38 research outputs found
Life-threatening hypophosphataemia in a cirrhotic patient with jaundice
We report the case of a 51-year-old patient with a history of liver cirrhosis, who presented with jaundice (total bilirubin 50 mg/dl [855 µmol/l], direct bilirubin 20 mg/dl [342 µmol/l]) and life-threatening hypophosphataemia (serum phosphate 0.5 mg/dl [0.16 mmol/l]), accompanied by inappropriate phosphaturia. The patient also manifested hypouricaemia (serum uric acid 1.7 mg/dl [101 µmol/l]) with renal uric acid wasting and renal glycosuria. This generalized proximal tubular defect may occasionally be seen in deeply jaundiced patients. Therefore, serum phosphate levels should be closely monitored in these patients
Safety and impact on cardiovascular events of long-term multifactorial treatment in patients with metabolic syndrome and abnormal liver function tests: a post hoc analysis of the randomised ATTEMPT study
Effects of Eprosartan on Serum Metabolic Parameters in Patients with Essential Hypertension
The effect of the anti-hypertensive drug eprosartan on metabolic parameters is currently not extensively documented. We evaluated the effect of eprosartan on parameters involved in atherogenesis, oxidative stress and clotting activity. This open-label unblinded intervention study included 40 adult patients with essential hypertension taking eprosartan. Eprosartan significantly reduced by 8% (p<0.001) the systolic and by 13% (p<.001) the diastolic blood pressure, and in-creased by 24% the time needed to produce oxidative by-products (p=0.001), a marker of oxidative stress. In contrast, ep-rosartan did not alter 8-isoprostane (8-epiPGF2a) levels, another marker of oxidative stress. Additionally, eprosartan re-duced by 14% aspartate aminotransferase and by 21% then alanine aminotransferase activity, while it had a neutral effect on the lipid profile and apolipoprotein levels and did not influence glucose homeostasis, creatinine and uric acid levels. Eprosartan did not affect the clotting/fibrinolytic status (estimated by plasminogen activator inhibitor 1, tissue plasmino-gen activator and a2 antiplasmin levels), or the enzymatic activity of the lipoprotein associated phospholipase A2 (Lp-PLA2) and paraoxonase 1 (PON1). In conclusion, eprosartan should be mainly considered as an anti-hypertensive agent with neutral effects on most of the metabolic parameters in hypertensive patients
Dapagliflozin in patients with type 2 diabetes mellitus
Dapagliflozin is a selective and reversible inhibitor of sodium–glucose linked transporter type 2 (SGLT2), which mediates approximately 90% of active renal glucose reabsorption in the early proximal tubule of the kidney. Dapagliflozin significantly reduces glucose reabsorption and decreases serum glucose concentration in an insulin-independent manner. The decrease of glucose reabsorption by dapagliflozin has also been associated with a reduction in body weight. Furthermore, the drug modestly reduces blood pressure levels through weight loss and its action as osmotic diuretic. Dapagliflozin has been approved as monotherapy in patients with type 2 diabetes mellitus (T2DM) who cannot tolerate metformin or in combination with other antidiabetic drugs, with the exception of pioglitazone due to the theoretical increased risk of bladder cancer. The drug should not be prescribed in patients with moderate or severe renal impairment or in patients at risk for developing volume depletion. Dapagliflozin is associated with increased incidence of genital and lower urinary tract infections, but these infections are usually mild to moderate and respond to standard antimicrobial treatment. Based on current evidence, dapagliflozin is a useful drug for patients with T2DM with a favorable safety profile. However, further research regarding the effects of dapagliflozin on cardiovascular outcomes is needed
Compliance with lipid-lowering therapy and its impact on cardiovascular morbidity and mortality
Non-Classical Aspects of Obesity Pathogenesis and Their Relative Clinical Importance for Obesity Treatment
Obesity is a chronic disease and a major public health problem due to its association with non-communicable diseases and all-cause mortality. An increased energy intake and decreased physical activity have been long recognized as the classical parameters that contribute to the development of obesity. However, several other, non-classical factors have also been associated with obesity through various complex mechanisms. Some of them are diet related, such as diet quality, dietary habits and speed of eating. Other factors are non-dietary, such as endocrine-disrupting chemicals, sleep quality and quantity, psychotropic medications and light at night. The scope of the present narrative review is to address these non-classical factors that are implicated in the pathogenesis of obesity, to clarify their potential role in the management of obesity and, where possible, to provide some practical clinical recommendations