Deep Learning CT-based Quantitative Visualization Tool for Liver Volume Estimation: Defining Normal and Hepatomegaly. Background Imaging assessment for hepatomegaly is not well defined and currently uses suboptimal, unidimensional measures. Liver volume provides a more direct measure for organ enlargement. Purpose To determine organ volume and to establish thresholds for hepatomegaly with use automated liver volume ± standard deviation was 1533 mL ± 375 and demonstrated a normal distribution. Patient weight was the major determinant of liver volume and demonstrated a linear relationship. From this result, a linear weight-based upper limit of normal hepatomegaly threshold volume was derived: hepatomegaly (mL) = 14.0 × (weight [kg]) + 979. A craniocaudal threshold of 19 cm was 71% sensitive (49
YAP-TEAD mediates PPAR α-induced hepatomegaly and liver regeneration in mice. Peroxisome proliferator-activated receptor α (PPARα, NR1C1) is a ligand-activated nuclear receptor involved in the regulation of lipid catabolism and energy homeostasis. PPARα activation induces hepatomegaly and plays an important role in liver regeneration, but the underlying mechanisms remain unclear. In this study , the effect of PPARα activation on liver enlargement and regeneration was investigated in several strains of genetically modified mice. PPARα activation by the specific agonist WY-14643 significantly induced hepatomegaly and accelerated liver regeneration after 70% partial hepatectomy (PHx) in wild-type mice and Ppara mice, while these effects were abolished in hepatocyte-specific Ppara-deficient (Ppara
NRF2 activates growth factor genes and downstream AKT signaling to induce mouse and human hepatomegaly. Hepatomegaly can be triggered by insulin and insulin-unrelated etiologies. Insulin acts via AKT, but how other challenges cause hepatomegaly is unknown. Since many hepatomegaly-inducing toxicants and stressors activate NRF2, we examined the effect of NRF2 activation on liver size ) and autoimmune hepatitis (AIH). RNA sequencing and cell signaling analyses were used to determine cellular consequences of NRF2 activation and diverse histological analyses were used to study effects of the different manipulations on liver and systemic pathophysiology. Hepatocyte-specific NRF2 activation, due to p62 accumulation or inhibition of KEAP1 binding, led to hepatomegaly associated with enhanced
if displaced downwards by lung disorders. An enlargedliver expands down and across towards the left iliac fossa (LIF). To avoid missing a really big liver, always begin liver palpation in the LIF and work towards the right upper quadrant[1] .The most common causes of hepatomegaly in the UK are alcoholic liver disease, malignancy (particularly metastases) and congestive cardiac failure.Hepatomegaly Hepatomegaly (Causes, Symptoms, and Treatment) We value your privacyWe and our partners store and/or access information on a device, such as cookies and process personal data, such as unique identifiers and standard information sent by a device for personalised ads and content, ad and content measurement, and audience insights, as well as to develop and improve products. With your permission we
Superselective Transarterial Chemoembolization as an Alternative to Surgery in Symptomatic/EnlargingLiver Hemangiomas. Transarterial embolization of liver hemangiomas has not been considered to be consistently effective. The charts of 25 patients who underwent superselective transarterial chemoembolization with the bleomycin-lipiodol emulsion were evaluated retrospectively. Twenty-two patients the first week. Seventeen of the 22 symptomatic patients (77%) reported resolution or marked amelioration of complaints. Regrowth after initial regression was not observed during median (range) 14 (8-39) months of follow-up (n:18). Transarterial chemoembolization with the bleomycin-lipiodol emulsion is a potential alternative to surgery for symptomatic/enlargingliver hemangiomas. Volume reduction
TCPOBOP-induced hepatomegaly & hepatocyte proliferation is attenuated by combined disruption of MET & EGFR signaling. TCPOBOP (1,4-Bis [2-(3,5-Dichloropyridyloxy)] benzene) is a constitutive androstane receptor (CAR) agonist that induces robust hepatocyte proliferation and hepatomegaly without any liver injury or tissue loss. TCPOBOP-induced direct hyperplasia has been considered signaling was achieved using MET knockout (KO) mice along with Canertinib treatment for EGFR inhibition. Combined elimination of MET and EGFR signaling [MET KO + EGFR inhibitor (EGFRi)], but not individual disruption, dramatically reduced TCPOBOP-induced hepatomegaly and hepatocyte proliferation. TCPOBOP-driven CAR activation was not altered in [MET KO + EGFRi] mice, as measured by nuclear CAR
