Serum uric acid in relation with the metabolic syndrome components and adiponectin levels in Lebanese University students.

BACKGROUND: The relation between serum uric acid (SUA) and metabolic syndrome (MetS) parameters has never been studied in a young Middle-Eastern population. In addition, the relation between SUA and adiponectin was poorly studied. METHODS: We looked at the relation between SUA, and both adiponectin and MetS components in 381 randomly selected Lebanese university students (201 males and 180 females). RESULTS: SUA was positively correlated with body mass index (BMI), systolic blood pressure (SBP), diastolic blood pressure (DBP), waist circumference (WC), fasting blood glucose (FPG), triglycerides, total and LDL-cholesterol, and homeostasis model assessment (HOMA) index (p<0.001 for all variables, p<0.01 for FPG) and inversely correlated with HDL-cholesterol and adiponectin (p<0.001 for both variables). In men, SUA was positively correlated with BMI, WC, SBP, DBP, FPG, triglycerides, total and LDL-cholesterol, and HOMA index and inversely correlated with adiponectin (p<0.001 for all variables, p<0.05 for adiponectin); these correlations persisted after BMI adjustment, for WC, FPG, triglycerides, total-cholesterol, LDL-cholesterol, and HOMA index. In women, SUA was positively correlated with total and LDL-cholesterol (p<0.001), independently of BMI. In a multiple regression analysis, SUA was independently associated with WC, triglycerides, total cholesterol, HDLcholesterol and adiponectin in the overall population while, in men, it was associated with triglycerides, total-cholesterol, and WC. CONCLUSION: Our results suggest, in young adults, a gender difference in the relation between SUA and both adiponectin and MetS parameters. In addition, we observed in both genders a strong relation of SUA with total cholesterol. Further studies are needed in larger populations in order to elucidate these findings.

Heparin-induced hyperkalemia in chronic hemodialysis patients: comparison of low molecular weight and unfractionated heparin.

Aldosterone suppression and subsequent hyperkalemia are well described reversible side effects of prolonged treatment with heparin. This study was designed to examine whether the discontinuous use of heparin three times a week to prevent thrombosis formation during hemodialysis sessions could also induce hypoaldosteronism and might contribute to increased predialysis kalemia in hemodialysis patients. Two different heparinization regimens were prospectively compared in a crossover study of 11 chronic hemodialysis patients. During 2 consecutive weeks, the patients were dialyzed each week with either their usual doses of unfractionated heparin (UH) (6,160 IU +/- 1,350 IU) or low molecular weight heparin (LMWH) (15 anti-Xa activity [aXa] U/kg + 5 aXa U/kg/h). In all but 2 patients, the predialysis level of plasma K+ was higher with UH than with LMWH, and the mean value was higher (5.66+/-0.83 versus 5.15+/-0.68 mM, p = 0.01) while no differences in the predialysis plasma concentrations of creatinine, phosphate, urea, and bicarbonate were observed, excluding the potential role of differences in diet and dialysis efficacy in explaining the higher plasma K+ concentration with UH. The mean plasma aldosterone to plasma renin activity (pRA) ratio was higher with LMWH than with UH (149.54+/-123.1 versus 111.91+/-86.22 pg/ng/ h, p < 0.05). Individual plasma aldosterone values were found to be correlated to pRAs both during the UH period and the LMWH period, and the slope of the positive linear relation between plasma aldosterone and pRA was lower during the UH treatment period (63 versus 105 pg/ng/h). Finally, a negative linear correlation was found between the differences in individual predialysis plasma K+ observed during the 2 protocols and the differences in the corresponding plasma aldosterone levels, suggesting a link between the higher kalemia and the lower aldosterone responsiveness to angiotensin with unfractionated heparin. Although it cannot be concluded whether or not LMWH inhibits aldosterone synthesis, should LMWH decrease aldosterone production, this side effect is 33% less marked than that of UH so that the predialysis plasma K+ levels are 10% lower. This property makes LMWH use preferable to that of UH in patients with elevated predialysis kalemia.

Unawareness of hypoglycemia by insulin-dependent diabetics.

After several years of insulin therapy, about 20% of insulin-dependent diabetics have little or no perception of hypoglycaemia because of a loss of the adrenergic warning symptoms. This defect, poorly correlated with the presence of autonomic neuropathy, has been classically explained by a defect in the catecholamine secretion. We compared the hormonal counterregulation during hypoglycaemia induced by subcutaneous injection of insulin in 7 insulin-dependent diabetics with poor perception of hypoglycaemia and experiencing repeated episodes of severe hypoglycaemia (group A) and 7 insulin-treated diabetics with very good perception of hypoglycaemia and not experiencing severe hypoglycaemia (group B). Groups A and B were similar in terms of age, duration of diabetes, HbA1c level and degenerative complications. The glucagon levels were identical and non-reactive in the two groups. The basal levels and secretion peaks of adrenaline, noradrenaline, growth hormone and cortisol were similar between the two groups, but there was a significant delay in secretion in group A with a blood glucose threshold of adrenergic secretion of between 3.1 +/- 0.5 and 1.6 +/- 0.2 mmoles/l in group A and between 4.6 +/- 0.3 and 3.2 +/- 0.2 mmoles/l in group B (P less than 0.05). This delayed secretion could be explained by desensitisation of the hypothalamic glucostat and could be due to the frequency and/or severity of hypoglycaemic episodes.

