The New Nation - Internet Edition

Jaundice: A slow killer disease

Jaundice, also known as icterus (attributive adjective: "icteric"), is yellowish discoloration of the skin, sclerae (whites of the eyes) and mucous membranes caused by hyperbilirubinemia (increased levels of bilirubin in the blood). This hyperbilirubinemia subsequently causes increased levels of bilirubin in the extracellular fluids. Typically, the concentration of bilirubin in the plasma must exceed 1.5 mg/dL, three times the usual value of approximately 0.5mg/dL, for the coloration to be easily visible. Jaundice comes from the French word jaune, meaning yellow.

Normal Physiology: In order to understand how jaundice results, it is important to understand where the pathological processes that cause jaundice take their effect. It is also important to further recognize that jaundice itself is not a disease, but rather a symptom of an underlying pathological process that occurs at some point along the normal physiological pathway of the metabolism of bilirubin.

Pre-hepatic events: When red blood cells have completed their life span of approximately 120 days, their membranes become fragile and prone to rupture. As the cell traverses through the reticuloendothelial system, their cell membranes rupture and the contents of the red blood cell is released into the blood. The component of the red blood cell that is involved in jaundice is hemoglobin. The hemoglobin released into the blood is phagocytosed by macrophages, and split into its heme and globin portions. The globin portion, being protein, is degraded into amino acids and plays no further role in jaundice. Two reactions then take place to the heme molecule. The first reaction is the oxidation of heme to form biliverdin.This reaction is catalyzed by microsomal enzyme heme oxygenase and it results in biliverdin (green color pigment), iron and carbon monoxide. Next step is reduction of biliverdin to yellow color tetrapyrol pigment bilirubin by cytosolic enzyme biliverdin reductase.

This bilirubin is known as "unconjugated", "free" or "indirect" bilirubin. Approximately 4 mg per kg of bilirubin is produced each day. The majority of this bilirubin comes from the breakdown of heme from expired red blood cells in the process just described. However approximately 20 per cent comes from other heme sources, including ineffective erythropoiesis, breakdown of other heme protrins such as muscle myoglobin and cytochrome enzymes.

Hepatic events: The unconjugated bilirubin then travels to the liver through the bloodstream. Because this bilirubin is not soluble, however, it is transported through the blood bound to serum albumin. Once it arrives at the liver, it is conjugated with glucuronic acid (to form bilirubin diglucuronide, or just "conjugated bilirubin") to become more water soluble. The reaction is catalyzed by the enzyme UDP-glucuronide transferase.

Post-hepatic events: This conjugated bilirubin is excreted from the liver into the biliary and cystic ducts as part of bile. Intestinal bacteria convert the bilirubin into urobilinogen. From here the urobilinogen can take two pathways. It can either be further converted into stercobilinogen, which is then oxidized to stercobilin and passed out in the faeces, or it can be reabsorbed by the intestinal cells, transported in the blood to the kidneys, and passed out in the urine as the oxidised product urobilin. Stercobilin and urobilin are the products responsible for the coloration of faeces and urine, respectively.

Causes: When a pathological process interferes with the normal functioning of the metabolism and excretion of bilirubin just described, jaundice may be the result. Jaundice is classified into three categories, depending on which part of the physiological mechanism the pathology affects. The three categories are:

Pre-hepatic: Pre-hepatic jaundice is caused by anything which causes an increased rate of hemolysis (breakdown of red blood cells). In tropical countries, malaria can cause jaundice in this manner. Certain genetic diseases, such as sickle cell anemia, spherocytosis and glucose 6-phosphate dehydrogenase deficiency can lead to increased red cell lysis and therefore hemolytic jaundice. Commonly, diseases of the kidney, such as hemolytic uremic syndrome, can also lead to coloration. Defects in bilirubin metabolism also present as jaundice. Jaundice usually comes with high fevers.

Hepatic: Hepatic jaundice causes include acute hepatitis, hepatotoxicity and alcoholic liver disease, whereby cell necrosis reduces the liver's ability to metabolise and excrete bilirubin leading to a buildup in the blood. Less common causes include primary biliary cirrhosis, Gilbert's syndrome (a genetic disorder of bilirubin metabolism which can result in mild jaundice, which is found in about 5% of the population), Crigler-Najjar syndrome and metastatic carcinoma. Jaundice seen in the newborn, known as neonatal jaundice, is common, occurring in almost every newborn as hepatic machinery for the conjugation and excretion of bilirubin does not fully mature until approximately two weeks of age.

