Cirrhosis - Science topic
Cirrhosis is a consequence of chronic liver disease characterized by replacement of liver tissue by fibrosis, scar tissue and regenerative nodules (lumps that occur as a result of a process in which damaged tissue is regenerated), leading to loss of liver function.
Questions related to Cirrhosis
Alcohol is associated with many diseases- pancreatic cancer, cirrhosis,etc and also violence, accidents and social breakdown
And yet, many in our Society are able to control their intake. And many abstain for religious reasons.
On balance, is it more harmful than useful?
Is it not time to re-consider its use?
What are your thoughts on this matter?
Hello, I am currently working on my project for my thesis in Pharmacovigilance. I found a case when a diabetic patient consumed glimepiride while at the same time he/she had Cirrhosis also CKD. I am confused about how to answer the fifth question, that is, "Are there alternative causes (other than the drug) that could on their own have caused the reaction?". Can I answer these by "Yes" because some resources stated that CKD stage 5 (kidney failure) dan Chirrhosis might cause hypoglycemia but on the other hand some sources stated CKD and Chirrosis as risk factors.
From your perspective should I answer it as a "No" or"Yes" Or "Do not Know"? Thank you, I am looking forward to your reply.
our team is looking for a tecnic bases on culture b cells from cirrhotic patients, and ACLF, in his own plasma and also do a crosslink betwen other plasma from healhy controls, please do you know some other groups that do the same, or with others ilness? Thank you.
HF management is with selective BB - Portal hypertension is with non selective. What is the evidence about the right BB to use when both diseases are present?
I would like to learn what is the median HBsAg value (as well as the range) in treatment-näive CHB patients. Please also show me the paper or guidance (AASLD, EASL, APASL, etc.)
I have found some documents, all of which tell the HBsAg level in patients treated or with advanced liver diseases (e.g. fibrosis, cirrhosis).
Thank you very much!
Basically, most of the literature declared that obesity will cause to up-regulation of inflammatory markers and macrophage infiltration in fat tissue. My question is that body weight loss other pathologic condition will decrease the inflammation and macrophage content of fat tissue?
A case with portal hypertension and Cirrhosis since 4 years having Ascitis since 1 month. What will be the prognosis specific to this case and in general as well?
Is the term “cryptogenic” as a term in human medicine ”clarifying/useful” Why or why not?
Liver biopsy is the gold standard for the most accurate diagnosis of MTX-induced hepatic fibrosis and cirrhosis, but routine liver biopsies in monitoring patients receiving long-term MTX is controversial. What may the alternate reliable laboratory test/tests to monitor hepatic fibrosis who is on long term MTX therapy?
the first table of the article describes the differences between cirrhotic and non cirrhotic hepatocellular carcinomas and notes that when the first is caused by alcoholic or viral insults to the organ, the later is, among other causes, derived of metabolic alterations. This statement, I consider should be revised because it has been widely studied the association of non-alcoholic fat liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) as cirrhosis causatives and their close link to metabolic origins.
I recently register a clinical trial in patients with liver cirrhosis. One of the study variables is hepatic vein velocity. There are three hepatic vein and determine hepatic vein velocity is possible to all three veins and in different regions (i.e. proximal to ivc or distal or in sinusoids)
Which hepatic vein velocity is more reliable in cirrhotic patient for determine of hepatic vein velocity? Which section of vein is beter for determine this value?
If a person can buy the alcohol at her/his own expense over decades, should we let the person also buy the liver transplant ?
The social cost of alcohol consumption is enormous. The cost of alcoholism to care givers is enormous.
Will this pattern continue indefinitely? Should it be allowed to?
I am working on ultrasound images of cirrhosis and normal liver. All the included liver images are captured via longitudinal scan, subcostal transverse scan and intercostal scan.
1) Now is it possible to do automatic segmentation or I have to take only specific view of liver for automatic segementation.
2) Or the manual segementation will be better as different view are present.
3) If automatic segmentaion is better for diffuse liver type of images, then please suggest the best segmentation approach.
