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Complementary and Alternative Medical Lab Testing Part 6: Liver and Gallbladder
Complementary and Alternative Medical Lab Testing Part 6: Liver and Gallbladder
Complementary and Alternative Medical Lab Testing Part 6: Liver and Gallbladder
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Complementary and Alternative Medical Lab Testing Part 6: Liver and Gallbladder

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Complementary and Alternative Medical Lab Testing (CAM Labs) contains summaries of the published research on lab tests, primarily from PubMed trials on humans. Each chapter (disease) begins with a brief summary of conventional lab tests, followed by additional lab tests, including diabetes, insulin resistance, metabolic syndrome, inflammation, etc. There are sections on endocrine hormones (thyroid, adrenal, sex steroids) and environmental medicine (toxic heavy metals). The nutritional assessments section includes minerals, vitamins and amino acids.

CAM Labs 6 – Liver and Gallbladder

1. Cirrhosis
2. Fatty Liver (Steatosis)
3. Gallstones (Cholelithiasis)
4. Gilbert's Disease
5. Hepatitis, Autoimmune
6. Hepatitis, Viral
7. Wilson's Disease

LanguageEnglish
Release dateJun 4, 2016
ISBN9781311411747
Complementary and Alternative Medical Lab Testing Part 6: Liver and Gallbladder
Author

Ronald Steriti

Dr. Ronald Steriti is a graduate of Southwest College of Naturopathic Medicine and currently is researcher for Jonathan V. Wright at the Tahoma Clinic.

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    Book preview

    Complementary and Alternative Medical Lab Testing Part 6 - Ronald Steriti

    Complementary and Alternative

    Medical Lab Testing

    Part 6: Liver and Gallbladder

    By Ronald Steriti, ND, PhD

    ©

    Complementary and Alternative Medical Lab Testing Clinician’s Guide Part 6: Liver and Gallbladder

    By Ronald Steriti, ND, PhD

    Copyright © 2016

    All rights reserved. No part of this book may be reproduced in any form or by any means, including photocopying, including in a web site, or stored in a retrieval system, or transmitted in any form by any means, without expressed, written permission of the copyright owner.

    The contents of this document are the sole property of the author.

    Disclaimer

    This book has not been evaluated by the FDA and is not intended to diagnose, treat, cure or prevent any disease.

    The information contained in this book is for educational purposes only, and should not be construed as medical advice or instruction. No action should be taken based solely on the contents of this book. Readers should consult appropriate health officials.

    While extensive efforts have been made to ensure the accuracy of the information contained, the possibility of errors, omissions, and misinterpretations cannot be ruled out. The reader is advised to consult the original references for verification and clarification.

    Foreward

    This book is a summary the published research on lab tests, primarily from PubMed. The studies are limited to those with trials on humans. As such, some labs may be excluded due to the lack of published research. That is simply a reflection of the current state of research - much more work is needed!

    Although this book may be useful for differential diagnosis, lab tests are can also be used to identify inderlying causes and associated conditions.

    The sections on conventional lab tests are purposefully brief. These tests are typically used to confirm a diagnosis. There are other more comprehensive sources of information on conventional medical lab testing.

    Table of Contents

    1. Cirrhosis

    2. Fatty Liver (Steatosis)

    3. Gallstones (Cholelithiasis)

    4. Gilbert's Disease

    5. Hepatitis, Autoimmune

    6. Hepatitis, Viral

    7. Wilson's Disease

    Chapter 1. Cirrhosis

    Conventional Lab Tests

    Albumin and total serum protein

    Partial thromboplastin time or prothrombin time/INR

    Bilirubin, AST, ALT, and LDH

    Antinuclear antibodies (ANA)

    Ferritin and iron tests

    Tests for hepatitis B and hepatitis C

    Blood alcohol level (BAL)

    Serum ceruloplasmin testing (Wilson's disease)

    Alpha1-antitrypsin

    Additional Lab Tests

    Fasting Glucose, Hemoglobin A1C

    About 30% of patients with cirrhosis have diabetes mellitus (DM). DM, which develops as a complication of cirrhosis, is known as hepatogenous diabetes. Treatment of the diabetes is complex due to liver damage and hepatotoxicity of oral hypoglycemic drugs. (Garcia-Compean et al., 2009)

    A study reviewed medical files for presence of Type 2 diabetes and potential confounders in 94 patients with cirrhosis (cases) and compared these with a control group of 107 patients with non-ulcer dyspepsia. The aetiology of our cirrhosis population was alcohol (59%), viral hepatitis (10%), biliary cirrhosis (3%) or cryptogenic (28%). Prevalence of Type 2 diabetes was significantly higher in patients with cirrhosis than in control subjects: 35/94 (37%) vs. 7/107 (7%) (OR 8.5, 95% CI 3.5-20.2, P < 0.001). After adjustment for age, sex, family history of Type 2 diabetes, alcohol use and BMI, cirrhosis remained significantly associated with Type 2 diabetes (OR 13.6, 95% CI 4.3-42.9, P < 0.001). Most cases of Type 2 diabetes were already diagnosed before diagnosis of cirrhosis (21/35, 60%) or were incidentally found together with cirrhosis (5/35, 14%). Liver cirrhosis had a strong, independent association with Type 2 diabetes. (Wlazlo et al., 2010)

