Multinodular fatty change in the liver in patients with chronic hepatic porphyria

1999 ◽  
Vol 24 (5) ◽  
pp. 481-483 ◽  
Author(s):  
H. Ishida ◽  
K. Konno ◽  
T. Komatsuda ◽  
H. Naganuma ◽  
Y. Hamashima ◽  
...  
Keyword(s):  
Fatty Change ◽  
Chronic Hepatic Porphyria

Multinodular fatty change in the liver in three patients with chronic hepatic porphyria: Contribution of sonography to the diagnosis

2018 ◽  
Vol 47 (3) ◽  
pp. 165-168 ◽  
Author(s):  
Hiroko Naganuma ◽  
Hideaki Ishida ◽  
Makoto Yoshida ◽  
Masato Funaoka ◽  
Shuichi Ito ◽  
...  
Keyword(s):  
Fatty Change ◽  
Chronic Hepatic Porphyria

Alteration of Mitochondria in Oxythiamine-Induced, Acute Thiamine Deficiency in the Mouse

1976 ◽  
Vol 34 ◽  
pp. 284-285
Author(s):  
Itaru Watanabe ◽  
Dante G. Scarpelli
Keyword(s):  
Electron Microscopy ◽  
Adult Male ◽  
Thiamine Deficiency ◽  
Light And Electron Microscopy ◽  
Fatty Change ◽  
Deficient Diet ◽  
Subcutaneous Injections ◽  
Swiss Mice ◽  
Time Period ◽  
Ad Libitum

Acute thiamine deficiency was produced in mice by the administration of oxythiamine, a thiamine analogue, superimposed upon a thiamine deficient diet. Adult male Swiss mice (30 gm. B.W.) were fed with a thiamine deficient diet ad libitumand were injected with oxythiamine (170 mg/Kg B.W.) subcutaneously on days 4 and 10. On day 11, severe lassitude and anorexia developed, followed by death within 48 hours. The animals treated daily with subcutaneous injections of thiamine (300 μg/Kg B.W.) from day 11 through 15 were kept alive. Similarly, feeding with a diet containing thiamine (600 μg/Kg B.W./day) from day 9 through 17 reversed the condition. During this time period, no fatal illness occurred in the controls which were pair-fed with a thiamine deficient diet.The oxythiamine-treated mice showed a significant enlargement of the liver, which weighed approximately 1.5 times as much as that of the pair-fed controls. By light and electron microscopy, the hepatocytes were markedly swollen due to severe fatty change and swelling of the mitochondria.

scholarly journals THU0492 MAGNETIC RESONANCE IMAGING OF THE SACROILIAC JOINTS IN PATIENTS WITH HYPERMOBILITY: A RETROSPECTIVE COHORT STUDY

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 482.4-483
Author(s):  
A. Jones ◽  
C. Ciurtin ◽  
H. Kazkaz ◽  
M. Hall-Craggs
Keyword(s):  
Magnetic Resonance Imaging ◽  
Bone Marrow ◽  
Back Pain ◽  
Lumbar Spine ◽  
Magnetic Resonance ◽  
Bone Marrow Oedema ◽  
Resonance Imaging ◽  
Sacroiliac Joints ◽  
Fatty Change ◽  
Subchondral Sclerosis

Background:The incidence of inflammatory and structural lesions on magnetic resonance imaging of sacroiliac joints (MRI SIJs) in patients with hypermobility related disorders has not been fully investigated. Hypermobile patients are more susceptible to pelvic instability and biomechanical stress of the SIJs, leading to MRI SIJ changes similar to those occurring in spondyloarthritis (SpA). Patients with hypermobility and suspected SpA pose a unique challenge owing to the high prevalence of back pain in the hypermobility cohort and the absence of spinal restriction on clinical examination.Objectives:In this study, we aim to investigate the incidence of MRI SIJ lesions in patients with hypermobility.Methods:We performed a retrospective study of all patients with a confirmed diagnosis of hypermobility related disorders (including hypermobility syndrome, hypermobility spectrum disorders and Ehlers-Danlos Syndromes) referred for an MRI lumbar spine and SIJ between 2011 and 2019 to investigate long-standing back pain. MRIs were examined by a musculoskeletal (MSK) radiologist with more than 25 years of experience, who was blinded to the clinical outcome of the patients. MRI SIJs were assessed for the presence of bone marrow oedema, subchondral sclerosis, erosion, fatty change, enthesitis, ankylosis, joint fluid and capsulitis.Results:51 patients with confirmed hypermobility related disorders were referred for MRI SIJ and lumbar spine between 2011 and 2019. 3 patients demonstrated clinical features in keeping with a diagnosis of SpA and were excluded from the study. 15/48 (31.3%) of patients with hypermobility and back pain (but no clinical picture of SpA) were found to have inflammatory and/or structural lesions on MRI SIJ. The most frequent lesions were small foci of bone marrow oedema (16.6%) followed by subchondral sclerosis (12.5%) and fatty change (10.4%). The incidence of erosions was 4.2%.Conclusion:There is a relatively high incidence of inflammatory and structural lesions on MRI SIJ of patients with hypermobility. The presence of hypermobility should be taken into consideration when interpreting MRI changes in patients with suspected SpA. Further research into long-term outcomes of MRI SIJs in patients with hypermobility and back pain is required to establish the clinical significance of these findings.Disclosure of Interests: :Alexis Jones: None declared, Coziana Ciurtin Grant/research support from: Pfizer, Consultant of: Roche, Modern Biosciences, Hanadi Kazkaz: None declared, Margaret Hall-Craggs: None declared

