The Severe Acute Respiratory Syndrome (SARS) dominated headlines a few months ago. However, at that time, SARS was not the only viral illness reported to the World Health Organization (WHO). As reported in Newsweek (May 5, 2003), an outbreak of Ebola fever in Central Africa had already entered its fifth month. In Belgium and the Netherlands, entire chicken farms were being wiped out by a virulent new strain of avian flu. 18 million birds were slaughtered by farmers in an attempt to curb the outbreak. Yet, the avian flu not only spread to several provinces, but also caused 83 human cases.

As recently as June 2003, the Centers for Disease Control (CDC) received reports of patients with a febrile rash illness who had close contact with pet prairie dogs and other animals. Investigations revealed that this outbreak was caused by the monkeypox virus (MMWR Weekly June 13, 2003). This was first identified in 1970 in the Democratic Republic of the Congo, in a region where smallpox had been eradicated in 1968. After an incubation period of 7-17 days, the disease is characterized by the onset of a prodrome of fever, headache, backache and fatigue. The monkeypox rash includes macules, papules, vesicles, pustules and crusts that evolve in the same stage over 14-21 days, similar to smallpox. A major clinical difference is pronounced lymphadenopathy in a majority of patients with monkeypox.

 

 At the mercy of the microbe

 

The history of mankind has been pockmarked with emerging pathogens and pandemics, whether it was the Spanish flu epidemic of 1918, or the Black Death, or more recently, Monkeypox. The list of emerging infectious diseases continues, each one confirming the vulnerability of our species. About 30 years ago, when smallpox was thought to be eradicated, a sense of jubilation prevailed, and the battle with the microbes was generally thought to have been won. At that time, infection with the Human Immunodeficiency Virus (HIV) had yet to emerge as today's holocaust. Floods, wars, earthquakes and famines have been known to wreak epidemics in the past. However, paradoxically, today the pace of our progress itself exerts a potent influence in nurturing future outbreaks. As an example, our crowded megacities, jet planes and blood banks open broad new avenues for infection. Dozens of new diseases have emerged since the mid-1970's - causing tens of millions of deaths. Forgotten scourges, such as plague, have resurfaced with alarming regularity. Moreover, as newer pathogens continue to evolve, it seems certain that infectious diseases will continue to emerge.

So what steps can we take to minimize the impact of emerging pathogens? As the SARS outbreak has shown, the key is surveillance. By spotting new infections whenever they occur, and taking global measures to contain them, we can greatly reduce their impact. However, preparedness alone cannot be our ultimate weapon. It is equally imperative to understand how newer pathogens evolve, and then ensure that conditions favouring such events do not arise in the first place.
 

Figure 1: Coronaviruses are a group of
viruses that have a halo or crown-like
(corona) appearance when viewed under
a microscope

The genesis of new diseases

 

Most new diseases begin when a person catches an infection from an animal (zoonotic transmission). This could possibly occur by chance, or perhaps due to a change in the weather. For example, ten years ago, healthy young adults started dying of a SARS-like syndrome in New Mexico in the United States. Intensive laboratory research revealed that the cause was a novel member of the hantavirus family. This family is a group of rodent viruses that sometimes spread through the air after rats or mice shed them in their urine. The previous outbreaks had occurred in Asia. Scientists believe that the American mice had harboured the virus all along, but had never been populous enough to scatter infectious doses in toolsheds and basements. But that year, the ocean disturbance called the El Nino phenomenon caused an unusually warm winter in the Southwest. This caused an explosion in the mouse population as well as the hantavirus.

Ecologists report that human enterprise is an equally significant force. This is because almost any activity that disrupts a natural environment can enhance the mobility of pathogenic microbes. For example, in the 1980s, farmers in Venezuela's Portuguese state cleared millions of acres of forest to create farms. These farms drew many rats and mice, which introduced a deadly new virus into the region. This Guanarito virus caused fever, shock and haemorrhaging. It infected more than 100 people, leaving one-third dead.

