Science topic

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.
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Hi, is hyperammonemia associated with worse outcomes of acute myocaridal infarction yet decreased risks of coronary and/or cerebrovascular events?
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ammonia plays an important role in maintaining cardiovascular health. Researchers say that non-toxic amounts of the gas could help prevent coronary artery disease. Coronary artery disease is caused by plaque buildup in the vessels that deliver blood to the heart.
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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?
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Hi Dr Fazleh Mahomed . Yes it should be banned because it sometimes lead to big crimes at least car accidents .
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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.
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When the amount of sugar in a person’s blood is too low to provide their body with sufficient energy, it can lead to something called hypoglycemia. Hypoglycemia is defined as a blood sugar level under 70 mg/dl (3.9 mmol/l) and can result in irritability, confusion, and even seizures and unconsciousness during extreme lows.
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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.
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Isolated B-cells were stimulated with anti-CD40 antibodies and TLR9 agonist to assess costimulation marker expression, cytokine production, immunoglobulin production, and CD4+ T-cell allostimulatory capacity.
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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?
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I agree. Carvedilol would be the best choice. ACC 2017 guidlelines recommend it a the drug of choice for HFrEF and the COPERNICUS trial showed it reduced death and hospitalizations in this group.
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Hello mates,
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!
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Hi Bingqian
I would suggest you refer to these articles.
Best
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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? 
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Many scientific studies have shown that inflammation (chronic) is a fundamental and common underlying factor in all major degenerative diseases, including weight gain and difficulty in losing weight.
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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?
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The prognosis of liver cirrhosis is determined by presence of portal hypertension.
As cirrhosis progressed from compensated to decompensated cirrhosis, portal hypertension worsen and prognosis worsen.
In cirrhosis without varices and ascites, the annual risk of death is 1%
In cirrhosis with varices alone without other complications, the annual risk of death is 3.4%
In cirrhosis with ascites, with or without varices, the annual risk of death is 20%
In cirrhosis with variceal bleeding, the annual risk of death is 57%
(D'Amico , J Hepatol 2006)
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Is the term “cryptogenic” as a term in human medicine ”clarifying/useful” Why or why not?
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Yes it is useful, cryptogenic means we had evaluated the disease thoroughly but unable to find a cause. So it's an entity we compare with known etiology to find a prognosis.
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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?
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When evaluating laboratory tests included in the non-invasive fibrosis diagnosis kits, it must be remembered that they were validated to diagnose fibrosis in chronic viral or alcoholic hepatitis.
In addition, the potential effect of metortexate on laboratory tests must be considered in order to avoid false positive and false negative results.
A liver biopsy is of course the gold standard. But it is very curious from the execution technique.
Elastography , in my opinion, may well be an alternative.
Sincerely,
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Dear Colleagues:
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.
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Metabolic syndrome is a constellation of problems including obesity, dyslipidemia, diabetes, and insulin resistance These diseases are associated with both increased risk for, and worsened outcomes of many types of cancer. In the liver, inflammatory and angiogenic changes due to underlying insulin resistance and fatty liver disease will likely lead to increased numbers of patients with HCC in the near future. Much work needs to be done to define more clearly the risks for development of HCC in those with underlying metabolic syndrome, the best methods of screening those at risk, and ultimately, the best treatments targeting the underlying mechanisms of pathogenesis.
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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?
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The left hepatic vein can sometimes be harder to profile if the liver is echogenic and the patient is large. But no difference in the middle and right that I am aware of.
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Excessive fat accumulation within hepaocytes seems pathological. Can it be a cause of cirrhosis or chronic liver disease?
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The pathogenesis of how the accumulated hepatic fat causes liver damage is a complicated issue.
According to “ 2 or multiple hits hypothesis”, the accumulated hepatic fat in some people causes injury to liver cells (nonalcoholic steatohepatitis or NASH) through direct lipotoxicity from free fatty acids (FFAs), oxidative stress, mitochondrial dysfunction, gut microbiota/LPS, activation of fibrogenesis, etc.
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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?
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Data on the matter in question may relate to many factors e.g. magnitude of alcohol related problems in a country [data from countries where alcohol is social or religious taboo will be very different from those that are not], alcohol related diseases [psychiatric, injuries, liver etc] alcohol related liver disease [which further include decompensated liver disease, acute on chronic liver failure, alcoholic hepatitis etc] and each of which will be different in different regions of the world. Added to this it must remembered that the above mentioned points may occur in unison which also affect outcomes depending on the multidisciplinary medical infrastructure in a country devoted to diagnosing and treating alcohol related problems [which is dismal in India] Alcohol problems are also under reported most times.
