| disease | Jaundice |
| alias | Jaundice |
Jaundice is the clinical manifestation of hyperbilirubinemia, which is characterized by the yellowing of the sclera, skin, mucous membranes, and other tissues and body fluids due to elevated bilirubin levels in the blood. Normally, the bilirubin level in the blood does not exceed 17 μmol/L (1.0 mg/dl). When the bilirubin level exceeds the normal range but jaundice is not yet visible to the naked eye, it is referred to as latent or subclinical jaundice. Jaundice is not an independent disease but rather a symptom and sign of many conditions, particularly those affecting the liver, biliary system, and pancreas.
bubble_chart Pathogenesis
It is known that bilirubin is derived from heme in hemoglobin. Normally, the human body produces about 250-350 mg of bilirubin daily, with 80-85% of it coming from senescent red blood cells in circulation. The average lifespan of red blood cells is 120 days, and approximately 1% of senescent red blood cells are lysed daily in the reticuloendothelial system (spleen, bone marrow, liver), releasing hemoglobin (4-6 g daily). The heme in hemoglobin is converted into biliverdin by heme oxygenase, and biliverdin is then catalyzed by biliverdin reductase into bilirubin. One gram of hemoglobin can produce 34 mg of bilirubin. The remaining small portion (15-20%) of bilirubin does not come from senescent red blood cells and is therefore called shunt bilirubin; it has two sources: the bone marrow and the liver.
Most of the bilirubin released from the reticuloendothelial system circulates in the blood as a bilirubin-albumin complex. This type of bilirubin has not yet conjugated with glucuronic acid in the liver, hence it is called unconjugated bilirubin, also known as indirect bilirubin, which is lipid-soluble.
After the formation of conjugated bilirubin, it, along with other components of bile, is secreted into the bile canaliculi through the bile secretory apparatus, transmitted from one meridian to the next, and then excreted from the liver into the intestines.
Conjugated bilirubin cannot pass through the intestinal mucosal cells and is reduced to urobilinogen by bacterial action in the terminal ileum and colon. Neijing Most of the urobilinogen in the intestines is excreted with feces, with the normal content of urobilinogen in feces being 68-473 μmol (40-280 mg) per 24 hours. A small portion of urobilinogen (10-15%) is reabsorbed by the intestinal mucosa, reaches the liver via the portal vein, and this is the enterohepatic circulation of bile pigments. The reabsorbed urobilinogen in the liver is mostly excreted into the biliary system and intestines either unchanged or converted back into bilirubin; only a small portion enters the systemic circulation and is excreted by the kidneys. The normal content of urobilinogen in urine does not exceed 68 μmol (4 mg) per 24 hours.
bubble_chart Clinical Manifestations
Due to the varying primary diseases causing jaundice, the clinical manifestations are diverse, stemming from both the primary disease and jaundice itself. Additionally, only the common manifestations seen in individuals with jaundice disease are briefly described.
(1) Yellow staining of tissues such as the skin and sclera: Bilirubin has a strong affinity for tissues containing elastin, so tissues like the sclera, skin, and mucous membranes are most prone to jaundice. As jaundice deepens, urine, sputum, tears, and sweat may also become yellow-stained, though saliva generally does not change color. The depth of yellow staining varies depending on the primary disease causing jaundice and the duration of the jaundice.
(3) Gastrointestinal symptoms: Cases of jaundice disease often present with symptoms such as abdominal distension and fullness, abdominal pain, loss of appetite, nausea, vomiting, diarrhea, or constipation, which may vary slightly depending on the primary disease.
(4) Manifestations of cholemia: Extrahepatic obstructive jaundice and intrahepatic cholestasis can lead to the retention of bile salts in the blood due to impaired excretion, known as cholemia. Its main manifestations include: ① cutaneous pruritus, though the pruritus may correlate with the degree of jaundice; ② bradycardia, seen in severe jaundice cases, related to bile salts stimulating the vagus nerve and inhibiting cardiac conduction; ③ intestinal issues due to a lack of bile salts, affecting fat digestion and the absorption of fat-soluble vitamins, leading to symptoms such as abdominal distension and fullness, bleeding tendencies, steatorrhea, and nyctalopia; ④ weakness, lethargy, and headache, likely related to the toxic effects of bile salts on the central nervous system.
There are numerous laboratory tests for jaundice disease, which aid in the differential diagnosis of the disease cause and should be reasonably selected.
