1.
THE RESTLESS LEGS SYNDROME (REVIEW).
Japaridze, G, Kasradze, S, Maisuradze, L, Popp, R, Wetter, T
Georgian medical news. 2018;(285):74-81
Abstract
The restless legs syndrome (RLS), also known as Willis-Ekbom disease, is a common sleep related neurological disorder with prevalence between 1 and 10%, increasing with age. Women are more frequently affected than men. RLS is characterized by an urge to move the legs accompanied by uncomfortable and unpleasant sensations in the legs, worsening of complaints during periods of rest, improvement by movement and an increase of symptoms in the evening or at night. In addition, affected patients may also suffer from severe sleep disorders and negative effects on daily activities. There is often a history of RLS among first-degree relatives, especially with the primary form. Among other, comorbidities or causal factors are iron deficiency, terminal renal insufficiency, pregnancy, polyneuropathy, or psychotropic drugs. The etiology of primary (idiopathic) RLS has not been clarified yet; however, genetic factors and dysfunctional dopaminergic neurotransmission as well as alterations of central iron metabolism play an important role. In addition to non-pharmacological treatment such as lifestyle modifications or behavioral strategies, levodopa, dopamine agonists, or anticonvulsants are effective. Opioids may be used in otherwise refractory forms. In the case of secondary or comorbid RLS, treatment of the underlying disease is necessary.
2.
Atrial natriuretic peptide and renal dopaminergic system: a positive friendly relationship?
Choi, MR, Rukavina Mikusic, NL, Kouyoumdzian, NM, Kravetz, MC, Fernández, BE
BioMed research international. 2014;:710781
Abstract
Sodium metabolism by the kidney is accomplished by an intricate interaction between signals from extrarenal and intrarenal sources and between antinatriuretic and natriuretic factors. Renal dopamine plays a central role in this interactive network. The natriuretic hormones, such as the atrial natriuretic peptide, mediate some of their effects by affecting the renal dopaminergic system. Renal dopaminergic tonus can be modulated at different steps of dopamine metabolism (synthesis, uptake, release, catabolism, and receptor sensitization) which can be regulated by the atrial natriuretic peptide. At tubular level, dopamine and atrial natriuretic peptide act together in a concerted manner to promote sodium excretion, especially through the overinhibition of Na+, K+-ATPase activity. In this way, different pathological scenarios where renal sodium excretion is dysregulated, as in nephrotic syndrome or hypertension, are associated with impaired action of renal dopamine and/or atrial natriuretic peptide, or as a result of impaired interaction between these two natriuretic systems. The aim of this review is to update and comment on the most recent evidences demonstrating how the renal dopaminergic system interacts with atrial natriuretic peptide to control renal physiology and blood pressure through different regulatory pathways.
3.
Prader-Willi syndrome as a model of human hyperphagia.
Tauber, M, Diene, G, Mimoun, E, Çabal-Berthoumieu, S, Mantoulan, C, Molinas, C, Muscatelli, F, Salles, JP
Frontiers of hormone research. 2014;:93-106
Abstract
Prader-Willi syndrome (PWS), first described in 1956, is considered as a paradigm of a neurodevelopmental disorder with severe and early obesity with hyperphagia and impaired satiety. The improved knowledge in the natural history and recent data on genetics offer new perspectives for understanding the metabolic and endocrine dysfunctions and possibly for treatment. Natural history of the disease has been described due to the early diagnosis performed in the first months of life and various nutritional phases have been described. In addition, there is clear evidence that the abnormal feeding behavior is included in the behavioral problems. Brain imaging studies have shown that some brain regions may be important in PWS. The role of SNORD116 gene cluster is detailed and its links with circadian rhythm and brain and hypothalamus development. Pathophysiology of the abnormal ghrelin levels and of OT dysfunction is documented. While no effect on appetite and weight regulation has been reported with ghrelin antagonists, OT has been shown to improve some of the behavioral problems in adults. We discuss our hypothesis of an abnormal ghrelin/OT/dopamine pathway which may explain the switch of nutritional phases and behavior. These new aspects offer an opportunity for therapeutic use and possible early intervention.