Steatorrhea

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

Steatorrhea is the formation of non-solid feces. Stools may also float due to excess fat from malabsorption, have an oily appearance and be foul smelling. An oily anal leakage or some level of fecal incontinence may occur. There is increased fat excretion, which can be measured by determining the fecal fat level. While definitions have not been standardized, fat excretion in feces in excess of 0.3 (g/kg) / day is considered indicative of steatorrhea. Based on underlying etiology steatorrhea can be classified into 3 types, intestinal, biliary, and pancreatic steatorrhea. Steatorrhea occurs as a result of either defect of the normal architecture of digestive tract or defect of synthesis or secretion of enzymes required for metabolism fats. Steatorrhea may be caused by Celiac disease, choledocholithiasis, cystic fibrosis, exocrine pancreatic insufficiency, hypolipidemic drugs, inflammatory bowel disease, small bowel bacterial overgrowth syndrome. Common risk factors in the development of steatorrhea include Celiac disease, cystic fibrosis, exocrine pancreatic insufficiency, inflammatory bowel disease, small intestinal bacterial overgrowth, hypolipidemic drugs. If left untreated, steatorrhea can lead to severe malnutrition due to inability of gastrointestinal tract to absorb fat soluble vitamins and ultimately severe weight loss. Complication of steatorrhea include anemia, intestinal obstruction, weight loss. Prognosis of steatorrhea is generally good with appropriate treatment. The 72 hr-fecal fat determination is the gold standard test for the diagnosis of steatorrhea. Mild steatorrhea can manifest as passage of frothy, foul smelling stool, greasy in appearance and difficult to flush, abdominal pain, bloating, heart burn. if severe it may cause malnutrition , dehydration, anemia, muscle weakness, weight loss, skin problems, neurological problems, osteoporosis. Patients with steatorrhea usually appear emaciated secondary to loss of subcutaneous fat. Physical examination of patients with steatorrhea is usually remarkable for distended abdomen, orthostatic hypo-tension and ecchymoses, Chvostek sign and Trousseau sign secondary to hypocalcemia. There are no specific laboratory findings associated with steatorrhea. Management of steatorrhea include treatment of underlying etiology, control of diarrhea and correction of nutritional deficiencies. Surgery is usually reserved for patients with refractory or pre-malignant complications, such as Enteropathy Associated T-cell Lymphoma (EATL) and ulcerative jejunitis (UJ). Effective measures for the primary prevention of steatorrhea include smoking cessation, alcohol cessation, minimizing the use of certain medications, such as antibiotics, that can alter normal bowel flora, and consuming diet rich in dietary fiber.

The history of celiac disease dates back to late 1800’s when an english scientist described celiac disease. In October 1887, Samuel Gee, a pediatrician, was the first to describe in detail celiac disease and its association with fatty stools. In 1950, Wim Dicke’s colleagues, Weijers and Van de Kamer, presented a way to diagnose mal-absorption syndromes by using stool fat measurement. In late 1960’s case of idiopathic steatoeehea and reticulosis of the small bowel as a late complication was reported.

Steatorrhea may be classified based on etiology into 3 types, intestinal, biliary, and pancreatic steatorrhea.

Stearorhea can be defined as loss of undigested fat in stools. The processes can be invoked by either defect of the normal architecture of digestive tract or it may involve defect of synthesis or secretion of enzymes of GI tract which are needed to metabolize fatty content of food.

Steatorrhea may be caused by Celiac disease, choledocholithiasis, cystic fibrosis, exocrine pancreatic insufficiency, hypolipidemic drugs, inflammatory bowel disease, small bowel bacterial overgrowth syndrome.

Steatorrhea must be differentiated from other causes of mal-absorption such as cystic fibrosis, Hartnup’sdisease, Whipple’s disease, Zollinger Ellison syndrome, acrodermatitis enteropathica, intestinal lymphangiectasia.

The demographic measures of steatorrhea can be explained by independent causes of steatorrhea.

Common risk factors in the development of steatorrhea include: Celiac disease, cystic fibrosis, exocrine pancreatic insufficiency, inflammatory bowel disease, small intestinal bacterial overgrowth, hypolipidemic drugs

There is insufficient evidence to recommend routine screening for steatorrhea

If left untreated, steatorrhea can lead to severe malnutrition due to inability of gastrointestinal tract to absorb fat soluble vitamins and ultimately severe weight loss. Complication of steatorrhea include anemia, intestinal obstruction, weight loss. Prognosis of steatorrhea is generally good with appropriate treatment.