Fever, pulmonary interstitial fibrosis, and hepatomegaly in a 15-year-old boy with Gaucher disease: a case report Gaucher disease is an autosomal recessive disorder resulting from the accumulation of glucocerebroside in the cells of the macrophage-monocyte system caused by deficiency in lysosomal glucocerebrosidase. Intravenously administered enzyme replacement therapy is the first-line therapy for Gaucher disease type 1 and substrate reduction therapy represents an alternative oral treatment. Here is a rare case report of Gaucher disease in South China. Our patient was a 15-year-old Han Chinese boy presenting with fever, edema, and gradually increasing abdominal girth. A physical examination revealed obvious hypoevolutism and hepatomegaly, and laboratory tests and imaging examinations showed
Glucose-free/high-protein diet improves hepatomegaly and exercise intolerance in glycogen storage disease type III mice Glycogen disease type III (GSDIII), a rare incurable autosomal recessive disorder due to glycogen debranching enzyme deficiency, presents with liver, heart and skeletal muscle impairment, hepatomegaly and ketotic hypoglycemia. Muscle weakness usually worsens to fixed myopathy of proteins against skeletal muscle degeneration, at least in some districts. Hepatomegaly was reduced by about 20%. Moreover, the long-term administration of GFD did not worsen serum parameters even after eight months of high-protein diet. A decreased phosphofructokinase and pyruvate kinase activities and an increased expression of Krebs cycle and gluconeogenesis genes were seen in the liver of GFD fed
Young Man with Hepatomegaly: A Case of Glycogenic Hepatopathy Glycogenic hepatopathy is a rare but potentially reversible condition characterized by hepatomegaly and elevated liver enzymes occurring in poorly controlled type 1 diabetes mellitus patients and often requires a liver biopsy to confirm the diagnosis. We present the case of a young man who was admitted with diabetic ketoacidosis
First-year medical students use of ultrasound or physical examination to diagnose hepatomegaly and ascites: a randomized controlled trial To compare point-of-care ultrasound and physical examination (PEx), each performed by first-year medical students after brief teaching, for assessing ascites and hepatomegaly. Ultrasound and PEx were compared on: (1) reliability, validity and performance, (2 ) diagnostic confidence, ease of use, utility, and applicability. A single-center, randomized controlled trial was performed at a tertiary centre. First-year medical students were randomized to use ultrasound or PEx to assess for ascites and hepatomegaly. Cohen's kappa and interclass coefficient (ICC) were used to measure interrater reliability between trainee assessments and the reference standard (a same
An Interstitial 4q Deletion with a Mosaic Complementary Ring Chromosome in a Child with Dysmorphism, Linear Skin Pigmentation, and Hepatomegaly Interstitial deletions of 4q are rarely reported, vary in size, and have limited genotype-phenotype correlations. Here, genome-wide array CGH analysis identified a 21.6 Mb region of copy number loss at 4q12-q21.1 in a patient diagnosed with dysmorphism , linear skin pigmentation, and hepatomegaly. An additional small ring chromosome was detected in 5/30 cells examined via G-banding. Confirmation of the origin of the ring chromosome was obtained by FISH analysis which identified that the ring chromosome contained material from the deleted region of chromosome 4 and was therefore complementary to the 21.6 Mb deletion. Further microarray studies
Deubiquitinase YOD1: the potent activator of YAP in hepatomegaly and liver cancer Advances in the understanding of the Hippo signaling as a key regulatory pathway of proliferation and apoptosis have provided mechanical insights for controlling organ size and tumorigenicity. Recently, much attention has been directed to the regulation of LATS1/2 (large tumor suppressor) kinases that phosphorylate by the differential expression of miR-21 in a cell-density-dependent manner. Using a transgenic mouse model, we showed that the inducible expression of YOD1 enhances the proliferation of hepatocytes and leads to hepatomegaly in a YAP/TAZ-activitydependent manner. Moreover, a strong correlation was observed between YOD1 and YAP expression in liver cancer patients. Overall, our data suggest that YOD1 is a novel
