Allergic colitis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qasim Salau, M.B.B.S., FMCPaed [2]

Allergic colitis is a non IgE immunological reaction against food protein antigens, particularly cow-milk and soy proteins. The exact mechanism is not known. It usually develops insidiously, and is believed to be T-cell mediated. Allergic colitis is most commonly caused by allergy to cow’s milk protein. Symptoms and signs of allergic colitis are non-specific and observed in other causes of colitis and some systemic diseases. Detailed history and physical examination is needed to make the diagnosis. In addition, endoscopy with biopsy may be required to confirm the diagnosis. The exact prevalence of allergic colitis is unknown. Allergic colitis typically develops in early infancy. Allergic colitis is benign, resolving completely in most children without any sequelae. The most common symptoms of allergic colitis is passage of blood streaked stool in an otherwise healthy young infant. There are no specific laboratory findings that are pathognomonic of allergic colitis. Laboratory studies should therefore be correlated with a carefully taken history and a detailed physical examination. Presence of eosinophils in the stool is suggestive of allergic colitis in the presence of typical clinical findings. The mainstay of treatment of allergic colitis is dietary management. Medical therapy includes allergen avoidance, treatment of severe manifestations of the allergy, and eventual reintroduction of the allergy into the diet.

Allergic colitis was first described by Kaijser in 1937. Allergic proctocolitis was described by Rubin in 1940. In the 1960s, Gryboski subsequently described proctocolitis and enterocolitis.

Allergic colitis can be classified into two subtypes based on the anatomical site involved, proctocolitis and enterocolitis. Allergic colitis manifests more commonly as proctocolitis. It is also more common among infants.

Allergic colitis is a non IgE immunological reaction against food protein antigens, particularly cow-milk and soy proteins. The exact mechanism is not known. It usually develops insidiously, and is believed to be T-cell mediated. The activated T-cells lead to recruitment of eosinophils and other polymorphonuclear cells into the intestinal tract, which then cause intestinal inflammation and damage. Some of these children may later develop specific IgE. Genetic influence may also play a role, since disease is sometimes present within families. On gross pathology, there is evidence of inflammation with ulcers and friable, erythematous mucosa. On microscopy, the mucosa architecture is preserved with eosinophil infiltrates.

Allergic colitis is most commonly caused by allergy to cow’s milk protein. 20-40% of patients with allergic colitis have allergies to both cow’s milk protein and soy protein.

Symptoms and signs of allergic colitis are non-specific and observed in other causes of colitis and some systemic diseases. Detailed history and physical examination is needed to make the diagnosis. In addition, endoscopy with biopsy may be required to confirm the diagnosis. In infancy, allergic colitis must particularly be differentiated from necrotizing enterocolitis, infectious colitis, anal fissure, intussusception, and volvulus. In adolescent and adults, allergic colitis must be differentiated from inflammatory bowel disease, infectious colitis, and colorectal malignancy.

The exact prevalence of allergic colitis is unknown. Prevalence of food protein-induced allergic proctocolitis (FPIAP) has been reported to range from a low of 16% to a high of 64% among infants with rectal bleeding. FPIAP is the most common cause of non-infectious colitis in infancy. Allergic colitis is mainly a disease of infants, with onset usually in the first two to three months of life. There is a slight male predominance (50–61.6%) for allergic colitis.

Risk factors for allergic colitis include family history of atopy and previous sibling with IgE mediated food allergy.

Screening is not recommended for allergic colitis.

Allergic colitis typically develops in early infancy. Allergic colitis is benign, resolving completely in most children without any sequelae. The infants with food protein-induced allergic proctocolitis are usually on exclusive breastfeeding while those with food protein-induced enterocolitis syndrome are often on infant formula. If left untreated, spontaneous resolution may occur in 20% of the children with allergic colitis without elimination of the triggering food. Most infants with allergic colitis will tolerate the offending food by 1 to 3 years of age.

The most common symptoms of allergic colitis is passage of blood streaked stool in an otherwise healthy young infant especially in FPIAP. History of failure to thrive may also be gotten in the infant with FPIES. There may be a family history of allergy.