Considering liver disease, data in meagre in India [for relapse rates check article: Narendra S. Choudhary, Naveen Kumar, Sanjiv Saigal,⁎ Rahul Rai, Neeraj Saraf, and Arvinder S. Soin. Liver Transplantation for Alcohol-Related Liver Disease. J Clin Exp Hepatol. 2016 Mar; 6(1): 47–53.] Data will vary according to nature of alcohol related liver disease that is being treated. I also personally feel that much of these data are biased in favour of selection of patients who have chance of better outcome on pretransplant check up. Also the follow up period is very variable and most studies do not report long term outcome.
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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,
Puja
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Dear Puja According to the information you provided, there are two possibilities:
1 - The images in a different planes refer to a specific sample liver, then you can use the 3D segmentation instead of the 2D segmentation,specially when 3D volume measurement is required . Of course, this requires image fusion. The whole process can be done both manually and (semi-)automated. thesis [1] has a suitable review about them. if your goal is to segment the particular part of the liver, then the algorithm should be directed in that context.
There are several software that performs it semi-automatically, like 3D-Doctor and ...
2. The images in different planes refer to multiple samples , in which case two-dimensional segmentation methods can work(manual/automated). texture-based Approaches were reviewed in[2].
In this case, the auxiliary softwares can do this process (semi-)automatically.
but, nowadays manually and semi-automated framework are more reliable in clinical used( [1] ).
[1] Childs, Jessie. "Development of a simple technique of measuring liver volume using 2D ultrasound including development of a reference range." (2016).
[2] Rathore, Saima, et al. "Texture analysis for liver segmentation and classification: a survey." Frontiers of Information Technology (FIT), 2011. IEEE, 2011.
I hope it can be useful.
Regards
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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?
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Yes can you help me regarding how to do it using SPSS??? Any presentation or booklet??
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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:
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Thank!
(I hope you will find the correct answers in the appendix section of the manuscript we are writing!)
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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?
Thank you
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@Fahimeh Kazemi
Thank you for your suggestion
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Fat induced hepatic injury/ fatty liver
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Dear Mohd Saleem Itoo
The accumulation of fats in the liver (liver steatosis "LS") causes variable damage in hepatocytes
The most common cause of LS is metabolic syndrome (MS), simple obesity or associated MS and DM2.
LS causes alteration in the function of hepatocytes and visualization under microscope and within the hepatocytes, of fat microvesicles in a nearby area and around the perivenular veins and minimal degree of inflammation:
  1. In grade I or incipient LS, histological changes can be stopped or reversed if the metabolic alteration that induces such changes is controlled or eliminated, such as MS and Hyperlipidemia control, weight loss in Obesity and adequate control of DM2.
  2. Failing to prevent or controlling the inducing factors of LS-GI, the condition evolves to a greater degree of fat infiltration and inflammatory changes; That is, to Steatohepatitis. In this case, with a good therapeutic control of the factors related to aggravation, in the best case, the changes can be reversed to a lower degree of LS.
  3. To continue and not to decrease the Steatohepatitis, areas of fibrosis appear histologically (healing by cicatrization of inflammatory areas). That is, it is histologically identified the maximum degree of intracellular fat infiltration and areas of fibrosis interspersed with zones of inflammation around the central vein of the lobules (Perivenular). Alterations similar to those observed in alcoholism, except for the accumulation of fat. This grade of histological lesion is irreversible in 80% of the cases, frequently leading the majority to the final stage of Liver Cirrhosis.
regards
Jose Luis
Estimado Mohd Saleem Itoo
La acumulación de grasas en el hígado (esteatosis hepática "EH") ocasionan daño variable en los hepatocitos
La causa más común de EH es el síndrome metabólico (SM), la obesidad simple o asociada el SM y DM2.
La EH ocasiona alteración en la función de los hepatocitos y visualización bajo microscopio y dentro de los hepatocitos, de microvesículas de grasa en una área cercana y alrededor de las vénulas (perivenular) y grado mínimo de inflamación: 
  1. En la EH grado I, o incipiente, los cambios histológicos pueden detenerse o revertirse si se controla o se elimina la alteración metabólica que induce tales cambios, como sería control del SM e Hiperlipidemia, bajar de peso en la Obesidad y control adecuado de DM2.
