Petar Gaćina

Doppler Ultrasound of Hepatic and System Hemodynamics in Patients with Alcoholic Liver Cirrhosis

OBJECTIVE The progression of liver cirrhosis eventually increases cardiac output, while blood pressure and systemic vascular resistance are reduced. A complex behavior of portal hemodynamic to hepatic artery and system circulation has not yet been presented. There is a lack in knowledge about the correlation of local and systemic circulation parameters to the degree of liver failure, with respect to presence of ascites and esophageal varices. PATIENTS AND METHODS The study sample was 76 patients hospitalized for established alcoholic liver cirrhosis. Patients were divided into groups according to Child-Pugh clinical score; grade A (n = 24), B (n = 18) and C (n = 18). Ascites was found in 28 patients and esophageal varices in 46. Portal vein flow velocity (PVFV), hepatic artery resistance index (HARI), heart and great vessels within mediastinal cavity were assessed with ultrasound devices equipped with spectral Doppler. RESULTS Significant differences in mean blood pressure, systemic vascular resistance index (SVRI) minute volume, cardiac index and PVFV were found in the group of patients with the most severe stage (C). In regard to presence of ascites statistically significant difference was observed in elevated mean blood pressure and SVRI. Correlation was found between conjugated HARI to blood pressure and to SVRI. CONCLUSIONS In patients with liver cirrhosis there is an inversely reciprocal relationship of conjugated HARI with PVFV, correlating to disease grade. PVFV in cirrhosis decreases and HARI values were over 0.7. Study demonstrated that combining echocardiography with abdominal Doppler ultrasound served as valuable non-invasive diagnostic insight in liver and systemic circulation among different grade of cirrhosis.

Pleural and pericardial effusions combined with ascites in a patient with severe sunitinib-induced hypothyroidism

To best of our knowledge, this is the first reported case of pericardial and pleural effusions combined with ascites, precipitated with severe sunitinib-induced hypothyroidism. A 58-year-old man presented in our emergency department due to dyspnoea and dry cough. Sixteen months earlier, the patient underwent left nephrectomy due to metastatic renal cell adenocarcinoma (RCC), and therapy with sunitinib was initiated postoperatively. Thyroid function was not assessed during the therapy. On admission, all laboratory findings were within normal range. Computed tomography of the chest detected voluminous bilateral pleural effusions and mild pericardial effusion, and echocardiography revealed pericardial effusion. Thoracocentesis was carried out three times, and cytological examination showed no signs of malignant cells. After assessment of the thyroid function, neglected hypothyroidism was registered. Substitution therapy with levothyroxine was initiated, and thyroid function normalised 2 weeks later. Few days after the last thoracocentesis, his condition suddenly got worse. Thoracocentesis was repeated, and microbiological analysis of the exudate came positive for Klebsiella pneumoniae and Streptococcus pneumoniae. Despite the implemented therapeutic measures, his clinical condition progressively deteriorated. The patient died 27 days after the admission, hospital-acquired pneumonia was identified as the cause of death. Our case emphasises the necessity of careful monitoring and management of side-effects in patients who receive sunitinib. Hypothyroidism is a known cause of pleural, pericardial and abdominal effusions, as reported in several case reports. Timely initiation of substitution levothyroxine therapy can decrease unnecessary pauses in the therapy with sunitinib, as well as prevent development of severe symptoms.

Complete response of adult-onset CNS Langerhans cell histiocytosis documented on 18F-FDG PET/CT.

We report a case of a 49-year-old woman with biopsy-proven multisystemic Langerhans cell histiocytosis (LCH) with hypothalamic involvement documented on F-FDG PET/CT. Chemotherapy with a combination of vinblastine, prednisolone, methotrexate, and 6-mercaptopurine was carried out. Two months later, a 90% reduction of the hypothalamic tumor mass was noted on magnetic resonance imaging, but with no signs of pathological F-FDG accumulation. The patient died 4 months later, and we found no signs of LCH on autopsy. Our case highlights the need for further studies regarding the role of F-FDG PET/CT in the assessment of treatment response in patients with LCH.