Differences

This shows you the differences between two versions of the page.

--- home:tests:liver [05.02.2011] – external edit 127.0.0.1
+++ home:tests:liver [10.12.2018] – [Patients experiences] sallieq
@@ Line 1: / Line 1: @@
-<IncompleteNotice>
 ====== Tests of liver function ======
-Liver function tests (LFTs or LFs), which include liver enzymes, are groups of clinical biochemistry laboratory blood assays designed to give information about the state of a patient's liver.
+Liver function tests (LFTs or LFs), which include liver enzymes, are groups of clinical biochemistry laboratory blood assays designed to give information about the state of a patient's liver. Normally, only very small amounts of these enzymes are present in your blood. However, a laboratory report of elevated liver enzymes is not uncommon. Further, it is not unusual to see liver enzymes elevate while on the Marshall Protocol even if liver disease was not previously suspected because temporary immunopathology is unavoidable as a part of recovery.
@@ Line 23: / Line 23: @@
 Abnormal liver function measures are expected to be seen in many MP patients because these measures are an indication of an inflammatory response to infection. The experience of Autoimmunity Research Foundation has, thus far, shows that as long as immunopathology is tolerable while liver function remains abnormal, there's no need to make any changes in dosing of the MP medications. However, physicians and patients should always assess if immunopathology is too strong. If this is the case, taking [[home:mp:managing_immunopathology|measures to reduce immunopathology]] is always recommended.
+Note that NSAIDs (non-steroidal anti-inflammatory drugs) such as Tylenol can increase liver enzymes. If pain medication is needed, an alternative should be considered. Nutritional and herbal supplements may also affect values of liver function.
-===== Beneficial effects of ARBs on liver disease =====
+===== Beneficial effects of olmesartan on liver disease =====
-Some of the documented protective effects of ARBs include the ability to:
+The renin-angiotensin system (RAS) is frequently activated in patients with chronic liver diseases. Angiotensin-II (AT-II) has been suggested to play an important role in the progression of liver fibrogenesis.(({{pubmed>long:11584371}})) (({{pubmed>long:16919500}}))
-  * inhibit liver fibrosis and aid liver healing(({{pubmed>long:12871826}}))
+Some of the documented protective effects of the angiotension receptor blocker, olmesartan, include the ability to:
-  * reduce liver fibrosis(({{pubmed>long:19303015}}))
+  * **inhibit liver fibrosis and aid liver healing** – Olmesartan medoxomil was given to fibrotic rats. Liver hydroxyproline content, the mRNA expression of collagen alpha1(I) and alpha-smooth muscle actin (alpha-SMA), and plasma levels of transforming growth factor-beta1 (TGF-beta1) were significantly reduced by olmesartan treatment, suggesting that olmesartan improved liver fibrosis.(({{pubmed>long:12871826}})) A second study came to similar conclusion.(({{pubmed>long:19303015}}))
+  * **reduce fatty liver** – Fatty liver developed in Zucker fatty rats was ameliorated by olmesartan treatment.(({{pubmed>long: 15082419}})) "Taken in sum," one team concluded, "ARB improves the overproduction and accumulation of TG in the liver associated with insulin resistance, and it does so through mechanisms independent of its hypotensive action."
-Br J Pharmacol. 2003 Jul;139(6):1085-94.
-An angiotensin II type 1 receptor antagonist, olmesartan medoxomil, improves experimental liver fibrosis by suppression of proliferation and collagen synthesis in activated hepatic stellate cells.
-Kurikawa N, Suga M, Kuroda S, Yamada K, Ishikawa H.
