondary causes are known. Potassium citrate is the primary treatment. In the case we present here we emphasise the need for metabolic screening, focussing on hypocitraturia, a less well-known cause of nephrolithiasis.

Haemosuccus pancreaticus, a rare cause of upper gastrointestinal bleeding.

Upper gastrointestinal bleeding is most commonly caused by lesions in the oesophagus, stomach or duodenum. In a minority of cases the bleeding originates from the pancreatic duct, and is known as haemosuccus pancreaticus. In many cases it is associated with chronic pancreatitis. Diagnostic strategies and therapeutic options are discussed.

Decreased cortisol production in male type 1 diabetic patients.

BACKGROUND: It is unclear whether cortisol production and the 11betaHSD-mediated cortisol to cortisone interconversion are different between type 1 diabetic patients and healthy subjects. MATERIALS AND METHODS: Fourteen male, nonobese, normotensive type 1 diabetic patients without severe complications (HbA1c < 8.5%) were studied twice during a daily sodium intake of 50 and 200 mmol, and were then compared with 14 individually matched healthy subjects. Cortisol production was assessed by the sum of urinary cortisol metabolite excretion. Urinary ratios of (tetrahydrocortisol + allo-tetrahydrocortisol)/tetrahydro-cortisone [(THF + allo-THF)/THE] and of free cortisol/free cortisone [UFF/UFE] were determined as parameters of 11betaHSD activity. RESULTS: Sum of urinary cortisol metabolite excretion during low- and high-salt diet was 7.4 +/- 2.5 vs. 7.7 +/- 2.3 nmol min-1 m-2 (NS) in diabetic patients and 9.7 +/- 2.1 vs. 11.2 +/- 4.1 nmol min-1 m-2 (NS) in healthy subjects, respectively (P < 0.05 vs. healthy subjects at both diets). The allo-THF excretion and allo-THF/THF ratios were lower in the diabetic than in the healthy males during both diets (P < 0.05). Urinary (THF + alloTHF)/THE and UFF/UFE were similar in both groups and remained unchanged after salt loading. CONCLUSIONS: The sum of urinary cortisol metabolite excretion as a measure of cortisol production is lower in nonobese, normotensive type 1 diabetic males with adequate glycaemic control and without severe complications, irrespective of sodium intake. We suggest that this is at least in part as result of diminished 5alpha reductase activity, resulting in a decreased cortisol metabolic clearance. In type 1 diabetic and in healthy males, the 11betaHSD setpoint is not affected by physiological variations in sodium intake.

Short-term moderate sodium restriction induces relative hyperfiltration in normotensive normoalbuminuric Type I diabetes mellitus.

AIMS/HYPOTHESIS: Type I (insulin-dependent) diabetes mellitus is associated with an increased extracellular volume. Sodium restriction might seem a logical form of treatment but data on its renal effects is conflicting. We therefore studied the effects of sodium restriction on renal haemodynamics in uncomplicated Type I diabetes mellitus. METHODS: Uncomplicated Type I diabetic patients ( n = 24) and matched control subjects ( n = 24) were studied twice in random order: after a week of 50 mmol or after 200 mmol sodium intake, respectively. The diabetic patients were studied under normoglycaemic clamp conditions. Glomerular filtration rate and effective renal plasma flow were measured as the clearances of iothalamate and hippuran, respectively. RESULTS: During liberal sodium intake, glomerular filtration, effective renal plasma flow and filtration fraction were similar between the diabetic patients and the control subjects. Sodium restriction decreased the effective renal plasma flow in both groups, whereas glomerular filtration rate only decreased in the control subjects. Consequently, in the diabetic patients, the filtration fraction was increased on low sodium (4.1 +/- 8.4 %, p < 0.05 vs liberal sodium). As a consequence, filtration fraction (24.0 +/- 2.6 vs 22.1 +/- 2.0 %, p < 0.05) and glomerular filtration (119 +/- 14 vs 110 +/- 13 ml/min, p < 0.05) were higher in the diabetic patients than in the control subjects during sodium restriction. CONCLUSION/INTERPRETATION: Short-term moderate sodium restriction induces relative hyperfiltration in uncomplicated Type I diabetes. This could indicate an increased intraglomerular pressure. Sodium restriction could be an unfavourable preventive approach in diabetes mellitus but its long-term effects are not known.