Thanks & Regards,
I have done a study comparing two different regimens for hepatitis C management. Sample sizes are equal and randomised. There are two confounding variables like presence or absence of cirrhosis and treatment experienced or not. There are 3 outcome variables like if patient achieved EVR, ETR and SVR. How to analyze this and what tests of significance may be applied?
Complications related to viral hepatitis, alcohol-related and non-alcoholic liver disease, are the main reason for seeking gastroenterologists and hepatologists advice. In addition, hepatocellular carcinoma often arise on the ground of hepatitis, representing the fifth most common cancer in men and the ninth in women. In 2015, the World Health Organization estimated that 325 million people were living with chronic hepatitis infections (hepatitis B or C) worldwide and that globally, 1.34 million people died of viral in 2015.
In front of this global health problem, gastroenterologists, hepatologists and hepato-biliary-pancreatic (HBP) surgeons, are daily involved in the clinical routine in taking difficult clinical decisions. As Sir William Osler quoted: “medicine is a science of uncertainty and an art of probability” and no doctor returns home from a busy day at the hospital without the nagging feeling that some of his/her diagnoses may turn out to be wrong, or some treatments may not lead to the expected cure. Probability is a recurring theme in medical practice and the ability of dealing with risk and uncertainty can be elicited through a special kind of intelligence. In 2012, The UK psychologist Dylan Evans defined it as “risk-intelligence” that is "a special kind of intelligence for thinking about risk and uncertainty", at the core of which is the ability to estimate probabilities accurately.
Consequently, doctors are routinely asked to make predictions, and their predictions would lead to a consistent payoff when regarding a patient’s life. At the basis of “wise” medical decisions, physician’s experience surely plays a vital role. However, doctors can assume that their competency in a given area can be significantly higher than it really is. Such illusory superiority, is described as the Dunning – Kruger effect, a meta-cognitive bias leading to a discrepancy between the way people actually perform and the way they perceive their own performance level. The concept of “risk-intelligence” relies on the confidence that each subject has with their own knowledge, thus returning accurate probability estimates, and a “wise” doctor should be aware that he/she do not known, thus, returning high risk-intelligence.
To date, little is known about risk-intelligence and the Dunning – Kruger effect between doctors, and, especially, among hepatologists, a specialty strongly involved in important clinical decisions. With this aim we conducted a survey to test how risk-intelligence affects medical decision making in this particular clinical setting and whether the Dunning – Kruger bias can effectively affect these physicians.
If you are a gastroenterologist, hepatologist or HBP surgeon please help us in investigate this issue by completing the following survey:
Inulin is used for detection of Glomerular filtration rate. I have seen in many of the papers in which they have used radiolabeled inulins or FITC inulin. Is there any problem in detecting ordinary inulin in mouse or rat plasma? Is there any problem with level of detection?
Or if it can be done, what is the best method to detect it?
How do you explain elevated AST (269 U/L) while ALT is normal (13 U/L). Is there any dietary guidelines for that?
A 15 year old female child with
1. Beta thalassemia major (on regular transfusion, HLA matched donor unavailable)
2. Splenomegaly with multiple splenic infarcts
3. Acute Pancreatitis (Amylase- 345, Lipase- 420) (non necrotising)
4. HCV infection with mild cholestasis
5. Severe autoimmune hemolytic anemia (DCT negative): Hb - 2.8 gm%
6. Widal Test 1:160 positivity with Blood culture negative
A 54-year old man had an episode of acute pancreatitis 4 years ago (drug related). He developed an obstruction of main pancreatic duct about 3 cm from the ampula of Vater. Since then the Wirsung is increasing. Now is 11 mm. He developed a type 2 diabetes and mild atrophy of the pancreas. He is not alcoholic. Should we leave this obstruction till develop pain or other symptoms or should we operate and perform a Roux-en-Y lateral pancreato-jejunostomy?