Patients with allergic colitis may appear well in the case of FPIAP or may appear lethargic when they have FPIES. Physical examination of patients with FPIES is usually remarkable for signs of dehydration, pallor, and poor weight.

There are no specific laboratory findings that are pathognomonic of allergic colitis. Laboratory studies should therefore be correlated with a carefully taken history and a detailed physical examination. Presence of eosinophils in the stool is suggestive of allergic colitis in the presence of typical clinical findings.

There are no diagnostic x ray findings associated with allergic colitis.

There are no diagnostic CT findings associated with allergic colitis.

There are no diagnostic MRI findings associated with allergic colitis.

There are no diagnostic ultrasound findings associated with allergic colitis.

Other imaging studies for allergic colitis include endoscopy. Endoscopy is not recommended in the routine diagnosis of allergic colitis. Endoscopy is usually required for atypical presentation in addition to detailed clinical assessment. The lesions in allergic colitis are most often observed in the the rectosigmoid area. Gross endoscopic findings associated with allergic colitis include; focal or diffuse erythema, edematous and friable mucosa, with nodular hyperplasia and/ or ulcerations. Characteristic circumscribed central pit-like erosions may also be observed.

There are no additional diagnostic studies associated with allergic colitis.

The mainstay of treatment of allergic colitis is dietary management. Medical therapy includes allergen avoidance, treatment of severe manifestations of the allergy, and eventual reintroduction of the allergy into the diet.

There is no indication for surgical intervention in allergic colitis.

There are presently no established methods to prevent allergic colitis.

There are presently no secondary preventive measures for allergic colitis. However, it is important to avoid food allergens identified in the individual until tolerance has been demonstrated.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qasim Salau, M.B.B.S., FMCPaed [2]

Allergic colitis was first described by Kaijser in 1937. Allergic proctocolitis was described by Rubin in 1940. In the 1960s, Gryboski subsequently described proctocolitis and enterocolitis.

• Allergic colitis was first described by Kaijser in 1937.^[1][2]
• In 1940, Rubin also described allergic proctocolitis.^[2][3]
• In 1966 and 1967, Gryboski published the first case series of cow milk induced colitis in neonates.^[4][5][6]
• In the 1970s, Powell described food induced enterocolitis following cow milk and soy milk introduction in young infants.^[4][7][8]
• Gryboski and Powell described acute severe symptoms following re-exposure to cow milk formula after an initial period of avoidance.^[4]
• In 1982, McDonald et al. first used the term food induced enterocolitis (FIE) to describe cow milk/soy protein induced enterocolitis and subsequently modified the nomenclature in 1984 to food protein-induced enterocolitis (FPIE).^[4][9]
• In 1998, Sicherer et al. suggested food protein-induced enterocolitis be called a syndrome, recognizing the disease was characterized by a constellation of shared clinical and laboratory features.^[4][10]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qasim Salau, M.B.B.S., FMCPaed [2]

Allergic colitis can be classified into two subtypes based on the anatomical site involved, proctocolitis and enterocolitis. Allergic colitis manifests more commonly as proctocolitis. It is also more common among infants.

Based on the anatomical area involved, allergic colitis may be classified into:^[1][2][3]

• Food protein-induced allergic proctocolitis (FPIAP)
• Food protein-induced enterocolitis syndrome (FPIES)

Based on age, allergic colitis can be classified into:^[2]

• Infantile
• Adolescent/Adult

Based on immune mechanism, it can be classified into:^[2][4]

• Atopic (IgE mediated)
• Non atopic (non-IgE mediated)

Based on the duration of symptoms and presentation, allergic colitis may be classified into:^[1]

• Acute: Minutes to few hours after coming in ingesting the offending protein.
• Chronic: Weeks after ingesting the offending protein. Presentation is due to accumulative effect of the protein.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qasim Salau, M.B.B.S., FMCPaed [2]

Allergic colitis is a non IgE immunological reaction against food protein antigens, particularly cow-milk and soy proteins. The exact mechanism is not known. It usually develops insidiously, and is thought to be T cell mediated. The activated T cells lead to recruitment of eosinophils and other polymorphonuclear cells into the intestinal tract, which then cause intestinal inflammation and damage. Some of these children may later develop specific IgE. Genetic influence may also play a role, since disease is sometimes present within families. On gross pathology, there is evidence of inflammation, with ulcers and friable, erythematous mucosa. On microscopy, the mucosa architecture is preserved with eosinophil infiltrates.

