scholarly journals Toxic Hepatitis Associated With the Use of Contraceptives: A Diagnosis to Bear in Mind

Cureus ◽  
2022 ◽  
Author(s):  
Alejandro Blanquicett ◽  
Maria Cristina Martinez-Ávila ◽  
Zulay Mondol ◽  
Pedro Imbeth Acosta
Keyword(s):  
Toxic Hepatitis

Two cases of toxic hepatitis caused by arrowroot juice

2009 ◽  
Vol 15 (4) ◽  
pp. 504 ◽  
Author(s):  
Seung Young Kim ◽  
Hyung Joon Yim ◽  
Jae Hong Ahn ◽  
Jeong Han Kim ◽  
Jin Nam Kim ◽  
...  
Keyword(s):  
Toxic Hepatitis

Toxic hepatitis associated with Polygoni multiflori

2010 ◽  
Vol 16 (2) ◽  
pp. 182 ◽  
Author(s):  
Sang Hoon Bae ◽  
Dong Hyun Kim ◽  
Young Seok Bae ◽  
Kwang Jae Lee ◽  
Dong Wan Kim ◽  
...  
Keyword(s):  
Toxic Hepatitis

Резекция печени изменяет механизмы выведения аммиака почками крыс с хроническим тетрахлорметановым гепатитом

2018 ◽  
pp. 72-79
Author(s):  
П.Н. Савилов ◽  
Д.В. Молчанов
Keyword(s):  
Body Weight ◽  
Toxic Hepatitis ◽  
Ammonia Excretion ◽  
Left Lobe ◽  
Free Form ◽  
Sham Operation ◽  
White Rats ◽  
Urea Reabsorption ◽  
Ambiguous Effect ◽  
Collecting Tubules

Цель исследования - изучение влияния резекции печени (РП) на аммиакэкскретирующую функцию почек при хроническом тетрахлорметановом гепатите. Методика. Опыты выполнены на 265 беспородных белых крысах (самках) массой 180-220 г. Хронический гепатит воспроизводили подкожным введением 50% раствора тетрахлорметана (CCl) на оливковом масле (0,1 мл/100 г массы тела, через сутки, c двумя двухнедельными перерывами между 6, 7 и 13-14 инъекциями). На 65-е сут. (последние) введения тетрахлорметана, удаляли часть левой доли печени (15-20% массы органа). На 3-и, 7-е и 14-е сут. после РП или лапаротомии («ложнооперированные» животные) в почках, артериальной и венозной крови, моче исследовали содержание аммиака, глутамина и мочевины. Результаты. Прогрессирование эндогенной аммиачной интоксикации после РП на фоне тетрахлорметанового гепатита сопровождается повышенной экскрецией аммиака почками. Однако это не устраняет артериальную гипераммониемию и не предотвращает накопление почками аммиака. Инкреция глютамина из почек в кровоток прекращается. К 14-м сут. послеоперационного периода возрастает потребление глютамина из артериальной крови, что приводит к его накоплению в почках. Стимулируя выведение мочевины из организма с мочой, РП одновременно активирует её образование в почках, с дальнейшим поступлением как в кровоток, так и в мочу. В зависимости от сроков послеоперационного периода это сопровождается изменением скорости реабсорбции мочевины в почках. Заключение. Полученные результаты свидетельствуют, что при РП на фоне тетрахлорметанового гепатита почки не предотвращают прогрессирование эндогенной аммиачной интоксикации, патологическое накопление аммиака и глутамина её клетками, но сохраняют способность принимать участие в регуляции повышенного содержания мочевины в артериальной крови. Mechanical (resection) or toxic (hepatitis) liver damage alone has an ambiguous effect on renal ammonia excretion during development of endogenous ammonia intoxication. The aim. The study investigated the effect of liver resection (LR) on renal ammonia excretion in chronic tetrachlorocarbon (CCl)-induced hepatitis. Methods. Experiments were conducted on 240 mongrel white rats (females) weighing 180-220 g. Chronic hepatitis was induced by subcutaneous injection of 50% solution of carbon tetrachloride (CCl) in olive oil (0.1 ml/100g body weight per day with two two-week breaks between injections 6-7 and 13-14). LR with removal of a part of the left lobe (15-20% of body weight) was performed on the 65th (last) day of CCl injections. The animals were examined on the 3rd, 7th and 14th day after LR or laparotomy (sham operation). Contents of ammonia (AM), glutamine (GN), and urea were measured in the kidney, arterial (AB) and venous ( v.renlis ) blood, and urine. Results. Progression of endogenous ammonia intoxication after LR associated with CCl-induced hepatitis and increased renal excretion of Am involves three mechanisms: 1) excretion of Am that is delivered to kidneys in the free form with AB; 2) stimulation of renal tubule secretion of Am that had formed in kidneys by deamidation of «arterial» Gn; and 3) contrary to rules, partial reabsorption of Am from collecting tubules into the blood. However, this does not eliminate arterial hyperammonemia or prevent accumulation of Am in kidneys. The stimulatory effect of LR in CCl-induced hepatitis on Gn incretion from kidneys to the circulation stops by the 14 day after surgery, and the accompanying increased consumption of Gn from AВ results in Gn accumulation in kidneys. LR stimulates urea excretion with urine and simultaneously activates kidney formation of urea, which further enters the bloodstream and urine. Depending on the postoperative period this is associated with changes in the rate of urea reabsorption in kidneys. Conclusions. In RP associated with CCl-induced hepatitis, kidneys cannot prevent progression of endogenous ammonia intoxication and pathological accumulation of ammonia and glutamine in kidney cells but retain the ability to participate in the regulation of the increased urea level in AB.

