ABSTRACT
Portal vein thrombosis (PVT) may occur at any time following liver transplantation. We describe our experience with portal vein recanalization in cases of thrombosis after liver transplantation. Twenty-eight children (5%) out of 566 liver transplant recipients underwent portal vein recanalization using a transmesenteric approach. All children received left hepatic segments, developed PVT, and had symptoms or signs of portal hypertension. Portal vein recanalization was performed via the transmesenteric route in all cases. Twenty-two (78.6%) patients underwent successful recanalization and stent placement. They received oral anticoagulants after the procedure, and clinical symptoms subsided. Symptoms recurred due to portal vein restenosis/thrombosis in seven patients. On an intention-to-treat basis, the success rate of the proposed treatment was 60.7%. Only 17 out of 28 children with posttransplant chronic PVT retained stent patency (primary + assisted) at the end of the study period. In cases of portal vein obstruction, the transmesenteric approach via minilaparotomy is technically feasible with good clinical and hemodynamic results. It is an alternative procedure to reestablish the portal flow to the liver graft that can be performed in selected cases and a therapeutic addition to other treatment strategies currently used to treat chronic PVT.
Subject(s)
Graft Rejection/prevention & control , Liver Diseases/surgery , Liver Regeneration , Liver Transplantation/adverse effects , Portal Vein/surgery , Venous Thrombosis/surgery , Child , Child, Preschool , Female , Follow-Up Studies , Graft Rejection/etiology , Graft Survival , Humans , Infant , Male , Portal Vein/pathology , Prognosis , Retrospective Studies , Risk Factors , Survival Rate , Venous Thrombosis/etiologyABSTRACT
BACKGROUND: Osteoporosis is one of the most important public health problems involving a high percentage of costs in the medical care system. Reliable diagnostic techniques for an early detection of bone deterioration and studies of factors that influence its development in menopausal women are crucial. The aim of the study was to determine the relationship between bone microarchitecture and anthropometry in climacteric women. METHODS: Women were recruited at the Menopause Clinic, University Hospital of FMRP/USP, and submitted to anthropometry and to the evaluation of bone quality (Ultrasound Bone Profile Index, UBPI) and quantity (Amplitudedependent Speed of Sound, AD-SoS-) by phalangeal quantitative osteosonography (DBM Sonic BP). Descriptive analysis of the data was reported and a multiple linear regression was performed using the software SAS® 9.0. RESULTS: 71 patients aged 58 ± 7 y were studied: 28% had BMI 18.5-24.9 kg/m(2), 35% BMI 24.9-29.9 and 37% BMI > 30. Mean AD-SoS was 2059 ± 79 m/s and mean UBPI was 0.67 ± 0.13. Considering AD-SoS the dependent variable, there was no statistically significant relationship between age (p = 0.20), BMI (p = 0.76), fat mass by bioelectrical impedance (p = 0.42) and by anthropometry (p = 0.95). The variables had very low effect on the UBPI when it was considered the dependent variable. CONCLUSIONS: The relation between bone microarchitecture and the anthropometry of the women studied shows that, the greater the bone quantity, the better the anthropometric parameters, without statistically significance. This work was a cross-sectional study on a small sample that needs to be validated in a prospective design.
Subject(s)
Bone Density/physiology , Bone and Bones/anatomy & histology , Climacteric/physiology , Absorptiometry, Photon , Anthropometry , Body Mass Index , Bone and Bones/diagnostic imaging , Electric Impedance , Female , Humans , Linear Models , Middle Aged , Skinfold Thickness , Ultrasonography , Waist-Hip RatioABSTRACT
Acute liver insufficiency, followed by heart disease, pneumopathy and infectious syndrome is reported in a 36 year old brown alcoholic man in which the necropsy revealed anatomopathological changes suggesting sickle cell trait. Acute ischemic lesions were noted in the heart, kidneys, central nervous system and liver. In the absence of other causes explaining the ischemic lesions, they were attributed to circulatory changes related to sickle cell trait. Hepatic failure was consequent to functional disturbances derived from the occlusion of sinusoids and necrosis of hepatocytes. The factor responsible for sickling, which caused recent ischemic lesions, may have been the respiratory insufficiency secondary to lung disease. Chronic ischemic lesions have been seen in the heart and may be related to previous sickling episodes. Subsequent to necropsy findings, screening of family members revealed a daughter with sickle cell trait.