The 72 hr-fecal fat determination is the gold standard test for the diagnosis of steatorrhea

Mild steatorrhea can manifest as passage of frothy, foul smelling stool, greasy in appearance and difficult to flush, abdominal pain, bloating, heart burn. if severe it may cause malnutrition , dehydration,anemia, muscle weakness, weight loss, skin problems, neurological problems, osteoporosis.

Patients with steatorrhea usually appear emaciated secondary to loss of subcutaneous fat. Physical examination of patients with steatorrhea is usually remarkable for distended abdomen, orthostatic hypo-tension and ecchymoses, Chvostek sign and Trousseau sign secondary to hypocalcemia.

Quantitative analysis of fat in the stool may be helpful in the diagnosis of steatorrhea. The various tests that may be helpful in the diagnosis are acid steatocrit, near-infrared reflectance analysis (NIRA) and sudan III stain.

There are no x-ray findings associated with steatorrhea. However, there are x-ray findings depends on the underlying causes.

There are no CT scan findings associated with steatorrhea. However, there are CT scan findings depends on the underlying causes

There are no MRI findings associated with steatorrhea. However, there are MRI findings depends on the underlying causes.

There are no other diagnostic studies associated with steatorrhea. However, there are no other diagnostic studies depends on the underlying causes.

Management of steatorrhea include treatment of underlying etiology, control of diarrhea and correction of nutritional deficiencies.

Surgical intervention is usually not recommended for the management of steatorrhea. Surgery is usually reserved for patients with refractory or pre-malignant complications, such as Enteropathy Associated T-cell Lymphoma (EATL) and ulcerative jejunitis (UJ). EATL patients presenting with ulcerative lesions, stenotic lesions, and perforation needs surgical intervention. Surgery also serves as a pre-therapy in order to prevent perforation of the small bowel during chemotherapy in case of EATL. After surgery patients receive immunotherapy, chemotherapy and/or stem cell transplantation

Effective measures for the primary prevention of steatorrhea include smoking cessation, alcohol cessation, minimizing the use of certain medications, such as antibiotics, that can alter normal bowel flora, and consuming diet rich in dietary fiber.

Secondary preventive measures of steatorrhea are similar to primary preventive measures.

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

Steato means relating to fatty matter or tissue and rrhea means discharge; flow. So the word means flow of fatty matter. Malabsorption is a condition which is associated with impaired absorption of one or all dietary nutrients. There are multiple etiologies with diminished intestinal absorption. Many of them present with diarrhea, especially steatorrhea. Some of the main causes of steatorrhea are celiac disease, cystic fibrosis, pancreatic insufficiency, small intestinal bacterial overgrowth syndrome. The history of celiac disease dates back to late 1800’s when an english scientist described celiac disease.

• In October 1887, Samuel Gee, an English leading authority in pediatrics, gained the full credit of explanation of celiac disease, presenting a lecture named “celiac affection” to medical students; which was published next year.
• In 1950, Wim Dicke, a Dutch pediatrician, suggested in his doctoral thesis that elimination of wheat, rye, and oats from diet would result in reasonable cure of celiac disease. He also described the pathological factor gluten in pathophysiology of Celiac disease.^[1]d
• At the same time, Wim Dicke’s colleagues, Weijers and Van de Kamer, presented a way to diagnose celiac disease by using stool fat measurement.^[2]

• In late 1960’s case of idiopathic steatoeehea and reticulosis of the small bowel as a late complication was reported.^[3]
• Pancreatic enzyme replacement therapy for pancreatic exocrine insufficiency ia an important land mark in the 21st century.^[4]
• The CFTR gene was discovered first in 1989.
• In 1990, scientists successfully added cloned normal gene to Cystic Fibrosis cells in the laboratory, which corrected the chloride transportation.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Vindhya BellamKonda, M.B.B.S [2] Sunny Kumar MD [3]

Steatorrhea may be classified based on etiology into 3 types, intestinal, biliary, and pancreatic steatorrhea.