Post-hepatic: Post-hepatic jaundice, also called obstructive jaundice, is caused by an interruption to the drainage of bile in the biliary system. The most common causes are gallstones in the common bile duct, and pancreatic cancer in the head of the pancreas. Also, a group of parasites known as "liver flukes" live in the common bile duct, causing obstructive jaundice. Other causes include strictures of the common bile duct, biliary atresia, ductal carcinoma, pancreatitis and pancreatic pseudocysts. A rare cause of obstructive jaundice is Mirizzi's syndrome.

The presence of pale stools and dark urine suggests an obstructive or post-hepatic cause as normal feces get their color from bile pigments.

Patients also can present with elevated serum cholesterol, and often complain of severe itching or "pruritus".

Neonatal jaundice: Main article: Neonatal jaundice Neonatal jaundice is usually harmless: this condition is often seen in infants around the second day after birth, lasting until day 8 in normal births, or to around day 14 in premature births. Serum bilirubin normally drops to a low level without any intervention required: the jaundice is presumably a consequence of metabolic and physiological adjustments after birth. In extreme cases, a brain-damaging condition known as kernicterus can occur; there are concerns that this condition has been rising in recent years due to inadequate detection and treatment of neonatal hyperbilirubinemia. Neonatal jaundice is a risk factor for hearing loss.

Jaundiced eye: It was once believed persons suffering from the medical condition jaundice saw everything as yellow. By extension, the jaundiced eye came to mean a prejudiced view, usually rather negative or critical. Alexander Pope, in 'An Essay on Criticism' (1711), wrote: "All seems infected that the infected spy, As all looks yellow to the jaundiced eye."[4] Similarly in the mid 19th century the English poet Lord Alfred Tennyson wrote in the poem 'Locksley Hall': "So I triumphe'd ere my passion sweeping thro' me left me dry, left me with the palsied heart, and left me with a jaundiced eye."

Jaundice in healthy newborns

A common condition in newborns, jaundice refers to the yellow color of the skin and whites of the eyes caused by excess bilirubin in the blood. Bilirubin is produced by the normal breakdown of red blood cells.

Normally, bilirubin passes through the liver and is excreted as bile through the intestines. Jaundice occurs when bilirubin builds up faster than a newborn's liver can break it down and pass it from the body. Reasons for this include:

Newborns make more bilirubin than adults do since they have more turnover of red blood cells.

A newborn baby's still-developing liver may not yet be able to remove adequate bilirubin from the blood.

Too large an amount of bilirubin is reabsorbed from the intestines before the baby gets rid of it in the stool.

High levels of bilirubin - usually above 25 mg - can cause deafness, cerebral palsy, or other forms of brain damage in some babies. In less common cases, jaundice may indicate the presence of another condition, such as an infection or a thyroid problem. The American Academy of Pediatrics (AAP) recommends that all infants should be examined for jaundice within a few days of birth.

Types of Jaundice: The most common types of jaundice are:

Physiological (normal) jaundice: occurring in most newborns, this mild jaundice is due to the immaturity of the baby's liver, which leads to a slow processing of bilirubin. It generally appears at 2 to 4 days of age and disappears by 1 to 2 weeks of age. Jaundice of prematurity: occurs frequently in premature babies since they are even less ready to excrete bilirubin effectively. Jaundice in premature babies needs to be treated at a lower bilirubin level than in full term babies in order to avoid complications.

Breastfeeding jaundice: jaundice can occur when a breastfeeding baby is not getting enough breast milk because of difficulty with breastfeeding or because the mother's milk isn't in yet. This is not caused by a problem with the breast milk itself, but by the baby not getting enough to drink.

Breast milk jaundice: in 1% to 2% of breastfed babies, jaundice may be caused by substances produced in their mother's breast milk that can cause the bilirubin level to rise. These can prevent the excretion of bilirubin through the intestines. It starts after the first 3 to 5 days and slowly improves over 3 to 12 weeks.

Blood group incompatibility (Rh or ABO problems): if a baby has a different blood type than the mother, the mother might produce antibodies that destroy the infant's red blood cells. This creates a sudden buildup of bilirubin in the baby's blood. Incompatibility jaundice can begin as early as the first day of life. Rh problems once caused the most severe form of jaundice, but now can be prevented with an injection of Rh immune globulin to the mother within 72 hours after delivery, which prevents her from forming antibodies that might endanger any subsequent babies.

Symptoms and Diagnosis: Jaundice usually appears around the second or third day of life. It begins at the head and progresses downward. A jaundiced baby's skin will usually appear yellow first on the face, followed by the chest and stomach, and finally, the legs. It can also cause the whites of an infant's eyes to appear yellow.