(1) Liver function tests
1. Serum bilirubin measurement: Serum bilirubin is divided into one-minute bilirubin and total bilirubin. The former is equivalent to conjugated bilirubin (CB), normally not exceeding 3.4 μmol/L (0.2 mg/dl), with a fluctuation range of 0.85 to 3.4 μmol/L (0.05 to 0.2 mg/dl). Total bilirubin (TB) is the sum of conjugated and unconjugated bilirubin, mainly unconjugated bilirubin, normally not exceeding 17 μmol/L (1.0 mg/dl).
2. Bilirubin in urine: Hemolytic jaundice does not contain bilirubin in urine, while hepatocellular and obstructive jaundice show positive reactions.
3. Urobilinogen in urine: In acute massive hemolysis, urobilinogen in urine significantly increases; in chronic minor hemolysis, the urobilinogen content changes little. In hepatocellular jaundice, urobilinogen in urine may increase; in intrahepatic cholestasis, it may decrease or even disappear. In extrahepatic obstruction, urobilinogen is mostly absent in urine, especially in cancerous jaundice.
4. Urobilinogen in feces: In obstructive jaundice, urobilinogen may decrease; stone obstruction is often incomplete, while cancerous obstruction can be complete. Long-term reduction of urobilinogen in feces (< mg/24 hours) suggests cancerous jaundice.
5. Protein metabolism tests: Serum protein quantification and protein electrophoresis analysis have little significance in the differential diagnosis of jaundice. Decreased plasma albumin is seen in severe liver parenchymal damage, such as chronic hepatitis, decompensated cirrhosis, and advanced stage liver cancer. Increased plasma globulin and inverted albumin/globulin ratio are seen in active chronic liver disease and connective tissue diseases. Changes in total plasma protein are more pronounced in hepatocellular jaundice. Long-term extrahepatic obstruction and gallstone cirrhosis show significant increases in plasma α 2 and β globulins.
6. Blood cholesterol, cholesterol ester, and protein X (LP-X) measurements reflect the lipid metabolism function of liver cells and the excretory function of the biliary system.
7. Serum bile acid measurement: Bile acids are synthesized and secreted in the liver, with normal serum levels not exceeding 10 μmol/L. In hepatobiliary diseases, bile acid metabolism is disordered. The mechanisms of uptake and excretion of bile acids and bilirubin by liver cells are different; in unconjugated hyperbilirubinemia such as Gilbert's syndrome and hemolytic jaundice, there is no bile acid retention, which aids in the differential diagnosis of jaundice.
8. Serum enzyme tests: Measurement of serum enzyme activity (referred to as serum enzymes) can be somewhat helpful in diagnosing the disease cause of jaundice. Clinically, serum enzymes are divided into two major categories: ① Enzymes reflecting liver cell damage, mainly alanine aminotransferase (ALT) and aspartate aminotransferase (AST), others include alanine amber acid lyase (ASAL), aldolase (ALD), arginase (ARG), and ornithine carbamoyltransferase (ChE), which decrease in hepatitis; ② Enzymes reflecting biliary tract lesions, such as alkaline phosphatase (ALP), γ-glutamyl transpeptidase (GGT), leucine aminopeptidase (LAP), and 5'-nucleotidase (5'-NT). Jaundice enzyme profile (enzymogram) testing, which involves a single micro-measurement of a series of enzymes, aids in the differential diagnosis of jaundice. For example, a single measurement of ALT, AST, OCT, ALP, GGT, and 5'NT enzymes. If the first three enzymes rise, it is hepatocellular jaundice; if the latter three increase, it is obstructive jaundice. However, serum enzyme tests do not help differentiate between intrahepatic cholestasis and extrahepatic obstructive jaundice (see "Viral Hepatitis").
9. Plasma Prothrombin Time Determination Vitamin K promotes the formation of prothrombin in liver cells. In hepatocellular jaundice, the formation of prothrombin is reduced, and the prothrombin time is prolonged. Vitamin K is fat-soluble and becomes water-soluble in the intestine Neijing under the action of bile salts, thus it can be absorbed. Therefore, the prothrombin time can also be prolonged in obstructive jaundice.
10. Dye Excretion Function Test Indocyanine Green (ICG) Excretion Test After ICG enters the bloodstream, it quickly binds to albumin and is taken up by liver cells. After being metabolized in the liver Neijing, it is directly excreted into the intestines via the bile ducts, thus accurately reflecting the excretory function of liver cells. In normal individuals, an intravenous injection of ICG at a dose of 0.5mg/kg body weight results in a venous retention rate of 0-10% after 15 minutes.