In the case of the monkeypox outbreak, a total of 51 patients reported direct or close contact with prairie dogs and one patient reported contact with a Gambian giant rat. Investigations into the source of the monkeypox introduced into the United States identified a common distributor, where prairie dogs and Gambian giant rats were housed together in Illinois. A search of imported animal records revealed that Gambian giant rats were shipped from Ghana in April and subsequently were sold to the Illinois distributor. The shipment contained about 800 small mammals of nine different species that might have been the actual source of introduction of monkeypox. Thus, the introduction of exotic species could pose a serious public health threat because of the potential for introduction of nonindigenous pathogens.

 

The spread of new diseases

 

Even when a microbe succeeds at leaping from one species to another, the new host is often a dead end. The Guanarito virus cannot spread from person to person. Relatively inefficient person-to-person transmission has been documented for monkeypox.

However, this is not how infections derived from primates and pigs behave. When the Ebola virus jumps from an ape into a human, it often quickly spreads through a family or a hospital. And HIV is still spreading steadily after two decades of person-to-person transmission. It has infected some 60 million people since crossing over from chimpanzees. It has been theorized that African hunters contracted HIV while butchering chimpanzees and monkeys (bush meat), and then passed it on through sexual contact. Until a few decades ago, the repercussions of that hunting accident would have been restricted locally. It became a global holocaust due to the ease of international travel, a breakdown of social traditions, and the advent of blood banking and needle sharing. These conditions virtually ensured that HIV infection became a global infection - a pandemic.

Both the volume and speed of travel possible today are unprecedented. SARS is only the latest reminder of how powerful those connections can be. The novel coronavirus that causes the syndrome emerged from the Chinese province Guangdong. Pigs, ducks, chickens and people live in close proximity on the district's primitive farms, exchanging flu and other viruses so rapidly that a single pig can easily incubate human and avian viruses simultaneously. The dual infections can generate hybrids that escape antibodies produced against the originals, setting off a whole new chain of human infection. These farms are a few miles away from Guangzhou, which is a busy city in which people, animals and microbes from the countryside mingle with travelers from around the world. So what began as a local outbreak spread to nearly a dozen countries, as far away as Canada, killing more than five hundred people.

 

The way ahead

Pandemic flu viruses have emerged in the past, and many experts believe that it is only a matter of time until it happens again. In fact, the World Health Organisation (WHO) has said that the world must tighten its defenses against infectious diseases because other potential killers like SARS are certain to arise.

Hence, it is key to have contingency plans in place to lessen the danger. It is said that the best defense against any infectious disease is a good offence. In this connection, surveillance is extremely important. It is important to be prepared, and have warning systems for potential outbreaks in place. Today, progress in information technology has made infectious diseases easier to track. The world's largest health agencies have created systems for sharing scientific research.

During the two-day international conference on SARS held in Toronto, Canada in May, a series of recommendations were made as to specific steps countries must now take to ensure that SARS is contained permanently. Many of these recommendations were based on issues that have been raised in the past - including the overwhelming importance of having a solid public health infrastructure in the face of a new contagion like SARS.

 

Table 1: Measures to prevent outbreaks of new infectious diseases

Active surveillance programmes   Global measures to limit spread   Modernize farming practices   Improve basic health care   Judicious use of land and wilderness preservation   Undertake epidemiologic research   Develop newer antivirals/antimicrobials, newer agents to fight infections   Restrict introduction of exotic species of animals   Systems for information sharing and updating physicians   Emphasize use of standard precautions in hospitals   Early and effective quarantine procedures

Dr Gardam, Director of Infection Prevention and Control, Toronto, Canada credited Toronto's aggressive approach to dealing with SARS with its successful containment. Among measures taken, he said, were closure of hospitals to all but urgent and emergency care, screening of all staff and patients before entry into hospitals; requiring all staff to wear appropriate protective clothing, cancellation of all visitors unless a patient was expected to die within 24 hours, and construction of negative pressure isolation units for probable or suspected SARS patients.