  2. De no prevenir o controlar los factores inductores de HE-GI, evoluciona el cuadro a un grado mayor de infiltración grasa y cambios inflamatorios; es decir, a Esteatohepatitis. En este caso, con un buen control terapéutico de los factores relacionados del agravamiento, en el mejor de los casos, se pueden revertir los cambios a un grado menor de EH.
  3. De continuar y no disminuir la Esteatohepatitis, histológicamente aparecen zonas de fibrosis (curación por cicatrización de áreas inflamatorias). Es decir, histológicamente se identifica grado máximo de infiltración grasa intracelular y areas de fibrosis intercaladas con zonas de inflamación alrededor de la Vena Central de los lobulillos (Perivenular). Alteraciones similares a las que se observan en el alcoholismo, excepto por la acumulación de grasa. Este grado de lesión histológica es irreversible en el 80% de los casos, llevando con frecuencia a la mayoría al estado final de Cirrosis Hepática.
Saludos
José Luis
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Dear scientists
How do you explain elevated AST (269 U/L) while ALT is normal (13 U/L). Is there any dietary guidelines for that?
Best regards
Aly
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Please look for disorders of muscle (heart, skeletal) by estimating CPK, aldolase and those of RBC by parameters of hemolysis like LDH, bilirubin (direct/indirect), hemoglobin and of course kidney function tests. Regards  
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Suggest me some natural remedies to recover liver that is damaged due to alcoholic consumption
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Nice question very practical-- before remedies first step must be to stop alcohol intake.
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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  
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Very difficult. How is HCV-RNA? 
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the medicinal plant,  root stem, leaf  or fruit
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Zhao, M.Q.; Han, D.W.; Ma, X.H.; Zhao, Y.C.; Yin, L.; Li, C.M. Preventive and therapeutic actions of glycyrrhizin, glycyrrhetic acid and crude saikosides on experimental liver cirrhosis in rats. Acta Pharm. Sin. 1983, 18, 325–331.
 Wang, J.; Guo, J.; Liu, S. [inhibitory effect of glycyrrhizin on nf-kappa b binding activity in ccl4 plus ethanol induced liver cirrhosis in rats]. Chin. J. Hepatol. 1999, 7, 42–43.
 Guo, C.; Xu, L.; He, Q.; Liang, T.; Duan, X.; Li, R. Anti-fibrotic effects of puerarin on ccl4-induced hepatic fibrosis in rats possibly through the regulation of ppar-gamma expression and inhibition of pi3k/akt pathway. Food Chem. Toxicol. An Int. J. Publ. Br. Ind. Biol. Res. Assoc. 2013, 56, 436–442.
 Qu, Y.; Zong, L.; Xu, M.; Dong, Y.; Lu, L. Effects of 18alpha-glycyrrhizin on tgf-beta1/smad signaling pathway in rats with carbon tetrachloride-induced liver fibrosis. Int. J. Clin. Exp. Pathol. 2015, 8, 1292–1301.
Zhang, B.J.; Xu, D.; Guo, Y.; Ping, J.; Chen, L.B.; Wang, H. Protection by and anti-oxidant mechanism of berberine against rat liver fibrosis induced by multiple hepatotoxic factors. Clin. Exp. Pharmacol. Physiol.
2008, 35, 303–309.
Li, J.; Pan, Y.; Kan, M.; Xiao, X.; Wang, Y.; Guan, F.; Zhang, X.; Chen, L. Hepatoprotective effects of berberine on liver fibrosis via activation of amp-activated protein kinase. Life Sci. 2014, 98, 24–30.
Wang, N.; Feng, Y.; Cheung, F.; Chow, O.Y.; Wang, X.; Su, W.; Tong, Y. A comparative study on the hepatoprotective action of bear bile and coptidis rhizoma aqueous extract on experimental liver fibrosis in rats. BMC Complement. Altern. Med. 2012, 12, 239.
Li, R.; Xu, L.; Liang, T.; Li, Y.; Zhang, S.; Duan, X. Puerarin mediates  hepatoprotection against ccl4-induced hepatic fibrosis rats through attenuation of inflammation response and amelioration of metabolic function. Food Chem. Toxicol. An Int. J. Publ. Br. Ind. Biol. Res. Assoc. 2013, 52, 69–75.