Fatty change in the endometrium

1992 ◽  
Vol 20 (4) ◽  
pp. 362-363 ◽  
Author(s):  
F.F. NOGALES ◽  
M. PAVCOVICH ◽  
M.T. MEDINA ◽  
M. PALOMINO
Keyword(s):  
Fatty Change

Fatty Change of the Pediatric Myocardium

1992 ◽  
Vol 12 (3) ◽  
pp. 325-331 ◽  
Author(s):  
N. Carter ◽  
S. Variend
Keyword(s):  
Fatty Change

scholarly journals Fatty Change in the Myocardium of the Newborn

BMJ ◽  
1961 ◽  
Vol 2 (5269) ◽  
pp. 1746-1749 ◽  
Author(s):  
J. M. Scott
Keyword(s):  
Fatty Change

Fatty change in the myocardium of newborn infants

1962 ◽  
Vol 64 (2) ◽  
pp. 283-284
Author(s):  
Jean M. Scott
Keyword(s):  
Newborn Infants ◽  
Fatty Change

scholarly journals Chronic hepatitis C associated with porphyria cutanea tarda which showed hepatic focal fatty change arising in a non-alcoholic patient.

Kanzo ◽  
1999 ◽  
Vol 40 (6) ◽  
pp. 350-354 ◽  
Author(s):  
Kazufumi DOHMEN ◽  
Shingo ONOHARA ◽  
Hironari AJIBE ◽  
Masafumi SHIRAHAMA ◽  
Yuichi MIYAMOTO ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis C ◽  
Chronic Hepatitis C ◽  
Porphyria Cutanea Tarda ◽  
Alcoholic Patient ◽  
Fatty Change

scholarly journals Nitrosative Stress and Lipid Homeostasis as a Mechanism for Zileuton Hepatotoxicity and Resistance in Genetically Sensitive Mice

2020 ◽  
Vol 175 (2) ◽  
pp. 220-235 ◽  
Author(s):  
Dahea You ◽  
Lascelles E Lyn-Cook ◽  
Daniel M Gatti ◽  
Natalie Bell ◽  
Philip R Mayeux ◽  
...  
Keyword(s):  
Liver Injury ◽  
Nitrosative Stress ◽  
Farnesoid X Receptor ◽  
Therapeutic Interventions ◽  
Mechanistic Study ◽  
Acid Oxidation ◽  
Fatty Change ◽  
Active Inhibitor ◽  
Mouse Population ◽  
Mechanisms Of Toxicity

Abstract Zileuton is an orally active inhibitor of leukotriene synthesis for maintenance treatment of asthma, for which clinical usage has been associated with idiosyncratic liver injury. Mechanistic understanding of zileuton toxicity is hampered by the rarity of the cases and lack of an animal model. A promising model for mechanistic study of rare liver injury is the Diversity Outbred (J:DO) mouse population, with genetic variation similar to that found in humans. In this study, female DO mice were administered zileuton or vehicle daily for 7 days (i.g.). Serum liver enzymes were elevated in the zileuton group, with marked interindividual variability in response. Zileuton exposure-induced findings in susceptible DO mice included microvesicular fatty change, hepatocellular mitosis, and hepatocellular necrosis. Inducible nitric oxide synthase and nitrotyrosine abundance were increased in livers of animals with necrosis and those with fatty change, implicating nitrosative stress as a possible injury mechanism. Conversely, DO mice lacking adverse liver pathology following zileuton exposure experienced decreased hepatic concentrations of resistin and increased concentrations of insulin and leptin, providing potential clues into mechanisms of toxicity resistance. Transcriptome pathway analysis highlighted mitochondrial dysfunction and altered fatty acid oxidation as key molecular perturbations associated with zileuton exposure, and suggested that interindividual differences in cytochrome P450 metabolism, glutathione-mediated detoxification, and farnesoid X receptor signaling may contribute to zileuton-induced liver injury (ZILI). Taken together, DO mice provided a platform for investigating mechanisms of toxicity and resistance in context of ZILI which may lead to targeted therapeutic interventions.

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