Lack of hypoglycemic symptoms and decreased beta-adrenergic sensitivity in insulin-dependent diabetic patients.

Plasma epinephrine, norepinephrine, and dopamine responses were studied in insulin-dependent diabetic patients at rest, on standing and during insulin-induced hypoglycemia. beta-Adrenergic sensitivity was evaluated by the isoproterenol sensitivity test. Five men who had adrenergic symptoms during hypoglycemia and no severe hypoglycemic accidents (coma, seizures) (group A) and five men who had repeated severe hypoglycemic accidents but lack of adrenergic symptoms of hypoglycemia (group B) were studied. The mean resting plasma epinephrine was lower in group B (147 +/- 22 pmol/L, SEM) than in group A (398 +/- 98 pmol/L, P less than 0.02). On standing plasma epinephrine increased significantly in both groups. During hypoglycemia blood glucose decreased identically in the two groups; plasma epinephrine and norepinephrine increased significantly and to the same extent in both groups; the mean maximal heart rate was significantly greater in group A than in group B. Isoproterenol sensitivity (defined as the dose of isoproterenol required to increase heart rate by 25 beats/min) was lower in group B (5.87 +/- 1.12 micrograms) than in group A (2.37 +/- 0.22 micrograms, P less than 0.01). The group B patients had significantly fewer hypoglycemic symptoms during insulin-induced hypoglycemia than did group A patients. We conclude that decreased beta-adrenergic sensitivity contributes to the lack of adrenergic symptoms of hypoglycemia in insulin-dependent diabetic patients.

[Panic attacks: a diagnosis to know in internal medicine. Analysis apropos of 11 patients and an attempt at a physiopathological explanation]. / Attaques de panique: un diagnostic à connaître en médecine interne. Analyse à propos de onze malades et tentative d'explication physiopathologique.

The authors report a series of 11 patients who consulted or were admitted to a hospital medical unit for organic symptomatology, especially hypertensive, diagnosed as panic attacks based on the criteria of the DSM III. Cardiovascular symptoms were dominant in 10 out of the 11 patients. In 7 cases, the symptoms were very suggestive of pheochromocytoma. Treatment based on tricyclic antidepressive drugs associated with behavioural therapy in 5 cases, led to the total regression of acute panic attacks in 9 out of 11 patients with a follow-up period ranging from 1 to 2 years. However, it did not prevent 2 of the patients from developing a chronic anxiety state. After reviewing the principal clinical features of panic attacks, the authors discuss their underlying physiopathological mechanisms. The results of catecholamine metabolic studies in 2 out of 3 patients suggest the possible role of an inhibitor of catecho-o-methyl-transferase, but this requires confirmation by further studies. Panic attacks are very prevalent in the general population (2 to 5 p. 100). The diagnosis must be born in mind to avoid long and costly investigations, and for specific treatment to be instituted. The main risk is the development of chronic severe morbidity with serious socio-familial consequences.

[Catecholamines and their derivatives in the study of pheochromocytoma]. / Les catécholamines et leurs dérivés dans l'exploration du phéochromocytome.

The biochemical diagnosis of pheochromocytoma is essentially based on the plasma and urinary levels of catecholamines and their derivatives, the metanephrines and vanyl-mandelic acid. The advantages and disadvantages of these investigations are reviewed, especially as regards the specificity and sensitivity of each test. The measurement of urinary metanephrine is the best test as its excretion is relatively higher, and it is rarely normal. The measurement of plasma catecholamines is more difficult but gives satisfactory results, but experience so far is limited.

Comparative study of urinary excretion rates of para-hydroxy-mandelic acid, homovanillic acid, vanylmandelic acid in cirrhotic patients with and without encephalopathy.

A comparative study of urinary excretion of octopamine, dopamine, and noradrenaline catabolic products, respectively parahydroxymandelic acid (PHMA) homovanillic acid (HVA) and vanylmandelic acid (VMA) was carried out in 27 cirrhotic patients with (11) and without (16) porto-systemic encephalopathy (P.S.E). PHMA, HVA and VMA were significantly higher in patients with PSE, and there was a positive correlation between PHMA and HVA, and between PHMA and VMA. Higher excretion of PHMA in patients with PSE strongly suggests an increased metabolism of octopamine. HVA and VMA increased excretion, and the positive correlations could be explained by the depletion of stored dopamine and noradrenaline. These observations support the hypothesis that octopamine acts as a false neurotransmitter, and the resulting depletion of dopamine and noradrenaline could explain the neuropsychic phenomena of PSE, and the awakening effect of L. Dopa treatment.