71 yo pacient with liver cirrhosis, admited for variceal bleeding, afebrile, torpor, with grade 1 ascites (negative exam for SBP),negative infectious workup with high level of procalcitonin ( >10ng/ml), CRP=1.34, normal leukocytes. We've been given Ciprofloxacin but Any ideas?
We know that ACE inhibitors reduces GFR and they are contraindicated in kidney failure..I wanna ask that how this reduced GFR affects the diseased or damaged ? Is that blood supply that reduces or any other factor..Please elaborate in detail that which factor is responsible and how it leads to further failure in kidney
I do have a patient with persistent asymptomatic low potassium level, about 2.5-3mmol/l. She's not on diuretics, oral antiviral. No alcoholic history. Mild to moderate ascites clinically. Renal profile and urine K are normal.
Any other explanations?
some transgenic mice have several white spots on the liver. Is this a kind of cirrhosis or HCA?
This liver is knocked out glucose regulation gene and several mice show these patterns.
this mouse is 20 week old with normal diet.
I recently came across a 60 year old lady who had been treated for HCV infection. She was documented during evaluation to have low serum immunoglobulins and the Immunoglobulin profile showed low IgG (312 mg/dl, normal being 700-1600), low IgM (30.5 mg/dl, range 40-230) and IgA (< 50, range 70-400). She did not have chronic diarrhoea, nephrotic syndrome or cirrhosis. Her LFT and RFT were normal. She gave no history of having consumed steroids or being given rituximab. Her CD4 and CD8 counts were normal.
A repeat test , 2 weeks later, showed normalisation of gammaglobulins level. Is it purely lab error or could there be some explanation for this phenomenon?
I am working on a bile duct ligation-induced liver fibrosis animal model. As part of the protocol, I stained collagen with picrosirius red staining and now I have to obtain the fibrotic area in each picture. I took 30 pictures for each animal. I use the Image J software to obtain the fibrotic area (RGB stack, threshold etc). However, I am having some problems with the analysis since, in this model fibrosis, is not as obvious as in CCl4 model. First, in the pictures I took, I don't know exactly how extent is the fibrosis, I mean I don't know if i am including part which are not collagen (picture1). Maybe someone who is familiarized with this animal model and the methodology could help help me analyzing just the picture 2 i joined , so i can better imagine which parts are fibrosis and which parts are not? Also, in my pictures, i can see that some nucleus of the hepatocytes are red-stained (picture 3), this problem definitely add noise to the results because the software consider these nucleus as fibrosis, have you had this problem? how did you resolve it? are they really nucleus?
Really I have a decrease in AST and ALT activities in liver fibrosis induced by CCl4 in a study in which 3ml /kg CCl4 40% in olive oil twice a week for 5 weeks and I can not find a cause but I think that may I got a late fibrosis or cirrhosis in my model which decreases the production of these parameters
could you please attach me a paper that explain this part in details?
Treatment for PBC is commonly ursodeoxycholic acid, but it does not seem to influence the development or resolution of the associate features of a Sjogren's syndrome.
Importantly, none of the medical treatments currently used for SS are contraindicated in patients with coexisting PBC.
In patients with major organ involvement, such as lymphocytic interstitial lung disease, we consider therapy with steroids and immunosuppressive agents, such as cyclophosphamide.
But, several studies showed that corticosteroids and Immunosuppressive agents are not effective in the treatment of PBC.
Rituximab seems to be a good alternative in such association.
Does anyone have any experience in treating these association with rituximab.
a 65 year old male, diagnosed to be a case of primary biliary cirrhosis, having recurrent attack of severe muscle cramp....how to precede for treatment?
Cirrhotic patient is exhibiting fever, leukocytosis and negative blood culture without an evident source of infection often. Could this be SIRS or culture-negative bacterial infection?
Well known, that the patient with decompensated liver cirrhosis has multiple predisposing factors and mechanisms for development of infection. In this connection the presence of fever, neutrophilic leukocytosis (or >10% immature forms) and negative blood culture without an evident source of infection in patients with decompensation cirrhosis – is this systemic inflammatory response syndrome or culture-negative bacterial infection?