It is in the nature of epidemics to be unpredictable. However, even if SARS may never be vanquished, its lessons are preparing scientists for whatever comes next.

Until recently, the presence or absence of reversibility was thought to be the major distinction between asthma and chronic obstructive pulmonary disease [COPD], with reversible airflow obstruction being the hallmark of asthma and mainly irreversible airflow obstruction the hallmark of COPD. Over the past few years, the thinking about COPD has changed appreciably. Consequently, there are now new definitions for both asthma and COPD that acknowledge the overlap and highlight the similarities and differences between them.

 

DEFINITIONS

Asthma: Global initiative for asthma (GINA) guidelines defined asthma as a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role. The chronic inflammation causes an associated increase in airway hyperresponsiveness that leads to recurrent episodes of wheezing, breathlessness, chest tightness and coughing, particularly at night or in the early morning. These episodes are usually associated with widespread but variable airflow obstruction that is often reversible, either spontaneously or with treatment.

COPD: Global initiative for chronic obstructive lung disease (GOLD) guidelines defined COPD as a disease state characterised by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal response of the lungs to noxious particles or gases.

 

SIMILARITIES AND DIFFERENCES

Asthma and COPD have important similarities and differences.

Similarities
1. Chronic inflammatory diseases
2. Involve small airways
3. Cause airflow limitation
4. Result from gene-environment interactions and
5. Both are usually characterised by mucus and bronchoconstriction

 

Differences

OVERLAP

It is well known that airway remodelling can occur in long-standing asthma and results in partially reversible airflow obstruction. Therefore, in many patients with long-standing asthma there is a component of chronic irreversible airflow obstruction with reduced lung function and incomplete response to a short-acting bronchodilator or to an oral or inhaled corticosteroid. This makes the diagnosis of asthma sometimes challenging in older adults and it requires adjustment of the goals of treatment with respect to the patient's age, as maintenance of normal lung function can no longer be a realistic goal.

 

CONCLUSION

It is important to distinguish between asthma and COPD so that the most appropriate therapies can be given. Failure to do so can result in the following scenarios:
 

Misdiagnosing COPD as Asthma

• Overtreatment with inhaled steroids and undertreatment with b2-agonists or inhaled anticholinergic drugs
   

• Failure to offer more appropriate therapy for COPD including consideration of oxygen therapy and pulmonary rehabilitation
   

Misdiagnosing Asthma as COPD

• Undertreatment with inhaled steroids (and possible failure to prevent airway remodelling) and overtreatment with b-agonists or inhaled anticholinergic drugs
   

• Predictable failure to improve the patient's lung function and achieve complete symptom control
   

• Failure to influence and probably improve the patient's symptom control.
  
   

VITILIGO

Vitiligo is a common skin disorder affecting approximately 0.5%-1% of the world population, irrespective of race or ethnic origin. It is mainly present on the skin where the loss of functioning melanocytes results in white patches. The hair and, rarely, the eyes may also lose colour. Any person of any age can develop vitiligo, but it is rarely reported at birth. Vitiligo patches can appear anywhere on the skin but common sites are usually around the orifices, the genitals, or areas exposed to the sun such as the face and hands.
 

Though neither lethal nor symptomatic, its effects can be cosmetically and psychologically devastating. Although the cause of vitiligo is uncertain, it seems to be dependent on the interaction of genetic, immunological and neurogenic factors. Vitiligo has sometimes been associated with autoimmune diseases such as pernicious anaemia, thyroid disorders, diabetes mellitus and Addison's disease. Hence a popular hypothesis is that vitiligo is an autoimmune disease.

