Hepatocellular Health Dictionary

Jaundice is a yellow discoloration of the skin due to the deposition of BILE pigment in its deeper layers. It is the main sign of several disorders of the liver and biliary system. Many babies develop jaundice soon after birth because of the accumulation of BILIRUBIN (yellow bile pigment) in the blood. In most, this is due to liver immaturity and soon disappears, but a serious disorder, HAEMOLYTIC DISEASE OF THE NEWBORN, is a potentially dangerous type of neonatal jaundice that requires treatment.

Types In adults, three types of jaundice occur. They are all the result of disturbance in the mechanism by which HAEMOGLOBIN from the breakdown of ageing red blood cells (erythrocytes) is not properly processed in the liver. Normally the breakdown product of this haemoglobin – bilirubin – is made water-soluble in the liver and excreted via the bile ducts into the small intestine, where it colours the stools dark brown. HAEMOLYTIC JAUNDICE In this type, the amount of bilirubin produced is too much for the liver to deal with, the excess usually being the result of an abnormal level of haemoglobin from the breakdown of blood cells. This haemolytic anaemia, as it is known, has several causes (see ANAEMIA). HEPATOCELLULAR JAUNDICE In this disorder, bilirubin builds up in the blood because liver cells have been damaged or have died – usually as a result of a viral infection (there are four types) causing HEPATITIS, or of liver failure. OBSTRUCTIVE JAUNDICE Also called cholestatic jaundice, this type is characterised by the inability of bile to be discharged from the liver because the bile ducts are blocked as a result of gall-stones (see under GALL-BLADDER, DISEASES OF) or a growth. Sometimes the ducts are absent (atresia) or have been destroyed in the liver as a result of CIRRHOSIS.

Symptoms Yellowness, appearing ?rst in the whites of the eyes and later over the whole skin, is the symptom that attracts notice. Indigestion, nausea, poor appetite and general malaise are other symptoms. The skin may itch, and the faeces are pale because of the absence of bile.

Treatment The essential step is to treat the underlying cause if possible: for instance, gallstones, if these be the cause of the jaundice. Comprehensive laboratory investigations are usually required, and supportive measures are needed. (See also LIVER, DISEASES OF.).... jaundice

Andrographis paniculata

Acanthaceae

San: Bhunimbah, Kiratatiktah

Hin: Kakamegh, Kalpanath

Ben: Kalmegh

Mal: Nilaveppu, Kiriyattu Tam: Nilavempu Kan: Kreata

Importance: Kalmegh, the Great or Green Chiretta is a branched annual herb. It is useful in hyperdipsia, burning sensation, wounds, ulcers, chronic fever, malarial and intermittent fevers, inflammations, cough, bronchitis, skin diseases, leprosy, pruritis, intestinal worms, dyspepsia, flatulence, colic, diarrhoea, dysentery, haemorrhoids and vitiated conditions of pitta (Warrier et al, 1993). It is used to overcome sannipata type of fever, difficulty in breathing, hemopathy due to the morbidity of kapha and pitta, burning sensation, cough, oedema, thirst, skin diseases, fever, ulcer and worms. It is also useful in acidity and liver complaints (Aiyer and Kolammal, 1962). The important preparations using the drug are Tiktakagheta, Gorocandi gulika, Candanasava, Panchatiktam kasaya, etc. (Sivarajan et al, 1994). A preparation called “Alui” is prepared by mixing powdered cumin (Cuminium cyminum) and large cardamom (Amomum subulatum) in the juice of this plant and administered for the treatment of malaria (Thakur et al, 1989). It is also a rich source of minerals.

Distribution: The plant is distributed throughout the tropics. It is found in the plains of India from U.P to Assam, M.P., A.P, Tamil Nadu and Kerala, also cultivated in gardens.

Botany: Andrographis paniculata (Burm.f.) Wall ex.