Yen, M.H.; Weng, T.C.; Liu, S.Y.; Chai, C.Y.; Lin, C.C. The hepatoprotective effect of bupleurum kaoi, an endemic plant to taiwan, against dimethylnitrosamine-induced hepatic fibrosis in rats. Biol. Pharm. Bull.
2005, 28, 442–448.
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How long should we wait after portal vein infusion of fructose in mice to reach 90%< to liver
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Dear Sezin,
The important issue is the time point of injection. Please try to do your experiment at late afternoon, if you work on rodents. You will get considerable results depending on the experimental time or you have to fasten the animals at least 8 hours before the injection.
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Chicken model are being used for the study of NAFLD. How does NAFLD differ from FLHS?
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Non-alcoholic fatty liver disease (NAFLD) is a tissue-clinico-pathological entity with histological characteristics similar to those caused by alcohol use in the hepatic parenchyma, but concerns patients with short or no history of alcohol abuse.
The NAFLD is characterized by makronodular hepatic steatosis histologically distinguishable as simple fat accumulation in hepatocytes (steatosis-fatty liver) and steatosis accompanied by necroinflammatory reaction with or without fibrosis. The form of the disease accompanied by fibrosis defined as nonalcoholic steatohepatitis (NASH).
FLHS is a non human fatal accumulation of fat in the liver of the female chickens.
So NAFLD is steatosis to cirrhosis and FLHS is Hepatocyte Damaged resulting in severe bleeding
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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?
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Actually with this new imformation, Prof. Marcel Machado gave a good answer.
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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?
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Bacterial infections occur in one third of hospitalized cirrhotic patients and in approximately half of those admitted with gastrointestinal bleeding. C-reactive protein (CRP) and procalcitonin (PCT) are two plasma biomarkers included among the inflammatory variables in the diagnosis of sepsis. Based on a serum PCT cut-off value of 0.5 ng/mL for the diagnosis of infections, the sensitivity and specificity were reported as 92.5% and 77%, respectively. Some studies suggested serum PCT levels with WBC/PLT ratios can be used as diagnostic biomarkers of cirrhotic patients with infections.
Elevation of PCT could be due to
1.Localized mild-to-moderate bacterial infection
2.Noninfectious systemic inflammatory response
3.Untreated end-stage renal failure
PCT levels may be elevated in patients who do not have sepsis. The plasma levels usually are not very high (<2 ng/mL), but they may increase significantly in certain conditions, e.g. following liver transplantation, during severe and prolonged cardiogenic shock, in patients with severe pancreatitis, and rhabdomyolysis (>2-10 ng/mL). In addition, certain types of autoimmune disorders may induce significant amounts of PCT. Therefore, the etiology of that patient's liver cirrhosis should be learnt.
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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
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There is a very detailed description on UpToDate. ACE inhibitors could cause renal failure (hypoperfusion) when the perfusion pressure cannot be sustained because of decrease in arterial pressure or when it is highly angiotensin II dependent.
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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?
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Thank you, Dr Luis.
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how safe is canagliflozin for diabetes in patients with compensated and decompensated cirrhosis?
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Do NOT use canagliflozin if:
you are allergic to any ingredient in canagliflozin
you have type 1 diabetes
you have high blood or urine ketone levels (diabetic ketoacidosis)
you have severe liver problems or severe kidney problems, or if you are on dialysis
... It does not give in liver cirrhosis...
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any guidelines for refractory ascites?
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some transgenic mice have several white spots on the liver. Is this a kind of cirrhosis or HCA?
1/4/2016 add
This liver is knocked out glucose regulation gene and several mice show these patterns.
this mouse is 20 week old with normal diet. 
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The only way to determine whether this is cirrhosis or some other alteration (inflammation, etc.) is by having a pathologist evaluate this liver histologically.
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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? 
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Interesting senario...
First at all, may I know why the Ig levels were offered to her? Do you worried of Autoimmune hepatitis? Does she has any other immunocompromised illness, such as HIV and Epstein-Barr virus? Haemophilic status?
