HEPATITIS - Clinical features, Differential diagnosis, Prophylaxis

The pathological features of hepatitis are liver cell necrosis and inflammatory cell infiltration. Hepatitis is divided into acute and chronic types on the basis of clinical and pathological criteria.

Acute hepatitis is most commonly caused by one of the hepatitis viruses (Fig. 4.5). Acute hepatitis is usually self-limiting with a return to normal structure and function. Occasionally there is progression to massive liver cell necrosis (p. 158). Clinically the patient may be jaundiced, with an enlarged and tender liver, and there is laboratory evidence of hepatocellular damage

Some causes of acute parenchymal damage

Fig. 4.5 Some causes of acute parenchymal damage.

with raised serum aminotransferase levels. Disease severity is assessed by the prothrombin time (p. 140) and serum bilirubin. Alcoholic hepatitis is distinguished from other causes of acute hepatitis by characteristic laboratory abnormalities (p. 175).

Chronic hepatitis is defined as sustained inflammatory disease of the liver lasting for more than 6 months (Table 4.2). Chronic viral hepatitis is the principal cause of chronic liver disease, cirrhosis and hepatocellular carci-noma (HCC) world-wide.

Viral hepatitisnd

The differing features of the common forms of viral hepatitis are summarized in Table 4.3. All cases must be notified(nd) to the appropriate public health authority. This allows contacts to be traced and provides data on disease incidence.

Hepatitis And Epidemiology

Hepatitis A (HAV) is the most common type of acute viral hepatitis. It occurs world-wide and affects particularly children and young adults. Spread is

Table 4.2 Causes of chronic hepatitis

Viral
Hepatitis B ± D
Hepatitis C
Autoimmune
Drugs

Methyldopa
Nitrofurantoin
Isoniazid
Ketoconazole
Hereditary
Wilson’s disease
Others
Inflammatory bowel disease
Alcohol

faecal-oral and arises from the ingestion of contaminated food (e.g. shellfish, clams) or water. The virus is excreted in the faeces of infected individuals for about 2 weeks before the onset of the illness and for up to 7 days after. It is most infectious just before the onset of the jaundice.

Clinical features

After an average incubation period of 28 days, the viraemia causes non-specific prodromal symptoms of nausea, anorexia and distaste for cigarettes. After 1 or 2 weeks some patients become jaundiced with dark urine and pale stools and the prodromal symptoms improve. There is moderate hepato-megaly and the spleen is palpable in 10% of cases. Occasionally lymph-adenopathy and a skin rash are present. The illness is self-limiting and usually over in 3-6 weeks. Rarely there is fulminant hepatitis (p. 158), coma and death.

Investigations

■ Liver biochemistry shows raised ALT and raised bilirubin when jaundice develops.

■ The blood count may show a leucopenia with relative lymphocytosis and a high erythrocyte sedimentation rate (ESR). The prothrombin time is prolonged in severe cases.

■ Acute HAV infection is diagnosed by IgM anti-HAV in the serum; the pres-ence of IgG anti-HAV indicates past infection.

Differential diagnosis

This includes other causes of jaundice and in particular other types of viral and drug-induced hepatitis.

Management

There is no specific treatment. Hospital admission is not usually necessary and avoidance of alcohol advised only when the patient is ill.

Prophylaxis

■ Active immunization with an inactivated strain of the virus is given to travellers to areas of high prevalence (Africa, Asia, South America, eastern Europe, the Middle East), patients with chronic liver disease (in whom the disease is more severe), patients with haemophilia treated with plasma-derived clotting factors, and persons who have occupational risk for exposure (staff and residents of homes who have severe learning difficulties, workers at risk of exposure to untreated sewage).

Control of hepatitis also depends on good hygiene. Travellers to high-risk areas should drink only boiled or bottled water and avoid risky foods.

■ Passive immunization with immunoglobulin is given to close contacts of confirmed cases of hepatitis A to prevent infection.

Hepatitis Bnd Epidemiology

Hepatitis B virus (HBV) is present world-wide and is particularly prevalent in parts of Africa, the Middle and Far East. Vertical transmission from mother to child during parturition is the most common means of transmission world-wide. HBV is also spread through blood and blood products, sexual inter-course, particularly in men who have sex with men, and horizontal transmission occurs particularly in children through minor abrasions or close contact with other children.