The exact pathophysiologic mechanism by which allergic colitis develops is not fully understood.

• It is a non-IgE immunological reaction against food protein antigens, which is thought to be T cell mediated.^{[1][2][3][4][5]}
  • Activation of T cells (CD8 and Th2) results in release of inflammatory cytokines TNF-α, and decreased expression of TGF-β in the intestinal mucosa, attracting polymorphonuclear cells (PMN) including eosinophils to the intestinal tract, subsequently causing intestinal inflammation and damage.^[6]

• Autoimmunity may play a role in the pathogenesis. Atypical perinuclear antineutrophil cytoplasmic antibodies (a-pANCA) have been found in some of the infants, with intestinal infiltration by neutrophils.^[7]

• Specific IgE antibodies against food proteins have been demonstrated in 4 to 24% the children suggesting a role in the pathogenesis of allergic colitis. These antibodies developed over time.^[8][9]

Allergic colitis is sometimes observed within families, suggesting genetic predisposition may play a role in the pathogenesis.^[7]

• Gross pathological findings are predominantly in the rectosigmoid region in patients with allergic colitis. The lesions are diffuse or patchy with or without necrosis, ulcers, abscesses within the crypts and hemorrhage. The mucosa is erythematous and friable. Nodular hyperplasia with characteristic circumscribed central pit-like erosions and ulcers may also be observed.^[10][11][12]

• Allergic colitis is characterized by marked eosinophil infiltrates (≥ 60/10 HPF) in the mucosa (especially the lamina propria) of the involved area.^[10][11][13]
• Typically, the mucosa architecture is preserved on microscopy.^[10][11]

• 
  Allergic colitis. H and E stain showing abundant eosinophils – By Nephron – Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=30671091

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qasim Salau, M.B.B.S., FMCPaed [2]

Allergic colitis is most commonly caused by allergy to cow’s milk protein. 20-40% of patients with allergic colitis have allergies to both cow’s milk protein and soy protein.

The most common cause of allergic colitis is cow’s milk protein allergy, which accounts for 50% to 65% of reports. Cow’s milk protein and soy protein together account for about 75% of the causes.^[1][2] Other causes include:

• Egg
• Peanut
• Cereals such as corn, rice, oat, barley
• Others include meats, fish, shellfish

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qasim Salau, M.B.B.S., FMCPaed [2]

Symptoms and signs of allergic colitis are non-specific and observed in other causes of colitis and some systemic diseases. Detailed history and physical examination is needed to make the diagnosis. In addition, endoscopy with biopsy may be required to confirm the diagnosis. In infancy, allergic colitis must particularly be differentiated from necrotizing enterocolitis, infectious colitis, anal fissure, intussusception, and volvulus. In adolescent and adults, allergic colitis must be differentiated from inflammatory bowel disease, infectious colitis, and colorectal malignancy.

The differential diagnosis of allergic colitis can be classified into two according to age group.

• Swallowed maternal blood syndrome
• Anorectal fissure
• Necrotizing enterocolitis especially in preterm babies
• Vitamin K deficiency hemorrhage
• Other coagulopathies (hereditary such as coagulation factor deficiency or acquired such as liver disease with clotting factor deficiency)
• Intussusception
• Infectious colitis
• Hirschsprung disease complicated by enterocolitis
• Volvulus
• Inflammatory bowel disease (early onset)
• Meckel diverticulum
• Dermatitis
• Gastrointestinal duplication cyst
• Vascular malformations
• Gastro-duodenal ulcers
• Lymphonodular hyperplasia

• Inflammatory bowel disease
• Behcet’s disease
• Arteriovenous malformation
• Diverticulosis
• Infectious colitis
• Coagulopathy
• Henoch-Schonlein purpura
• Systemic lupus erythematosus (SLE)
• Colorectal malignancy