Pathophysiology of hypogammaglobulinemia:
(a)Conditions that cause an abnormal loss or increased catabolism of Ig:
Nephrotic syndrome and other severe renal diseases
Severe burns
Sepsis
Protein-losing enteropathy
Intestinal lymphangiectasia
(b)Conditions/factors affecting Ig production
Nutritional due to malnutrition or alcoholism
Drugs e.g. phenytoin, carbamazepine, immunosuppressive drugs
Malignancies, especially haemato malignancies
Rheumatological disease, e.g. rheumatoid arthritis or SLE
Viruses including HIV, Epstein-Barr virus, rubella, cytomegalovirus
HCV with low Ig levels - we should think of:
-HCV Related Cryoglobulinemia
-HCV Related Lymphoproliferation
-Drug induced, e.g. rituximab
Few articles did mentioned about the relationship between low Ig levels with Hepatitis C:
IgA deficiency is a risk factor for HCV infection in some patients - IgA deficiency associated with chronic hepatitis C virus infection. A cause or an effect?
by Ilan Y et al. Arch Intern Med. 1993 Jul 12;153(13):1588-92.
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Hi experts
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?
thank you
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Hi Florent,
looking at your pictures, the second analysis is much closer to what I would expect than the first one. If you are in doubt which of the staining is really collagen, looking at your PSR-stained slides using polarized light microscopy might help. Collagen bundles will light up brightly. In our hand imageanalysis in these kind of slides with ImageJ works best by making a RGB-stack and threshold the green slice using the Yen method. It looks like your pictures are slightly underexposed which makes things harder as well.
good luck,
Reinout
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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? 
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According to this article, the AST/ALT ratio can decrease when uremia sets in. Any idea if your research subjects began experiencing uremia when these readings were taken?
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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.
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Dear Dr Rosas,
thank you for your very pertinent idea.
eventhough, in our patient we didn't observed, lymphadenopathy, pancreatitis, tubbulointertitial nephritis, nor retropetoneal fibrosis, and that there was no storiform pattern in the histology of major salivary glands biopsy, and also that PBC ARE VERY RARELY REPORTED in IG4 related disease...we will look for Ig4 elevation in our case.
thank you again. 
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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?
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L-carnitine for Muscle Cramps in Patients with Cirrhosis
Nakanishi H et al. Clin Gastroenterol Hepatol 2015 Aug.
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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?
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Another point to remember is the infection of the ascitic fluid itself [spontaneous bacterial peritonitis] which is quite common in decompensated chronic liver disease and may be the source of sepsis. Other less common variants called monomicrobial non neutrocytic bacterascites [earlier stage in development of SBP] and culture negative neutrocytic bacterascites [where organisms cannot be grown in culture as Dr Biddulph mentioned] also occur and can be the source of SIRS. Even fungal infections are common in late stages of the disease
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is there any protocol for using bee honey for cirrhosis
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Thanks dear Dr Nader, 
That is good,
and to know the basic nutrients that honey contains I will do so, and results will be discussed with you and all other researchers who are interested in this topic
thanks. .
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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)?
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 I think manual cell counter is a best method. I was see sometimes strong difference betwen this 2 methods and in my experience normally the manual method y more consistent with the others clinical and laboratories parameters
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Have you seen other location of this sign?
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It is a very interesting question, Zmicer. Actually, spider angiomas also called as telangiectasias, are not specific to liver cirrhosis or portal hypertension. Nevertheless, they are frequent (not exclusive) in liver cirrhosis and located on skin and mucosa of superior vena cava territory. It is certain that hyper estrogenic theory of genesis is the most mentioned, however it has never been proved. We can see them all the long of GI tract from mouth to rectum without relation to liver cirrhosis, neither plasma estrogen high levels nor portal hypertension. In these locations they are frequent cause of bleeding and risk factors are genetics, advanced age and renal insufficiency.
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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.
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Luisa, the most likely reasons are 1) Tissue is differentially homogenized, some being more completely homogenized than others (i.e., TUBA levels are reflective of degree of homogenization, 2) Tissue composition is different for each sample, some with more cells than others (i.e., TUBA levels is reflective of cellular content in tissue), and 3) TUBA expression is impacted by the disease conditions (i.e., TUBA levels reflect degree of pathology.
Other possible reasons are you have loaded an unequal amount of total protein, not likely assuming you have performed a good protein quantitation assay. If the protein levels vary widely between your samples, this could be a source of your variation, even with appropriate quantitation. Ideally, your lysates should have protein at a concentration of about 1-3ug/uL. Much less or more can result in some issues. Depending on what you are attempting to detect (very low abundant protein?), I don't know that 50ug of total protein is necessary. 10-20ug is sufficient for most tissues, and I go down as low as 5 ug for cells from culture. At or above 50ug you start to run into problems with protein migration, especially in mini-gels with 12+ wells.