Viral structure

The whole virus is the Dane particle, which consists of an inner core or nucleocapsid surrounded by an outer envelope of surface protein (hepatitis B surface antigen, HBsAg). The inner core contains incomplete double-stranded circular DNA and DNA polymerase/reverse transcriptase and is surrounded by the core proteins (HBcAg and HBeAg). These two proteins have most of their sequence in common but HBeAg is secreted since it is processed differently from the HBcAg and not assembled into the progeny virus. HBsAg is also secreted into the serum and is a marker of HBV infection.

Mutations can occur in all regions of the HBV genome. They can emerge in patients with chronic HBV infection (escape mutants) or can be acquired by infection. HBV mutations can potentially modulate the severity of liver disease by altering the level of HBV replication or the expression of immunogenic epitopes (the site against which T cells respond). Mutants in HBsAg result in changes in the antibody binding domain and the usual tests for HBsAg may be affected. Other mutants stop production of HBeAg (a serum marker of active viral replication) but the virus can continue to replicate with the presence of HBV DNA in the serum and elevated liver enzymes. HBV DNA must therefore always be measured in an HBsAg-positive patient to determine the level of viral replication.

Acute HBV infection

HBV penetrates the hepatocyte and in immunocompetent adults there is a strong cellular immune response to the foreign HBV proteins expressed by hepatocytes. This response leads to clearance of the infection in 99% of infected adults and is marked by the disappearance of HBsAg from the serum, the development of antibodies to surface antigen (anti-HBs) and immunity to subsequent infection (Fig. 4.6A and Table 4.4). Acute infection may be asymptomatic or produce symptoms and signs similar to those seen in hepa-titis A. Occasionally it is associated with a rash or polyarthritis affecting the small joints. One per cent of patients develop fulminant liver failure (p. 158). Investigation is generally the same as for hepatitis A. There is no specific therapy for acute HBV infection and management is supportive.

Fig. 4.6 Time course of the events and serological changes seen following infection with hepatitis B virus.

Development of chronic hepatitis followed by seroconversion

(A) Acute infection.

Antigens

HBsAg appears in the blood from about 6 weeks to 3 months after an acute infection and then disappears.

HBeAg rises early and usually declines rapidly.

Antibodies

Anti-HBs appears late and indicates immunity.

Anti-HBc is the first antibody to appear and high titres of IgM anti-HBc suggest an acute and continuing viral replication. It persists for many months. IgM anti-HBc may be the only serological indicator of recent HBV infection in a period when HBsAg has disappeared and anti-HBs is not detectable in the serum. Anti-HBe appears after the anti-HBc and its appearance relates to a decreased infectivity, i.e. a low risk.

(B) Development of chronic hepatitis followed by seroconversion.

HBsAg persists and indicates a chronic infection (or carrier state).

HBeAg persists and correlates with increased severity and infectivity and the development of chronic liver disease. When anti-HBe develops (seroconversion) the Ag disappears and there is a rise in ALT.

HBV DNA suggests continual viral replication. For mutants, see text.

Chronic HBV infection

The persistence of HBsAg in the serum for more than 6 months after acute infection defines chronic infection. Progression from acute to chronic infec-tion depends on several factors including the virulence of the virus, and the immunocompetence and age of the patient. When HBV infection is acquired

Table 4.4 Serologic markers of hepatitis B infection

HBsAg

anti-HBc

anti-HBs

IgM anti-HBc

Susceptible to infection

Negative

Negative

Negative

Negative

Immune due to natural infection

Negative

Positive

Positive

Negative

Immune due to hepatitis B vaccination

Negative

Negative

Positive

Negative

Acutely infected

Positive

Positive

Negative

Positive

Chronically infected

Positive

Positive

Negative

Negative

at birth (vertical transmission) or early childhood there is a high level of immunological tolerance and cellular immune responses to hepatocyte-membrane HBV proteins do not occur and chronic infection is the norm. This immune tolerant phase is characterized by minimal hepatic inflammatory activity and normal or near-normal serum ALT despite positive HBeAg and high levels of HBV replication (reflected by high levels of serum HBV DNA). This phase may persist for 2-3 decades before an immune clearance phase that lasts for a variable period of time and is characterized by high HBV DNA levels as before but now is an active hepatitis (that might lead to fibrosis and cirrhosis) with elevated serum ALT. This phase ends with clearance of HBeAg and development of anti-HBe (HBeAg seroconversion) with a marked decrease in serum HBV DNA and normalization of serum ALT (the inactive HBsAg cariier State). Some patients during the immune clearance phase will develop viral mutations (see above) that do not produce HBeAg but continue to replicate at high levels and have progressive liver damage with fluctuating serum levels of aminotransferases (reactivation phase). Acquisition of infec-tion later in life is associated with a very short immune tolerant phase or not at all. Most patients clear the virus (see acute infection) and only a small percentage will progress to chronic infection (Fig. 4.6B).

