World Kidney Day (March 13)
Eminent Author, Medical Biochemist and Scientist, Technical Education consultant.
AGD Biomedicals (Pvt) LTD. Andheri East, Mumbai.
Food therapy along with self-screening and yearly performed ‘Liver Function Tests’ (LFTs), could be useful to prevent and detect early liver diseases(1) (refer to answers of Q2 and case studies:1-3). Presence of jaundice indicates early clinical events, which exhibit or predict progression of liver disease. Jaundice is a sign of Pre-hepatic, hepatic and post-hepatic conditions, which can be diagnosed very well by routinely performed IVD laboratory tests such as complete hemogram (CBC) and LFTs, backed by fifth generation point of care (POCT) tests based of multi-stick and immuno-chromogenic tests(2,3)(Refer to case studies:1-3). Early detection of liver disease with effective treatment can prevent complete liver failure and will be able to avoid in future; very expensive treatment options like liver transplantation(4). There is a need to focus on prevention of liver disorders, and to find out effective ways to treat patients suffering from liver diseases without exposing their households to the fateful effects of out of pocket (OOP) expenditure(5,6).
Q1. What is the theme of ‘World Liver Day’ (2025)?
ANS: ‘Food is medicine’ is the theme of ‘World Liver day’.
Q2. Describe the foods that could protect liver.
ANS: Foods that contain adequate protein, lipids, complex sugars (polysaccharides), minerals, micronutrients and fibers could protect liver well. Foods containing the following lipotropic factors are useful to protect liver: Choline, betaine, inositol (all these function like B-complex vitamins), and methionine (sulfur containing essential amino acid). These components act like antioxidants, decrease oxidative stress, help in detoxification process and prevent accumulation of fats in the liver cells. The following foods in balanced amounts contain liver protective substances: Fish, eggs, nuts, cereals, dry fruits, oatmeal, leafy green vegetables, barries, grape fruits, beet roots, citrous fruits and cruciferous vegetables (Cauliflower, Broccoli, cabbage, etc).
Q3. What food types are responsible for liver damage?
ANS: High intake of fried foods, refined sugars, excess of salts (present in fast foods), and alcohol. These food types, facilitate infiltration of fats in the liver cells and the process of cirrhosis of liver.
Q4. What is jaundice?
ANS: Jaundice means yellow coloration of blood (serum, plasma), skin, eyes(sclera) due to increase in serum bilirubin above 2.0 mg/dl. Jaundice occurs in pre-hepatic, hepatic and post-hepatic conditions. Normal serum bilirubin is <1.0 mg/dl. In acute and chronic liver diseases, serum bilirubin increases in blood.
Note:
(A) Clinical conditions related to jaundice and reasons: Refer to the following table:
| Prehepatic conditions)(PC) | Hepatic conditions (HC) | Posthepatic conditions (PHC) |
| Hemolytic anemia | Viral, bacterial, amebic Hepatitis | Obstruction to bile passages and duct |
| Gilbert’s disease (GD) | Drug-induced hepatitis | Gall bladder bile stones |
| Crigler-Najjar syndrome (CNS) | Fatty liver | Cancer of gall bladder |
| Alcoholic cirrhosis | Congenital anomaly of bile duct | |
| Non-alcoholic steatohepatitis | Acute pancreatitis | |
| Autoimmune disorders |
(B) Congenital deficiencies of enzymes responsible to convert water insoluble bilirubin into water soluble bilirubin lead to GD and CNS.
(C) Acute hepatitis (AH) is sudden severe injury to liver and Chronic hepatitis (CH) is long-term liver disease.
(D) AH can occur due to severe viral or bacterial infections or it can be drug-induced. CH can occur due to any one of clinical condition associated with PC, HC or PHC.
Note
(A) Pre-hepatic jaundice is a type of jaundice (yellowing of the skin and eyes) that occurs before the bilirubin reaches the liver for processing and excretion.
(B) Pre-hepatic conditions, also known as hemolytic jaundice, are caused by excessive red blood cell breakdown (hemolysis), leading to an overproduction of bilirubin that overwhelms the liver’s ability to process it, resulting in unconjugated hyperbilirubinemia and jaundice
(C) Post-hepatic jaundice refers to the obstruction of biliary drainage. The excess bilirubin that is not excreted will get conjugated (made water-soluble, more in amount) by the liver, hence the result is a conjugated hyperbilirubinaemia.