To determine if you have loaded grossly different amounts of total protein then consider staining your gel with commassie blue, or your membrane with Ponceu S. These will show whether or not your loaded equal protein. I bet you have, so then you may consider the more likely reasons I've stated above for future tissue processing.
Best of luck.
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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. 
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Just to add some suggestions when we have cirrhosis of unknown origin we always check for non alcoholic steatohepatitis (metabolic syndrome, overweight/obesity, insulin resistance...), iron overload (genetic or secondary), Wilson Disease and alpha1antitripsin. Furthermore a number of cirrhosis in India might depend from vascular disease causing macro or micro thrombosis in the liver (Budd Chiari ...) 
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The patient is S/P TAH. BSO and has been taking oral Estradiol.
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Hormon replacement, as well as oral contraceptives remain as two-edged  sword, since sexual hormones are capable of inducing protective or deleterious effects on liver diseases, depending on several factors, the very disease, age, estrogens or progestins type administered to women, genetic propensity, etc. Given the complexity of primary billiary cirrhosis, as it has been recognized as an autoimmune injury; I invite you to read my last article wherein you may find any further information which perhaps helps you. You will please find it attached.
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The distinction between HRS and ATN can be clinically uncertain (if biopsy is under risk).
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Dear Adrian and Dear Zmicer
Adrian, I agree with your last comment.  Then, one can conclude that HRS is a prerenal, non responding to vascular volume expanders and non renal parenchimal condition,  exclusive of cirrhotic patients ,occurring spontaneously or secondary to a precipitating factor. Right?
It leads to answer  Zmicer´s question :Type 1 hepatorenal syndrome (HRS) does not  lead to acute tubular necrosis (ATN) in the absence of other insult.
Best regards both
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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?
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Dear Dr.Strebel,
I agree with what you have pointed out. With reference to the  discussion, I have mentioned that there is no role of the drugs in cirrhosis. The other point is that NASH by itself is not a fully curable disease and hence both UDCA and Vitamin E are given for short time periods [may 6m - 1 year] for normalisation of liver enzymes if found elevated. There is no question of giving both drugs for years together. At least I have found it extremely useful in my patients. 
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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.
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I thank all for the responses.
I think, that rapid deterioration or “critically ill cirrhotic” could be regarded as acute decompensation and as acute-on-chronic liver failure (ACLF).
ACLF is potentially reversible, but acute decompensation could also be potentially reversible condition. ACLF usually results following a precipitating event (bacterial infection, GI bleeding, HBV etc.), and the AD develops because of the same events.
It is important to know, why one patient is tolerant to accelerating events, but others are not.
Excellent research CANONIC has given us the tool for stratification of risk for critically ill cirrhotic (CLIF-SOFA score).
Identification of risk defines early specific treatments and intensive management.
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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.
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Here are a few things that I’ve learned from my experience using CCl4 injections to induce liver inflammation and fibrosis in mice.
For the experiments that I was doing, the goal was to induce chronic inflammation/fibrosis – the dosage and injection regimen will be different (namely, a higher dose with fewer injections) if the goal is to induce acute liver damage.
Starting at 8 weeks of age, I injected male C57BL/6J mice intraperitoneally with a solution of 10% CCl4 in mineral oil. Mice were injected with ~2.5ul per gram body weight twice a week for 12 weeks. This protocol was sufficient to induce chronic liver inflammation, steatosis, and fibrosis that was maintained until at least 65 weeks of age.
I’ve tried both corn oil and mineral oil. In either case, with repeated IP injection the oil ends up forming small white inclusion bodies attached to the exterior of the peritoneal organs (liver, intestines, etc.). This is likely because the amount of oil injected is too much for the animals to completely process, so the excess gets sequestered in these inclusion bodies. (They are also formed with repeated injection of oil alone, so this is not an effect of the CCl4). In my experience, corn oil induced a stronger reaction in the mice, leading to a larger number and size of these inclusion bodies, as compared to mineral oil. As they are likely to affect the animals’ physiology in some way, my conclusion was that mineral oil was a more appropriate vehicle for delivery.
