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02
November 06, 2017
GASTROINTESTINAL DISORDERS IN CHILDREN PART II
Dra. Ruby Ann Punongbayan
Department of Pediatrics

TOPIC OUTLINE
I. Peptic Ulcer Disease
a. Role of Helicobacter pylori
b. Clinical Manifestations
c. Diagnosis
d. Treatment
II. Stress Ulcer Disease
III. Gastroenteritis
a. General Etiology
b. Risk Factors
c. Complications
d. General Approach to Diarrhea
e. Common Causative Organisms with Corresponding
Presentations and Treatment
Figure 1. Peptic Ulcer Disease
- Five Major Groups of E.coli
- Management
- Diagnosis of E.coli  Ulcers are deep lesions that breach the integrity of the epithelium
and penetrate through the muscularis mucosa with exposure of
- Indications for PCR and DNA Probes
submucosa
- Treatment
f. Clinical Syndromes  Erosions are superficial lesions that stop short of the muscularis
IV. Chronic Diarrhea propria
a. Evaluation of Chronic Diarrhea  Both lesions occur in the presence of gastric inflammation or
b. Treatment gastritis
V. Diseases of the Pancreas
a. Acute Pancreatitis
- Pathogenesis
- Clinical Manifestations
- Diagnosis
- Treatment
- Prognosis
VI. Diseases of the Liver
a. Manifestations of Liver Disease
- Viral Hepatitis
- Hepatitis B Antigens and Antibodies

PEPTIC ULCER DISEASE

 Clinical spectrum encompasses conditions that involve gastric acid
and pepsin in the pathogenesis (esophagitis -> gastritis ->duodenitis
-> PUD) Figure 2. Pathogenesis of PUD
 Peptic ulcer (genetic predisposition and cigarette smoking)
o Discontinuation of gastric or duodenal mucosa with Role of Helicobacter pylori
penetration to the muscularis mucosa and exposure of the  Spiral, microaerophilic Gram negative bacterium with sheathed
submucosa flagella
 Other possible causes: drugs, physical agents, stress,  Can increase pH of gastric antrum
immunologic/allergic, granulomatous inflammation, hypersecretory  Gastroduodenal inflammation due to H. Pylori is found primarily in
states the mucus layer covering gastric epithelial cells
 Primary (duodenal in nature) and secondary (gastric in  H. pylori produce urease that catalyzes conversion of urea in the
location) gastric juice to NH3 and HCO3 which buffer the gastric acid
 Pathogenesis is incompletely understood  H. pylori may be present in either parent of an affected child
 Ulceration occurs when aggressive factors (gastric acid, digestive  It is an important cause of recurrent ulcers and abdominal pain
enzymes, H. pylori) overwhelm the natural barriers (mucosal
defensive factors) that protect the gastroduodenal lining
(bicarbonate-mucus barrier, gastric epithelial cells, mucosal blood
flow, PGs)
o The mucus layer serves as a barrier preventing access of
pepsin onto the apical surface of the epithelial cells and
neutralizing the acid through the presence of bicarbonate
secreted into the mucus layer

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Highly sensitive & specific but the

Urea Breath Test method has not yet been
standardized in children

Figure 3. Role of H.pylori in PUD

Clinical Manifestations
Figure 4. Difference of DU and GU
 Classic symptom of epigastric pain alleviated by ingestion of food is
present only in a minority of children
Treatment
 Majority of children present with poorly localized pain
 After 6 years old, clinical features may be similar to those of adults  With H. pylori who have ulcers, MALT lymphoma, atrophic gastritis
o Dull or aching pain with intestinal metaplasia; cost-benefit ratio of eradicating H.
o GI blood loss Pylori
o Exacerbations and remissions  PPI + Clarithromycin + Amoxicillin or
 <33% of patients presenting with typical ulcer pain experience  PPI + Clarithromycin + Metronidazole
prompt relief after intake of antacids  Taken for 4 to 6 weeks

