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Organophosphate (OP) poisoning continues to represent an important medical issue through its high prevalence among toxic pathologies and through its severity. In diagnosing this toxicological disorder, the most frequently utilized and available laboratory test remains the assessment of plasma cholinesterase – butyrylcholinesterase (BChE) – activity. Despite the reluctance of many researchers on the usefulness of serum BChE for kinetic analysis in OP intoxications, we have tested a recently proposed protocol, which is safe, non-expensive, easy to perform, appropriate to distinguish between an aged cholinesterase and a still reactivable one. Our aim was to validate the usefulness of this protocol, studying a series of 23 consecutive patients acutely intoxicated with OP, admitted in a regional Emergency Hospital, over a 1-year period. Introducing the proposed test in the routine of monitoring OP-intoxicated patients has resulted in the identification of a pattern with a funnel aspect, consequence of the initial possibility to increment the degree of BChE activity. This funnel shape defines the presence of reactivability, while its absence demonstrates the lack of obidoximes effect, due to cholinesterase’s ageing process. This method consisted in an advantage for the diagnosis, having the potential of improving prognostic evaluation and therapeutic orientation in OP intoxications. [ABSTRACT FROM PUBLISHER]

Thromboembolic (TE) risk scores used for atrial fibrillation (AF) patients do not include mitral annular calcification (MAC) as a potential indicator of vascular disease. This research evaluated the correlation between MAC and TE risk scores (CHADS2 and CHA2DS2-VASc). We compared TE risk score values and clinical and echocardiographic data in patients with and without MAC. We included, prospectively, 103 patients: 40.8% with AF, 83.5% with hypertension, 30.1% with type II diabetes mellitus, 79.6% with chronic heart failure, and 7.8% with a history of stroke. We identified MAC in 50.5% of patients. The mean CHADS2 and CHA2DS2-VASc scores were 2.56 ± 1.135 and 4.57 ± 1.61, respectively. In MAC patients, both scores tended to increase significantly compared with the control (2.88 ± 1.114 versus 2.24 ± 1.06, p = 0.005, and 5.21 ± 1.51 versus 3.92 ± 1.46, p < 0.001, respectively). The left ventricular ejection fraction negatively correlated with the presence of MAC (r = −0.254, p = 0.01). The presence of MAC was a risk factor for vascular disease (OR = 2.47, χ2 = 34.32, p < 0001). Conclusions: The presence of MAC is associated with greater TE risk scores and a higher risk of vascular disease. It appears that adding MAC as a vascular disease parameter to TE risk scores may have benefits for patients by improving their predictive value. [ABSTRACT FROM AUTHOR]

Despite being one of the most debilitating conditions encountered in the field of toxicology, there is a lack of neutralization measures for the toxins involved in acute corrosive poisoning, and this promotes progressive contact injury of deep tissues after poisoning has occurred. Multiple controversies still surround management strategies during the acute phase of poisoning and the long-term follow-up of the patient. Here, we report a severe case of intentional poisoning with nitric acid complicated by extensive injury of the upper digestive tract, multiple stricture formation, and complete dysphagia. Serial endoscopic dilation and insertion of a jejunostomy feeding tube were necessary, and underlying psychiatric illness negatively affected the outcome of the patient. We conclude that an interdisciplinary approach is necessary to properly reduce the extent of lesions and sequelae induced by corrosion. Early endoscopic mapping of injuries is of major importance to better predict the evolution and possible complications of poisoning. Interventional and reconstructive surgical procedures may significantly improve the life expectancy and quality of life of patients following intoxication with corrosive substances. [ABSTRACT FROM AUTHOR]

Hyponatremia is commonly encountered in the setting of heart failure, especially in decompensated, fluid-overloaded patients. The pathophysiology of hyponatremia in patients with heart failure is complex, including numerous mechanisms: increased activity of the sympathetic nervous system and the renin–angiotensin–aldosterone system, high levels of arginine vasopressin and diuretic use. Symptoms are usually mild but hyponatremic encephalopathy can occur if there is an acute decrease in serum sodium levels. It is crucial to differentiate between dilutional hyponatremia, where free water excretion should be promoted, and depletional hyponatremia, where administration of saline is needed. An inappropriate correction of hyponatremia may lead to osmotic demyelination syndrome which can cause severe neurological symptoms. Treatment options for hyponatremia in heart failure, such as water restriction or the use of hypertonic saline with loop diuretics, have limited efficacy. The aim of this review is to summarize the principal mechanisms involved in the occurrence of hyponatremia, to present the main guidelines for the treatment of hyponatremia, and to collect and analyze data from studies which target new treatment options, such as vaptans. [ABSTRACT FROM AUTHOR]

Aim. Non-alcoholic fatty liver disease (NAFLD) and type 2 diabetes mellitus (T2DM) are in a bidirectional relationship. This prospective study focused on associations between parameters common to the pathogenesis of insulin resistance, inflammation and hepatic steatosis in T2DMpatients with metabolic imbalance. Methods. We used clinical data, insulin resistance and inflammation indices, and hepatic steatosismarkers from 120 patients. Results. The patients (44% men, mean age 58) had a mean body mass index (BMI) of 32 kg/m2 and mean T2DM history of 6 years. With exceptions, significant correlations were found between metabolic, inflammatory and hepatic parameters. Conclusions. In T2DM patients with poor glycemic control, hepatic steatosis correlates significantly with insulin resistance and inflammation. Increased prevalence and poor prognosis of these diseases together justify the need for NAFLD screening of diabetic patients. [ABSTRACT FROM AUTHOR]