ROLE OF THE STROMAL CELLULAR COMPONENT IN COMPENSATORY PROCESSES IN DIFFUSE LIVER DAMAGE

2018 ◽  
pp. 32-37 ◽  
Author(s):  
Z. A. Shafigullina ◽  
S. Yu. Medvedeva ◽  
I. G. Danilova
Keyword(s):  
Toxic Hepatitis ◽  
Intraperitoneal Administration ◽  
Sharp Decrease ◽  
Cellular Component ◽  
Ki 67 ◽  
Sinusoidal Cells ◽  
Toxic Damage ◽  
Stromal Component ◽  
Regeneration Processes

The aim of the study was to assess the role of the cellular component of the stroma in liver regeneration after its toxic damage. The experimental model of toxic hepatitis caused by intraperitoneal administration of tetrachloromethane (CCl4) showed that regeneration processes in the liver on the 3rd day are manifested in an increase in binuclear hepatocytes, Ki-67 + cells and hepatocytes dividing by mitosis. The reaction of the stromal component is expressed in an increase in the number of CD45 +, mast and sinusoidal cells (SC). On the 7th day of the development of toxic hepatitis the hepatocyte alteration increases, that is accompanied by a sharp decrease in the mitotic index and the number of Ki-67 + cells. In the stromal component there is a decrease in the number of sinusoidal cells, CD45 + and a significant increase in mast cells with a high secretion granule content.

Multifocal Osteonecrosis Glucocorticoid Induced

2017 ◽  
Vol 68 (1) ◽  
pp. 200-202
Author(s):  
Alexandru Patrascu ◽  
Liliana Savin ◽  
Olivera Lupescu ◽  
Dan Mihailescu ◽  
Dana Nicoleta Mihai ◽  
...  
Keyword(s):  
Wilson Disease ◽  
Toxic Hepatitis ◽  
Left Shoulder ◽  
Hepatic Transplantation ◽  
Number Of Patients ◽  
Cementless Prosthesis ◽  
Chronic Toxic Hepatitis ◽  
Aseptic Osteonecrosis ◽  
Hemi Arthroplasty ◽  
Protective Treatment

The present study describes a 29 years old patient diagnosed with aseptic osteonecrosis with multiple localization occurred after a corticoid treatment for chronic toxic hepatitis. The clinical and para-clinical examinations determined the diagnosis of Wilson disease and avascular necrosis with multiple localizations. The evolution of the disease was favourable following the surgical treatment consisting of bilateral total hip arthroplasty with cementless prosthesis, hemi-arthroplasty of the left shoulder with cementless prosthesis, orthotopic hepatic transplantation with an entire liver from donor in cerebral death and immunosuppressive, anticoagulant, antiretroviral and gastro-protective treatment. There is an increase of the number of patients undergoing a glucocorticoids treatment for several months, years or lifelong periods. This type of treatment increases the risk of osteonecrosis depending on the dosage and the duration of the treatment.

scholarly journals A possible interaction between favipiravir and methotrexate: Drug-induced hepatotoxicity in a patient with osteosarcoma

2021 ◽  
pp. 107815522110313
Author(s):  
Emre Demir ◽  
Osman Sütcüoğlu ◽  
Beril Demir ◽  
Oktay Ünsal ◽  
Ozan Yazıcı
Keyword(s):  
Drug Interactions ◽  
Toxic Hepatitis ◽  
Antiviral Agents ◽  
Antiviral Agent ◽  
Aldehyde Oxidase ◽  
Chemotherapeutic Agents ◽  
High Dose ◽  
Drug Induced ◽  
Metastatic Osteosarcoma ◽  
Grade 3

Introduction Favipiravir is an antiviral agent that is recently used for SARS-CoV2 infection. The drug-drug interactions of favipiravir especially with chemotherapeutic agents in a patient with malignancy are not well known. Case report The patient diagnosed with metastatic osteosarcoma was given high dose methotrexate treatment, and favipiravir was started on the third day of the treatment with suspicion of SARS-CoV2 infection. Grade 3 hepatotoxicity developed after favipiravir. Management & outcome: The acute viral hepatitis panel and autoimmune liver disease panel were negative. The ultrasound of the abdomen was unremarkable for any hepatobiliary pathology. The all viral and hepatobiliary possible etiological factors were ruled out. The patient’s liver enzymes increased just after (12 hours later) the initiation of favipiravir, and we diagnosed toxic hepatitis caused by favipiravir-methotrexate interaction. Therefore, methylprednisolone 1 mg/kg dose was started for a presumed diagnosis of toxic hepatitis. Hepatotoxicity completely regressed after favipiravir was discontinued. Discussion Favipiravir may inhibit methotrexate elimination by inhibiting aldehyde oxidase and its sequential use may cause hepatotoxicity in this case. The clinicians should keep in mind possible drug interactions while using new antiviral agents against SARS-CoV2 like favipiravir.

TOXIC HEPATITIS

1940 ◽  
Vol 65 (3) ◽  
pp. 465 ◽  
Author(s):  
J. D. KIRSHBAUM
Keyword(s):  
Toxic Hepatitis
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