Diagnosis

Method of Choice
Esophagogastroduodenoscopy
Direct Visualization
Gold standard for diagnosis is
histologic demonstration or
isolation
To test for:
• Undocumented duodenal
or gastric ulcer
• MALT lymphoma
(anrtalmicronodules
representing lymphoid
follicles)
Taken from
Biopsy
• Antrum
• Body
• Transition zone

Preferably while off acid suppression

Figure 5. Urea Breath Test
for at least 2 weeks
For H pylori: gold standard for
diagnosis is the histologic STRESS ULCER DISEASE
demonstration or isolation by  Underlying cause of secondary PUD not fully understood
bacteriologic culture of the  Similar in symptomatology with PUD
organism  Comorbid conditions must be identified
Rapid Urease Test Done in biopsy sample  Factors that interfere with host defense mechanisms are involved
• Blood o Mucosal blood flow
• Urine o PG synthesis
• Saliva o Acid/mucus production
Ab Detection • Stool  Infants: related to infection or dehydration
 Older children: related to trauma
Low sensitivity & specificity in low  Curling ulcers: associated with burns (>25%)
prevalence areas  Cushing ulcers: head trauma with surgery
Ag Detection • Stool  Associated with hemorrhage or perforation
 Drug-related: due to NSAIDs

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o Thought to damage mucosa by inhibiting PG synthesis, cell  Malabsorption

proliferation and mucosal HCO3 and mucus secretion  Endocrinopathies
o Cimetidine 20-40 mkday q6h;  Food poisoning
o Ranitidine 4-6 mkday q12h  Neoplasms
 Inciting cause must be removed  Miscellaneous
o Milk allergy
Treatment o Immunodeficiency states
 Goal: To control gastric acidity for 6-8 weeks with use of: o Laxative abuse
o Ulcerative colitis
o Motility disorders
Neutralize acid
Antacids
AlMgOH
Suppress acid secretion From Dr. Punongbayan’s PPT
H2 Receptor Blockers
Ranitidine
Antibiotics are given to selected patients with bacterial enteritis to
Undergoes acidic activation within
shorten the clinical course, to decrease excretion of the causative
parietal cell to allow it to be ionized
organism, or to prevent complications.
and form covalent disulphide bonds
PPI with cysteines of H-K-Adenosine
Triphosphatase
From 2017
Esomeprazole (ideal PPI)
 ETEC colonizes the enterocytes of the small intestine and produces
the heat-labile (LT) and heat-stable (ST) enterotoxins.
GASTROENTERITIS o LT is structurally similar to V. cholera toxin and activates
 Infections of the GIT which are caused either by bacterial, viral or adenylate cyclase, resulting in increased cGMP
parasitic pathogens.  Shigella invades the superficial colonic mucosa through the M cells of
 Can either be acute or chronic Peyer’s Patches. Bacteria spread leads to release of inflammatory
 Two types of acute infectious diarrhea: cytokines (IL-1 and IL-8) which cause neutrophil migration and
o Non-inflammatory necrosis leading to mucosal destruction (reason why there is bloody
 enterotoxin production by bacteria stool).
 destruction of villus by viruses
 adherence by parasites
o Inflammatory – due to bacteria that invade the intestine Risk Factors
directly or produce cytotoxins  Environmental contamination
 Chronic or persistent diarrhea – more than 14 days duration  Measles
may be due to:  Inadequate breastfeeding
 infection  Immunodeficiency
 any enteropathogen infecting an immunocompromised  Malnutrition
host or  Young age
 residual symptoms due damage to the intestine
Complications
General Etiology
 Severe Dehydration - Death
o Secondary infections
Type Cause o Electrolyte deficiencies
 Campylobacter jejuni o Micronutrient deficiencies
 Clostridium difficile
 Enteroinvasive Escherichia coli (EIEC) General Approach to Diarrhea
Inflammatory  Salmonella  Assess the degree of dehydration & provide fluid &
 Shigella – most common cause of bloody electrolyte replacement.
diarrhea  Prevent spread of the enteropathogen.
 Yersinia  Determine etiologic agent in selected cases & provide specific
 Enteropathogenic Escherichia coli (EPEC) therapy if indicated.
 Enterotoxigenic Escherichia coli (ETEC) –
Non-inflammatory most common cause of traveler’s diarrhea WHO ASSESSMENT CHART
 Vibrio cholera – fish odor, rice watery A B C
stool Clinical
No Some Severe
 Rotavirus – most common cause of Parameter
Dehydration dehydration dehydration
infantile diarrhea (NSP4 as
General Lethargic
viralenterotoxin) Alert Irritable
Condition Unconscious
Viral  Adenovirus
Eyes Normal Sunken Sunken
 Astrovirus
Thirst None Drinks eagerly Drinks poorly
 Norwalk
Skin
 Calicivirus Quick Slow Very slow >2s
Retraction
 Giardia lamblia Weight loss % <5% 5-10% >10%
 Entamoeba histolytica – bloody stool with
Fluid Deficit <50ml/kg 50-100 ml/kg >100 ml/kg
mucus
Parasitic *Made for far flung areas
 Balatidium coli
 Strongyloides
 Spore-forming protozoa
Other causes  Anatomic defects

