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The short-term effect of the blockade of the beta-adrenergic receptors on serum lipoproteins and the plasma activities of the enzymes involved in the metabolism of the serum lipoproteins: lipoprotein lipase (LPL), hepatic lipase (HL) and lecithin: cholesterol acyltransferase (LCAT) was evaluated in ten healthy normolipemic and normotensive subjects. In the first part of the study, the first three-day period of placebo was followed by another three-day period during which propranolol (120 mg/d) was given. In the second, third, and fourth part of the study, the same schedule was used but pindolol (15 mg/d), nadolol (160 mg/d), atenolol (100 mg/d) were given respectively instead of propranolol. The four drugs induced a significant blockade of the beta-adrenergic receptors as evaluated by the measurement of the double two-step test of Master (-45%). Despite similar blockade, the effect on serum lipid concentrations depended on the type of drug: propranolol induced an increase in triglycerides and apoprotein B-concentrations and a decrease in serum high density lipoprotein cholesterol (HDL-C) and apoprotein AI-concentrations. Pindolol provoked only a slight decrease of serum HDL-C concentration. Nadolol and atenolol elicited a lowering of the same magnitude in HDL-C. Except for a possible slight increase in plasma LCAT activity on propranolol, there was no significant change in the plasma activities of LPL, HL, and LCAT during the blockade of the beta-adrenergic receptors with the drugs used. It is difficult to draw firm conclusions in regard to the mechanism by which beta blockers given to patients for much longer periods of time alter lipoprotein metabolism from results obtained in normolipemic subjects receiving beta blockers for only three days. It seems that pindolol modifies the serum lipoprotein pattern less likely than propranolol, nadolol, or atenolol. This difference could be attributed to the intrinsic sympathomimetic activity of pindolol of which the other beta blocking drugs that were used are devoid. The mechanism by which the serum lipid changes can be induced by beta blockade does not involve a lower activity of any of the plasma enzymes regulating the intravascular metabolism of lipoproteins. [ABSTRACT FROM AUTHOR]

Unlabelled: Since heterozygous familial hypercholesterolemia (HeFH) is a disease that exposes the individual from birth onwards to severe hypercholesterolemia with the development of early cardiovascular disease, a clear consensus on the management of this disease in young patients is necessary. In Belgium, a panel of paediatricians, specialists in (adult) lipid management, general practitioners and representatives of the FH patient organization agreed on the following common recommendations. 1. Screening for HeFH should be performed only in children older than 2 years when HeFH has been identified or is suspected (based on a genetic test or clinical criteria) in one parent.2. The diagnostic procedure includes, as a first step, the establishment of a clear diagnosis of HeFH in one of the parents. If this precondition is satisfied, a low-density-lipoprotein cholesterol (LDL-C) levelabove 3.5 mmol/L (135 mg/dL) in the suspected child is predictive for differentiating affected from non-affected children. 3. A low saturated fat and low cholesterol diet should be started after 2 years, under the supervision of a dietician or nutritionist.4. The pharmacological treatment, using statins as first line drugs, should usually be started after 10 years if LDL-C levels remain above 5 mmol/L (190 mg/dL), or above 4 mmol/L (160 mg/dL) in the presence of a causative mutation, a family history of early cardiovascular disease or severe risk factors. The objective is to reduce LDL-C by at least 30% between 10 and 14 years and, thereafter, to reach LDL-C levels of less than 3.4 mmol/L (130 mg/dL)., Conclusion: The aim of this consensus statement is to achieve more consistent management in the identification and treatment of children with HeFH in Belgium., (Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.)

The market of generic drugs is in continuous development in all countries, including Belgium. Their low cost explains their success in western and developed countries. However, clinical concerns have been raised when generics are used. Indeed, various studies suggest that generic substitution can be associated with reduced efficacy or (and) increased side-effects, particularly with drugs used in severe diseases or pathological states such as epilepsy, cardiac arrhythmia, prevention of graft-rejection, ... The generic drugs must have systemic bioavailability similar to that of the original drug. Thus, they have supposed similar therapeutic bioequivalence. However, similar pharmacokinetics does not imply identical therapeutic activity, particularly with drugs having narrow therapeutic indices such as anti-epileptics, anti-arrythmics ... In this case, switchability rather than prescribability may cause problems. Low pharmaceutical quality is more frequent when drugs are produced in certain countries, in some cases causing a real concern when activity and safety are considered.

