Paolo Lentini

Augmentation index is increased in patients with inflammatory bowel disease, a meta-analysis

In a work published in a recent issue of the European Journal of Internal Medicine [1], Cappello et al. found that, despite the lower prevalence of dyslipidemia, carotid-femoral pulsewave velocity, ameasure of arterial stiffness, and augmentation index, ameasure of wave reflection, were significantly increased in patients with inflammatory bowel disease (IBD), a disease characterized by chronic inflammation. This finding confirms the results of our previous works [2,3] and is of clinical interest because it helps explain why IBD patients have an increased cardiovascular risk despite the low prevalence of traditional cardiovascular risk factors [4]. In this regard, the significantly higher augmentation index reported by Cappello et al. in IBD patients treated with salicylates are consistent with current evidences showing that chronic inflammation could play a role in the arterial stiffening of patients with IBD [2–6]. This finding is also in accordance with the results of two recent meta-regression analyses that has suggested a lack of efficacy of salicylates in protecting IBDpatients fromarterial stiffening [7] and the destiffening effect of anti-tumor necrosis factorα (anti-TNFα) therapy [5]. At the light of the results of Cappello et al. [1], we reanalyzed data of our recentmeta-analysis [5] and performed a newmeta-analysis to test whether augmentation index is increased in patients with IBD. A total of 6 studies published within the last 5 years (5 studies included in our

Kidney and heavy metals - The role of environmental exposure (Review)

Heavy metals are extensively used in agriculture and industrial applications such as production of pesticides, batteries, alloys, and textile dyes. Prolonged, intensive or excessive exposure can induce related systemic disorders. Kidney is a target organ in heavy metal toxicity for its capacity to filter, reabsorb and concentrate divalent ions. The extent and the expression of renal damage depends on the species of metals, the dose, and the time of exposure. Almost always acute kidney impairment differs from chronic renal failure in its mechanism and in the magnitude of the outcomes. As a result, clinical features and treatment algorithm are also different. Heavy metals in plasma exist in an ionized form, that is toxic and leads to acute toxicity and a bound, inert form when metal is conjugated with metallothionein and are then delivered to the liver and possible causing the kidney chronic damage. Treatment regimens include chelation therapy, supportive care, decontamination procedures and renal replacement therapies. This review adds specific considerations to kidney impairment due to the most common heavy metal exposures and its treatment.

Digoxin and Hypermagnesuria

In a recent issue of Nephron, Abu-Amer et al.[1] reported the presence of hypermagnesuria in patients following acute intravenous administration of digoxin and suggested that the Na+/K+-ATPase γ-subunit, which is the pharmacological target of digoxin, can play a role in this process. Hypermagnesuria induced by digoxin may have important clinical consequences, particularly in the presence of inherited and acquired conditions associated with hypermagnesuria and hypomagnesemia. Moreover, the co-administration of digoxin with other drugs that reduce gastrointestinal absorption (i.e., proton pump inhibitors) or increase urinary excretion (i.e., loop diuretics) may increase the likelihood of developing hypomagnesemia. In this article, we reviewed the main causes of hypermagnesuria and discussed potential drug interactions that can enhance the magnesuric effect of digoxin. We suggest that during the administration of digoxin, clinicians should consider the presence of other causes of hypomagnesemia and hypermagnesuria that could enhance the magnesuric effect of digoxin, monitor the urinary and serum levels of magnesium and prescribe an oral supplementation of magnesium.

The effect of tumor necrosis factor antagonists on functional aortic stiffening

To the Editor: In an aggregate data meta-analysis published in a recent issue of Clinical Rheumatology Journal [1], Vlachopoulos et al. found that tumor necrosis factoralpha (TNF-alpha) antagonists may have a beneficial effect on aortic stiffness. This finding is of clinical interest and is in accordance with the current hypothesis that inflammation could be associated with aortic stiffening in chronic inflammatory diseases [2], and with the results of a small longitudinal study and two metaregression analyses performed in patients with inflammatory bowel diseases, showing that aortic stiffness was reduced in patients treated with TNF-alpha antagonists and increased in those treated with salicylates [3–5]. TNF-alpha can affect arterial wall properties reducing the endothelial nitric oxide (functional arterial stiffening) or promoting white blood cell infiltration into blood vessels and changes in vascular smooth muscle phenotypes (structural arterial stiffening) [2]. In patients with chronic inflammatory diseases, whether inflammation is associated with functional or structural arterial stiffness is not completely known. In this regard, three small studies included in the meta-analysis of Vlachopoulos et al. [1] have evaluated the effect of treatment with TNF-alpha antagonists on both aortic stiffness and endothelial function after a follow-up of 6–12 weeks (Table 1) [6–8]. The findings that endothelial function was improved [6–8] and that the duration of follow-up was not associated with the magnitude of the reduction in aortic stiffness in the meta-analysis of Vlachopoulos et al. [1] could suggest that few weeks of treatment with TNF-alpha antagonists have a beneficial effect on functional arterial stiffening. Further studies are necessary to test the long-term effect of TNF-alpha antagonists on structural arterial stiffening.