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WHO-CDC PROTOCOL ON REHYDRATION AVERAGE COMPOSITION OF STOOL AND VOMITUS IN

1. Fluids: Give ORS after every loose stool. GASTROENTERITIS
Ideally, volume of stool should be estimated, Electrolyte Stool (mEq/L) Vomitus (mEq/L)
and replaced with same volume of ORS. Sodium 55 60
Treatment Plan 2. Feeding: Continue breastfeeding or regular Potassium 25 10
A feeding to prevent malnutrition (do not Chloride 55 90
(No change dilution of milk formula). Bicarbonate 15 ---
Dehydration) 3. Follow-up: If the child does not improve in
3 days or shows repeated vomiting, frequent
COMPOSITION OF COMMONLY USED FLUIDS
watery stools, marked thirst, eating, and
drinking poorly, fever, bloody stools. Fluid Na (mmol/L) K (mmol/L) Osmolarity
1. Give 75cc/kg ORS per orem over 4 hours. Apple juice 114-251 2.2-17 290-507
Orange juice 0.6-2.5 41-65 290-507
 Example: 10kg child with dehydration
o 10kg x 75cc/kg 750cc or (3/4) L Coke/Pepsi 1.3-1.7 0.1 591-601
Treatment Plan ORS is given 7-up 5.0-5.5 1.0-2.0 523-548
B 2. Re-assess hydration status after 4 hours and Coconut 0-5.4 32.6-53.5 255-333
(Some adjust treatment as needed. Gatorade 14.6 3.5 58 gm (S+G/Fr)
dehydration) 3. May be repeated if same signs of dehydration Powerade 8 4 80 gm (Sucrose)
are still present after 4 hours. Pocari sweat 21 5 641
4. Continue feeding as in Plan A. Grape juice 1.3-2.8 28-32 1167-1190
5. Follow-up as in Plan A. Comm’l soup 114-251 2.2-17 290-507
1. Give a total of 100cc/kg pLR IV as follows: WHO recomm’n 50-75 20 210-269
 First: 30cc/kg over 1 hour for infants and
30 min for children From 2017
 Next: 70cc/kg over 5 hours for infants  Apple juice - Na is too high
and 2.5 hours for children  Orange juice - K is too high
2. Re-assess the patient every hour and re-  Softdrinks consumption – not enough Na and K
classify.  Gatorade / Powerade – not enough Na and K
Treatment Plan  No urine output for the past 6 hours is  Comm’l soup – Na is too high
C alarming (may lead to acute renal
(Severe failure).
dehydration)  Low BP and Capillary refill time are also From 3A 2018
alarming
 Hyponatremia: cold, clammy skin, cell will swell
 Early signs of shock -> tachycardia  Hypernatremia: doughy, hot velvety skin, cell will shrink
3. May be repeated if there are still signs of
 Both hypo and hyper could cause seizure
severe dehydration.
Precaution: d/t electrolyte imbalance secondary to AGE
4. Start ORS as soon as the patient can drink.
 Can also give crystalloids as these are
volume expanders
COMPOSITION OF STANDARD ORS:
*Add ZINC: for repair / re-epithelialization (2 weeks)
Standard WHO-ORS Reduced osmolarity
(mEq or mmol/L) ORS (mEq or mmol/L)
ASSESSMENT OF DEHYDRATION Glucose 111 75
 Normal mental status Sodium 90 75
 Slightly thirsty Chloride 80 65
Mild  With tears, eyes and fontanel not sunken Potassium 20 20
Dehydration (3-  Slightly dry mucous membranes Citrate 10 10
5%)  Normal pulses Osmolarity 311 245
 Immediate skin retraction
 Normal CRT and UO
From 3B 2018
 Irritable, moderately thirsty
 Rationale of using Reduced Osmolarity ORS
 Sunken eyes and fontanel; reduced to absent o Significantly reduced vomiting
Moderate tears; dry mucous membranes
o Significantly higher urine output
Dehydration (6-  Rapid, weak pulses o As efficacious as standard WHO-ORS for cholera patients
9%)  Slightly reduced UO o However, Patients have increased risk for hyponatremia
 Slightly cool extremities
 CRT and skin retraction >2s
 Lethargic to comatose Space filler =)) Insert anything here xD
 Very thirsty or unable to drink
 Absent tears, sunken eyes and fontanel
Severe
 Parched mucous membranes
Dehydration
 Cool, mottled skin; acryocyanosis
(>10%)
 CRT and skin retraction >2s
 Anuria
 Deep/rapid respiration