How often you meet false negative results at the relatively low but pathological levels of PMN in ascitic fluid (for example, polymorphonuclear cell count <500 cells/mm3)?
I tried to detect alpha tubulin, I used total protein (50 ug) from liver tissue with cirrhosis and/or hepatocarcinoma and liver tissue with cirrhosis and/or hepatocarcinoma associated to Hepatitis C virus infection. I stored the lysate on -20 degree and use a dilution 1:500.
Do you have any suggestion why the tubulin have bands of different thickness? You can see my WB result on my attachment.
Add your valuable opinion
he was known case of hypertension since 30 years, having hypersensitivity to penicillins group of antibiotic, sulpha, tetracycline group.
Was on montelukast 10 mg for past 3 years due to high IgE.
No history of Alcohol consumption and no History of. Hepatitis B nor C.
Does anybody have any information about clinical trials of Vitamin E in cirrhosis (of the kind not related to alcohol abuse)? There are reports in the literature of its use in CCl4 induced cirrhosis in animals. Also, does anybody know about the pathophysiology and prognostic significance of functional heart murmurs in the same kind of liver disease?
In a recently prospective study (CANONIC) it has been shown that the patients without a prior history of acute decompensation, acute-on-chronic liver failure was characterized by higher mortality compared with acute-on-chronic liver failure in patients with a prior history of acute decompensation.
Do we have to use corn oil or olive oil?
It is necessary for corn oil has to be sterile?
Is there any protocol where pure CCl4 is used?
I need articles with IF>5.
An asterixis severity scale is mentioned in a number of journal articles. However, whenever I try to access the reference source the journal article provides, the authors simply make reference to the scale, but does not provide information on the actual contents of the scale or what it looks like.
One of the manifestations of liver cirrhosis is hyperdynamic system circulation. There seems to be several issues open in relation and clinical implications of those two.
Left ventricular diastolic dysfunction occurs in 50-70 % of decompensated cirrhosis. However with the development of left ventricular systolic dysfunction or mean arterial pressure < 82mm of hg or Cardiac Index < 1.5 L or refractory ascites; non selective beta blocker should be abandoned.
Patient, 55 years old, diaphragm hernia operation.
Cirrhosis is detected intraoperatively (no clinical manifestations). This patient doesn't show history of viral infection of the liver or the use of toxic substances.
The only laboratory parameter which was without normal range: prothrombin 28% with INR 2.36, in postoperative period.
The patient shows no signs of active bleeding, the response to administration of vitamin K (10mg) was minor (TP 40% after 6 hours).
What it is your opinion about indication to transfuse FFP in this case to correct prothrombin complex?
It would be sufficient reserves liver cells that respond to the vitamin K?
Thank you in advance for your help.
Ideally would like to know cirrhosis diagnosis by U.S. state, including other characteristics like age, race, sex, etc, and would like the actual data set (rather than just viewing published tables).
Nonalcoholic steatohepatitis is a common clinic-pathological entity with a worldwide distribution. The disease is often indolent, but 15%-20% of patients may progress to fibrosis and 7%-17% may insidiously develop cirrhosis which is a strong warning finding in patients’ liver biopsies. Which factors can predict this event in NASH patients?
Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) are intracellular enzymes. I am not sure if these enzymes are secreted by the cell like prothrombin. In my opinion ALT and AST may be predictive of liver cell damage but not the functional capability (If function and damage are not considered synonyms) whereas prothombin may be predictive of liver function.
GGT is reported to be localized on the canalicular region of the hepatocytes and cholangiocytes(cells linning the bile duct). GGT has been used as marker of liver damage after excessive alcohol intake.
The treatment of a cirrhotic dog with Octreotide, a somatostatin analog, that should lower glucagon levels has been proposed. Cirrhosis is secondary to phenobarbital treatment over extended periods to control epilepsy.
Can anyone explain what's the different between congestive hepatopathy, congestive cirrhosis and cardiac cirrhosis?