Nees belongs to the family Acanthaceae. It is an erect branched annual herb, 0.3-0.9m in height with quadrangular branches. Leaves are simple, lanceolate, acute at both ends, glabrous, with 4-6 pairs of main nerves. Flowers are small, pale but blotched and spotted with brown and purple distant in lax spreading axillary and terminal racemes or panicles. Calyx-lobes are glandular pubescent with anthers bearded at the base. Fruits are linear capsules and acute at both ends. Seeds are numerous, yellowish brown and sub-quadrate (Warrier et al,1993).

Another species of Andrographis is A. echioides (Linn.) Nees. It is found in the warmer parts of India. The plant is a febrifuge and diuretic. It contains flavone-echiodinin and its glucoside-echioidin (Husain et al, 1992).

Agrotechnology: The best season of planting Andrographis is May-June. The field is to be ploughed well, mixed with compost or dried cowdung and seedbeds of length 3m, breadth 1/2m and 15cm height are to be taken at a distance of 3m. The plant is seed propagated. Seeds are to be soaked in water for 6 hours before sowing. Sowing is to be done at a spacing of 20cm. Seeds may germinate within 15-20 days. Two weedings, first at one month after planting and the second at 2 month after planting are to be carried out. Irrigation during summer months is beneficial. The plant is not attacked by any serious pests or diseases. Flowering commences from third month onwards. At this stage, plant are to be collected, tied into small bundles and sun-dried for 4-5 days. Whole plant is the economic part and the yield is about 1.25t dried plants/ha (Prasad et al, 1997).

Properties and activity: Leaves contain two bitter substances lactone “andrographolid” and “kalmeghin”. The ash contains sodium chloride and potassium salts. Plant is very rich in chlorophyte. Kalmeghin is the active principle that contains 0.6% alkaloid of the crude plant. The plant contains diterpenoids, andrographolide, 14-deoxy-11-oxo-andrographolide, 14-deoxy-11,12-dihydroandrographolide, 14-deoxy andrographolide and neoandrographolide (Allison et al, 1968). The roots give flavones-apigenin-7,4-dio-O-methyl ether, 5-hydroxy-7,8,2’,3’- tetramethoxyflavone, andrographin and panicolin and -sitosterol (Ali et al, 1972; Govindachari et al, 1969). Leaves contain homoandrographolide, andrographosterol and andrographone.

The plant is vulnerary, antipyretic, antiperiodic, anti-inflammatory, expectorant, depurative, sudorific, anthelmintic, digestive, stomachic, tonic, febrifuge and cholagogue. The plant is antifungal, antityphoid, hepatoprotective, antidiabetic and cholinergic. Shoot is antibacterial and leaf is hypotensive(Garcia et al, 1980). This is used for the inflammation of the respiratory tract. In China, researchers have isolated the andrographolide from which soluble derivative such as 14-deoxy-11, 12-dehydro-andrographolide which forms the subject of current pharmacological and clinical studies. Apigenin 7,4’-O-dimethyl ether isolated from A. paniculata exhibits dose dependent, antiulcer activity in shay rat, histamine induced ulcer in guinea pigs and aspirin induced ulcers in rats. A crude substance isolated from methanolic extract of leaves has shown hypotensive activity. Pre-treatment of rats with leaf (500mg/kg) or andrographolide (5mg/kg) orally prevented the carbon tetrachloride induced increase of blood serum levels of glutamate-oxaloacetate transaminase in liver and prevented hepatocellular membrane.... green chiretta

Also known as BILHARZIASIS. This infection results from one of the human Schistosoma species. It is common in Africa, South America, the Far East, Middle East, and, to a limited extent, the Caribbean. The life-cycle is dependent on fresh-water snails which act as the intermediate host for the ?uke; the cercarial stage of the ?uke enters via intact human skin and matures in the portal circulation. Clinically, ‘swimmers’ itch’ may occur at the site of cercarial skin penetration. Acute schistosomiasis (Katayama fever) can result in fever, an urticarial rash (see URTICARIA), and enlargement of LIVER and SPLEEN. The adult male is about 12 mm and the female 24 mm in length.