(II) Immunological Tests
1. Immunoglobulins In chronic active hepatitis, IgG levels are significantly elevated, while in primary biliary cirrhosis, IgM levels are markedly increased. In cases of extrahepatic obstruction, immunoglobulins remain normal.
2. Alpha-fetoprotein (AFP) The AFP content in the blood of normal adults is extremely low (<20ng/ml).
3. Autoantibody Detection The positivity rate of mitochondrial antibodies in jaundice disease cases varies. In primary biliary cirrhosis, it is about 95%, in chronic active hepatitis 30%, and in long-term extrahepatic obstruction, it is occasionally positive (<5%).
4. Specific Markers for Viral Hepatitis For example, a positive anti-HAV-IgM indicates hepatitis A virus infection; positive HBsAg and anti-HBc-IgM are helpful for diagnosing hepatitis B; abnormal ALT with positive anti-HCV suggests hepatitis C; and positive anti-HEV-IgM indicates hepatitis E virus infection.
(III) Hematological Tests In hemolytic jaundice, besides anemia, there is an increase in reticulocytes in the peripheral blood (usually 5-50%, occasionally over 90%), and polychromatic red blood cells appear. Bone marrow examination also shows compensatory changes such as nucleated red blood cell hyperplasia.
(IV) X-ray Examination
1. Plain X-ray of the liver area helps to understand the size and shape of the liver. Combined with fluoroscopy, it can also determine the position of the diaphragm, whether the diaphragmatic surface is smooth, and whether diaphragmatic movement is restricted.
2. Upper gastrointestinal barium meal imaging may reveal esophageal varices. Hypotonic duodenography may assist in the diagnosis of extrahepatic obstruction.
3. Routine oral and intravenous cholangiography often fails to image due to deep jaundice. However, using certain contrast agents (such as 40% cholovue), imaging is still possible when total bilirubin is greater than 102-119μmol/L (6-7mg/dl).
4. Endoscopic retrograde cholangiopancreatography (ERCP) and percutaneous transhepatic cholangiography (PTC) can show the location and extent of biliary obstruction, aiding in the differentiation between intrahepatic and extrahepatic obstructive jaundice. To avoid complications of liver puncture cholangiography such as bleeding and biliary peritonitis, some advocate for jugular vein catheterization cholangiography, where a catheter is inserted from the jugular vein to the hepatic vein, then punctured into the bile duct for imaging.
5. Selective celiac angiography has limited significance in the differential diagnosis of jaundice. The vascular changes displayed can suggest the location and extent of the lesion, which may be helpful for pancreatic diseases.
6. Splenoportography and umbilical venography can show the vascular morphology of the portal system, aiding in the diagnosis of portal hypertension, liver space-occupying lesions, and preoperative assessment for portosystemic shunt. Jaundice disease cases rarely undergo such examinations.
7. Computed Tomography (CT) Abdominal CT can display cross-sectional images of abdominal organs such as the liver, bile ducts, and pancreas, providing significant reference value for the presence of space-occupying lesions in the liver and pancreas, and whether the bile ducts and gallbladder are dilated. It aids in the diagnosis of obstructive jaundice.
(V) Ultrasound Examination Abdominal B-mode ultrasound helps differentiate between medical and surgical jaundice. In the latter, the common bile duct diameter is often dilated (>6mm), intrahepatic bile ducts are dilated with branch-like anechoic dark bands or small light rings, the gallbladder is enlarged with an often irregular inner membrane; liver echoes are mostly similar to normal.
(VI) Radionuclide Examination
(7) Duodenal Drainage This method does not have special significance in the differential diagnosis of jaundice, but it has reference value in determining extrahepatic obstruction.
(8) Liver Biopsy Helpful in the diagnosis of diffuse liver diseases, such as chronic hepatitis, early cirrhosis, and drug-induced jaundice, as well as in the determination of borderline diseases, such as the differentiation of stages of chronic hepatitis; the differentiation between drug-induced intrahepatic cholestasis and extrahepatic obstruction.
(9) Laparoscopy Although laparoscopy is not a primary method for the differential diagnosis of jaundice, it allows direct visualization of parts of the liver, falciform ligament, gallbladder, and peritoneal membrane, as well as the intra-abdominal condition. Based on the size, shape, color, surface condition of the liver, the degree of venous engorgement and varicosity of the falciform ligament, and the nature of ascites, it aids in the diagnosis of certain causes of jaundice, especially diffuse liver diseases.