Since many babies are now released from the hospital at 1 or 2 days of life, it is best for the baby to be seen by a doctor within 1 to 2 days of leaving the hospital to check for jaundice. Parents should also keep an eye on their infants to detect jaundice.

If you notice your baby's skin or eyes looking yellow you should contact your child's doctor to see if significant jaundice is present.

At the doctor's office, a small sample of your infant's blood can be tested to measure the bilirubin level. Some offices use a light meter to get an approximate measurement, and then if it is high, check a blood sample. The seriousness of the jaundice will vary based on how many hours old your child is and the presence of other medical conditions.

When to Call the Doctor

Your doctor should be called immediately if:

jaundice is noted during the first 24 hours of life

the jaundice is spreading or getting more intense

your baby develops a fever over 100° Fahrenheit (37.8° Celsius) rectally

if your child starts to look or act sick

Also call the doctor right away if the color deepens, your baby is not feeding well, or if you feel your baby is sleepier than usual. It is difficult to tell how significant jaundice is just by looking at a baby, so any baby who has yellow eyes or skin should be checked by the doctor.

Treatments: In mild or moderate levels of jaundice, by 1 to 2 weeks of age the baby will take care of the excess bilirubin on its own. For high levels of jaundice, phototherapy - treatment with a special light that helps rid the body of the bilirubin by altering it or making it easier for your baby's liver to get rid of it - may be used.

More frequent feedings of breast milk or supplementing with formula to help infants pass the bilirubin in their stools may also be recommended. In rare cases, a blood exchange may be required to give a baby fresh blood and remove the bilirubin.

If your baby develops jaundice that seems to be from breast milk, your doctor may ask you to temporarily stop breastfeeding. During this time, you can pump your breasts so you can keep producing breast milk and you can start nursing again once the condition has cleared.

If the amount of bilirubin is high, your baby may be readmitted to the hospital for treatment. Once the bilirubin level drops and the treatment is stopped, it is unlikely that treatment for jaundice will need to be restarted.

Nutrition care for mothers, children

Health Report

National Nutrition Program (NNP) of the government over the years has generated huge response across the country. The government's aim to combat large-scale malnutrition problem through this program is on the way to meet success.

The program is designed and directly supervised by the Ministry of Health and Family Welfare of the government.

Voluntary Organization for Social Development (VOSD), one of the non-government organizations (NGO), engaged in implementing the Program in cooperation with the NNP.

Through its skilled and sincere services VOSD has already earned wide reputation. In a recent finding of performance of the Ministry of Health and Family Welfare, VOSD has been adjudged as "A+" (Excellent) for its highly satisfactory performance.

VOSD has been running this program in two Upozilas in Barisal, 4 Upozilas in Jhalakhati, 1 Upozila in Faridpur, 1 in Munshigonj, 7 Upozila in Chandpur, 4 in Laximpur and 1 Upozila in Barguna.

It has so far provided nutrition facilities to 56 lakh 91 thousand and 484 women and children by 4 thousand 641 Community Nutrition Providers (CNP) through establishing 4641 Community Nutrition Centers (CNC).

Huge number of severely mal nutrition affected children, pregnant women, breast feeding mothers, adolescent (13-19 years) and newly married women at 'sidr' affected Amtali Upozila of Barguna has been brought under nutrition care of this program. Everyday from 9 am to 11 am, the children and pregnant women who come under supplementary feeding are provided with health knowledge and food at the nutrition centers established in Amtoly.

Each pack of nutrition food contains 20 gram fried rice powder, 10 gram of fried lentil powder, 5 gram molasses and 3 gram Soyabean Oil.

A VOSD high official said reducing the rate of malnutrition of under 2 children is possible below 5 per cent; increasing weight of 50 per cent pregnant women upto 9 Kg or more; bringing the number of less weight children (during birth) below 30 per cent; reducing the rate of less blood of adolescents and pregnant women by one third, limiting the rate of nyctapolic among 1-5 year children within 0.5 per cent and lessening the rate of less iodine by 50 per cent are successfully being implemented through this program.

While visiting the CNP No 143 of Amtoly Upazila a beneficiary Taslima Begum said the this correspondent, "we really could not know what is mal nutrition if there were no 'Pusti Apa'. "

Severely mal nutrition affected children are fed two packs and pregnant women who are of below 17 of Body Mass Index (BMI) are fed 4 nutrition packs as supplementary food. A total of 2,52,480 children and 61, 816 pregnant women (from 4 months of pregnancy) have so far come under feeding of nutrition pack.