S. haematobium causes CYSTITIS and haematuria – passage of blood in the urine; bladder cancer and ureteric obstruction, giving rise to hydronephrosis and kidney failure, are long-term sequelae in a severe case. S. mansoni can cause colonic symptoms and in a severe case, POLYPOSIS of the COLON; diarrhoea, which may be bloody, can be a presenting feature. In a heavy infection, eggs surrounded by granulomas are deposited in the liver, giving rise to extensive damage (pipe-stem ?brosis) associated with PORTAL HYPERTENSION, oesophageal varices, etc. However, unlike in CIRRHOSIS, hepatocellular function is preserved until late in the disease. S. japonicum (which is con?ned to the Far East, especially Indonesia) behaves similarly to S. mansoni infection; liver involvement is often more severe.

Diagnosis can be made by microscopic examination of URINE or FAECES. The characteristic eggs are usually detectable. Alternatively, rectal or liver BIOPSY are of value. Serological tests, including an ELISA (see ENZYME-LINKED IMMUNOSORBENT ASSAY (ELISA)), have now largely replaced invasive procedures used in making a parasitological diagnosis.

Treatment CHEMOTHERAPY has been revolutionised by the introduction of praziquantel (administered orally); this compound has no serious side-effects, although its cost may limit its use in developing countries. Oxamniquine is cheaper and e?ective in S. mansoni infection, although evidence of resistance has been recorded in several countries. Metriphonate is also relatively cheap and is of value in S. haematobium infection. Prevention is by complete avoidance of exposure to contaminated water; all travellers to infected areas should know about this disease. It is increasing in frequency as new expanses of fresh water appear as a result of irrigation schemes and dam projects. Molluscicides can be employed for snail-control.... schistosomiasis

ACUTE LIVER DISEASE The hepatitis viruses (A– F) are of paramount importance. Hepatitis E (HEV) often produces acute hepatic failure in pregnant women; extensive epidemics – transmitted by contaminated drinking-water supplies – have been documented. HBV, especially in association with HDV, also causes acute liver failure in infected patients in several tropical countries: however, the major importance of HBV is that the infection leads to chronic liver disease (see below). Other hepatotoxic viruses include the EPSTEIN BARR VIRUS, CYTOMEGALOVIRUS (CMV), the ?avivirus causing YELLOW FEVER, Marburg/Ebola viruses, etc. Acute liver disease also occurs in the presence of several acute bacterial infections, including Salmonella typhi, brucellosis, leptospirosis, syphilis, etc. The complex type of jaundice associated with acute systemic bacterial infection – especially pneumococcal PNEUMONIA and pyomiositis – assumes a major importance in many tropical countries, especially those in Africa and in Papua New Guinea. Of protozoan infections, plasmodium falciparum malaria, LEISHMANIASIS, and TOXOPLASMOSIS should be considered. Ascaris lumbricoides (the roundworm) can produce obstruction to the biliary system. CHRONIC LIVER DISEASE Long-term disease is dominated by sequelae of HBV and HCV infections (often acquired during the neonatal period), both of which can cause chronic active hepatitis, cirrhosis, and hepatocellular carcinoma (‘hepatoma’) – one of the world’s most common malignancies. Chronic liver disease is also caused by SCHISTOSOMIASIS (usually Schistosoma mansoni and S. japonicum), and acute and chronic alcohol ingestion. Furthermore, many local herbal remedies and also orthodox chemotherapeutic compounds (e.g. those used in tuberculosis and leprosy) can result in chronic liver disease. HAEMOSIDEROSIS is a major problem in southern Africa. Hepatocytes contain excessive iron – derived primarily from an excessive intake, often present in locally brewed beer; however, a genetic predisposition seems likely. Indian childhood cirrhosis – associated with an excess of copper – is a major problem in India and surrounding countries. Epidemiological evidence shows that much of the copper is derived from copper vessels used to store milk after weaning. Veno-occlusive disease was ?rst described in Jamaica and is caused by pyrrolyzidine alkaloids (present in bush-tea). Several HIV-associated ‘opportunistic’ infections can give rise to hepatic disease (see AIDS/HIV).