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GENERAL APPROACH Five Major Groups of E.coli

 Oral intake  ETEC – infantile explosive diarrhea with dehydration; few or no
 Frequency, volume of stool output structural changes in the gut mucosa
 General appearance and activity of the child  EIEC – causes colonic lesions like dysentery
 Frequency of urination  EPEC – non bloody diarrhea with mucus; prolonged
 Recent travel  EAEC – significant dehydration; prolonged diarrhea
Ask about the  Use of antimicrobials  EHEC – shiga – toxin producing E.coli; bloody diarrhea
following  Intake of seafood, contaminated water,
uncooked meat, or unwashed vegetables Strain Age grp Watery Bloody Duration
 Duration of diarrhea at risk diarrhea diarrhea
 Presence of blood in stool
 Other symptoms such as fever, tenesmus,
ETEC >1y/o +++ Little ---- Acute
vomiting and to no
 If HUS is suspected travelers fever
 Bloody diarrhea EIEC >1y/o + ++ Acute
Stool culture  Stool with fecal leukocytes Dysentery
 During outbreak EPEC <2y/o +++ ---- Acute or
 Immunocompromised patients
esp<6 Vomiting Persistent
 Management of dehydration is the
mos old and low
 cornerstone
 Rapid rehydration with replacement of grade
ongoing losses during the first 4 to 6 hours fever
Rehydration
 Reintroduce food once rehydration is EHEC 6 mos – + +++ Acute
complete 10y/o Afebrile
 Encourage breastfeeding, small frequent and the
feedings
elderly
Anti-diarrheal Generally not recommended
Routine culture of EAEC <1y/o +++ ---- Acute or
Not mandatory and Persistent
E. coli
travelers
Common Causative Organisms with Corresponding
Presentations and Treatments Diagnosis of E.coli
 Clinical features of illness are seldom distinctive
Presentation Treatment  Routine laboratory tests are of very limited value
C. difficile  History of antibiotic  Metronidazole or  Practical methods primarily for EHEC
use Vancomycin  For the others: based on tissue cultures or identification of specific
S. aureus  Sx within 12 hrs  None virulence factors of the bacteria by phenotype or genotype
due to pre formed
toxin with a Indications for PCR and DNA Probes
common source  Severe or life threatening complications
E. histolytica  Infects the colon  Metronidazole  Persistent diarrhea
 Acute bloody  Outbreak investigations
diarrhea
G. lamblia  Cysts are ingested  Metronidazole Treatment
from contaminated  Fluid and electrolyte therapy
food and water  Early refeeding(within 8-12 hrs of initiation of rehydration)
 Watery diarrhea  Specific antimicrobial therapy is problematic due to difficulty of
Cholera  Profuse watery  Azithromycin, making a diagnosis and the unpredictability of antibiotic
diarrhea Tetracycline, susceptibilities
 Rice watery stools Trimetoprim-  ETEC responds to TMP - SMZ
with fishy odor Sulfamethoxazole