Like in other medical specialities, training in internal medicine is confronted with the duty hours regulation. A reduction to a maximum of 48 duty hours has been introduced in Belgium in 1999 for all residents and is still under debate in the European Communities. A reduction of duty hours to a maximum of 80 hours per week was recently adopted in the USA. Several surveys were conducted in this country before and after the introduction of the new system to evaluate its impact on training and patient care. A reduction of duty hours appears to improve the mental health and the security and the quality of life of the trainees. On the other hand, it is suspected that reducing training hours can have a negative effect not only on education but also on patient safety and satisfaction giving the fragmentation of care. This appears to be a key problem, particularly in internal medicine, as it implies more frequent transfers of medical information, a source of medical errors and a loss of responsibility.

Surveillance for early detection of hepatocarcinoma (HCC) in patients with cirrhosis is widely accepted. In a cohort of 141 patients with cirrhosis collected during the year 1995, we conducted a surveillance program by performing liver ultrasonography and blood alpha-foetoprotein measurement every 6 months. The median follow-up was 34 months. This study addressed to two questions: the compliance to the surveillance schedule according to the aetiology of cirrhosis and the results in terms of emergence of HCC and outcome. Aetiology of cirrhosis was alcohol-induced in 86 (61%), HCV-related in 30 (21%) and from other origins in 25 (18%). Compliance to the program schedule was good in patients with HCV-related cirrhosis (29/30--97%) and patients with cirrhosis of "other origins" (20/25--80%) but was poor in patients with alcoholic cirrhosis (45/86--52%). The lack of compliance was significantly linked to the failure to achieve alcohol abstinence. During follow-up, 6 HCC lesions were observed in 6 male patients with median age of 68 years. All 6 HCC were single nodule, less than 4 cm and accessible to percutaneous acetic acid injection. Nevertheless, the outcome was disappointing, four patients dying 3-15 months later (median: 8 months), two of them with extensive HCC. One of the two patients still alive developed extensive HCC, 36 months after percutaneous acetic acid injection.

Studies in which hypolipidemic therapy were used for preventing cardiovascular diseases are analyzed on the basis of the number of patients to treat to avoid a clinical event, one of the most accepted evidence-based medicine criteria. The benefit of treatment appears to be related to the risk profile of the population and to the reduction of LDL-Cholesterol concentration but not to the type of therapy. Total mortality is decreased only when statins are used. Special groups of patients (women, aged patients, diabetics) also appear to benefit from the treatment.

Out of a prospective series of 142 consecutive episodes of hypoxic (ischemic) hepatitis (HH), we identified 17 episodes associated with an acute exacerbation of chronic respiratory failure (CRF) without left cardiac failure. In the aim to evaluate the role of arterial hypoxemia in the pathogenesis of HH associated with respiratory failure, these 17 episodes of HH (study group) were hemodynamically compared with a control group of 17 episodes of HH associated with congestive heart failure (CHF) (control group 1) and a group of 16 episodes of acute respiratory failure (ARF) not complicated by HH (control group 2). Arterial hypoxemia was significantly more severe in the study group (arterial blood tension in O2 [PaO2], 34 mm Hg) than in control group 1 (PaO2, 70 mm Hg; P <.0001) and control group 2 (PaO2, 45.5 mm Hg; P =.002). The role of arterial hypoxemia, however, appeared weakened by comparable degrees of systemic hypotension and liver passive congestion in episodes of HH associated with CRF and episodes of HH associated with CHF. Finally, the causative role of arterial hypoxemia emerged from hemodynamic measurements of cardiac index (CI), systemic vascular resistances (SVR), and oxygen transport: systemic hypotension in HH associated with CHF (control group 1) was the result of a fall in CI (median, 2. 33 L/min. m2; range, 1.21-3.14 L/min. m2) associated with high SVR (median, 2,492 dyn. s/cm5. m2; range, 1,382-4,053 dyn. s/cm5. m2), whereas in HH associated with respiratory failure (study group), systemic hypotension was the result of a fall in SVR (median, 1,053 dyn. s/cm5. m2; range, 646-3,148 dyn. s/cm5. m2), resulting in high CI (median, 4.23 L/min. m2; range, 1.9-5.32 L/min. m2) (P =.0087 and. 0038 for cardiac index and SVR, respectively). Moreover, measurements of oxygen transport in patients with HH associated with respiratory failure showed low values of O2 delivery (DO2) (median, 376 mL/min. m2; range, 253-427 mL/min. m2) as a result of extreme arterial hypoxemia despite high CI. In conclusion, these hemodynamic results and additional measurements of hepatic blood flow (HBF) by the method of galactose clearance at a low concentration suggest that in the setting of HH associated with respiratory failure, the liver is not "ischemic," despite hypotension, but rather "hypoxic" as a result of the combination of severe arterial hypoxemia and elevated central venous pressure (CVP).

