Jaundice

Jaundice is a term that refers to a yellowing of the skin, sclerae (whites of the eyes), and other tissues caused by an excess of circulating bilirubin. Bilirubin is a water-insoluble waste product derived mostly from the heme portion of degenerating RBCs, as well as from RBC precursors in the marrow and heme proteins of liver and other tissues. Bilirubin is released by phagocytes and other cells into circulation where it is bound with albumin, transported and taken up by the liver. Bilirubin is then conjugated with glucoronic acid to form bilirubin diglucuronide, and is then secreted into the bile. Within the colon the bacterial flora deconjugate bilirubin into stercobilinogen, most of which is excreted in the feces as a brownish coloured pigment. Significant amounts are absorbed however, and then directed back to the liver where they are again excreted in the bile, or via the kidneys in urine as urobilinogen. (Berkow 1992; Rubin and Farber 1990, 396-400)

Abnormalities in the production and excretion of bilirubin often result in jaundice. Elevated levels of unconjugated bilirubin in the blood can be the result of an increased production of bilirubin, an impairment in liver uptake, or inefficient conjugation by the liver. In contrast, elevated levels of conjugated bilirubin is caused by impaired biliary excretion. In both liver disease and cholestasis the patient will often present with a mixed hyperbilirubinemia, with both conjugated and unconjugated serum bilirubin. (Berkow 1992; Rubin and Farber 1990, 396-400)

Cases of mild jaundice in the absence of a dark-coloured urine would tend to indicate an unconjugated hyperbilirubinemia, caused by either hemolysis or Gilbert's syndrome (see below). In contrast, more severe indications of jaundice, and/or a very dark urine is a definite indication of an overt liver or biliary disorder. Accompanying signs such as ascites or pruritis usually suggests a chronic rather than acute pathology. Patients will often report a darkening of their urine before the skin discoloration of jaundice occurs, and in the case history is a better indication of the original onset of the pathology and should be noted. Where nausea and vomiting proceeds jaundice this is most often an indication of acute hepatitis or an obstruction of the cystic duct by a stone – when abdominal pain is a dominant symptom it is more likely to be caused by cholecystitis. Jaundice concurrent with symptoms such as poor appetite, weight loss and fatigue suggest alcoholic liver disease or chronic hepatitis. (Berkow 1992; Rubin and Farber 1990, 396-400)

Common disorders of bilirubin metabolism include unconjugated hyperbilirubinemia, Gilbert's syndrome, obstructive jaundice, and neonatal jaundice. Other more rare causes include inherited diseases such as Crigler-Najjar disease, which like Gilbert’s syndrome is manifested by decreased bilirubin conjugation, and Dubin-Johnson syndrome, which relates to the decreased intracellular transport of conjugated bilirubin. (Berkow 1992; Rubin and Farber 1990, 396-400)

Unconjugated hyperbilirubinemia is the result of a hemolytic anemia, a premature destruction of the RBCs, occurring in association with some infectious diseases, with certain inherited red-cell disorders, or in response to drugs and other toxic agents. (Berkow 1992; Rubin and Farber 1990, 396-400)

Gilbert's syndrome is an inherited autosomal dominant, mild and chronic, unconjugated hyperbilirubinemia often misdiagnosed as chronic hepatitis. It may affect as many as 5-10% of the population. The pathogenesis appears to be related to defects in the liver's uptake of plasma bilirubin. While Gilbert’s syndrome is not associated with any overt liver pathology, patients will often experience some degree of malaise and weakness. (Berkow 1992; Rubin and Farber 1990, 396-400)

Obstructive jaundice, or cholestasis, results from impaired bile flow, from any point between the liver cell canaliculi and the ampulla of Vater. Typically, a distinction is made between intrahepatic and extrahepatic causes. The most common intrahepatic causes are hepatitis from drug toxicity and alcoholic liver disease, but less common forms include primary biliary cirrhosis, cholestasis in pregnancy and metastatic carcinoma. The most common extrahepatic causes are a common duct stone and pancreatic cancer, with less common causes being a benign stricture of the common duct (usually related to surgery), ductal carcinoma, pancreatitis and sclerosing cholangitis. (Berkow 1992; Rubin and Farber 1990, 396-400)

Neonatal jaundice is in most cases a normal event experienced by up to 70% of newborns, called “physiologic jaundice,” the cause of which is poorly understood. It is usually a transient condition that can be easily treated by having the baby lie in the direct sunlight for 5-10 minutes each day. Other causes of neonatal jaundice are more serious such as infection or extrahepatic biliary atresia. (Berkow 1992; Rubin and Farber 1990, 396-400)

Medical treatment of jaundice

As jaundice is often a symptom of an underlying liver pathology (with the exception of inherited disorders of bilirubin metabolism), the treatment is thus orientated towards resolving the underlying condition. Intrahepatic cholestasis is often treated with the drugs cholestyramine or ursodeoxycholic, which combine with the bile acids in the intestine to form an insoluble complex that is excreted by the feces. This allows excess bile acids to be properly eliminated, and thus can help with systemic symptoms such as itching. Extrahepatic biliary obstruction is usually treated by some kind of surgical intervention, including stone extraction, and/or the insertion of stents and catheters. In some patients benefit is to be had by undergoing biliary lithotripsy through endoscopic methods or shockwave therapy. (Berkow 1992)

Holistic treatment of jaundice

A careful assessment should be made to determine the origin of the jaundiced state before undertaking any kind of therapy, which could range from cholangitis (inflammation and infection), cholecystitis (gall stones), a malignancy, hepatitis or cirrhosis, or infection with parasites such as liver flukes (e.g. Clonochoris sinensis) or intestinal parasites (e.g. Ascaris). Caution should be taken whenever there is any kind of abdominal pain. Nonetheless herbal treatment should be considered as a beneficial, non-invasive method to enhance the metabolism of bilirubin, to ease the itching and aesthetic problems associated with jaundice, while determining the underlying cause. In Therapeutic Herbalism, David Hoffman recommends among others, the usage of cholagogues and hepatics, lymphagogues and anti-pruritics (3-31), e.g.

• cholagogues and hepatics, to improve liver catabolism, e.g. Dandelion (Taraxacum officinale), Milk Thistle (Silybum marianum), Barberry (Berberis vulgaris), Boldo (Peumus boldus), Fringe Tree (Chionanthus virginicus), Black-root (Leptandra virginica), Celandine Poppy (Chelidonium majus)
  
• lymphagogues, to mobilize and discharge cellular wastes, e.g. Cleavers Galium aparine), Pipsissewa (Chimaphila umbellata), Purple Coneflower (Echinacea angustifolia), Marigold (Calendula officinalis), Nettles (Urtica dioica), Poke Root (Phytolacca americana)
  
• anti-pruritics, used topically as a bath to ease itching, e.g. Chickweed (Stellaria media), Milky Oats (Avena sativa), Plantain (Plantago spp.)