-Pharmacology and Molecular Biology Research Laboratories, Sankyo Co., Ltd, 2-58, Hiromachi 1-chome, Shinagawa-ku, Tokyo 140-8710, Japan. kurikuri@shina.sankyo.co.jp
-Abstract
-. We studied the effect of a new angiotensin II type 1 (AT(1)) receptor antagonist, olmesartan medoxomil (olmesartan), on the fibrogenic responses in rat hepatic stellate cells (HSCs) and liver fibrogenesis. 2. Olmesartan (1 mg kg(-1) per day) was orally administered to fibrotic rats, induced by bile duct ligation. Liver hydroxyproline content, the mRNA expression of collagen alpha1(I) and alpha-smooth muscle actin (alpha-SMA), and plasma levels of transforming growth factor-beta1 (TGF-beta1) were significantly reduced by olmesartan treatment, suggesting that olmesartan improved liver fibrosis. Interestingly, AT(1) receptors were found to be expressed in alpha-SMA-positive cells in the fibrotic area of livers in bile duct-ligated rats by immunohistochemical analysis. Olmesartan treatment reduced the number of these cells. 3. In vitro experiments showed that angiotensin II (Ang II) treatment induced proliferation and collagen synthesis, and upregulated the profibrogenic cytokines, TGF-beta1 and connective tissue growth factor (CTGF), in rat primary HSCs. Olmesartan blocked all these effects of Ang II. 4. Based on these results, since activated HSCs were found to express AT(1) receptors and Ang II is thought to play an important role in the pathogenesis of liver fibrosis by binding to these receptors, olmesartan may act as a potent antifibrotic drug to suppress the proliferation, collagen synthesis and the expression of profibrogenic cytokines in activated HSCs by blocking these receptors.
-PMID: 12871826
-Am J Physiol Endocrinol Metab. 2004 Aug;287(2):E227-32. Epub 2004 Apr 13.
-Angiotensin II type 1 receptor blocker ameliorates overproduction and accumulation of triglyceride in the liver of Zucker fatty rats.
-Ran J, Hirano T, Adachi M.
-First Department of Internal Medicine, Showa University School of Medicine, Tokyo 142-8666, Japan.
-Abstract
-The effects of angiotensin II type 1 receptor blocker (ARB) on triglyceride (TG) metabolism associated with insulin resistance were explored in Zucker fatty (ZF) rats. Olmesartan medoxomil, a newly developed ARB, was given as a 0.01% drinking solution ad libitum to ZF and Zucker lean (ZL) rats for 4 wk. Olmesartan lowered blood pressure in both strains to the same extent. ZF rats had a markedly low insulin sensitivity index (SI) and glucose effectiveness (SG), together with significantly increased glucose levels. Olmesartan treatment substantially elevated both SI and SG. The ZF rats were hyperlipidemic, with plasma TG levels sixfold higher than those of the ZL rats. Olmesartan remarkably decreased the plasma free fatty acid level in the ZF rats, but it did not exert a significant effect on the plasma TG level. The TG secretion rate assessed by the Triton WR-1339 technique was almost six times higher in the ZF than in the ZL rats, and olmesartan treatment suppressed this TG overproduction by one-half. The TG content in the liver was ten times higher in the ZF than in the ZL rats, and olmesartan halved this high hepatic TG content without affecting the cholesterol content. The fatty liver developed in the ZF rats was ameliorated by olmesartan treatment. Olmesartan treatment had no significant effects on TG metabolism or insulin sensitivity in the ZL rats. Taken in sum, ARB improves the overproduction and accumulation of TG in the liver associated with insulin resistance, and it does so through mechanisms independent of its hypotensive action.
-PMID: 15082419
-Hepatology. 2001 Oct;34(4 Pt 1):745-50.
-Angiotensin-II type 1 receptor interaction is a major regulator for liver fibrosis development in rats.
-Yoshiji H, Kuriyama S, Yoshii J, Ikenaka Y, Noguchi R, Nakatani T, Tsujinoue H, Fukui H.