 

Treatment

In the absence of a clear understanding of the etiopathogenesis, there is no ideal treatment. Disguising vitiligo with make-up, self-tanning compounds or dyes, is a safe and easy method of camouflage. Medical treatment of vitiligo includes corticosteroids, psoralens, phenylalanine, PABA, levamisole and dapsone etc. Surgery for vitiligenous lesions is indicated for stable vitiligo (when it is resistant to the conventional medical line of treatment) and secondary leukoderma (post-burns and chemicals etc). Vitiligo surgery has progressed from tattooing to various procedures described below.
 

Tattooing: Tattooing is the uniform implantation of minute metabolically inert pigment granules into the dermis. It is found more useful if lesions are few and small (less than 3-4 inches in diameter).
 

Skin Grafting: This treatment is available only in some parts of the country and is useful only for a small group of vitiligo patients. It does not generally result in total return of pigment in the treated areas.

The different types of grafting are miniature punch grafting, suction blister grafting, thin Thiersch's split thickness skin grafting and skin cultures.

Miniature Punch Grafting is carried out under local anesthesia. Thin, miniature punch skin autografts of sizes 1.5 to 2.0 mm from normal pigmented donor sites are taken and individually grafted in the appropriately punched out chambers at the recipient site. Common complications are graft rejection, scarring and reactivation of vitiligo.

Suction Blister Grafting consists of obtaining split thickness skin grafts containing only the epidermis. This is followed by securing this sheet to the dermabraded recipient site. It is a safe and simple procedure. Re-pigmentation after grafting is cosmetically well accepted. There is no scarring at the donor site, which can be reutilized for future grafting.

Thin Thiersch's Split Thickness Skin Grafting consists of obtaining a very thin, split thickness skin grafts consisting of epidermis and part of upper papillary dermis. This is grafted on the dermabraded patch of stable vitiligo and further secured with pressure and local immobilization. The advantage is that larger areas can be covered in a single sitting. It is quick and less time consuming than other procedures of grafting for vitiligo. The disadvantage is that thin grafts are more vulnerable to trauma.
 

Melanocyte transplantation: Cells are cultured from the patient's unaffected skin and injected into blisters on the depigmented areas or directly into dermabraded skin. This technique is expensive and there is a concern that the culture medium is a potent tumour promoter.

 

NAIL SURGERY

Like all other cutaneous structures, the nail also gets affected by various medical and surgical problems. The broad objectives of nail surgery are to alleviate pain, treat infections, correct deformities and remove local tumours. Some common and simple surgeries are nail avulsion, nail unit biopsy, treatment of peri-ungual or sub-ungual warts, drainage of sub-ungual haematomas etc.

 

NAIL AVULSION

This is the most commonly performed nail operation, in which the nail plate is separated from the matrix and nail bed. This is achieved either surgically or chemically. It is done for diagnostic purposes in nail bed/nail matrix biopsy or therapeutic purposes for onychomycosis, ingrown nails, nail bed defects, sub-ungual or peri-ungual warts. The complications are pain, bleeding, infection, necrosis, trauma to matrix and nail bed giving rise to nail deformities and dystrophies.

Nail unit biopsy consists of obtaining specimens of either the nail plate, nail bed, nail matrix, proximal or lateral nail fold, hyponychium, alone or in any combination for diagnostic purposes. It is indicated to differentiate between mycotic and psoriatic nails and between sub-ungual haematoma and melanoma. It also helps to diagnose cutaneous disease when it is limited to nails and causes nail dystrophies e.g. lichen planus. It is contraindicated in peripheral vascular diseases and uncontrolled diabetes mellitus.

SUB-UNGUAL/PERI-UNGUAL WARTS
The surgical approaches to this condition include excision, electrodesiccation and curettage, and cryotherapy with liquid nitrogen spray.
 

LIPOSUCTION

Liposuction surgery is a safe technique when performed by a fully trained, experienced physician. Patients under 40 years of age with good skin elasticity are the best candidates, but patients ranging in age from 16 to over 70 can be successfully treated. Fat is removed through half-inch incisions during liposuction.
 