Table 4.4 summarizes the serological markers of HBV infection at various stages.

Treatment of chronic infection: whom to treat

Patients who present with detectable HBsAg and clinical and/or epidemiologi-cal factors suggestive of chronic infection can be considered for treatment without waiting for the 6-month period that defines chronicity after acute infection. In HBsAg-positive individuals there is a strong relationship between ongoing HBV replication and the risk of progression of chronic liver disease to cirrhosis, HCC or both. Serum HBV DNA is a direct measure of the level of viral replication and should be obtained for all patients with chronic infection. Treatment is given to patients who are most likely to develop progressive liver disease (i.e. high levels of HBV replication) and to those who are most likely to respond to treatment. Thus patients with chronic HBV infection (HBsAg-posi-tive), high serum levels of HBV DNA (>20 000 IU per ml) and elevated serum ALT should be given antiviral treatment (see below). Antiviral therapy is not used for inactive HBV carriers (normal ALT and HBV DNA <2000 lU/mL) who are at low risk for Progressive liver disease. However, they should have annual assessment of hepatitis B serology and liver biochemistry, since some will develop progressive disease and require treatment. Patients who lie outside these categories may require treatment if significant inflammation or necrosis is found on a liver biopsy or serum ALT increases on follow-up.

Antiviral agents

The aim of treatment is the seroconversion of HBeAg (when present) and the reduction of HBV DNA to undetectable levels. In addition, normalization of ALT and histological improvement in inflammation and fibrosis reflects a good response. Pegylated interferon alfa (IFN), and lamivudine, adefovir, entecavir and tenofovir, are the most commonly used drugs. IFN is administered by subcutaneous injection and inhibits viral replication and enhances the immune response to the virus. The nucleoside/nucleotide analogues are given orally and work through incorporation into viral DNA causing chain termination and inhibiting viral replication. For HBeAg-positive disease, IFN is given for 1 year and the oral antiviral agents are given long term. HBeAg-negative disease (indicating a mutant) requires long-term treatment with oral agents.

Hepatitis B and HIV co-infection

Routes of infection are similar for HBV and the human immunodeficiency virus and rates of co-infection are 10-20%. All patients with chronic HBV infection should have a test for HIV antibody and vice versa. Testing should be repeated if there is ongoing risk of HIV, particularly before antiviral treatment for HBV is contemplated. HIV infection makes it more likely that an individual exposed to HBV will develop chronic infection and this will progress to more severe liver disease. Treatment of co-infection is complex and is best managed in a specialist unit.

Prophylaxis

The avoidance of high-risk factors (needle sharing, prostitutes and multiple male homosexual partners) and counselling patients who are potentially infec-tive are key aspects of prevention. Active immunization with a recombinant yeast vaccine is universal in most developed countries. In the UK it is only recommended for those at increased risk, e.g. healthcare workers, homo-sexual and bisexual men and prostitutes, intravenous drug users, people with haemophilia and haemodialysis patients. The immunity that develops after active immunization lasts for over 10 years. Combined prophylaxis (i.e. active immunization and passive immunization with specific antihepatitis B immunoglobulin) is given to non-immune individuals after high-risk exposure, e.g. a needle-stick injury from a carrier, newborn babies of HBsAg-positive mothers and HBV-negative sexual partners of HBsAg-positive patients.

Hepatitis D (delta or 5 agent)nd

Hepatitis D virus (HDV) is an incomplete RNA virus enclosed in a shell of HBsAg. It is unable to replicate on its own, but is activated by the presence of HBV. It can affect all risk groups for HBV infection, but is seen particularly in intravenous drug users. Infection can occur as a co-infection with HBV or as a superinfection in an already HBsAg-positive patient, and thus presents as an illness indistinguishable from acute HBV infection or as a flare-up (with a rise in serum transferases) of previously quiescent chronic HBV infection. Diagnosis is by finding HDV RNA or IgM anti-HDV in the serum.