42,864 progenitress mothers have been brought under other nutrition care facilities (giving vitamin-A tablets) and 3,25,445 adolescent girls have been given nutrition care. An adolescent girl's forum has been formed and all it's members are given wormicide tablets at a gap of 6 months. Besides, VOSD has been contributing to eliminating anemia through distributing iron tablets among 61556 pregnant women and 3,25,445 adolescent girls.

A total of 26,784 newly married women have been given nutrition care, who are also being given lessons to contribute in building sound and healthy children through the adolescent forum.

VOSD Executive Director, A K M Mostafizur Rahman said, "A mentionable portion of total population of the country has been suffering from mal nutrition. Especially women and children are most vulnerable among the people in terms of nutrition".

He said, mal nutrition is not only a physical problem, it also spread harmful impact on the education receiving power and productivity of human body, so the government's initiative of undertaking this program is great and as the Executive Director of VOSD, I really feel proud to be an associate of this program.

Indigenous plants and knowledge in hill districts

Niaz Ahmed Khan and A.Z.M. Manzoor Rashid

Part-II

Drawing the respondents' comments and responses, the following major problems and challenges concerning the practice of Baidya may be identified:

· The most widely used species in the preparation and practice of medicine are becoming increasingly rare and difficult to procure for such reasons as rapid destruction of the neighbouring natural forests (mainly prompted by organised illicit commercial logging), bureaucratic complications and harassment (e.g. by the Forest Department), and inaccessibility and difficulties in communication and transportation.

· There is no formal arrangement or institution to train and nurture this knowledge in the locality. The institutional mechanisms for dissemination or extension of the knowledge and practice are also absent.

· The time of collection and harvesting of medicinal plants is a vital factor in ensuring efficacy of the medicines prepared thereof. The time factor is often ignored or by-passed by the Baidyas due to acute shortage and great demand of these plants.

· Competition Local people nowadays prefer 'modern' mainstream medication. The reduced number of patients, coupled with the difficulty in obtaining raw materials, makes the practice of Baidya almost unsustainable.

· The young generation does not show much interest in learning the traditional practice. They feel that Baidya as a profession is not promising for the above reasons.

· Majority of the existing Baidyas buy the raw material (spices, plants, stamp, seeds, roots etc.) of their practice from the local markets. Many respondents reported that these materials are generally of low quality and poor stock.

· The Baidyas, who want to ensure a sustained source of quality seed and seedling, badly feel the absence of a central propagation nursery.

· Institutional and external support and patronisation, especially from the government, for the development and promotion of indigenous medicinal plants and knowledge are nearly absent in the study areas.

Drawing on the respondents' comments and our observation during the fieldwork, the following ideas and clues on possible improvement may be considered:

· With the active participation of the local people, the existing medicinal plants should be systematically documented and recorded.

· Organised motivational and awareness raising campaign regarding medicinal plants and their benefits (e.g. free from negative side effects, low cost) may be carried out at the community level, especially amongst the younger population, by involving the community leaders and local community based organisations (e.g. schools and religious institutions) and NGOs.

· Experimental propagation nurseries may be established under government and non-government initiatives to ensure sustained supply of seedlings.

· The mainstream research institutions in the country, especially the forest and agricultural research institutes and universities may be encouraged to provide the much-needed research support for proper documentation and dissemination of the knowledge on medicinal plants and associated folk and herbal treatment methods.

· The local press, media and folk cultural practices (e.g. folk theatres) may be utilised as community-based extension and dissemination media to highlight the importance of conserving this traditional practice and heritage.

· Local base and community relations-two of the major benefits of some of the local NGOs and community based organisations may also be exploited for initiating a network or platform to bring the Baidyas together.

The age-old indigenous practice of Baidya is currently threatened by a host of problems including limited availability of the required plants and herbs; rapid destruction of natural forests; lack of formal arrangement or institution to train and nurture this knowledge; lack of organised propagation nurseries; inadequate Institutional and external support and patronisation (especially from the government); low quality and poor stock of raw materials in the open market; and unwillingness among the youngsters to learn and adopt the practice. Despite the rather dismal present state of affairs, this deeply rooted social practice, which has significant value as a community service, still holds great potential, remains too important to be ignored, and therefore, deserves the attention and support of all concerned.

[ Dr. Niaz Ahmed Khan is Professor of Development Studies at the University of Dhaka, Bangladesh and Honorary Research Fellow, Centre for Development Studies, University of Wales, UK. Contact: niaz.khan@yahoo.com; and A.Z.M.Manzoor Rashid is Assistant Professor of Forestry and Environmental Science at the Shahjalal University of Science &Technology, Sylhet, Bangladesh.]