Lipoprotein(a) Lp(a) is an independent cardiovascular risk factor. We present real-life characteristics of patients with increased Lp(a) levels attending a University Lipid Clinic.
We retrospectively ...studied patients attending the University of Ioannina Hospital Lipid Clinic with Lp(a) levels ≥30 mg/dL who were followed-up for a median of 22 months.
One hundred eight patients (median age 59 years, 49% females) were included with median Lp(a) levels 67 mg/dL (30–320). Of patients, 25.1% had established atherosclerotic cardiovascular disease (ASCVD): 11.1 and 5.6% positive personal history of myocardial infarction (MI) and stroke, respectively, 6.5% carotid artery disease and 1.9% lower extremities arterial disease (LEAD). In addition, 35.2% of participants had heterozygous familial hypercholesterolemia (heFH), 37.9% positive family history of premature ASCVD, 29.6% hypertension, 12.0% diabetes and 5.5% chronic kidney disease (CKD). Of patients, 67.6% were receiving statin therapy and 16.6% additional ezetimibe at baseline visit, and 83 and 35% were receiving statin treatment and additional ezetimibe, respectively, during follow-up. Low-density cholesterol (LDL-C) levels and LDL-Ccorrected for Lp(a) levels were significantly reduced in lipid-lowering therapy naive patients by 37 and 40% (p <0.05), in lipid-lowering therapy intensified patients by 31 and 36% (p <0.05), and in patients on stable lipid-lowering treatment by 15% (p <0.05) and 10% (p >0.05), respectively, during follow-up. Lp(a) levels increased by 9% (p <0.05).
Our data confirm the high prevalence of established ASCVD, hFH and positive familial history of premature ASCVD in patients with elevated Lp(a) levels. Lp(a) levels slightly increased during follow-up.
Diuretics are one of the most common causes of severe hyponatremia. The responsible pathogenetic mechanisms remain unclear. Serum uric acid concentration has been proposed as an index of ...differentiating between two pathophysiologic constructs of diuretic-induced hyponatremia-extracellular volume depletion and syndrome of inappropriate antidiuretic hormone secretion (SIADH)-like state-but its discriminating value has not been verified in large series of patients. Here we attempt to illuminate the pathophysiology of diuretic-induced hyponatremia by focusing on uric acid homeostasis. Additionally, we analyze the epidemiology and clinical characteristics of the disorder.
We studied prospectively 158 adult patients with hyponatremia on admission to our internal medicine clinic. Here we report on those with diuretic-induced hyponatremia.
Forty patients (13 male and 27 female) had diuretic-induced hyponatremia, rendering it the most common cause of the disorder (25.3%). These patients had lower mean (Na+) (121.2 +/- 7.2 vs 126.4 +/- 4.1 mEq/L, p = .0001) than the remaining hyponatremic patients. Patients with serum uric acid levels < 4 mg/dL (n = 14) exhibited a biochemical profile consistent with a SIADH-like state, whereas patients with serum uric acid levels > or = 4 mg/d (n = 26) were consistent with extracellular volume depletion.
Diuretics are the most common cause of community-developed hyponatremia. The serum uric acid level effectively discriminates between two biochemical profiles of diuretic-induced hyponatremia, one consistent with extracellular volume depletion and another that simulates SIADH.
: Hypertriglyceridemia is associated with both the development of cardiovascular disease (CVD) when mild-to-moderate and high risk of pancreatitis when more severe. The residual CVD risk after ...low-density lipoprotein cholesterol (LDL-C) lowering is, in part, attributed to high triglyceride (TG) levels. Therefore, there appears to be a need for effective TG-lowering agents.
: This review presents the most recent advances in hypertriglyceridemia treatment; specifically, it discusses the results of clinical trials and critically comments on apolipoprotein C-III inhibitors, angiopoietin-like 3 inhibitors, alipogene tiparvovec, pradigastat, pemafibrate and novel formulations of omega-3 fatty acids.
: In the era of extreme lowering of LDL-C levels with several agents, there seems to be space for novel therapeutic options to combat parameters responsible for residual CVD risk, among which are elevated TGs. Furthermore, a significant number of individuals have very high TG levels and encounter the risk of acute pancreatitis. The most recently developed TG-lowering drugs appear to have a role in both conditions; the choice is mainly based on baseline TG levels. Dyslipidemia guidelines are likely to change in the near future to include some of these agents. Of course, long-term data regarding their safety and efficacy in terms of CVD outcomes and pancreatitis are warranted.
MECHANISMS OF HYPONATRAEMIA IN ALCOHOL PATIENTS Liamis, George L.; Milionis, Haralampos J.; Rizos, Evangelos C. ...
Alcohol and alcoholism (Oxford),
11/2000, Letnik:
35, Številka:
6
Journal Article
Recenzirano
Odprti dostop
Hyponatraemia is commonly reported in chronic alcoholic patients. However, the underlying pathogenetic mechanisms are not well delineated. In the current study, we analysed the possible ...pathophysiological mechanisms of hyponatraemia in a group of alcoholic patients (n = 127) admitted to our hospital for causes related to alcohol misuse. Hyponatraemia (serum sodium <134 mmol/l) was found in 22 patients (17.3%). The most common cause of hyponatraemia in our cohort was hypovolaemia (12 patients); pseudohyponatraemia was diagnosed in six patients with alcohol-induced severe hypertriglyceridaemia. It is of interest that two patients fulfilled the criteria of the so-called ‘beer potomania’ syndrome, while in two others, hyponatraemia was due to reset osmostat or to cerebral salt wasting syndrome, not previously described in alcoholic patients. It is concluded that hyponatraemia is a frequently observed electrolyte disorder in hospitalized alcoholic patients and is related to various pathophysiological mechanisms.