Hepatitis Cnd Epidemiology

Hepatitis C virus (HCV) is present world-wide, but is more common in south-ern Europe, Africa and Egypt. In the UK, the main mode of acquisition is via recreational intravenous drug use and in developing countries via transfusion of blood products and exposure to poorly sterilized instruments (Table 4.3). There are six viral genotypes, of which type 1 is the most common in Europe and the USA.

Clinical features

Acute infection is usually mild, with jaundice developing in less than 10% of cases. Most patients infected with HCV go on to develop chronic liver disease and will not be diagnosed until they present, years later, with elevated serum aminotransferase levels found on routine biochemistry (e.g. at health checks) or with symptoms and signs of chronic liver disease and cirrhosis (Fig. 4.1). Patients with cirrhosis secondary to chronic HCV are at increased risk for the development of HCC. Extrahepatic manifestations of chronic infection include arthritis, glomerulonephritis associated with cryoglobulinaemia, and porphy-ria cutanea tarda.

Diagnosis

This is made by finding HCV antibody in the serum. Antibodies may take 8 weeks to appear after acute infection, and thus an early negative result does not exclude acute HCV infection. Patients with antibodies to HCV should undergo further tests to look for the presence of HCV RNA in the serum. A positive RNA result indicates ongoing infection and HCV genotype should be characterized in those considered for treatment. A liver biopsy is performed if treatment is dependent on the degree of hepatitis but is not always necessary. Non-invasive testing (p. 143) is also used to assess the stage of fibrosis/cirrhosis without the need for biopsy.

Management

All patients with chronic infection are candidates for antiviral therapy but the risks and benefits of treatment must be carefully weighed on an individual basis. The aim of treatment is sustained viral clearance, i.e. the absence of HCV RNA in the serum 6 months after treatment. For genotypes 2 and 3 this is achieved in 80% of patients and most patients, even those with mild disease, are treated. In patients with less responsive genotypes (1 and 4, sustained viral clearance 40-50%) treatment is given to those with moderate or severe activity/fibrosis on liver biopsy. Treatment is with subcutaneous pegylated IFN-alfa once weekly and oral ribavirin daily for 24 weeks (geno-types 3 and 4) or 48 weeks (genotypes 1 and 4).

Hepatitis End

This is due to an RNA virus which causes enteral (epidemic or water-borne) hepatitis, similar to hepatitis A, particularly in developing countries (Table 4.3). Diagnosis is by detection of IgG and IgM anti-HEV in the serum or HEV RNA is serum or stools.

Fulminant hepatic failure

This is hepatic failure with encephalopathy (a neuropsychiatric condition developing as a consequence of liver disease) developing in less than 2 weeks in a patient with a previously normal liver, or in patients with an acute exacerbation of underlying liver disease. Cases that evolve at a slower pace (2-12 weeks) are called subacute or subfulminant hepatic failure. It is an infrequent complication of acute liver damage from any cause (Fig. 4.5) and occurs as a result of massive liver cell necrosis. In the UK, viral hepatitis and paracetamol overdose are the most common causes. Presentation is with hepatic encephalopathy (Table 4.5) of varying severity accompanied by severe jaundice and a marked coagulopathy. The complications include cer-ebral oedema, hypoglycaemia, severe bacterial and fungal infections, hypo-tension and renal failure (hepatorenal syndrome). Most patients should be managed with supportive treatment in a specialist liver unit (Table 4.6). Emergency liver transplantation has become a useful treatment, depending on the cause, for the very severe cases (grade IV encephalopathy), of which 80% might otherwise die.

Autoimmune hepatitis

Autoimmune hepatitis is usually a progressive liver disease which is often associated with other autoimmune diseases, e.g. pernicious anaemia,

Table 4.5 Clinical grading of hepatic encephalopathy

Grade

Neurological findings

0

No alteration in consciousness, intellectual function, personality or behaviour

1 Daytime somnolence, short attention span, mild asterixis*

2

Lethargic, drowsiness, disorientated usually in time, inappropriate behaviour, obvious asterixis*

3

Asleep but rousable, confusion, incomprehensible speech

4

Coma

*Asterixis (liver flap), involuntary flapping movements of the hand when the arm is
extended and wrist held in a backward position.

Table 4.6 Transfer criteria for patients with acute liver injury to specialized units
International normalized ratio >3.0
Presence of hepatic encephalopathy
Hypotension after resuscitation with fluid
Metabolic acidosis
Prothrombin time (seconds) >interval (hours) from overdose (paracetamol cases)

thyroiditis. It is most common in young and middle-aged women but can occur in any age in either sex.