A homozygous M694V mutation of the MEFV gene in a patient with periodic fever and thoracic pain.

A Turkish patient with episodic fever and thoracic pain is described in whom a homozygous M694V mutation of the MEFV gene confirmed the clinical diagnosis of familial Mediterranean fever. The role of DNA analysis is discussed with respect to understanding the pathogenesis of the fever and assessing the risk of amyloidosis in specific mutations of the MEFV gene.

Cardiac arrhythmia as initial presentation of aneurysmal subarachnoid hemorrhage.

Cardiac arrhythmia and sudden death are most frequently caused by preexisting heart disease. Rarely, cardiac arrhythmia is a first symptom of an acute neurological event. We describe a patient with asystole and other cardiac arrhythmias, as initial symptoms of acute aneurysmal subarachnoid hemorrhage. Several aspects of cardiac arrhythmias and acute aneurysmal subarachnoid hemorrhage are discussed.

Angiotensin-converting enzyme gene I/D polymorphism and renal disease.

In recent years a vast amount of data has been published on the association between the insertion/deletion (I/D) polymorphism of the gene coding for angiotensin-converting enzyme and renal disease. It has become clear that the polymorphism does not affect the prevalence of renal disease. However, data on the association with progression of renal disease and therapy response are still contradictory. Moreover, sufficient data on the physiological significance of this polymorphism are still lacking. This contribution provides an overview of the available studies and the potential pitfalls in interpreting the data. We also discuss the putative mechanisms for the association between the DD genotype and progression of renal disease and suggest directions for the future that might be employed to further clarify the role in renal pathophysiology.

Imported rickettsioses: think of murine typhus.

Murine typhus is a disease still prevalent in many parts of the world. Because the incidence in the US and Europe has declined rapidly, physicians in these continents have become unfamiliar with the clinical picture. Murine typhus is associated with significant morbidity and fatalities do occur, especially in the elderly and when late recognized. We present a patient with murine typhus that illustrates the wide variety of symptoms in this disease, which makes diagnosis difficult. However, if one keeps the possibility of murine typhus in mind, it is easily diagnosed and treated.

ACE polymorphism does not determine short-term renal response to ACE-inhibition in proteinuric patients.

BACKGROUND: The renal response to ACE inhibition is known to vary between individuals. The ACE genotype is a determinant of the ACE concentrations in plasma and tissue, and therefore might affect the renal response to ACE inhibition in renal patients. METHODS: To test this hypothesis we studied the short-term response to ACE inhibition (enalapril or lisinopril 10/20 mg/d) in 61 stable proteinuric patients (> 1.0 g/day) in relation to the ACE genotype (DD N = 16, ID N = 32, II N = 13). RESULTS: Baseline values were not significantly different for the three groups. ACE inhibition significantly reduced proteinuria, mean arterial pressure, GFR and FF in all genotype groups. The reduction in proteinuria, MAP, GFR and FF was not different between the genotype groups. ERPF increased significantly and to the same extent in all three groups. CONCLUSIONS: We conclude that in proteinuric patients the short-term responses to ACE inhibition of proteinuria, blood pressure, and renal haemodynamics are not determined by ACE genotype. Thus, ACE gene polymorphism does not account for the known interindividual variation in the short-term renal response to ACE inhibition.

Angiotensin converting enzyme insertion/deletion polymorphism and short-term renal response to ACE inhibition: role of sodium status.