Biochemical mechanism underlying hypertriglyceridemia and hepatic steatosis/hepatomegaly induced by acute schisandrin B treatment in mice It has been demonstrated that acute oral administration of schisandrin B (Sch B), an active dibenzocyclooctadiene isolated from Schisandrae Fructus (a commonly used traditional Chinese herb), increased serum and hepatic triglyceride (TG) levels and hepatic mass in mice. The present study aimed to investigate the biochemical mechanism underlying the Sch B-induced hypertriglyceridemia, hepatic steatosis and hepatomegaly. Male ICR mice were given a single oral dose of Sch B (0.25-2 g/kg). Sch B-induced changes in serum levels of biomarkers, such as TG, total cholesterol (TC), apolipoprotein B48 (ApoB 48), very-low-density lipoprotein (VLDL), non
Transjugular Liver Biopsy in a Multiple Myeloma Patient with Hepatomegaly, Portal Hypertension and “Miliary†Liver Lesions: A Case Report The present report describes a 50-year-old female recently diagnosed with multiple myeloma who presented with hepatosplenomegaly, miliary-type hyper enhancing liver tumors, and esophageal varices. We performed a transjugular liver biopsy when liver biopsy
Proximal 21q deletion as a result of a de novo unbalanced t(12;21) translocation in a patient with dysmorphic features, hepatomegaly, thick myocardium and delayed psychomotor development IInterstitial 21q deletions can cause a wide spectrum of symptoms depending on the size and the location of the deletion. It has previously been suggested that the long arm of chromosome 21 can be divided into three regions based on the clinical severity of the patients and deletion of the region from 32.3 Mb to 37.1 Mb was more crucial than the deletion of other regions. In this study we describe a female patient with dysmorphic features, hepatomegaly, thick myocardium and psychomotor delay. Conventional karyotyping was initially interpreted as full monosomy 21, but subsequent chromosome microarray
Carotenemia and hepatomegaly in an atopic child on an exclusion diet for a food allergy. Eczema is a frequent childhood manifestation and a few atopic children are allergic to certain foods or aeroallergens. Anxious parents of atopic children often have a fear of topical steroid-related side-effects, and some may try a range of elimination diets to avoid allergies. Elimination diets increase a child with eczema on an exclusion diet presenting with anaphylaxis to dairy food. He had carotenemia with hepatomegaly, which resolved on dietary management.
Clinical, Biochemical, and Genetic Characterization of Glycogen Storage Type IX in a Child with Asymptomatic Hepatomegaly Glycogen storage disease type IX (GSD IX) is caused by a defect in phosphorylase b kinase (PhK) that results from mutations in the PHKA2, PHKB, and PHKG2 genes. Patients usually manifest recurrent ketotic hypoglycemia with growth delay, but some may present simple hepatomegaly . Although GSD IX is one of the most common causes of GSDs, its biochemical and genetic diagnosis has been problematic due to its rarity, phenotypic overlap with other types of GSDs, and genetic heterogeneities. In our report, a 22-month-old boy with GSD IX is described. No other manifestations were evident except for hepatomegaly. His growth and development also have been proceeding normally. Diagnosed
Peliosis hepatis presenting with massive hepatomegaly in a patient with idiopathic thrombocytopenic purpura Peliosis hepatis is a rare condition that can cause hepatic hemorrhage, rupture, and ultimately liver failure. Several authors have reported that peliosis hepatis develops in association with chronic wasting disease or prolonged use of anabolic steroids or oral contraceptives . In this report we describe a case in which discontinuation of steroid therapy improved the condition of a patient with peliosis hepatis. Our patient was a 64-year-old woman with a history of long-term steroid treatment for idiopathic thrombocytopenic purpura . Her symptoms included abdominal pain and weight loss; the only finding of a physical examination was hepatomegaly. We performed computed tomography (CT