Introduction. Celiac disease is a chronic bowel disease with a prevalence of 1% in the general population. This condition, immune-mediated, may exhibit multiple extra-intestinal changes, including the liver. Case presentation. We present the case of a 43-year-old patient presenting in our clinic for fatigue, associated with cytolytic and cholestatic hepatic syndrome with an onset of 10 years. During this time, the patient performed multiple investigations with the exclusion of viral, autoimmune etiology, primitive biliary cirrhosis and Wilson's disease. An abdominal ultrasound recorded an elongated, with an infundibular septum gallbladder. Abdominal computer tomography did not detect any changes. The final diagnosis is chronic alithiasic cholecystitis receiving hepatoprotective treatment with symptom relief and improved hepatic disorders. Over the past 2 years, the patient was diagnosed with osteoporosis (T score = -2.7 followed by treatment with Calcium and Vitamin D and improvement in T score to -2.1), and an iron deficiency anemia corrected with oral iron treatment. Upon resuming the anamnesis, we notice the presence of an intermittent bloating associated with diarrhea. Positive antitransglutaminase antibodies required upper endoscopy with biopsy witch confirmed celiac disease. Conclusion. Despite the rather low prevalence of celiac disease in the etiology of hepatocytolysis, it is important to investigate its presence in the context of hepatic changes with uncertain etiology. This case motivates us to be rigorous in looking for secondary causes of hepatic impairment even in patients with apparently benign changes. [ABSTRACT FROM AUTHOR]

In recent decades, lifestyle and increase of life duration in developed countries predetermined the appearence of atherosclerotic “epidemy“. Peripheral artery disease (PAD) is a disease with high incidence, as well as an indirect status indicator of coronary and cerebral arteries. PAD outcome, including the subclinical stage, can be improved by developing an algorithm of early diagnosis, identification of the factors that determine the evolution of the disease and achieving of optimal pharmacological effect. [ABSTRACT FROM AUTHOR]

Introduction. Idiopathic polymyositis (PMI) is the main acquired myopathy, characterized by inflammatory and degenerative changes in the skeletal muscle. The incidence is 2-10 cases/1,000,000 people. Clinical case. A 63-year-old woman was found at home in confusion and was brought to the “Sf. Spiridon” Hospital Emergency Unit. Upon admission, laboratory investigations showed electrolyte imbalance without ECG signs and rhabdomyolysis. The clinical examination revealed a pale, confused and afebrile patient. Recommended neurological and toxicology tests ruled out a specialized pathology. Treatment aim to correct electrolyte imbalance and the at-home treatment with thiazide diuretic, sartan and statin was stopped, resulting in partial ionogram correction and the persistence of rhabdomyolysis. Two days after admission, patient experienced fever, fatigue and diffuse myalgias. Laboratory investigation showed increased rhabdomyolysis syndrome (CK =4213 U/l, LDH =970 U/l, TGO =197 U/l), inflammatory syndrome (VSH =50 mm/h, CRP =123.36 mg/L), myositis profile (anti-SRP ++, anti-Jo-1 ++) and immunological profile (ssDNA =118 U/ml, SSA Ro =91 U/ml), which informed the decision to transfer the patient to the Rheumatology Clinic with suspected polymyositis. The electromyography showed a myogenic route and confirmed the diagnosis of polymyositis (PMI) according to the Bohan and Peter criteria. Corticosteroid and immunosuppressive treatment was initiated and lead to the improvement of the clinical and enzymatic profile. Conclusion. The particularity of the case lies in the fulminant onset of polymyositis, atypical symptoms and prompt response to corticosteroids and immunosuppression. [ABSTRACT FROM AUTHOR]

In the present study we have analyzed the clinical evolution of the patients intoxicated with organophosphate insecticides, depending on the prescribed treatment, being a well-known fact that the reactivators of cholinesterase are administered only in the first 48-72 hours from the ingestion of the toxin, while after this period there appears a dezalkylation of the complex cholinesterase - organophosphorate substance (OPs), which triggers the irreversibility of the process of blocking the cholinesterase. Material and method: we have analyzed retrospectively a number of 137 patients hospitalized in the period 2003-2009. Results: all the patients were given supportive treatment and the association of Atropine, Obidoxime (Toxogonin) and plasma was administered only for 25,5% of the intoxications with OPs. There are no statistically significant differences between the evolution of the patients intoxicated with OPs treated only with Atropine and those treated with Atropine and Toxogonin [ABSTRACT FROM AUTHOR]

In the present study we have analyzed the clinical evolution of the patients intoxicated with organophosphate insecticides, depending on the prescribed treatment, being a well-known fact that the reactivators of cholinesterase are administered only in the first 48-72 hours from the ingestion of the toxin, while after this period there appears a dezalkylation of the complex cholinesterase - organophosphorate substance (OPs), which triggers the irreversibility of the process of blocking the cholinesterase. Material and method: we have analyzed retrospectively a number of 137 patients hospitalized in the period 2003-2009. Results: all the patients were given supportive treatment and the association of Atropine, Obidoxime (Toxogonin) and plasma was administered only for 25,5% of the intoxications with OPs. There are no statistically significant differences between the evolution of the patients intoxicated with OPs treated only with Atropine and those treated with Atropine and Toxogonin [ABSTRACT FROM AUTHOR]