Rotavirus  Watery diarrhea 7  Supportive Clinical Syndromes
to 10 days  Vomiting / diarrhea occurring in<1 hr = Chemical poisoning,
Entero  From nurseries and  toxins from fish or shellfish
Pathogenic daycare  Vomiting / diarrhea in1 – 6 hrs = S. aureus
E.coli  Watery diarrhea, abdominal cramps in8 – 72hrs = Salmonella
Entero  Hemorrhagic colitis   Bloody diarrhea in>15hrs = Shigella
Hemorrhagic  HUS  Neurologic symptoms:
E.coli o 0 – 6 hrs : Fish, shellfish, MSG
Salmonella  Eggs, milk and  Treat only S. typhi o 0 – 24 hrs: Mushroom
poultry and if <3 mos old o 8 – 24 hrs: C. botulinum
 Tx prolongs carrier  Diagnosis of food borne or water borne illness is considered when
state >2 persons have ingested common food/water develop similar
Shigella and  Person to person  Ciprofloxacis; acute illness
Campylobacter contact through Cefixime;
contaminated food Erythromycin

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CHRONIC DIARRHEA
 Increased total daily stool output with increased stool water content
 Diarrhea that lasts more than 2 weeks
 Results from altered intestinal water and electrolyte transport
 GI tract of an infant handles 285 ml/kg/day of fluid (intake plus
intestinal secretion) with a stool output of 5 – 10 g/kg/day
 Stool output in infants & children contains approximately per liter
(20-25 meq of na, 50-70 meq of k, 20-25 meq of cl)
 Mechanisms responsible for the absorptive capacity are caused by
the function of several transport proteins located at the brush
border membrane of the small and large intestine 

Evaluation of Chronic Diarrhea

 Phase I:Increased total daily stool output with increased stool water
content; Diarrhea that lasts more than 2 weeks
 Phase II: sweat chloride, 72-hr stool collection for fat, stool
electrolytes & osmolality, stool for phenolphthalein, Mg sulfate, PO4
 Phase III: endoscopy, small bowel biopsy, sigmoidoscopy or Figure 6. Pathogenesis of Acute Pancreatitis
colonoscopy, barium
 Phase IV: hormonal studies (VIP, gastrin, secretin) Clinical Manifestations
 Abdominal pain (epigastric, steady, appears acutely ill) PQRST
Treatment  Persistent vomiting
 Maintain adequate nutritional intake to permit normal growth &  Fever
development  Pain increases in intensity for 24-48 hours with vomiting
 If diarrhea is due to CHO intolerance, have a trial period of  Severe acute type: rare in children
decreased lactose or sucrose o Severe nausea, vomiting
 Use predigested formula pregestimil or alimentum for o Shock
postgastroenteritis malabsorption syndrome o Jaundice
 Secretory type: consider nutritional support (most likely due to o High fever
congenital defect in transport proteins) o Necrotic pancreas
o Mortality rate: 50%
o Cullen’s sign (bluish discoloration around umbilicus)
DISEASES OF THE PANCREAS o Grey turner sign (bluish discoloration of flanks)