Angiotensin converting enzyme (ACEi) inhibition retards renal function loss, but the therapeutic benefit varies between individuals. Renoprotection is poor in patients with the ACE DD genotype. ACE genotype is reported to affect short-term antiproteinuric response to ACEi, a predictor of long-term renoprotection, in some studies but not in others. Short-term responses to ACEi are enhanced by stimulating the renin-angiotensin system, that is, sodium restriction. We hypothesized that the ACE genotype influences sodium dependency of the response to ACEi. Therefore, we performed a cross sectional analysis of short-term responses to ACEi (enalapril or lisinopril) in 88 patients with stable non-diabetic proteinuria (> 1.0 g/day) and variable sodium intake. ACE genotype distribution was: DD, N = 25; ID, N = 40; II, N = 23. Baseline proteinuria (5.9 +/- 0.7; 5.8 +/- 0.07; 4.8 +/- 0.8 g/day, respectively) and mean arterial pressure (108 +/- 3; 106 +/- 2; 107 +/- 2 mm Hg, respectively) were similar for the three genotypes. ACEi similarly reduced proteinuria (-49 +/- 5; -55 +/- 4, -48 +/- 6%, respectively) and blood pressure (-12 +/- 3; -14 +/- 1 and -12 +/- 2%, respectively) in the three groups. Interestingly, the responses to ACEi of proteinuria (r = 0.42, P < 0.05) and blood pressure (r = 0.41, P < 0.05) correlated with urinary sodium excretion in DD genotype but not in the ID (r = 0.05 and 0.17, resp) or II genotype (r = 0.09 and 0.08, respectively). Thus, in the DD group, individuals with a high sodium excretion had a less effective response to ACEi. We conclude that differences in sodium status could account for disparities between studies on the relationship between ACE genotype and response to ACEi, and that sodium restriction might be a strategy to circumvent treatment resistance in the DD genotype.

Diagnostic value of dumping provocation in patients after gastric surgery.

BACKGROUND: In patients after gastric surgery it is often difficult to discern symptoms from dumping from other postcibal complaints. Strict criteria for dumping provocation test have not been defined. METHODS: The sensitivity and specificity of a dumping provocation using 50 g of glucose orally was assessed in 48 patients after gastric surgery, of whom 19 had a typical history of early dumping and 11 had a history of late dumping. Factors were heart rate, packed cell volume, breath hydrogen excretion, and blood glucose concentration. RESULTS: An increase in heart rate of > or = 10 beats/min in the 1st h had a sensitivity of 100% and a specificity of 94% in detecting early dumping. An early rise in breath H2 excretion showed a sensitivity of 84% and specificity of 94%. The nadir blood glucose concentration was not a sensitive or specific indicator for late dumping. CONCLUSIONS: Both an increase in heart rate of > or = 10 beats/min and a positive breath hydrogen excretion are sensitive indicators for early dumping. Late dumping is better recognized by the occurrence of subjective symptoms during provocation.

Effect of antrectomy and truncal vagotomy on erythromycin induced pancreatic polypeptide secretion.

Erythromycin, a motilin agonist, enhances gastrointestinal motility but also stimulates endogenous pancreatic polypeptide (PP) secretion. We investigated whether the effect of erythromycin on PP release is dependent on (1) prokinetic activity of erythromycin generated from the antrum and (2) the long vagus nerve since erythromycin acts via cholinergic neurons. Erythromycin induced PP secretion was determined in 14 patients with antrectomy (6 patients with Billroth I type anastomosis, 8 patients with Billroth II type anastomosis), in 6 patients with truncal vagotomy and pyloroplasty but without gastric resection and in 8 healthy controls. Plasma PP levels in response to erythromycin (3 mg/kg i.v.) were determined at regular intervals for 180 min. Erythromycin induced a significant increase in plasma PP in the control subjects from 22 +/- 4 pmol/l (basal) to 49 +/- 4 pmol/l at 10 min. In the patients with truncal vagotomy plasma PP secretion after erythromycin was significantly (P < 0.05) increased (peak increment vs. basal: 98 +/- 10 pmol/l vs. 27 +/- 2 pmol/l) and prolonged compared to controls. In the patients with antrectomy no significant increases in plasma PP over basal were observed after erythromycin infusion. It is concluded that erythromycin stimulates PP secretion in healthy controls. The PP response to erythromycin is exaggerated after truncal vagotomy but absent after antrectomy indicating that the antrum is essential for erythromycin induced PP secretion.