Hyponatremia is a common electrolyte abnormality with the potential for significant morbidity and mortality. Endocrine disorders, including adrenal deficiency and hypothyroidism, are uncommon causes ...of hyponatremia. Primary adrenal insufficiency (i.e. Addison's disease) may well be recognized by clear hall-marks of the disease, such as pigmentation, salt craving, hypotension, and concomitant hyperkalemia. Addison's disease is an important diagnosis not to be missed since the consequences can be grave. On the other hand, hypothyroidism and secondary adrenocortical insufficiency originating from diseases of the hypothalamus and/or pituitary (hypopituitarism) require a high index of suspicion, because the clinical signs can be quite subtle. This review focuses on clinical and pathophysiological aspects of hyponatremia due to endocrine disorders.
Statins reduce low-density lipoprotein cholesterol (LDL-C) and are currently the mainstay in the treatment of hyperlipidaemia and subsequently the prevention of atherosclerotic cardiovascular disease ...(CVD). Nevertheless, there is a need to further lower LDL-C, especially in subjects with severe forms of hypercholesterolaemia despite maximum doses of conventional drugs and/or in those intolerant to existing therapies.
Emerging therapeutic approaches to lowering LDL-C involve blocking LDL-receptor degradation by serum proprotein convertase subtilisin kexin 9 (PCSK9). Human monoclonal antibodies that target PCSK9 and its interaction with the LDL-receptor (AMG145, REGN727 and RN316) have been tested in Phase I - III clinical trials for the treatment of hyperlipidaemia in patients at high CVD risk.
These new agents are administered subcutaneously and have been shown to have major LDL-C and apoB lowering effects either alone or in combination with statins. These novel agents are generally well tolerated and once long-term safety data are available they appear promising therapeutic platforms for the treatment of patients with hypercholesterolaemia at risk for or with CVD not controlled by conventional therapies.
Heart failure (HF) is considered an epidemic disease with considerable morbidity, mortality, and immense healthcare costs. Electrolyte abnormalities are often encountered in patients with HF, posing ...a diagnostic and therapeutic challenge for clinicians. Hyponatremia affects up to one-third of HF patients and represents an unfavorable prognostic factor.
Low sodium levels in HF are mainly attributed to the neurohormonal activation secondary to decreased effective circulating volume. However, patients with HF often have several comorbidities which may cause or exacerbate the preexisting hyponatremia. Factors that provoke HF, such as alcohol overconsumption, may also be involved in hyponatremia development. Furthermore, drugs which are frequently prescribed to HF patients, especially diuretics, are potential culprits of hyponatremia and should always be addressed since their withdrawal may reverse hyponatremia. Despite the great prevalence and deleterious effects of hyponatremia in these patients, it is often overlooked and consequently undertreated. In this review, we present the mechanisms involved in the development of hyponatremia focusing on those besides neurohormonal activation. We also discuss the proper management of this electrolyte disorder which is frequently complex in patients with HF.
Hyponatremia in patients with HF is not only the result of neurohormonal activation; several comorbidities and frequently used drugs should also be addressed. Hence, a holistic approach is required both for the diagnosis and optimal treatment.
Background. Rapid correction of dysnatraemias is frequently associated with increased morbidity and mortality. Therefore, it is important to estimate the proper volume and type of infusate required ...to change the serum sodium concentration predictably. The aim of this study is to evaluate the utility or/and the accuracy of the Adrogue–Madias formula in managing patients with hyponatraemia and hypernatraemia. Methods. Among the 317 patients who either on admission to our internal medicine clinic or during their hospitalization were found to have hyponatraemia or hypernatraemia, we studied 189 patients (59.6%) in whom the administration of intravenous solutions was required for the correction of dysnatraemias. Results. Twelve hours after starting the administration of intravenous solutions the anticipated as well as the achieved serum sodium concentration were as follows: in volume depleted patients 130.2±4.1 vs 131.3±5.2 meq/l (n = 45; P = NS), in syndrome of inappropriate antidiuretic hormone secretion (SIADH) patients 127.4±5.7 vs 128.9±5.9 meq/l (n = 10; P = NS), in patients with diuretic-induced hyponatraemia 123.8±6 vs 125.5±5.6 meq/l (n = 29; P = NS), in patients with primary polydipsia 122.5±0.7 vs 129±1.4 meq/l (n = 2; P = 0.02), while in patients with hypernatraemia 153.6±7.5 vs 156.5±8.9 meq/l (n = 92; P = 0.021). Furthermore, 24 h from the initiation of the therapeutic intervention the expected and the achieved serum sodium concentrations were 130±4 vs 135.6±3.3 meq/l (n = 15; P = 0.002) in patients with volume depletion, 128.1±4.8 vs 130±4.5 meq/l (n = 15; P = NS) in patients with diuretic-induced hyponatraemia and 151.5±6.4 vs 153.3±8.3 meq/l (n = 67; P = NS) in patients with hypernatraemia. Conclusions. The formula that has been proposed by Adrogue and Madias predicted with relative accuracy the changes in serum sodium concentration in almost all patients. Thus, it should be considered as a very useful tool for the management of dysnatraemias. However, special attention should be paid when this equation is used in patients with hyponatraemia due to extracellular volume depletion after euvolaemia's restoration and primary polydipsia in order to avoid rapid correction of hyponatraemia.
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