 CASE: A 10 yr old girl was diagnosed to have systemic viral infection

1 week PTC. She was managed conservatively. Two days PTC, she
had epigastric pain that increased in intensity associated with 6
vomiting episodes for the past few hours.
 PE: Febrile, toxic-looking, flat, tensed, abdomen with tenderness
radiating to the back
 What is your Impression? Acute Pancreatitis

Acute Pancreatitis
 Most common pancreatic disorder in children
 Most common causes: CULLEN’S SIGN GREY TURNER SIGN
o Blunt abdominal injury
o Mumps and other viral illnesses (Measles, VIRAL)
o Multisystem disease
o Congenital abnormalities
o Biliary microlithiasis
o Drugs and toxins

Pathogenesis
 Theory: Following an insult, lysosomal hydrolase co-localizes with
pancreatic proenzymes within the acinar cell pancreatitis with
continued synthesis of enzymes occur  proenzymes are activated
by cathepsin leading to autodigestion, further activation and release DIAGNOSIS
of active proteases lecithin is activated by phospholipase A2 AMYLASE LIPASE
into the toxic lysolecithin (which attack the pancreatic cells) Serum levels elevated for up to 4 More specific in acute
days inflammatory pancreatic disease
Rises by 4-8 hours
Peaks at 24-48 hours
Remains elevated 8-14 days
longer than serum amylase

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Other laboratory findings: o Tumors

o Hemoconcentration  Clinical Manifestations:
o Coagulopathy o Hepatomegaly – increase in the number or size of the cells in
o Leukocytosis the liver, inflammation, infiltration, increased size or vascular
o Hyperglycemia space, increased size of biliary space
o Hyperbilirubinemia o Jaundice – unconjugated type may indicate increased
o High glutamyltranspeptidase production, hemolysis, reduced hepatic removal or altered
metabolism; conjugated type reflects decreased excretion by
Abnormal X-ray (20% of children may have normal findings):
damaged hepatic parenchymal cells or disease of biliary tract
o Sentinel loop due to sepsis, endocrine or metabolic disease, inflammation of
o Dilated transverse colon the liver or obstruction
(CUTOFF Sign): Abrupt o Pruritus – multifactorial; retained bile components
termination at level of o Spider angioma – due to altered estrogen metabolism in the
splenic flexure  yellow presence of liver dysfunction
arrowheads o Palmar erythema – due to vasodilation & increased blood
o Blurring of psoas margin flow
o Peripancreatic o Xanthoma – elevated cholesterol may cause deposition of lipid
extraluminal gas bubbles in the dermis & subcutaneous tissue
o Portal hypertension – >10mmHg difference between the
o Abdominal UTZ and CT portal vein & systemic veins
scan: o Ascites – portal hypertension & hepatic insufficiency are also
 Pancreatic present
enlargement o Variceal hemorrhage – results from increased pressure
 Hypoechoic, sonolucent, edematous within the varix which leads to changes in the diameter of the
 Pancreatic masses varix & increased wall tension
 Fluid collections o Encephalopathy – prominent or subtle neurologic
 Abscess dysfunctions; may be due to altered ammonium metabolism,
 20% of children may have normal findings synergistic neurotoxins, or “false neurotransmitters” with
plasma amino acid imbalance
o Endocrine abnormalities – adults>children
o Renal dysfunction – systemic disease or toxins may affect
Treatment both organs simultaneously; altered water & sodium activity,
 GOAL: To relieve pain and restore metabolic hemeostatis impaired concentrating ability; hepatorenal syndrome –
 Analgesia functional renal failure in patients with end-stage liver disease
 Fluid electrolyte and mineral balance restored and maintained o Pulmonary involvement – hepatopulmonary syndrome –
 Prophylactic antibiotics useful in severe cases to prevent infected triad of hypoxemia, intrapulmonary vascular dilations & liver
pancreatic necrosis disease
 Reefed when vomiting has resolved serum amylase in falling and o Recurrent cholangitis – ascending infection of the biliary
clinical symptoms are resolving system due to gram (-) enteric organisms
 Endoscopic therapy: If due to anatomic abnormalities (strictures
or stones)
Viral Hepatitis
 Severe acute type: Enteral or TPN, antibiotics, gastric acid
suppression, peritoneal lavage  Identified antibodies
o Anti-HAV, IgM anti-HAV
o Anti-HBsAg, IgM anti-HBsAg, anti-HBcAg, anti-HBeAg
Prognosis o Anti-HCV
 Uncomplicated cases: Recover over 2-5 days o Anti-HDV
 If associated with trauma or systemic disease: Prognosis is o Anti-HEV, IgM anti-HEV
related to the associated medical condition o Anti-HGV
 Ranson’s criteria and APACHE score: Prognostic systems used in
adults are inappropriate for use in children Lifted from 2018