• The symptoms of colitis, such as diarrhea (especially bloody diarrhea and abdominal pain)) are observed in all forms of colitis. The table below lists the differential diagnosis of common causes of colitis:^[1][2]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qasim Salau, M.B.B.S., FMCPaed [2]

The exact prevalence of allergic colitis is unknown. Prevalence of food protein-induced allergic proctocolitis (FPIAP) has been reported to range from a low of 16% to a high of 64% among infants with rectal bleeding. FPIAP is the most common cause of non-infectious colitis in infancy. Allergic colitis is mainly a disease of infants, with onset usually in the first two to three months of life. There is a slight male predominance (50–61.6%) for allergic colitis.

The exact prevalence and incidence of allergic colitis is unknown.

• Prevalence of food protein-induced allergic proctocolitis (FPIAP) has been reported to range from a low of 16% to a high of 64% among infants with rectal bleeding^[1][2][3]
• A population based study reported a prevalence of 1.6 in 1000 children under 1 year had cow’s-milk protein induced rectal bleeding^[4]
• The incidence of milk FPIES was estimated as 0.34% of the newborn population in a population based study^[4]
• 60% of infants with FPIAP are babies on exclusive breastfeeding^[1][5]

• FPIAP is the most common cause of non-infectious colitis in infancy^[6]

Allergic colitis is mainly a disease of infants, with onset usually in the first 2-3 months of life. An adolescent form may develop in adolescence or early adulthood.^[1][2][3][7]

There is a slight male predominance (50–61.6%) for allergic colitis.^[8][9]

There is no racial predilection for allergic colitis.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qasim Salau, M.B.B.S., FMCPaed [2]

Risk factors for allergic colitis include family history of atopy and previous sibling with IgE mediated food allergy.

Risk factors for allergic colitis include:^[1]

• Family history of atopy, asthma, environmental allergies
• Previous sibling with IgE mediated food allergy
• IgA deficiency
• Use of formula feeds
• Gastroenteritis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qasim Salau, M.B.B.S., FMCPaed [2]

Screening is not recommended for allergic colitis.

Screening is not recommended for allergic colitis.^[1][2]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qasim Salau, M.B.B.S., FMCPaed [2]

Allergic colitis typically develops in early infancy. Allergic colitis is benign, resolving completely in most children without any sequelae. The infants with food protein-induced allergic proctocolitis are usually on exclusive breastfeeding while those with food protein-induced enterocolitis syndrome are often on infant formula. If left untreated, spontaneous resolution may occur in 20% of the children with allergic colitis without elimination of the triggering food. Most infants with allergic colitis will tolerate the offending food by 1 to 3 years of age.

• The symptoms of allergic colitis typically develops in early infancy (within the first two or three months of life). The infants with food protein-induced allergic proctocolitis are usually on exclusive breastfeeding while those with food protein-induced enterocolitis syndrome are often on infant formula. Typically, the episodes resolve within 48 to 96 hours following avoidance of the trigger protein. Spontaneous resolution of symptoms may occur in 20% of the children without elimination of the offending protein. Most infants with food protein-induced allergic proctocolitis will be able to tolerate the offending protein by 1 to 3 years of age, while those with food protein-induced enterocolitis syndrome tolerate the offending protein later usually by 2 to 5 years of age.^[1][2][3][4]

• The natural history of allergic colitis that develops in adolescence or early adulthood especially if due to solid food is poorly characterized with the resolution of symptoms often prolonged.^[5]

Complications of allergic colitis are more common with food protein-induced enterocolitis syndrome (FPIES) than food protein-induced allergic proctocolitis (FPIAP). The complications include:^[6][7]

• Dehydration
• Electrolyte imbalance
• Iron deficiency anemia
• Hypoalbuminemia (from protein-losing enteropathy)
• Failure to thrive (especially in infants with FPIES)

• The prognosis of allergic colitis is excellent when it presents in infancy.
• The disease is benign, self-limiting, and resolves completely, with the child outgrowing the allergy with age.
• The prognosis for allergic colitis that presents in adolescence or adulthood is not fully understood.^[1][3][6]

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