Hospital Chronicles http://hospitalchronicles.gr/index.php/hchr Hospital Chronicles en-US Hospital Chronicles 1790-7306 Authors who publish with this journal agree to the following terms:<br /><p>a. Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a <a href="http://creativecommons.org/licenses/by/3.0/" target="_new">Creative Commons Attribution License</a> that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.</p><p>b. Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.</p><p>c. Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work (See <a href="http://opcit.eprints.org/oacitation-biblio.html" target="_new">The Effect of Open Access</a>).</p> Reducing diagnostic errors — Recognizing monoclonal gammopathy of renal significance (MGRS) http://hospitalchronicles.gr/index.php/hchr/article/view/810 Recently, the term monoclonal gammopathy of renal significance (MGRS) was used to describe monoclonal gammopathies capable of causing kidney damage resulting in chronic kidney impairement and end-stage renal disease. By definition, patients with MGRS have small plasma-cell or B-cell clones that do not meet the criteria for multiple myeloma or lymphoma, and are frequently mistaken as monoclonal gammopathies of undetermined significance (MGUS). As treatment is not recommended for MGUS, appropriate therapy is commonly withheld. Therefore, a high index of clinical suspicion for MGRS and a multidisciplinary approach are essential to avoid delayed diagnosis and the development of MGRS-related end-stage renal disease. Myrto Kostopoulou Androniki Bechli Konstantina Tsantila Hariklia Gakiopoulou Konstantinos Liapis ##submission.copyrightStatement## 2018-07-18 2018-07-18 12 1-4 3 10 10.2015/hc.v12i1.810 Diabetic Nephropathy: from bench to bedside http://hospitalchronicles.gr/index.php/hchr/article/view/812 <p>Diabetes mellitus together with arterial hypertension are the most common causes of chronic kidney disease (CKD). Notably, diabetic kidney disease (DKD) remains a major and independent risk for premature mortality. Therefore, continuous and accurate control of risk factors for the development of diabetic nephropathy is mandatory. Measurement of serum creatinine levels and calculation of estimated glomerular filtration rate (eGFR) according to CKD-EPI equation must be performed annually, Also, measurement of urine albumin and calculation of the urine albumin to creatine ratio rate (uACR) is recommended to be performed annually, too, as  uACR &gt; 30 mg/g creatinine is considered to be a continuous risk factor for cardiovascular disease. Equally important is good glycemic control, as determined by glycated hemoglobin levels of &lt; 7%, as well as control of hypertension, often with more than three anti-hypertensive drugs needed to achieve this goal. Inhibition of the renin-angiotensin-aldosterone system (RAAS) is not only effective in managing hypertension, but seems to reduce albuminuria levels among patients with diabetic nephropathy. However, combination of  angiotensin converting enzyme inhibitors  (ACE’s) with angiotensin receptor antagonists (AT2) or with direct renin inhibitors is not recommended due to the increased risk of hyperkalemia, hypotension and acute kidney injury.  Other antihypertensive drugs which decrease albuminuria levels are the newer dihydropyridines calcium blockers manidipine and the latest b-blockers (carvedilol). Dyslipidemia parameters should be improved, too, especially the serum LDL-cholesterol levels &lt;100 mg/dl. Vitamin D analogues have been shown to decrease albuminuria if eGFR &lt; 60 ml/min/1.73 cm2 on account of a) inhibition of RAAS b) immunomodulatory and anti-inflammatory effects and c) inhibition of interstitial fibrosis in conjunction with FGF-23 (Fibroblast Growth Factor-23). Besides, sodium glucose co-transporter 2 inhibitors, which produce glucosuria seem to possess nephroprotective properties among type 2 diabetic patients. In particular, the EMPAREG study has documented that empagliflozin reduces the relative risk of serum creatinine doubling by 44%, while the relative risk of introducing hemoperfusion has been decreased by 55% within four years. It seems likely that atrasentan, a selective antagonist of the receptor of endothelin A also reduces albuminuria by approximately 35%. Moreover, the significance of substances with anti-inflammatory properties, such as oxidase inhibitors, pentoxyfilline, and N-acetyl-cysteine remains to be elucidated. It is noteworthy that weight loss together with dietary consultation, not only are implicated in better glycemic control and dyslipidemia management, but also  in improving diabetic nephropathy per se.</p> Natalia Vallianou Kyriakos Trigkidis George Ioannidis ##submission.copyrightStatement## 2018-07-18 2018-07-18 12 1-4 11 14 10.2015/hc.v12i1.812 EPILEPSY IN CHILDREN AND ADOLESCENTS: WHAT A PSYCHIATRIST SHOULD KEEP IN MIND http://hospitalchronicles.gr/index.php/hchr/article/view/817 <p>Certain types of epileptic seizures can be mistaken for psychiatric manifestations. Complex partial seizures may present with changes in autonomic nervous system function, somatosensory auras, difficulties in speech, attention or movement, stupor, intense motor behavior, posturing, aimless wandering, changes in perception of place, time or persons, illusions and hallucinations. These phenomena are not usually accompanied by loss of consciousness.