Q5. What are routinely performed Liver Function Tests (LFTs)?
ANS:
- Routine urine examination
- Complete hemogram
- Serum total, direct (water-soluble) and indirect (water-insoluble) bilirubin
- SGPT, SGOT and serum alkaline phosphatase (ALP)
- Serum total proteins, albumin and globulins
- Serum cholesterol and triglycerides(2,3).
Q6. How routine IVD laboratory ‘Liver Function Tests (LFTS)’ are useful to detect and differentiate Jaundice?
ANS: Refer to the following Tables:
Table 2A(2):
| Examination / Parameter | Prehepatic conditions (PC) | Hepatic conditions (HC) | Posthepatic conditions (PHC) |
| Urine Physical Examination | Normal color | Yellow color | Yellow color |
| Urine Chemical Examination | |||
| Bile pigments | Absent | Present | Present |
| Bile salts | Absent | Increased | Increased |
| Urobilinogen | Highly Increased | Moderate increase | Moderate increase |
| Complete Hemogram | |||
| Hemoglobin | Very low | Normal | Normal |
| MCV, MCH, MCHC | Low or high | Normal | Normal |
Table 2B
| Examination / Parameter | Prehepatic conditions | Hepatic conditions | Post-hepatic condition |
| Liver Function Tests | |||
| Serum total bilirubin | High | High | High |
| Serum indirect bilirubin | Very high | High | High |
| Serum direct bilirubin | Normal | High | High |
| SGPT | Normal | Very high | High |
| SGOT | Moderately increased | Very high | High |
| Serum ALP | Normal | High | Very high |
Note
High serum cholesterol and triglycerides are observed mainly in fatty liver and NASH conditions.
Q7. What is the percentage of obese persons that may suffer from non-alcoholic steatohepatitis (NASH) in future?
ANS: The prevalence rates of steatosis and steatohepatitis are approximately 15% and 3%, respectively in non-obese persons, 65% and 20% respectively in persons with class I and II obesity (BMI>30.0), and 85% and 40% respectively in extremely obese patients (BMI ≥40). The relationship between BMI and Non-alcoholic fatty liver disease (NAFLD) is influenced by racial/ethnic background and genetic variation in specific genes(8).
Q8. What is the percentage of uncontrolled diabetic persons that may develop liver disease in future?
ANS:There are about 70% of persons with type 2 diabetes that have non-alcoholic fatty liver disease (NAFLD)(9).
Q9. What is the prevalence of autoimmune hepatitis that may develop end stage liver disease?
ANS: Autoimmune hepatitis incidences and prevalence have increased significantly in the past two decades and exhibit substantial variations across various region in the world(10).
Q10. What is hepatotoxicity caused by drugs and the prevalence of drug-induced hepatitis (DIH)?
ANS: Hepatotoxicity is a potential complication of nearly all classes of medicines including allopathic, ayurvedic, unani and other types of medicines. However, most cases of DIH are benign, and improve after the withdrawal of the specific drug. It is necessary to recognize and withdraw the offending drug as quickly as possible to prevent the progression to chronic liver disease and to fulminant hepatic failure(11,12).
Q11. What are the recent innovations in IVD that have significantly impacted the management and monitoring of kidney functions?
ANS: Advancements in the fifth generation point of care test (POCT) methods for blood and urine can diagnose liver risk factors by performing urine bile pigments, and urobilinogen (dipstick method), serum bilirubin (bilirubinometer) serum cholesterol, and triglycerides (Rapid immunochromatographic tests) in few minutes with accuracy and precision at patient’s bed side(2). Moreover, genetic predisposition to CKD could be detected by advanced DOT-BLOT molecular tests(2).
