Mortal consequences of a cooperative action between Takotsubo syndrome and increased intracranial pressure.

An elderly patient with head injury was registered to the emergency room. Because the patient arrived to the hospital unconscious, her cranial, cerebrovascular, and cardiac function was studied. The cardiac function measurements were (i) heart rate, (ii) blood pressure, (iii) oxygen saturation level, (iv) electrocardiogram (ECG), (v) coronary angiogram, (vi) chest computerized tomography (CT), and (vii) echocardiogram. The head damage was studied by cerebral CT and magnetic resonance imaging (MRI). The serum ischemia and inflammatory biomarkers were analysed. For the immediate treatment, the patient received cardiovascular system supporting medication. The cardiac diagnostic results were (i) the ECG suggested an elevation in the left ventricular systolic function, (ii) the blood test showed neutrophilia, increased creatine and increased troponin I kinase values, and (iii) the coronary angiogram and ECG analysis demonstrated a lack of a myocardial infarction but identified apical akinesia. The patient did not have previous symptoms of cardiovascular disease. The brain imaging demonstrated (iv) an acute ischemia in the left occipital area and (v) increased intracranial pressure. Brain MRI indicated (vi) aqueductal stenosis and (vii) multiple gliomatotic foci demonstrating hydrocephalus caused by gliomatosis cerebri. A chest CT indicated (viii) chronic obstructive pulmonary disease (COPD). One week later, the patient died because of cardiac arrest. The diagnosis was Takotsubo syndrome enforced by gliomatosis cerebri and COPD. To our knowledge, this is the first reported case in which the cardiac dysfunction of the patient is associated with gliomatosis cerebri-derived hydrocephalus and increased intracranial pressure that together with COPD may have enhanced the negative clinical outcome.

A Fatal Case of Neuroleptic Malignant Syndrome After Paralytic Bowel in a Patient Taking Antiparkinson Medication.

OBJECTIVES: We report a fatal case of neuroleptic malignant-like syndrome, which occurred as a consequence of paralytic bowel in a 72-year-old woman on treatment with antiparkinson medication. CASE DESCRIPTION: Contrast enhanced computerized tomography of the chest and abdomen demonstrated the presence of paralytic bowel. RESULTS: The patient died. CONCLUSIONS: Physicians involved in the treatment of patients affected by Parkinson's disease should take into consideration the possibility of dopaminergic drug malabsorption due to paralytic bowel as a possible cause of neuroleptic malignant-like syndrome. LEARNING POINTS: Clinical features of neuroleptic malignant-like syndrome (NMLS) in parkinsonian patients are similar to those of neuroleptic malignant syndrome (NMS), which is a potentially fatal condition associated with the withdrawal of antipsychotic medication.Paralytic bowel is a condition frequently impairing medication absorption in the absence of modifications to the normal daily intake of antiparkinson drugs.The present case report describes the fatal outcome of NMLS following paralytic bowel in a parkinsonian patient on levodopa and amantadine therapy.

Could inflammatory markers help diagnose nonalcoholic steatohepatitis?

BACKGROUND: Nonalcoholic fatty liver disease describes a set of conditions that range from fatty liver to nonalcoholic steatohepatitis (NASH), and is considered the hepatic manifestation of metabolic syndrome. Obesity and insulin resistance are strongly associated with systemic markers of inflammation. OBJECTIVE: Focusing on this aspect, we have attempted to find a noninvasive method that could likely assess the presence of NASH and help to decide the liver biopsy performance. METHODS: Using histology as a gold standard to diagnose nonalcoholic fatty liver disease, we consecutively studied 43 patients with NASH and 40 with fatty liver, comparing their data with those of 48 healthy control participants. The outcomes evaluated were ultrasonographic spleen longitudinal diameter coupled with the splenic artery resistive index, serum IL-6 and vascular endothelial growth factor concentrations. RESULTS: The NASH group had higher spleen longitudinal diameter values (P=0.0001) as well as significantly higher IL-6 and vascular endothelial growth factor concentrations than the other groups (P=0.0001). The optimal cut-off value for spleen longitudinal diameter that best discriminated NASH from fatty liver patients was 116 mm (specificity 95% and sensitivity 88%); the sensitivity and specificity of this parameter was better than both IL-6 and vascular endothelial growth factor in the same setting (area under the receiver operating characteristic curve 0.920 vs. 0.817 and 0.678). Splenic artery resistive index was similar between patients with NASH and those with fatty liver, but differed when compared with controls, P=0.0001. CONCLUSIONS: IL-6 was highly specific in confirming the absence of NASH at normal values. In our series, normal values of spleen longitudinal diameter and IL-6 were strongly associated with fatty liver.

The contribution of omental adipose tissue to adipokine concentrations in patients with the metabolic syndrome.

PURPOSE: To examine differences in peripheral vascular endothelial growth factor (VEGF), interleukin-6 (IL6) and cortisol concentrations between patients with both visceral obesity and metabolic syndrome, and lean controls. In a subsample of metabolic patients underwent abdominal surgery, the adipokine concentrations were measured in venous blood from the omentum to determine information on some processes of synthesis. METHODS: Forty-two healthy lean controls and 46 overweight-obese patients with central adiposity and stigmata of metabolic syndrome were studied. In a subsample of 11 metabolic patients undergoing non-bariatric surgery, blood samples from omental and peripheral veins were taken intraoperatively to determine VEGF, IL6 and cortisol concentrations. RESULTS: Median levels (range) of peripheral VEGF and IL6 were higher in patients than in controls [31.5 (3-112) pg/mL vs 21.35 (9-41.9) pg/mL (P < 0.05) and 5.50 (1.40-13) pg/mL vs 1.15 (0.3-1) pg/mL (P < 0.0001)]. On the other hand, concentrations of VEGF and IL6 from the omental and peripheral veins were similar in the surgery sub-group. Peripheral cortisol concentrations were not higher in patients than in controls, nor were omental concentrations different from the peripheral. Omental and peripheral VEGF and cortisol values were correlated, whereas no association was found between omental and peripheral IL6. CONCLUSIONS: In the presence of abdominal obesity, VEGF and IL6 concentrations are increased in the systemic circulation. The contribution of visceral adipose tissue to circulating levels of VEGF and IL6 was modest.

Metabolic factors involved in the therapeutic response of patients with hepatitis C virus-related chronic hepatitis.

BACKGROUND: The purpose of the present paper was to investigate the factors possibly involved in the failure of pegylated interferon (Peg IFN) plus ribavirin treatment at standard dosage in hepatitis C virus (HCV) 1b patients, with chronic hepatitis. METHODS: A fully screened population of 40 virological non-responders (NR) to combined antiviral therapy was selected and matched, 1:1, with a similar cohort of end-therapy virological responders (R). RESULTS: Waist circumference, glucose metabolic impairment, body mass index, non-genetic iron overload, steatosis and fibrosis severity and, finally, arterial hypertension were statistically more frequent in the NR group on Peg IFN plus ribavirin. Increased waist circumference was the strong independent predictor of therapeutical failure. Interestingly, the concomitant presence of cofactors was more significantly represented in NR, whereas in the R cohort this association was found in a few cases only. CONCLUSION: Insulin-resistance syndrome could contribute to non-response in treated chronic HCV patients, suggesting the presence of dysmetabolic factors that frequently cluster in a critical combination.