In a clinical setting of cardiac or circulatory failure, the diagnosis of hypoxic (ischaemic) hepatitis is easy and can be elicited on mere clinical and biochemical features. We report two cases of hypoxic hepatitis where cardiomyopathy remained unrecognized at admission due to the lack of conventional signs of congestive heart failure and where the increase in liver enzymes activities followed an atypical pattern, characterized by only moderate elevation of serum aminotransferases activities, low ASAT/ALAT ratio and elevated ALAT/LDH ratio. This atypical pattern not suggestive of hypoxic hepatitis, could be explained by a delay between the onset of hypoxic injury of the liver and admission to hospital. Moreover one case was complicated by frank jaundice, an unusual feature in hypoxic hepatitis. Consequently, diagnosis and appropriate inotropic treatment were delayed resulting in progressive deterioration and eventually death of both patients. The report of these two cases and the review of other similar cases previously published, enlighten some atypical features of hypoxic hepatitis.

The peroxidation step of lipid transormation is considered to be essential in the pathogenesis of atherosclerosis. Although data concerning the mechanisms by which lipid peroxidation occurs in vivo are scarce, several lines of evidence suggest that some endogenous and exogenous compounds with antioxidant activity could have some beneficial effects in the prevention of atherosclerosis. Ascorbic acid (vitamin C) and alpha-tocopherol (vitamin E) act as the most important hydrophilic and lipophilic antioxidants, respectively in vivo. Accordingly, animal and human studies suggest that these compounds may have some preventive effect against the development of clinical coronary heart disease. Many plant phenols and flavonoids may be important dietary antioxidants and it has been speculated that these compounds in red wine or in the Mediterranean diet could explain the 'French paradox'. Several studies show that antioxidants such as probucol and butylated hydroxytoluene can inhibit development of atherosclerotic lesions in Watanabe and cholesterol-fed rabbits. Some drugs such as beta-blockers, calcium antagonists, hypolipodemic drugs,...appear to have at least in vitro antioxidant effects but the clinical relevance of these properties remains unkonwn. Moreover, some interventions aimed to decrease the LDL-oxidative susceptibility have not been shown to attenuate atherogenesis when cholesterol levels remain markedly elevated.

Early distinction between acute alcoholic pancreatitis is important, because of possible emergency endoscopic sphincterotomy in case of biliary pancreatitis. The aim of this study was to evaluate the value of L/A ratio in the diagnosis of acute alcoholic pancreatitis. From 1990 to end 1993, 133 patients with acute pancreatitis were reviewed. Inclusion criteria were: 1) abdominal pain, 2) pathological serum amylase or serum lipase on admission or within 24 hours after beginning or abdominal pain, 3) acute pancreatitis at the echography or CT scan within 48 hours after admission. 60 patients met the inclusion criteria (31 alcoholic pancreatitis, 19 biliary pancreatitis and 10 pancreatitis of other causes). L/A ratio was studied in terms of delay from beginning of abdominal pain. There was no statistical difference between alcoholic and biliary pancreatitis at any time of the study, with the exception of admission. AST, ALT and alkaline phosphatase were higher in biliary pancreatitis than in alcoholic pancreatitis. AST and ALT were the best biochemical tests to diagnose biliary pancreatitis. Blamey's criteria can also contribute to diagnose biliary pancreatitis. These biochemical tests are the most helpful if they are collected very soon in the evolution of acute pancreatitis. It is concluded that L/A ratio is not helpful in the diagnosis of alcoholic acute pancreatitis.

Objectives: To analyze the role of the liver function on the serum levels of lipoprotein(a) (Lp(a)), a lipoprotein considered to be a risk factor for atherosclerosis., Methods: To measure the Lp(a) levels in patients with liver disease (n = 68) due to various causes and in patients with no liver disease and of similar age and sex-ratio (n = 62) and to analyze the relationship between Lp(a) levels on one hand and liver function and lipid and apoprotein levels on the other hand., Results: Patients with liver disease had significantly lower levels of Lp(a). Lp(a) levels were significantly lower in patients with more severe liver disease (Child Turcotte classification) and significantly correlated with liver function tests, in particular those related to the microsomal function and the synthetic capacity of the liver (albumin, coagulation tests, apoprotein A-II). In patients with liver disease, mean Lp(a) levels were not significantly different between those with and those without chronic alcohol intake., Conclusions: Patients with liver disease have low levels of Lp(a) that are related to reduced synthetic capacity of this organ and are not linked to a specific cause of liver disease, in particular excess alcohol intake.

We report a case of association between genetic haemochromatosis and mixed gonadal dysgenesis. To our knowledge, this case is the first reported in the literature. We discuss the mechanisms of hypogonadism observed in this patient.