</p><p>Temporal epilepsy exhibits prodromal symptoms, such as headache, irritability, insomnia, personality changes and a sense of imminent harm. Common symptoms include auras, déjà vu - jamais vu, dreamy states, feelings of fear and strangeness, automatisms, tonic-dystonic posturing of extremities, transpiration, dizziness, faintness, tachycardia, hypoxia, disordered consciousness. The seizure may be followed by confusion, tiredness, disorientation, headache, automatisms, impaired attention, memory and learning, hyperactivity, oppositionality, panic attacks, dissociation, and obsessive-compulsive symptoms.</p><h4>In frontal lobe epilepsy, three types of seizures may be mistaken for psychiatric problems:  hyperkinetic seizures, tonic seizures of complementary movement area, and absences. In absences, the EEG reveals pathological findings, whereas in one third of hyperkinetic seizures the EEG findings are normal. The complex and emotionally charged behavior of hyperkinetic seizures, and occasionally of  tonic seizures, combined with a normal EEG, may lead to the misdiagnosis of  a psychiatric disorder such as psychosis, dissociation, conversion disorder, panic attacks or  parasomnias.</h4><p>Auras are sensory or psychic seizure phenomena. Sensory auras resemble simple hallucinations. Psychic auras are complex hallucinatory experiences that comprise autoscopic phenomena, a sense of someone’s presence, déjà vu - jamais vu, fear and elation.</p><p>The limbic system has a prominent role in the initiation and persistence of psychokinetic seizures. Limbic seizures are  associated with  the emergence of psychiatric symptoms.</p><p>The diagnosis of epilepsy is mainly clinical; thorough history-taking is of paramount importance. A single surface EEG can neither confirm nor exclude epilepsy. Serial EEGs during wakefulness, in combination with prolonged sleep recordings or video-EEG monitoring, increase diagnostic accuracy.</p><p>Antiepileptic drugs may have a negative impact on mental functioning. Possible adverse effects can be reduced with gradual dose titration, dose reduction, use of extended release medications and drug selection according to its adverse effects profile.</p> Kalliopi Prokopaki ##submission.copyrightStatement## 2018-07-18 2018-07-18 12 1-4 15 22 10.2015/hc.v12i1.817 The era of molecular taxonomy of neoplasms – Neoplasms of the urinary tract http://hospitalchronicles.gr/index.php/hchr/article/view/824 <p>Urothelial carcinoma of the bladder is a common malignancy causing an estimated 150,000 deaths per year.  Treatment for muscle-invasive bladder cancer has not advanced beyond cisplatin-based combination chemotherapy and surgery in the past 30 years and no new drugs for the disease have been approved during that time. In contrast to other malignancies, molecular diagnostics are not established yet for routine clinical management for patients with urothelial cancer of the bladder. Studies have identified gene expression patterns that classify tumors into clinically relevant molecular subtypes. Molecular subtypes were defined by distinct gene expression signatures which are specific for cell cycle, cytokeratins, cell adhesion, receptor tyrosine kinases and immune response. These distinct molecular profiles may help define subsets of patients who are expected to respond positively to chemotherapy and to molecularly targeted therapy. In the current review, two molecular taxonomies of bladder cancer are investigated.</p> Athanasios Taliadoros Christine Vourlakou ##submission.copyrightStatement## 2018-07-18 2018-07-18 12 1-4 23 25 10.2015/hc.v12i1.824 “Chasing-the-Dragon” – Toxic Leukoencephalopathy. A Case Report http://hospitalchronicles.gr/index.php/hchr/article/view/726 <p>Toxic leukoencephalopathy occurs as a result of exposure to a wide variety of drugs such as cocaine, ethanol, 3,4-ethylenedioxymethamphetamine, intravenous heroin, psilocybin, toluene as well as inhaled heroin pyrolysate. The leukoencephalopathy caused by inhaled heroin called “chasing the dragon” results in characteristic signal abnormalities on MRI but may present similarities to other toxic leukoencephalopathies as well. We present a case of heroin vapour abuse with a cerebral MRI presenting symmetrical T2 hyperintensities in both of the temporal lobes, the centrum semiovale, the right occipital lobe, and the splenium of the corpus callosum, with restricted diffusion. The MRI findings quickly improved and the patient gradually recovered.</p> Despina Kriketou Santroninos Papadakis Antonios Tavernarakis Demetrios Exarhos ##submission.copyrightStatement## 2018-07-18 2018-07-18 12 1-4 26 29 10.2015/hc.v12i1.726 Dexmedetomidine for paroxysmal sympathetic hyperactivity in a patient with traumatic brain injury: a case report in the intensive care unit http://hospitalchronicles.gr/index.php/hchr/article/view/818 <p>In this case report we describe the course of a patient with severe traumatic brain injury who, upon withdrawal of sedation, presented the characteristic clinical signs of paroxysmal sympathetic hyperactivity and responded to the combination of dexmedetomidine infusion and oral metoprolol. We present the diagnostic and therapeutic rationale that guided our decisions and summarize the current knowledge on the topic.</p> Ismini Lasithiotaki Aikaterini Megalou Stefanos Korfias Stamatis Banos Charikleia Vrettou ##submission.copyrightStatement## 2018-07-18 2018-07-18 12 1-4 30 34 10.2015/hc.v12i1.818