I would suggest using sterile oil – it may not be absolutely necessary, but its minimal expense is justified by the enhanced experimental control it provides. Sterile mineral oil is available from Sigma (product #M5310).
Given CCl4’s high volatility, I think it would be harder to maintain a consistent effective dose without mixing it into some sort of delivery vehicle.
I’d be happy to send a more detailed protocol and/or example images of what I described if you’re interested.
Good luck!
Jesse
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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.
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Thank you Huy. It will help me greatly. Sincere thanks.
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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.
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common sense
hyperdynamic changes are related to the severity of the liver disease, therefore ... 
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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.
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Window concept for beta blocker is new in portal hypertension. So window period for beta blocker is very short from primary prophylaxis to decompensated cirrhosis without the risk factors (I have already mentioned). Recent studies have shown increased renal failure (HRS) and mortality with beta blocker in refractory ascites, MAP < 82 mm hg, CI < 1.5. In these high risk group endoscopic vareceal ligation is the best alternative
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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.
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Of course!
There is a decrease of several coagulation factors, but also an umpaired anticoagulation proteins realease and cleavage!, and a fbrinolysis disbalance, with a trend to hyperfibrinolisis and disfibrinogenemia!
Unnecessary plasma transfusion (with citrate as anticoagulant) could modify this fragil balance
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What implications in response to exercise for patients with cirrhosis?
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Dear Alexandra
I totally agree with the previous answer (Thomas Riley)
According to ACSM's guidelines("ACSM's exercise management for persons with chronic diseases and disabilities" by Durstine JL, Moore GE), patients with liver failure have reduced VO2 peak, decrease in muscle mass & strength and alcoholic myopathy. Special considertions during exercise: avoid Valsalva (d/t esophageal or gastric varices), and be aware of potential bleeding (d/t coagulation disorders - so avoid contact exercise, and ensure safe environment). Exercise intensity - fatigue dependent so monitor RPE.
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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).
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Another resource: the group at Inova Health Systems (Fairfax, VA) reported its analysis of chronic liver disease trends using data from National Health and Nutrition Examination Surveys. You might give Dr Younossi a call about how to access that database. Article: "Changes in the Prevalence of the Most Common Causes of Chronic Liver Diseases in the United States From 1988 to 2008" Clinical Gastroenterology and Hepatology Vol 9, No 6 (June 2011) pp 524-530
See full text at:
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The literature is mixed up between the two
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In stable patients without signs of metabolic decompesation, there is no need to reduce protein intake. In patients with hyperammoniemia or clinical signs of encephalopathy it is opportune to reduce proteins in the diet, which could been supplemented by branched chain amyno-acids.
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There are many reports for hepatic adverse effects of statins
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Dear Ahad,
there are reports on liver injury by statins, yet this adverse event is relatively rare in the general population. In fact, drug-induced liver injury does not occur more often in patients with cirrhosis or other liver diseases, but its consequences might be more severe due to a lower functional reserve in the already impaired liver.
The problem of statins and liver disease was reviewed by Russo and Jacobson quite comprehensively (http://ccjm.org/content/71/1/58.short) as well as Tandra and Vuppalanchi (http://www.ncbi.nlm.nih.gov/pubmed/19627660). These papers conclude that close monitoring can protect from unintended toxicity and recommend strategies for dose adjustment to minimize risks for hepatotoxicity.
In terms of drug-induced liver injury you are never completely save, but in the case of statins there seems to be compelling evidence, that the benefit outweighs the risks by far.
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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?
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... at least in children and adolescents there seems to be an association of age/ pubertal stage with surrogate markers of steatosis and steatohepatitis. For more in-depth information, I'd like to refer to our paper "Gender-specific prevalences of fatty liver in obese children and adolescents: roles of body fat distribution, sex steroids, and insulin resistance" (The Journal of clinical endocrinology and metabolism 09/2009; 94(10):3872-81).
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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.
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Look at the brief summary of liver functions:
1. Synthetic: albumin, coagulation proteins, some binding proteins etc.
2. Metabolic/homeostatis: glucose, lipids etc.
3. Storage: glycogen, iron, copper, lipid etc.
4. Catabolic: ammonia/urea, hormones, detoxification of drugs, chemicals etc.
5. Excretory: bile excretion
Why you are focusing on AST and ALT? You should define what exactly you want to know/study and further build very accurately your questions.
Generally speaking – you should read classical hepatology textbooks.
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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.