Indications
With a variety of new instruments and techniques, virtually any area can be treated - the small pot belly, the spare tire, hips and lateral thighs. Other appropriate areas include the male breasts (gynecomastia), the chin, the neck, anterior axillary fat folds, and the proximal arms. Lipomas are easily extracted. Liposuction is used by some surgeons during face-lift surgery.
 

Technique
Aradial tunneling procedure is used. A small cannula with a rounded aperture is inserted through an half inch incision. The cannula is pushed into the fat to break it loose from the fibrous stroma. Multiple to-and-fro movements mechanically disrupt the fat and create tunnels. The loosened fat is removed with powerful suction.
 

 

CONCLUSION

Dermatosurgical techniques have gained importance in recent years and are poised to increase in future. Dermatosurgeries offer a better cosmesis, and can ameliorate distressing symptoms of conditions such as vitiligo, acne scars, actinic keratoses and nail disorders.

 

INTRODUCTION

Urinary tract infections (UTIs) are common in infants and children. However, they are often undiagnosed, since the signs are distinct from those in adults. The diagnosis of UTI in this age group is also complicated by the difficulty of collecting uncontaminated urine specimens for culture.

Infections of the urinary tract are more common in neonatal boys as a result of anatomical abnormalities while after age one both bacteriuria and UTI are more frequent in girls. Accurate diagnosis and treatment is extremely important in preventing complications such as impaired renal function, hypertension, bacteremia and renal scarring.

 

ETIOLOGY AND PATHOGENESIS

Among infectious causes, almost 80% of UTIs are caused by Escherichia coli. Other pathogens include Staphylococcus and Streptococcus species, a wide variety of enterobacteria like Klebsiella, Proteus & Pseudomonas and occasionally Candida albicans. Bacterial virulence factors play a major pathophysiologic role in UTI. Almost all UTIs are ascending in origin and are caused by the bacteria in the GI tract that have colonized the periurethral area. Uncircumcised infants and toddlers are at greater risk of UTI.

In addition to bacterial virulence factors, other mechanical, immunologic and hydrodynamic host factors play important roles in UTI. Dysfunctional voiding is a major cause of childhood UTI. Infrequent voiding can lead to high residual urine, a source of infection. Vesicoureteral reflux (VUR) is responsible for recurrent pyelonephritis. Subsequent renal scarring depends on the severity of VUR. Other congenital urologic anomalies may also be responsible.

 

CLINICAL PRESENTATION

Paediatric UTI is a spectrum of disease that includes urethritis, asymptomatic bacteriuria, cystitis and pyelonephritis. Signs and symptoms of UTI are variable and depend on the age of the child and comorbid conditions. Neonates may be lethargic, hypotensive, irritable and anorectic. The most common presentation in infants is of fever, diarrhea, vomiting, irritability, and foul smelling diapers. Toddlers may have pyrexia of unknown origin, accompanied by signs of feeding problems and debility. In older children, symptoms of cystitis are most easily noted such as dysuria, abdominal pain, hematuria, cloudy urine, and enuresis or hesitancy. Lower tract symptoms do not always represent an infection - urethritis, vulvitis or dysfunctional voiding may also be responsible. Acute pyelonephritis is the most severe form of UTI and the most common form in infants. Cystitis is rarely associated with long-term morbidity.

 

DIAGNOSIS

The physical examination includes the examination of the abdomen for bladder tenderness, constipation, and renal or pelvic masses, back for costovertebral tenderness, perineum and genitalia for evidence of foreign bodies or irritation. Laboratory diagnostic tests include:

• Urinalysis with microscopic evaluation for presence of bacteria and pyuria
   
• Positive urine culture
   
• CBC with differential count showing leukocytosis
   
• Antibody coated bacteria may be seen with pyelonephritis
   

Recent guidelines issued by the American Academy of Pediatrics for the evaluation of fever of unknown origin higher than 102.2o F suggests urinalysis in all cases and a urine culture in all boys younger than 6 months of age and all girls younger than 2 years of age. In neonates less than 3 months old a catheterized urine analysis or suprapubic bladder aspiration is a standard procedure while older children can provide a clean midstream urine specimen.