-Third Department of Internal Medicine, Nara Medical University, Kashihara, Nara, Japan. yoshijih@naramed-u.ac.jp
-Abstract
-The renin-angiotensin system (RAS) is frequently activated in patients with chronic liver diseases. Angiotensin-II (AT-II) has been suggested to play an important role in liver fibrogenesis. It induces hepatic stellate cell (HSC) proliferation and up-regulates the transforming growth factor beta(1) (TGF-beta(1)) expression via AT-II type 1 receptor (AT(1)-R) in vitro. The aim of the present study was to examine the in vivo effect of candesartan (CA), a clinically used AT(1)-R blocker (ARB), and perindopril (PE), an angiotensin-converting enzyme (ACE) inhibitor (ACE-I), on pig serum-induced liver fibrosis development in rats. The clinically available comparable doses of CA and PE significantly attenuated the fibrosis development. These inhibitory effects of PE and CA were also found in the on-going liver fibrosis model. The hepatic hydroxyproline and serum fibrosis markers were significantly suppressed by CA and PE treatment. Furthermore, the alpha smooth muscle actin (alpha-SMA) positive cells in number were markedly suppressed by CA and PE treatment. Similarly, the hepatic TGF-beta(1) protein and messenger RNA (mRNA) levels were significantly suppressed. Our in vitro study showed that AT-II increased the TGF-beta(1) mRNA expression in the activated HSCs, and this effect was totally blocked by CA. These results suggested that the RAS, especially AT-II and AT(1)-R interaction plays a pivotal role in liver fibrosis development through HSC activation. Because both CA and PE are widely used in clinical practice without serious side effects, these drugs may provide an effective new strategy for anti-liver fibrosis therapy.
-PMID: 11584371
-Hepatol Res. 2006 Oct;36(2):124-9. Epub 2006 Aug 17.
-Angiotensin-II and vascular endothelial growth factor interaction plays an important role in rat liver fibrosis development.
-Yoshiji H, Kuriyama S, Noguchi R, Ikenaka Y, Kitade M, Kaji K, Yoshii J, Yanase K, Yamazaki M, Asada K, Tsujimoto T, Akahane T, Uemura M, Fukui H.
-Third Department of Internal Medicine, Nara Medical University, Shijo-cho 840, Kashihara, Nara 634-8522, Japan.
-Abstract
-Both angiotensin-II (AT-II) and vascular endothelial growth factor (VEGF) have been shown to play important roles in the progression of liver fibrosis. However, the interaction of AT-II with VEGF in the liver fibrosis has not been elucidated yet. The aim of the current study was to elucidate a possible association between these molecules, especially in conjunction with the hepatic stellate cells (HSC). The effect of AT-II type 1 receptor blocker (ARB) was assessed on several indices of choline-deficient l-amino acid-defined (CDAA)-induced liver fibrogenesis. This ARB significantly suppressed liver fibrosis development along with suppression of the VEGF expression and neovascularization in the liver. In the cultured activated HSC, AT-II induced VEGF in a dose- and time-dependent manner. ARB and LY333531, a protein kinase C (PKC) inhibitor, attenuated this augmentation. These results indicated that AT-II and VEGF interaction played an important role in liver fibrosis development, and that in the activated HSC, AT-II utilized type 1 receptor and PKC as an intracellular signaling pathway to induce VEGF.
-PMID: 16919500
@@ Line 95: / Line 57: @@
-{{tag>incomplete}}
+<blockquote>
-===== Notes and comments =====
+I also wanted to note that a couple of years ago independent of the MP I had a slightly elevated ALT reading. My doc wasn't too worried because he said typically it was a fairly high reading which caused medical concern but he had no clue why it was just slightly elevated. A couple of months later I decided to google it and found a newly released study from UNC-CH that Tylenol could raise ALT levels slightly even in healthy people. The weird thing was that it didn't take much and the elevation lasted several days after the Tylenol was stopped. I also found that environmental toxins and junk food could raise the values according to some sources.It just sounds like the ALT reading is very sensitive in some of us. Just think what a total bacterial dump would do to something this sensitive.