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Atta, excellent question. In biliary disorders, the literature suggests a cholangiocyte origin of increased serum GGT. However, in non-biliary chronic alcohol liver disorder, the origini of increased serum GGT is more likely the injured hepatocyte, disruption and extrusion of GGT into the canalicular region, and eventual absorption into the bloodstream. See excellent study by Irie et al:
"Hepatic expression of gamma-glutamyltranspeptidase in the human liver of patients with alcoholic liver disease" Hepatology Research (Nov 2007) 37(11):966-973. Abstract at: http://www.ncbi.nlm.nih.gov/pubmed/17854466
I cannot find a weblink for the full article. Here is Abstract:
Background: Gamma-glutamyltranspeptidase (GGT) has been recognized as an enzyme that converts glutathione into cysteine, and it is localized predominantly within the liver. Serum GGT is clinically recognized as the most useful marker for diagnosis of alcoholic liver disease (ALD). Methods: GGT localization within the liver was examined immunohistochemically using an anti-GGT antibody and was visualized by confocal laser scanning microscopy in ALD and normal livers. Double immunostaining for GGT and dipeptidylpeptidase-IV (DPP-IV) was carried out to evaluate GGT localization in greater detail. Results: Expression of GGT protein and mRNA was studied with immunoblot analysis and in situ hybridization, respectively. Immunohistochemically, the expression of GGT in the normal liver was faintly demonstrated in the bile canaliculi of hepatocytes and in biliary epithelial cells. In ALD livers, GGT was clearly demonstrated at the same sites. Double immunostaining demonstrated that GGT and DPP-IV were colocalized in hepatocytes in the ALD liver. In situ hybridization clearly demonstrated GGT-mRNA within the cytoplasm of hepatocytes and biliary epithelial cells. Immunoblot analysis revealed that GGT protein expression was increased in the ALD livers compared with that seen in the normal livers. Conclusion: These findings indicate that GGT in control and alcoholic livers is synthesized in hepatocytes and biliary epithelial cells, and is localized within the bile canalicular membrane and the luminal membrane in those cells, respectively. In conclusion, GGT synthesis and protein expression are increased in ALD livers, leading to the elevation of serum levels of GGT that are commonly noted in patients with the disease
For source of increased serum GGT in biliary cholestasis disorder, see Bulle at:
"Mechanism of gamma-glutamyl transpeptidase release in serum during intrahepatic and extrahepatic cholestasis in the rat: a histochemical, biochemical and molecular approach." in Hepatology. 1990 Apr;11(4):545-50 Abstract on web at:
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What is the pathophysiology of ILD with PBC.
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Thanks for very useful information Dr Mooney.
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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.
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Thank you
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Mesh versus tissue repair?
Intraperitoneal drain?
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There are some crucial questions in such cases: which organ exactly is incarcerated, and wheter the incarcerated content is vital or not, and is there an infection? So in my opinion laparoscopy is the most reliable option – you can reduce the hernia, can see what is incarcerated and wheter there are signs of necrosis, and also take fluid for culture. If there is a bowel necrosis the need of resection is clear. But if it is not the problem is always whether there is an infected ascites, as there is never been a good idea to place a mech in infected conditions. So better reduce the hernia, apply external pressure of the sac, for example with gauzes and fix them with adhesive bands or folio drape. Start antibiotics keeping the guidelines for the treatment of bacterial peritonitis in cirrhosis. Do not remove ascites if not visibly purulent, no drains, as they usually caused nearly uncontrollable homeostatic disturbances due to huge amount of fluid losed. When the patient is stable and infection is controlled by antibiotics you can move back to OR and do that what you prefer. I think the laparoscopic repair is better. So the philosophy is that there is absolutely no need to address both problems – incarceration and hernia itself in one stage in a patient that is usually not fit for surgery and had severe comorbidities. The exception might be the patients requiring bowel resection.
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Alcoholic Cirrhosis
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There are 2 widely used ones in the UK:
1. Maddrey's discriminate function
2. Glasgow Score
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Can anyone explain what's the different between congestive hepatopathy, congestive cirrhosis and cardiac cirrhosis?
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HI
You can find your answer by reading this paper: Cardiovascular Diseases and the Liver
Clinics in Liver Disease - Volume 15, Issue 1 (February 2011) written by: Ilan S. Weisberg, and Ira M. Jacobson, The paper is attached
I hope it helps
Hossein