Effect of erythromycin on gallbladder emptying in patients with antrectomy or truncal vagotomy.

OBJECTIVES: Erythromycin, a motilin-like agent, stimulates gallbladder contraction in healthy control subjects. Because the action of erythromycin is cholinergic dependent and possibly related to premature phase III migrating motor complex activity in the antrum, we investigated the effect of erythromycin on gallbladder volume in six patients with truncal vagotomy without gastric resection and 14 patients with antrectomy (6 with Billroth I anastomosis, 8 with Billroth II anastomosis), and we compared the results obtained with those in eight healthy controls. In addition, the effect of meal ingestion on gallbladder volume was studied. METHODS: Gallbladder volumes, measured with ultrasonography, were determined every 15 min for 180 min after erythromycin infusion (3 mg/kg i.v.), as well as 30 and 60 min after meal ingestion. RESULTS: Basal gallbladder volumes were not significantly different among the four groups. Erythromycin induced a significant (p < 0.01-0.05) gallbladder contraction of maximal 46 +/- 6% in the controls, 49 +/- 9% in the patients with truncal vagotomy, and 38 +/- 7% in the patients with antrectomy and Billroth I anastomosis. In the patients with antrectomy and Billroth II anastomosis, no significant reduction in gallbladder volume after erythromycin was observed. Meal-induced gallbladder contraction was normal in all patients, including those with Billroth II anastomosis. CONCLUSIONS: These results indicate that neither the long vagus nerve nor the antrum is essential for erythromycin-induced effects on the gallbladder. Because no significant reduction in gallbladder volume in response to erythromycin was observed in the patients with antrectomy and Billroth II anastomosis, we suggest that duodenojejunal anatomical integrity is essential for erythromycin-induced gallbladder contraction.

Effect of duodenal juice on bombesin-stimulated cholecystokinin release during loxiglumide administration in man.

Stimulation of cholecystokinin release by bombesin in augmented by cholecystokinin receptor blockade with loxiglumide. We hypothesize that this augmented cholecystokinin release results from inhibition of the pancreatico-biliary response to bombesin during cholecystokinin receptor blockade. To test this hypothesis, we infused bombesin for 180 min in six healthy subjects Three bombesin-infusion experiments were performed in each subject in random order on different days. In two of these experiments loxiglumide was co-infused with bombesin, while in the third experiment saline was co-infused with bombesin. In one of the loxiglumide experiments, duodenal juice, collected on the previous day during infusion of cholecystokinin-GIH, was reperfused intraduodenally during the second hour of bombesin infusion. In the saline experiment, the integrated cholecystokinin response during the first hour of bombesin-infusion (262 +/- 63 pmol 60 min-1) was significantly (P < 0.01) higher than during the second (88 +/- 26 pmol 60 min-1) and third (87 +/- 31 pmol 60 min-1) hour of bombesin-infusion. Loxiglumide augmented bombesin-stimulated cholecystokinin secretion from 262 +/- 63 pmol 60 min-1 to 453 +/- 63 pmol 60 min-1 in the first hour of bombesin infusion (P < 0.01). Integrated cholecystokinin values in the second (489 +/- 90 pmol 60 min-1) and third (450 +/- 74 pmol 60 min-1) hour of the loxiglumide experiment, were significantly (P < 0.01) higher than in the saline experiment.(ABSTRACT TRUNCATED AT 250 WORDS)