-TECHREVISE
-  * Legacy content
+//**Mindy**, MarshallProtocol.com// </blockquote>
-    * f200:
-A laboratory report of elevated liver enzymes is common. It doesn't indicate a specific disease. Liver enzymes help maintain a variety of chemical and metabolic processes that occur in the liver. Normally, only very small amounts of these enzymes are present in your blood. Treatment of elevated liver enzymes depends on the underlying cause. It is important to tell your doctor about any nutritional or herbal supplements you are taking.
-Th1 inflammation commonly affects the liver, although it may be subclinical and most liver diseases cause only mild symptoms initially. Patients may be told they have "fatty liver disease" or cirrhosis.
-An initial step in detecting liver damage is a simple blood test to determine the presence of certain liver enzymes in the blood. Under normal circumstances, these enzymes reside within the cells of the liver. But when the liver is injured, these enzymes are spilled into the blood stream.
-Liver function tests (LFTs or LFs), which include liver enzymes, are groups of clinical biochemistry laboratory blood assays designed to give information about the state of a patient's liver.
-Among the most sensitive and widely used of these liver enzymes are the aminotransferases. They include aspartate aminotransferase (AST or SGOT) and alanine aminotransferase (ALT or SGPT). These enzymes are normally contained within liver cells. If the liver is injured, the liver cells spill the enzymes into blood, raising the enzyme levels in the blood and signaling the liver damage. AST and ALT are the two most useful liver enzymes.
+{{tag>tests}}
+===== Notes and comments =====
-See What do my lab tests mean?
-It not unusual to see liver enzymes elevate while on the MP even if liver disease was not previously suspected because immunopathology is unavoidable during recovery. Your doctor should consider the risk/benefit ratio of treatment with the MP because liver damage will not resolve unless the CWD bacteria are killed.
-We cannot define the upper limits of liver enzymes for someone on the MP who needs to recover liver function. The usual scenario that docs see is expected worsening of liver function whereas immunopathology, even if relatively severe, is temporary and probably justified in terms of expected long-term benefit. If this is pointed out to doc, s/he may not be so concerned.
-"Any signs of damage to your liver are just that - signs. Any suggestion that there might be liver damage due to any of the MP drugs is totally unfounded in science."
-~Trevor
-Angiotensin receptor blocking drugs, such as Benicar, are known to have organ-protective effects.
-An angiotensin II type 1 receptor antagonist, olmesartan medoxomil, improves experimental liver fibrosis by suppression of proliferation and collagen synthesis in activated hepatic stellate cells.
-NSAIDs (non steroidal anti inflammatory drugs)
-These commonly prescribed pain medications can increase liver enzymes. If pain medication is needed, an alternative should be considered. See What should I do for liver or gallbladder pain?
- * f202:
-Cell death (apoptosis) elevates ALT and resolves fibrotic tissue
-(filelink)
+Couldn't find a study to support this:
+<blockquote>Cell death (apoptosis) elevates ALT and resolves fibrotic tissue
 The sensitive enzyme ALT is elevated when there is liver inflammation and cell death (apoptosis). We know that when the immune system is effectively fighting infection, the result is cell death. But this is the road to recovery.
@@ Line 152: / Line 87: @@
 ~Belinda
+</blockquote>
-<blockquote>
-I also wanted to note that a couple of years ago independent of the MP I had a slightly elevated ALT reading. My doc wasn't too worried because he said typically it was a fairly high reading which caused medical concern but he had no clue why it was just slightly elevated. A couple of months later I decided to google it and found a newly released study from UNC-CH that Tylenol could raise ALT levels slightly even in healthy people. The weird thing was that it didn't take much and the elevation lasted several days after the Tylenol was stopped. I also found that environmental toxins and junk food could raise the values according to some sources.It just sounds like the ALT reading is very sensitive in some of us. Just think what a total bacterial dump would do to something this sensitive.
-//**Mindy**, MarshallProtocol.com// </blockquote>
 ===== References =====

home/tests/liver.txt · Last modified: 09.14.2022 by 127.0.0.1