(10) Adrenocortical Hormone Treatment Trial The use of prednisone or other trial treatments, such as administering 10-15mg of prednisone 3-4 times a day, can result in a decrease in serum bilirubin concentration by more than 40-50% compared to before medication, which is beneficial for diagnosing hepatocellular jaundice and intrahepatic cholestasis (clinically similar to extrahepatic obstruction), whereas extrahepatic obstructive jaundice often shows no significant change.
(11) Exploratory Laparotomy
(1) Medical History A detailed understanding should be obtained regarding: 1. Age, 2. Gender, 3. Occupation and place of origin, 4. Diet and nutrition, 5. Family history, 6. History of hepatitis contact, 7. History of blood transfusion, injections, surgeries, and medication, 9. Onset and progression of current jaundice, 10. Abdominal pain, 11. Other gastrointestinal symptoms, 12. Fever and shivering, 13. Other relevant information, analyzing its possible relationship with jaundice.
(2) Physical Examination A comprehensive and systematic physical examination is crucial. First, determine the presence of jaundice, which should be examined under adequate natural light.
Focus on understanding the following aspects:
1. Skin Color The severity of hepatocellular jaundice varies; acute jaundice often presents with a golden-yellow skin color. In chronic intrahepatic cholestasis, the skin color is darker. Obstructive jaundice has the deepest skin color, which correlates with the degree of obstruction. In the initial stage [first stage], the skin appears golden-yellow, then turns from deep yellow to green, and in the late stage [third stage], it becomes dull gray or even dark brown, related to the oxidation of bilirubin to biliverdin and then to cholecyanin.
2. Other Skin Manifestations Pigmentation is seen in chronic liver disease and long-term biliary obstruction, generalized but more pronounced on the face, especially around the eyes. Xanthomas or xanthelasma are often related to lipid retention in the blood (though not entirely consistent). Xanthomas may shrink or disappear with decreased blood lipids or severe liver failure. Skin and mucosal petechiae are common in hepatocellular jaundice, with bleeding from the nasal mucosa, gums, and oral mucosa. In fulminant liver failure, large subcutaneous ecchymoses and bleeding sites appear, related to coagulation factor deficiency, thrombocytopenia, or accompanying DIC. Bleeding in obstructive jaundice is generally milder.
3. Superficial Lymphadenopathy Acute jaundice accompanied by generalized superficial lymphadenopathy should raise suspicion of infectious mononucleosis. Acute viral hepatitis usually does not present with superficial lymphadenopathy. Progressive jaundice with supraclavicular and other superficial lymphadenopathy should also consider cancerous jaundice. Lymphoma, malignant histiocytosis, miliary tuberculosis, and pulmonary infiltrative diseases can present with both jaundice and superficial lymphadenopathy.
4. Abdominal Signs
(1) Abdominal Contour Localized bulging in corresponding areas can be seen in hepatic space-occupying lesions, massive splenomegaly, retroperitoneal tumors, and pelvic tumors. Massive ascites present with a frog-belly appearance and protruding umbilicus, possibly leading to abdominal wall hernias and umbilical hernias. Abdominal wall varices are seen in portal hypertension, portal vein, or inferior vena cava obstruction. Abdominal surgical scars can sometimes aid in analyzing the cause of jaundice, such as gallbladder stones and cholecystitis.
(2) Liver Condition In acute viral hepatitis, jaundice and hepatomegaly coexist, with a soft liver, significant tenderness, and percussion pain. In acute and subacute liver necrosis, jaundice deepens rapidly, while hepatomegaly is not prominent or even decreases. In chronic hepatitis and cirrhosis, hepatomegaly is less pronounced than in acute hepatitis, with increased firmness and possibly no tenderness; cirrhosis may also present with irregular edges and nodules. In liver cancer, hepatomegaly is more prominent, possibly losing normal shape, firm, with palpable large masses or smaller nodules, and tenderness may not be significant, but a smooth liver surface does not rule out deep-seated or subclinical "small liver cancer." When a liver abscess is close to the liver surface, local skin may show redness, swelling, and tenderness. In massive liver abscess, hepatic echinococcosis, polycystic liver, and hepatic cavernous hemangioma, the liver area may have a cystic or fluctuating sensation.