Diagnostic imaging techniques such as ultrasonography and intravenous pyelography are used only for serious and recurrent cases of pyelonephritis, or if structural abnormalities are suspected, or if infections do not respond to treatment.

 

MANAGEMENT

Treatment goals include symptomatic relief of the acute infection and prevention of UTI & new or progressive renal scarring. Subsequent management depends on the severity of the condition and age group of the patient. Initial therapy should be based on the culture sensitivities of uncontaminated urine samples. Parenteral broad-spectrum antimicro-bials such as ampicillin, plus an aminoglycoside (e.g. gentamicin) or a third generation cephalosporin such as ceftriaxone or ceftazidime are often used. Children who can take antibiotics orally are frequently treated with cotrimoxazole, cefixime or nalidixic acid. Generally, the duration of treatment is about 5 days for children with acute uncomplicated UTI and 10-14 days for acute pyelonephritis. Studies show that larger cortical renal defects correlate with longer delay of treatment and longer length and severity of infection.

Figure 1 depicts the treatment algorithm outlined by the American Academy of Paediatrics, 1999.

 

 

CONCLUSION

Urinary tract infections in infants and children often go undiagnosed since the signs and symptoms are usually non specific and overlap with other common childhood illnesses. Prompt management of UTIs in infants and children is required to reduce morbidity & improve outcomes.

 

INTRODUCTION

The term "non-alcoholic fatty liver disease" (NAFLD) is used to describe a wide spectrum of fatty liver changes ranging from steatosis on one side and non-alcoholic steatohepatitis (NASH) on the other. Liver steatosis is a benign, non-progressive condition, in contrast to NASH, which can progress to liver fibrosis and cirrhosis. NAFLD can affect any age group, and occurs equally in men as well as in women.

 

HISTORICAL PERSPECTIVES AND RISK FACTORS

In the 1970s, "fatty liver hepatitis" was thought to affect mostly morbidly obese patients who had a jejunoileal bypass. One-third of these patients developed fibrosis and several needed liver transplantation after correction of the digestive anatomy. Later, NASH was described in patients taking drugs such as perhexiline-maleate, steroids, amiodarone, isoniazid and tamoxifen.

Most cases occur in persons with hyperlipidaemia and hyperglycaemia. Insulin resistance (IR) is probably a central pathogenic factor. Other risk factors include severe rapid weight loss, lipodystrophic syndromes and use of total parenteral nutrition.

 

PATHOGENESIS AND NATURAL HISTORY

It is postulated that IR leads to an increased hepatic production and circulation of free fatty acids (FFAs). The increased uptake of FFAs by the liver exceeds its capacity to metabolize and remove them. Consequently, hepatic steatosis develops, generally as a "benign" prerequisite of NASH. Various mechanisms (oxidative stress, iron overload, endotoxins etc.) have been proposed to explain the progression of fatty liver to NASH.

There are several histologic stages in the progression of NAFLD to cirrhosis. The earliest stage is a simple fatty liver alone. Over time, steatohepatitis may become associated with increasing fibrosis. Eventually, cirrhosis may develop. Cirrhosis secondary to NASH may also be complicated by the development of hepatocellular carcinoma.

About 12 percent of patients with NASH may progress to cirrhosis within seven years, which is a progression compatible with that of hepatitis C.