A localised (focal) form of liver disease in all tropical/subtropical countries results from invasive Entamoeba histolytica infection (amoebic liver ‘abscess’); serology and imaging techniques assist in diagnosis. Hydatidosis also causes localised liver disease; one or more cysts usually involve the right lobe of the liver. Serological tests and imaging techniques are of value in diagnosis. Whilst surgery formerly constituted the sole method of management, prolonged courses of albendazole and/or praziquantel have now been shown to be e?ective; however, surgical intervention is still required in some cases.

Hepato-biliary disease is also a problem in many tropical/subtropical countries. In southeast Asia, Clonorchis sinensis and Opisthorchis viverini infections cause chronic biliary-tract infection, complicated by adenocarcinoma of the biliary system. Praziquantel is e?ective chemotherapy before advanced disease ensues. Fasciola hepatica (the liver ?uke) is a further hepato-biliary helminthic infection; treatment is with bithionol or triclabendazole, praziquantel being relatively ine?ective.... liver disease in the tropics

An acute arbovirus (see ARBOVIRUSES) infection caused by a ?avivirus of the togavirus family, transmitted from animals to humans by various species of forest mosquito (jungle/sylvan yellow fever), and from human to human by Aëdes aegypti (urban yellow fever). Mosquito transmission was shown by Walter Reed and his colleagues in 1900. It is ENDEMIC in much of tropical Africa and Central and South America but does not occur in Asia. In the urban cycle, humans constitute the reservoir of infection, and in the jungle/sylvan variety, mammals – especially subhuman primates – are involved in transmission. Historically, yellow fever was enormously important, causing devastating epidemics (see EPIDEMIC); it also carried a high mortality rate in travellers and explorers. Differentiation from other infections associated with JAUNDICE was often impossible.

Clinically, yellow fever is characterised by jaundice, fever, chills, headache, gastrointestinal haemorrhage(s), and ALBUMINURIA. The incubation period is 3–6 (up to 10) days. Differentiation from viral hepatitides, other viral haemorrhagic fevers, severe Plasmodium falciparum malaria, and several other infections is often impossible without sophisticated investigative techniques. Infection carries a high mortality rate. Liver histology (biopsy is contraindicated due to the haemorrhagic diathesis) shows characteristic changes; a fulminating hepatic infection is often present. Acute in?ammation of the kidneys and an in?amed, congested gastric mucosa, often accompanied by haemorrhage, are also demonstrable; myocardial involvement often occurs. Diagnosis is primarily based on virological techniques; serological tests are also of value. Yellow fever should be suspected in any travellers from an endemic area.

Management consists of instituting techniques for acute hepatocellular (liver-cell) failure. The affected individual should be kept in an isolation unit, away from mosquitoes which could transmit the disease to a healthy individual. Formerly, laboratory infections were occasionally acquired from infected blood samples. Prophylactically, a satisfactory attenuated VACCINE (17D) has been available for around 60 years; this is given subcutaneously and provides an individual with excellent protection for ten years; international certi?cates are valid for this length of time. Every traveller to an endemic area should be immunised; this is mandatory for entry to countries where the infection is endemic.... yellow fever

(hepatocellular carcinoma) n. the most common primary malignant tumour of the liver. In Western countries patients with chronic hepatitis B or C or cirrhosis are at significantly increased risk of developing hepatoma. The higher incidence of hepatomas in non-Western societies (particularly the Far East and Africa) is partly due to increased hepatitis B endemicity but other factors contribute, including exposure to fungi (see aflatoxin) and other ingested toxins. Hepatomas often synthesize *alpha-fetoprotein, which is a useful serum tumour marker. The treatment options depend on the number and size of hepatomas and the staging of the disease. They include surgical resection, chemotherapy, *chemoembolization, local ablative treatment, and liver transplantation.... hepatoma