CASE STUDY
A 16-year-old girl suffered from nausea, loss of appetite, mild fever, generalized weakness and pain in the right hypochondrium. His laboratory test reports were as follows:
| PARAMETER | VALUE | REFERENCE RANGE (NORMAL VALUES) |
| ROUTINE URINE EXAMINATION | ||
| Colour | Yellow | Normal colour |
| Bile pigments | Present | Absent |
| Bile salts | Present | Absent |
| Urobilinogen | Increased | Normal |
| COMPLETE BLOOD COUNT Hb, Blood indices, WBC and Platelet counts and blood smear impressions: Normal | ||
| LIVER FUNCTION TESTS | ||
| Serum Total bilirubin | 5.7 mg/dl | Up to 1.0 mg/dl |
| Serum Direct bilirubin | 3.5 mg/dl | Up to 0.5 mg/dl |
| Serum indirect bilirubin | 2.2 mg/dl | Up to 0.5 mg/dl |
| SGPT | 585 IU | 5–35 IU |
| SGOT | 368 IU | 8-40 IU |
| Serum alkaline phosphatase | 120 IU | 20-80 IU |
| Serum total proteins | 6.4 g/dl | 6–8 g/dl |
| Serum albumin | 4.2 g/dl | 3.3–4.8 g/dl |
| Serum total globulins | 2.2 g/dl | 1.8–3.6 g/dl |
Evaluation of the laboratory report
(1) Diagnosis by referring to Table 2: Hepatic jaundice.
(2) It is necessary to find out cause from the history of the patient. Whether it was a viral infection (mainly HAV or HBV), drug-induced or autoimmune; by using additional Hepatitis surface antigen test or PCR tests.
CASE STUDY 2
A 11-year-old boy presented with significant loss of weight, weakness, yellow colored skin, eyes (sclera), and chronic ulcers on his internal and external malleoli. His laboratory test reports were as follows:
Blood indices
| PARAMETER | VALUE | REFERENCE RANGE (NORMAL VALUES) |
| ROUTINE URINE EXAMINATION | ||
| Colour | Normal | Normal colour |
| Bile pigments | Absent | Absent |
| Bile salts | Absent | Absent |
| Urobilinogen | Increased, very high | Normal |
| COMPLETE BLOOD COUNT | ||
| Hb | 5.6 g/dl | 14-16 g/dl |
| MCV | 72.2 fL | 82-92 fL |
| MCH | 23.0 pg | 27-32 pg |
| MCHC | 28.6% | 32-36% |
| Blood smear impressions | Hypochromia ++++ | Presence of significant numbers of target cells, poikilocytes, microcytes |
| WBC and Platelets counts and cells | Normal | |
| LIVER FUNCTION TESTS | ||
| Serum Total bilirubin | 7.8 mg/dl | Up to 1.0 mg/dl |
| Serum Direct bilirubin | 0.5 mg/dl | Up to 0.5 mg/dl |
| Serum indirect bilirubin | 7.3 mg/dl | Up to 0.5 mg/dl |
| SGPT | 30 IU | 5–35 IU |
| SGOT | 70 IU | 8-40 IU |
| Serum alkaline phosphatase | 28 IU | 20-80 IU |
| Serum total proteins | 6.0 g/dl | 6–8 g/dl |
| Serum albumin | 3.7 g/dl | 3.3–4.8 g/dl |
| Serum total globulins | 2.3 g/dl | 1.8–3.6 g/dl |
Evaluation of the laboratory report
(1) Diagnosis by referring to Table 2: Prehepatic jaundice. Additional hematological tests are required to find out the cause of prehepatic condition.
(2) The patient was suffering from hemolytic anemia. Considerable decrease in the life span of RBCs take place, due to primary diseases such as thalassemia major, sickle cell anemia, leukemia etc. Excessive breakdown of RBCs leads to increase in indirect bilirubin, that imparts yellow color to skin and eyes. Increased indirect is unable to pass in urine, hence urine color was normal. The end product of protoporphyrin ring of Hb) is bilirubin.
CASE STUDY 3
A 66-year-old man presented with nausea, loss of appetite, weakness, yellow eyes and skin and pruritus (generalised itching). His laboratory test reports were as follows:
Blood indices
| PARAMETER | VALUE | REFERENCE RANGE (NORMAL VALUES) |
| ROUTINE URINE EXAMINATION | ||
| Colour | Yellow | Normal colour |
| Bile pigments | Present | Absent |
| Bile salts | Present | Absent |
| Urobilinogen | Increased | Normal |
| LIVER FUNCTION TESTS | ||
| Serum Total bilirubin | 11.5 mg/dl | Up to 1.0 mg/dl |
| Serum Direct bilirubin | 7.3 mg/dl | Up to 0.5 mg/dl |
| Serum indirect bilirubin | 4.2 mg/dl | Up to 0.5 mg/dl |
| SGPT | 360 IU | 5–35 IU |
| SGOT | 410 IU | 8-40 IU |
| Serum alkaline phosphatase | 390 IU | 20-80 IU |
| Serum total proteins | 6.4 g/dl | 6–8 g/dl |
| Serum albumin | 4.2 g/dl | 3.3–4.8 g/dl |
| Serum total globulins | 2.2 g/dl | 1.8–3.6 g/dl |
Evaluation of the laboratory report
(1) Diagnosis: By referring to Table 2: Post-hepatic jaundice
(2) The patient was suffering from obstruction to the flow of normal amount of bile to the small intestine. Increased bilirubin due to obstruction lead to yellow coloration of skin and eyes. Increased bile salts caused pruritus. It was necessary to find out the cause of obstruction to the flow (gall stones, tumor, etc) and consideration of removal of the obstruction to the flow of bile.