Aetiology

The aetiology is unknown but the disease is characterized by immunological abnormalities including hypergammaglobulinaemia with high IgG levels, the presence of circulating autoantibodies and interface hepatitis with portal plasma cell infiltration on liver histology.

Clinical features

The onset is often insidious, with anorexia, malaise, nausea and fatigue. Twenty-five per cent present as an acute hepatitis, with rapidly Progressive liver disease. The signs of chronic liver disease are often present, with palmar erythema, spider naevi, hepatosplenomegaly and jaundice. Features of other autoimmune diseases may be present.

Investigations

Circulating autoantibodies (antinuclear, smooth muscle, soluble liver antigen, liver/kidney microsomal antibodies) are present in most patients. There is hypergammaglobulinaemia (particularly IgG), and serum bilirubin and aminotransferases are elevated. Liver histology will show the non-specific changes of chronic hepatitis, with interface hepatitis and often cirrhosis.

Prednisolone 30 mg daily is given for 2-3 weeks. A subsequent reduction in the dose depends on clinical response, but maintenance doses of 10-15 mg are usually required. Azathioprine should be added as a steroid-sparing agent and is usually continued lifelong. Mycophenolate, ciclosporin and tacrolimus are used in treatment failures.

Prognosis

Steroid and azathioprine therapy induce remission in over 80% of cases. Liver transplantation may be necessary if treatment fails although the disease can recur.

Ebook Essentials of Kumar and Clark's Clinical Medicine, 5e

1. Ethics and communication

Ethics and communication

2. Infectious diseases

Infectious diseases

3. Gastroenterology and nutrition

Gastroenterology and nutrition

4. Liver, biliary tract and pancreatic disease

Liver, biliary tract and pancreatic disease
LIVER BIOCHEMISTRY AND LIVER FUNCTION TESTS
SYMPTOMS AND SIGNS OF LIVER DISEASE
JAUNDICE
HEPATITIS
NON - ALCOHOLIC FATTY LIVER DISEASE (NAFLD)
CIRRHOSIS
COMPLICATIONS AND EFFECTS OF CIRRHOSIS
LIVER TRANSPLANTATION
TYPES OF CHRONIC LIVER DISEASE AND CIRRHOSIS
PRIMARY SCLEROSING CHOLANGITIS
BUDD - CHIARI SYNDROME
LIVER ABSCESS
LIVER DISEASE IN PREGNANCY
LIVER TUMOURS
GALLSTONES
THE PANCREAS
CARCINOMA OF THE PANCREAS
NEUROENDOCRINE TUMOURS OF THE PANCREAS

5. Haematological disease

Haematological disease
ANAEMIA
Assessment and treatment of suspected neutropenic sepsis
HAEMOLYTIC ANAEMIA
INHERITED HAEMOLYTIC ANAEMIAS
ACQUIRED HAEMOLYTIC ANAEMIA
MYELOPROLIFERATIVE DISORDERS
THE SPLEEN
BLOOD TRANSFUSION
THE WHITE CELL
HAEMOSTASIS AND THROMBOSIS
THROMBOSIS
THERAPEUTICS

6. Malignant disease

Malignant disease
MYELOABLATIVE THERAPY AND HAEMOPOIETIC STEM CELL TRANSPLANTATION
THE LYMPHOMAS
THE PARAPROTEINAEMIAS
PALLIATIVE MEDICINE AND SYMPTOM CONTROL

7. Rheumatology

Rheumatology
COMMON INVESTIGATIONS IN MUSCULOSKELETAL DISEASE
COMMON REGIONAL MUSCULOSKELETAL PROBLEMS
BACK PAIN
OSTEOARTHRITIS
INFLAMMATORY ARTHRITIS
THE SERONEGATIVE SPONDYLOARTHROPATHIES
Clinical features, Investigations
INFECTION OF JOINTS AND BONES
AUTOIMMUNE RHEUMATIC DISEASES
SYSTEMIC INFLAMMATORY VASCULITIS
DISEASES OF BONE
THERAPEUTICS