(3) Splenomegaly Jaundice accompanied by splenomegaly is commonly seen in decompensated stages of various types of cirrhosis, chronic hepatitis, acute hepatitis, hemolytic jaundice, systemic infectious diseases, and infiltrative diseases. Cancer invading the portal vein and splenic vein can also cause splenomegaly. Rare splenic infarction and splenic abscess can present similarly with splenomegaly and tenderness.
(4) Gallbladder Enlargement
5. Other conditions: Presence of hepatic odor, flapping tremor, hepatic encephalopathy, and other neuropsychiatric abnormalities; sparse axillary hair, testicular atrophy, clubbing of fingers, hyperkeratosis of the skin, spoon-shaped nails, multiple venous thromboses (seen in pancreatic cancer), and bradycardia, etc. In advanced stages of cancerous jaundice disease, patients may also exhibit signs related to cancer metastasis. Liver failure may manifest as encephalopathy and intracranial hemorrhage. Hemoperitoneum, gall bladder peritonitis, gall bladder nephropathy, and shock can also be seen in cases of cancerous jaundice disease.
A diagnosis can be made in conjunction with laboratory tests.
(1) Hemolytic jaundice
1. There may be a history of factors causing hemolysis, such as blood transfusion, medication, infection, or family history (genetic factors).
2. In cases of acute massive hemolysis or hemolytic crisis, the onset is sudden, with severe hemolytic reactions such as shivering, high fever, vomiting, abdominal pain, headache, general malaise, lack of strength, and even shock, unconsciousness, severe anemia, jaundice, and acute renal failure.
3. In cases of chronic minor hemolysis, symptoms are usually mild, including pale complexion, lack of strength, and other anemia symptoms, with jaundice being less obvious. The spleen may be enlarged to varying degrees, and liver enlargement is also common.
4. Bilirubin tests: Except during a hemolytic crisis when there may be deep jaundice, the total serum bilirubin is usually less than 85μmol/L (5mg/dl), with unconjugated bilirubin accounting for more than 80%. Urine urobilinogen is weakly positive, and bilirubin is negative; 24-hour urine urobilinogen is significantly increased, and can exceed 1,000mg in cases of massive hemolysis. Fecal urobilinogen is also increased, with a 24-hour excretion exceeding 300mg, and can even exceed 1,000mg.
5. Hematological tests: Besides anemia, reticulocytes in peripheral blood are increased (usually 5-20%, occasionally over 90%), with polychromatic red blood cells present. Bone marrow examination also shows compensatory changes such as nucleated red blood cell hyperplasia.
6. Other tests: In autoimmune hemolysis, the Coombs test is positive. In paroxysmal nocturnal hemoglobinuria, the Ham test is positive. Acute massive hemolysis may result in hemoglobinuria; hemosiderinuria is more common in chronic hemoglobinuria, especially in paroxysmal nocturnal hemoglobinuria.
(2) Hepatocellular jaundice
1. If caused by acute hepatitis, patients often have fever, lack of strength, loss of appetite, liver pain, and other symptoms, with liver enlargement and significant tenderness. In chronic hepatitis, the liver texture increases, and tenderness is usually not significant. Cirrhosis patients are often thin, with dark skin, spider angiomas, and possibly varicose veins on the abdominal wall. The liver may not be enlarged, is firm, and usually not tender; the spleen may be enlarged; advanced stages often have ascites, bleeding tendencies, renal impairment, and even hepatic encephalopathy.
2. Serum bilirubin tests: Total serum bilirubin usually does not exceed 170μmol/L (10mg/dl), with conjugated bilirubin often increased, accounting for more than 30%.
3. Urine bilirubin tests: Urine bilirubin is positive. Due to abnormal enterohepatic circulation, urobilinogen from the intestines cannot be oxidized in the liver and re-excreted into the intestines, so it is excreted by the kidneys, making urine urobilinogen positive. In the early stages of acute hepatitis (such as the pre-jaundice phase), the intrahepatic bile capillaries are compressed by swollen liver cells, affecting bilirubin excretion into the intestines, so urine urobilinogen and urobilin may be temporarily negative, usually for about a week. In intrahepatic cholestasis, the liver cells' ability to excrete bilirubin is reduced, and urine urobilinogen is often decreased or absent.
4. Fecal tests: In intrahepatic cholestasis or obstruction, fecal urobilinogen is decreased, and stool color is lighter, even clay-colored.