Q11. How do early detection of liver diseases (LDs) impact patient outcomes and overall healthcare costs
ANS: Liver diseases accounts for two million deaths annually and is responsible for 4% of all deaths (1 out of every 25 deaths worldwide). Approximately two-thirds of all liver-related deaths occur in men. Early detection of LDs could prevent serious liver damage, related therapy, other expenses and cases of liver transplantation.
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AGD CLINIPAK Reagents
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LFT Parameters:
- Albumin
- Total Protein
- Alkaline Phosphatase (ALP)
- Bilirubin (Total & Direct)
- SGOT (AST)
- SGPT (ALT)
- GGT
References
(1) American Association for the study of liver diseases. AASLD Family of Websites: AASLD.org
(2) Godkar PB, Godkar DP. Text book of Medical laboratory technology (4th edition, 2024), Bhlani Publishers, Mumbai. India.
(3) Godkar PB, Godkar DP. Medical Biochemistry, Theory and Practicals (1st edition, 2024), CBS Publishers, New Delhi,India.
(4) Shukla A, Vadeyar H, Rela M, Shah S. Liver transplantation: East Vs West. J Clin Exp Hepatol 2013;3:243‐253.
(5) Nneka N Ufere, Nishant Satapathy, Lisa Philpotts, Jennifer C Lai, Marina Serper. Financial burden in adults with chronic liver disease: A scoping review. Liver Transpl. 2022 Dec;28(12):1920-1935. doi: 10.1002/lt.26514. Epub 2022 Jul 7.
(6) Shankar Prinja 1, Pankaj Bahuguna 2, Ajay Duseja 3, Manmeet Kaur 2, Yogesh Kumar Chawla. Cost of Intensive Care Treatment for Liver Disorders at Tertiary Care Level in India. Pharmacoecon Open, 2018 Jun;2(2):179-190. doi: 10.1007/s41669-017-0041-4.
(7) Xiao-Ning Wu, Feng Xue, Nan Zhang, Wei Zhang, Jing-Jing Hou, Yi Lv, Jun-Xi Xiang & Xu-Feng Zhang. Global burden of liver cirrhosis and other chronic liver diseases caused by specific etiologies from 1990 to 2019. BMC Public Health volume 24, Article number: 363 (2024)
(8) Subrat Kumar Acharya. Acute Liver Failure: Indian Perspective. Clin Liver Dis (Hoboken). 2021 Jul 22;18(3):143–149. doi: 10.1002/cld.1135.
Elisa Fabbrini, Shelby Sullivan, Samuel Klein. Obesity and Nonalcoholic Fatty Liver Disease: Biochemical, Metabolic and Clinical Implications. PMCID: PMC3575093 NIHMSID: NIHMS441289 PMID: 20041406
(9) Spectrum of Liver Disease in Type 2 Diabetes and Management of Patients With Diabetes and Liver Disease.
(10) Jong Woo Hahn, Hye Ran Yang, Jin Soo Moon, Ju Young Chang et al. Global incidence and prevalence of autoimmune hepatitis, 1970–2022: a systematic review and meta-analysis. Clinical Medicine. 2023 Oct 17;65:102280. doi: 10.1016/j.eclinm.2023.102280
(11) Stefan David, James P Hamilton. Drug-induced Liver Injury. US Gastroenterol Hepatol Rev. 2010 Jan 1;6:73–80.
(12) Bjornsson ES. Liver injury associated with drugs and complementary and alternative medicines in India (Editorial). J Clin Exp Hepatol 2021;11:281‐283.