 

DIAGNOSTIC APPROACH

Most patients are asymptomatic and abnormal liver tests are often discovered fortuitously. When symptoms occur, they are relatively non-specific (fatigue, right upper quadrant discomfort, edema and pruritus). On examination, the liver may be normal in about 19-30% of cases. Hepatomegaly is commonly encountered. Stigmata of liver disease, edema, jaundice, splenomegaly and ascites may be present. The ALT:AST ratio is usually less than one. Frequently, IR-related diseases (obesity, type 2 diabetes mellitus and hyperlipidemia) coexist.

NASH may be considered a diagnosis of exclusion. Chronic alcohol consumption must be excluded. Chronic ethanol intake of 20 g/day is considered the hepatotoxic threshold for women and 40 g/day for men. Other liver diseases, such as hepatitis B and C, haemochromatosis and Wilson's disease must be excluded.

Imaging studies may help with diagnosing fatty infiltration of the liver, but they do not help in distinguishing between fatty liver, steatohepatitis, and steatohepatitis with fibrosis. A biopsy is usually required when the diagnosis is in doubt or if the disease must be staged.

Histologic findings in NAFLD are very similar to those found in alcoholic liver disease. Liver histology has prognostic implications since liver steatosis without inflammation is a benign, non-progressive condition and the presence of ballooning degeneration, Mallory hyaline or fibrosis is associated with a liver-related mortality that is ten times higher than in patients with a pure steatosis. Lastly, the histological assessment of hepatic iron stores is of importance.

 

TREATMENT OPTIONS

Gradual weight loss should be advocated in overweight individuals. Weight reduction by 10 percent or more has been associated with normalization of elevated serum ALT levels and with a decrease in hepatomegaly. However, a rapid weight loss may cause progression of NAFLD. A heart-healthy diet is also recommended. Effects of pharmacologic agents used to induce weight loss on liver histology are not well-known. The decision to use these agents or to proceed with surgical approaches should be dictated by the degree of obesity, the presence of other end-organ damage and the potential for severe hepatic decompensation due to surgery or rapid weight loss.

Patients with diabetes should have their disease controlled appropriately. Since NAFLD is associated with insulin resistance, the use of insulin-sensitizing agents may be logical. The thiazolidinediones (e.g. pioglitazone) improve peripheral insulin sensitivity. A small study of patients treated with troglitazone showed improvement in mean ALT levels and in hepatocellular inflammation. Metformin has been shown to improve serum aminotransferase levels. However, there are no definitive data on the use of these drugs in the treatment of NAFLD. The risks of hepatotoxicity associated with these agents have not yet been well characterized in this population.

Lipid-lowering agents may be beneficial in NASH. In a prospective, randomized and placebo-controlled study with 46 patients using oral gemfibrozil for 4 weeks, a significant improvement in liver tests and triglyceride levels was observed independent of weight loss. Rare cases of fibrate-induced hepatitis have been reported.

Several hepatoprotective drugs, such as vitamin E, ursodeoxycholic acid, lecithin, beta-carotene, taurine, selenium and betaine have been used. Vitamin E has been shown to significantly decrease liver enzymes. Betaines are trimethyl amino acids which function as methyl donors and reduce lipid accumulation in the liver. In a trial with seven NASH patients, a significant improvement in serum transaminase levels was noted, and in six patients in whom a second liver biopsy could be obtained, a marked improvement in the degree of steatosis, necroinflammation and fibrosis occurred. Thus, betaine is a promising compound which may play a role in the future treatment of NASH.

Ursodeoxycholic acid (UDCA) at a dose of 13-15 mg/kg/day for one year has been found to improve transaminases and steatosis. It is believed to have cytoprotective, chemoprotective, antioxidant and immunomodulatory properties.

Early treatment of recurrent NASH with antioxidants or UDCA has been advocated.
 

CONCLUSION

NAFLD is a common cause of chronic liver disease and is most often associated with obesity. Its incidence is reportedly on the rise worldwide. An improved understanding of its pathogenesis and treatment approaches is the key to managing this enigmatic disorder of the liver.