DISEASES OF THE LIVER Hepatitis A

o Reported to be sexually transmitted esp. among MSM
 Metabolic functions of the liver: o Viremia occurs within 1-2 weeks after HAV exposure
o Carbohydrate metabolism
o Peak fecal excretion and infectivity occurs before the onset of
o Protein metabolism
symptoms and declines after jaundice appears
o Lipid metabolism
o Most infections (70%) are subclinical in <6 years old
o Biotransformation
o Anti-Hav IgM detected at or prior to the onset of clinical illness
o Hepatic excretory function
and decline in about 3-6 months
Hepatitis B
Manifestations of Liver Disease o Philippines: 8-12% prevalence rate for HbsAg
 Alteration in liver structure & function
 Pathologic manifestations:
o Inflammation or necrosis: viruses, drus, toxins, hypoxia, IEM,
immunologic disorders
o Cholestasis: response to injury due to extra- or intrahepatic
obstruction to bile flow; accumulation in serum of substances
normally excreted in bile
o Cirrhosis

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HAV HBV HCV

Nucleic acid RNA DNA RNA
Incubation 30d 100-120d 7-9 weeks
Percutaneous Rare Common Common
Fecal-oral Common No No
transmission
Sexual Rare Common Rare
transmission
Transplacental No Common Rare
transmission
Chronic No Yes Yes
infection
Fulminant Rare Yes Rare
disease
HDV HEV HGV
Nucleic acid RNA RNA RNA
Incubation 2-4 mos 40d Unknown
Percutaneous Common No Common
Fecal-oral No Common No
transmission
Sexual Rare Rare Rare
transmission
Transplacental No Prob. No Rare
transmission
Chronic Yes No Yes
infection
Fulminant Yes Rare Prob. No
disease

Hepatitis B Antigens and Antibodies

 First clinical evidence of HBV infection is elevation of ALT levels
which occur at about 6-7 weeks after exposure

Ag/Ab Features
Anti-HBcAg • Most valuable single serologic marker foracute
HBV infection because it is present asearly as HBsAg
and continues to be presentlater in the course of the
disease whenHBsAg has disappeared
HBcAg • Inner portion of the virion that encodes viralDNA
HBeAg • Serves as a marker of active viral replication
• Identification of infected individuals at
increased risk of transmitting HBV
HBsAg First serologic marker to appear and its rise
coincides with onset of symptoms; detectionof
acutely or chronically infected people;antigen used in
hepatitis B vaccine
Anti-HBs • Identification of people who have
resolvedinfections with HBV; determination of
immunity after immunization
Anti-HBe • Identification of infected people with lower
risk of transmitting HBV
Anti-HBc Identification of people acute, resolved or
chronic HBV infection
IgM Anti-HBc Identification of people acute or recent HBV
infections (including HBsAg-negative people
during the “window” phase of infection)

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