5. Other liver function tests: In hepatocellular jaundice, the following tests are often abnormal: ① Serum transaminase levels are elevated; ② Plasma prothrombin time is prolonged, related to impaired production of vitamin K-dependent clotting factors by liver cells, and vitamin K often cannot correct it; ③ In severe liver damage, plasma cholesterol, cholesterol esters, and serum cholinesterase may decrease; ④ Serum alkaline phosphatase activity is mostly normal, but increases in intrahepatic cholestasis; ⑤ Serum prealbumin and albumin decrease, serum globulin increases, and the albumin/globulin ratio is imbalanced; in biliary cirrhosis, α and β globulins are often significantly increased.
6. Immunological Examination The determination of mitochondrial antibodies by immunofluorescence is helpful for the diagnosis of primary biliary cirrhosis. Detection of serological markers for various types of hepatitis viruses aids in the diagnosis of viral hepatitis (refer to "Viral Hepatitis"). Serum alpha-fetoprotein (AFP) also has reference value for the diagnosis of primary liver cancer.
7. Liver biopsy has diagnostic significance for jaundice caused by diffuse liver diseases, such as viral hepatitis, cirrhosis, fatty liver, and intrahepatic cholestasis. In addition to optical microscopy, electron microscopy, fluorescent immunoassay, immunohistochemistry, and ultramicro measurement of liver tissue enzymes can also be performed.
8. Liver radionuclide scanning, B-ultrasound, and CT imaging techniques are helpful in diagnosing space-occupying lesions in the liver.
(3) Obstructive jaundice
1. Clinical manifestations Acute cholecystitis and gallbladder stones often present with sudden onset, usually accompanied by upper abdominal colicky pain, and may also include fever, vomiting, tenderness in the gallbladder area, and muscle guarding. Jaundice appears and disappears rapidly; it can recur if caused by stones. Early symptoms of pancreatic head cancer may be subtle, with jaundice progressively deepening; in advanced stages, abdominal pain, loss of appetite, weight loss, and lack of strength become apparent. In obstructive jaundice, the retention of bile salts in the blood stimulates skin nerve endings, often leading to cutaneous pruritus; the lack of bile in the intestines affects the absorption of fat-soluble vitamin K, which can cause a tendency to bleed, often corrected by vitamin K injections.
2. Jaundice condition mainly depends on the location, degree, and duration of biliary obstruction. In early incomplete obstruction, jaundice is mild; as biliary obstruction gradually worsens, jaundice can deepen, appearing yellow, brown, or even black (referred to as black jaundice). In complete biliary obstruction, serum bilirubin can exceed 510μmol/L (30mg/dl), with conjugated bilirubin accounting for more than 35% (up to about 60%). Stone-induced jaundice often fluctuates, while cancerous obstruction presents with progressive jaundice, although ampullary cancer may show temporary relief of jaundice due to tumor ulceration.
3. Urine bilirubin test Urine bilirubin is positive, but urobilinogen is reduced or absent. If urobilinogen in urine remains negative for more than a week in obstructive jaundice, cancer-induced obstruction should be highly suspected. Complete biliary obstruction easily leads to secondary infections, and urobilinogen in urine may also be positive.
4. Stool color characteristics The more complete the obstruction, the lighter the stool color, which may appear clay-colored. The quantitative urobilinogen in stool over 24 hours is significantly reduced or completely absent. Ampullary cancer with ulceration or obstructive jaundice accompanied by bile duct membrane inflammation or ulceration may present with black stools or positive fecal occult blood.
5. Liver function tests Serum ALP activity and cholesterol levels may significantly increase. Long-term biliary obstruction often leads to secondary liver parenchymal damage, resulting in elevated serum transaminases. Plasma albumin may also decrease.
6. Other examinations Abdominal (liver, gallbladder, pancreas) plain films, gallbladder and biliary tract X-ray imaging, abdominal B-ultrasound and CT scans, endoscopic retrograde cholangiopancreatography (ERCP), and percutaneous transhepatic cholangiography (PTC) are all helpful in diagnosing obstructive jaundice. Tumor markers such as carcinoembryonic antigen (CEA), CA19-9, ferritin, and α1-antitrypsin may assist in the auxiliary diagnosis of cancerous obstruction, but they are not specific.
(4) Congenital non-hemolytic jaundice
This condition is discussed as a separate disease; for detailed information, please refer to the disease—congenital non-hemolytic jaundice.