8. Water, electrolytes and acid–base balance

WATER AND ELECTROLYTE REQUIREMENTS
BODY FLUID COMPARTMENTS
REGULATION OF BODY FLUID HOMEOSTASIS
PLASMA OSMOLALITY AND DISORDERS OF SODIUM REGULATION
DISORDERS OF POTASSIUM REGULATION
DISORDERS OF MAGNESIUM REGULATION
DISORDERS OF ACID - BASE BALANCE
THERAPEUTICS

9. Renal disease

Renal disease
INVESTIGATION OF RENAL DISEASE
GLOMERULAR DISEASES
NEPHROTIC SYNDROME
URINARY TRACT INFECTION
TUBULOINTERSTITIAL NEPHRITIS
HYPERTENSION AND THE KIDNEY
RENAL CALCULI AND NEPHROCALCINOSIS
URINARY TRACT OBSTRUCTION
ACUTE RENAL FAILURE/ACUTE KIDNEY INJURY
CHRONIC KIDNEY DISEASE
RENAL REPLACEMENT THERAPY
CYSTIC RENAL DISEASE
TUMOURS OF THE KIDNEY AND GENITOURINARY TRACT
DISEASES OF THE PROSTATE GLAND
TESTICULAR TUMOUR
URINARY INCONTINENCE

10. Cardiovascular disease

COMMON PRESENTING SYMPTOMS OF HEART DISEASE
INVESTIGATIONS IN CARDIAC DISEASE
CARDIAC ARRHYTHMIAS
HEART FAILURE
ISCHAEMIC HEART DISEASE
RHEUMATIC FEVER
VALVULAR HEART DISEASE
PULMONARY HEART DISEASE
MYOCARDIAL DISEASE
CARDIOMYOPATHY
PERICARDIAL DISEASE
SYSTEMIC HYPERTENSION
ARTERIAL AND VENOUS DISEASE
ELECTRICAL CARDIOVERSION
DRUGS FOR ARRHYTHMIAS
DRUGS FOR HEART FAILURE
DRUGS AFFECTING THE RENIN - ANGIOTENSIN SYSTEM
NITRATES, CALCIUM - CHANNEL BLOCKERS AND POTASSIUM - CHANNEL ACTIVATORS

11. Respiratory disease


Respiratory disease
TUBERCULOSISnd
DIFFUSE DISEASES OF THE LUNG PARENCHYMA
OCCUPATIONAL LUNG DISEASE
CARCINOMA OF THE LUNG
DISEASES OF THE CHEST WALL AND PLEURA
DISORDERS OF THE DIAPHRAGM

12. Intensive care medicine

Intensive care medicine

13. Drug therapy, poisoning, and alcohol misuse

Drug therapy, poisoning, and alcohol misuse

14. Endocrine disease

Endocrine disease
PITUITARY HYPERSECRETION SYNDROMES
THE THYROID AXIS
MALE REPRODUCTION AND SEX
FEMALE REPRODUCTION AND SEX
THE GLUCOCORTICOID AXIS
THE THIRST AXIS
DISORDERS OF CALCIUM METABOLISM
DISORDERS OF PHOSPHATE CONCENTRATION
ENDOCRINOLOGY OF BLOOD PRESSURE CONTROL
DISORDERS OF TEMPERATURE REGULATION
THERAPEUTICS

15. Diabetes mellitus and other disorders of metabolism

DIABETES MELLITUS
DIABETIC METABOLIC EMERGENCIES
COMPLICATIONS OF DIABETES
SPECIAL SITUATIONS
HYPOGLYCAEMIA IN THE NON - DIABETIC
DISORDERS OF LIPID METABOLISM
THE PORPHYRIAS

16. The special senses

THE EAR
THE NOSE AND NASAL CAVITY
THE THROAT
THE EYE

17. Neurology

COMMON NEUROLOGICAL SYMPTOMS
COORDINATION OF MOVEMENT
THE CRANIAL NERVES
COMMON INVESTIGATIONS IN NEUROLOGICAL DISEASE
UNCONSCIOUSNESS AND COMA
STROKE AND CEREBROVASCULAR DISEASE
EPILEPSY AND LOSS OF CONSCIOUSNESS
NERVOUS SYSTEM INFECTION AND INFLAMMATION
HYDROCEPHALUS
HEADACHE, MIGRAINE AND FACIAL PAIN
SPINAL CORD DISEASE
DEGENERATIVE NEURONAL DISEASES
DISEASES OF THE PERIPHERAL NERVES
MUSCLE DISEASES
MYOTONIAS
DELIRIUM
THERAPEUTICS

18. Dermatology

Dermatology

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