    Insulin Resistance, Metabolic Syndrome

    This review summarizes the available data documenting a detrimental role of obesity and insulin-resistance on the risk of appearance of clinical events in patients with cirrhosis. (Berzigotti and Abraldes, 2013)

    Forty-nine patients with cirrhosis and portal hypertension (PH) were included. Mean HOMA-2 index was 3 +/- 1.4. Fifty-seven percent of patients had IR. A weak correlation between HOMA-2 index and HVPG was observed. Eighty-six percent of patients had clinically significant PH (CSPH). HOMA-2 index was an independent predictor of CSPH. However, in patients with CSPH, the correlation between HOMA-2 index and HVPG was lost. HVPG, but not IR, predicted the presence of esophageal varices. (Erice et al., 2012)

    C-Reactive Protein (CRP)

    One-hundred and forty-eight consecutive cirrhotic patients with Child-Pugh score >/= B8 and without hepatocellular carcinoma were prospectively included and followed for 182 days. The primary end point was 6-month survival. In Child-Pugh score >/= B8 cirrhotic patients, persistent CRP levels >/= 29 mg/L predicted short-term mortality independently of age, MELD, and co-morbidities, and better than infection or clinically-assessed systemic inflammatory response syndrome (SIRS). (Cervoni et al., 2012)

    In 45 stable patients with cirrhosis on the basis of alcohol consumption, hsCRP levels were significantly higher in patients compared with controls (P<0.05) and the highest in patients belonging to Child-Pugh class C. hsCRP levels correlated with markers of liver dysfunction and with the hepatic venous pressure gradient (r=0.48, P<0.001). hsCRP values above the median level of 5.3 mg/l were associated with a highly increased mortality (P=0.001). Model for End-Stage Liver Disease score (P=0.01) and hsCRP (P<0.05) provided independent prognostic information. Cytokines had no discernible value in predicting survival. hsCRP is elevated in patients with cirrhosis and is associated with portal hypertension and decreased survival. hsCRP is a promising prognostic marker in cirrhosis, which may improve the selection of candidates for liver transplantation. (Mortensen et al., 2012)

    A prospective study was designed to clarify whether serum CRP value could be used as an indicator of bacterial infection in patients with cirrhosis. A total of 129 sessions of admission (bacterial infection 46, bacterial infection and gastrointestinal hemorrhage 5, gastrointestinal hemorrhage 24, other causes 54) from 94 patients with cirrhosis were studied. Serum CRP value was determined on admission. The normal range of CRP value was < 6 micrograms/ml. The serum CRP values obtained on admission ranged from 3 to 232 micrograms/ml in patients with bacterial infection, 17 to 178 micrograms/ml in patients with bacterial infection and hemorrhage, < 1 to 44 micrograms/ml in patients with gastrointestinal hemorrhage, and < 1 to 54 micrograms/ml in patients with other causes of admission. Using the normal upper limit of CRP value as a cut-off value did not differentiate those patients with from those without bacterial infection. However, using the CRP value of 20 micrograms/ml which was obtained from receiver-operating characteristic curves could differentiate between two groups of patients (sensitivity 80.39%, specificity 80.77%, accuracy 80.62%). In conclusion, serum CRP determination can be used in the detection of bacterial infection in patients with cirrhosis. However, a new cut-off value should be applied. (Lin et al., 2002)

    Cholesterol

    A retrospective observational cohort study included consecutive patients with liver cirrhosis (n = 191). Thirty-eight patients died in the follow-up period. Significant difference was observed in the level of total serum cholesterol between surviving and deceased patients (2.27 +/- 1.02 mmol/L vs. 2.97 +/- 1.00 mmol/L, P < 0.0001 respectively). Cholesterol was confirmed as a significant predictor of mortality in univariate logistic regression analysis, and independent predictor beside bilirubin, creatinine and MELD score in multivariate logistic regression analysis. Addition of serum cholesterol level to a prognostic model based on total bilirubin, creatinine and INR increased its accuracy by 4%. Adding cholesterol to the MELD score improved prediction accuracy by 3%. There was no significant difference in serum levels of triglycerides between surviving and deceased patients. Serum cholesterol is a routinely measured parameter, which has independent prognostic value in patients with liver cirrhosis. (Janicko et al., 2013)

    Nutritional Assessments

    Magnesium Loading Test

    Serum ionized magnesium represents less than 1% of the total body magnesium. The most reliable method to evaluate magnesium status is the magnesium loading test: In magnesium depletion its uptake is increased (20-50%) and is about 6% in normal magnesium status. There are no studies on magnesium status in chronic cirrhotics who may be

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