Steatorrhea may be classified based on etiology into 3 types, intestinal, biliary, and pancreatic steatorrhea.^[1][2][3][4]

• Intestinal causes:
  • Infections
  • Celiac disease
  • Food allergies
  • Inflammatory disease
  • Short bowel syndrome
• Biliary tract causes:
  • Biliary atresia
  • Biliary Stricture
  • Tumor of biliary tract
  • Gallbladder stones
• Pancreatic causes:
  • Congenital lipase enzymes deficiency
  • Cystic fibrosis
  • Inflammation of pancreas
  • Pancreatic tumors

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Sunny Kumar MD [2]

Steatrorhea can be defined as loss of undigested fat in stools. The processes can be invoked by either defect of the normal architecture of digestive tract or it may involve defect of synthesis or secretion of enzymes of GI tract which are needed to metabolize fatty content of food.

To understand the pathophysiology of fat malabsoption we need to understand normal physiology of fat metabolization:^{[1][2][3][4][5][6][7][8]}

• Absorption of fat requires a complex interaction of
  • Digestive enzymes
  • Bile salts
  • An intact intestinal mucosa
• Ingested fats are initially emulsified in the stomach.
• By the action of digestive enzymes emulsified lipids are hydrolyzed subsequently.
• Once hydrolyzed, they aggregate to form micelles with the help of bile salts.
• These micelles are absorbed across the intact intestinal villi of proximal small intestine.
• After absorption, micelles are packaged into chylomicrons within intestinal epithelial cells and transported to the circulation via the lymphatic system.

Any disturbance in the normal physiology results in decreased absorption of the fats.

• Disturbance in intact intestinal mucosa
  • Marked acceleration of intestinal transit can increase nutrient malabsorption and induce symptoms due to:
    • High osmotic load
    • Increased bacterial metabolism in the colon
  • Delayed intestinal transit may promote small intestinal bacterial overgrowth.
  • This bacterial overgrowth also causes malnutrition by consuming ingested nutrients.
  • In addition, de-conjugation of bile acids also sets in by the action of bacterial enzymes
    • Compromises bile acid absorption in the terminal ileum
    • Depletes the bile acid pool
    • Disturb lipid absorption

• Impaired Bile Acid Synthesis and Secretion
  • Bile acids support the emulsification of triglycerides and form micelles with fatty acids and monoglycerides to enable absorption from the intestinal lumen.
  • Thus, decreased luminal availability may result in or contribute to steatorrhea.
  • While there are rare inborn errors of bile acid synthesis and transport
    • Interruption of the enterohepatic circulation is the clinically most important pathomechanism which leads to decreased luminal availability of bile acids and lipid malabsorption.

The development of steatorrhea is the result of multiple genetic mutations. Common genetic conditions associated with steatorrhea include:

• Cystic fibrosis
• Crohn’s disease
• Ulcerative colitis
• Abetalipoproteinemia 

On gross pathology the gastro-intestinal tract looks normal in conditions which involves enzyme deficiencies. However in condition which involves obstruction of ducts involved in secretion of enzymes will look narrowed. The luminal causes which damage the luman of GIT and does not allow the absoption of faty products will also look ulcerated.

On microscopy the GIT looks normal in conditions which involves enzyme deficiencies. However in condition which involves obstruction of ducts involved in secretion of enzymes will look narrowed. The luminal causes which damage the luman of GIT and does not allow the absoption of faty products will also look ulcerated.

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

Steatorrhea may be caused by Celiac disease, choledocholithiasis, cystic fibrosis, exocrine pancreatic insufficiency, hypolipidemic drugs, inflammatory bowel disease, small bowel bacterial overgrowth syndrome.

Steatorrhea may be caused by.^{[1][2][3][4][5]}

• Celiac disease
• Choledocholithiasis
• Cystic fibrosis
• Exocrine pancreatic insufficiency
• Hypolipidemic drugs
• Inflammatory bowel disease 
• Small bowel bacterial overgrowth syndrome

Less common causes of steatorrhea include:^[6][7][8][9]

• Olestra
• Orlistat
• Jojoba oil
• Escolar and oilfish

Cardiovascular	No underlying causes
Chemical/Poisoning	No underlying causes
Dental	No underlying causes
Dermatologic	No underlying causes
Drug Side Effect	Hypolipidemic agent,  Lanreotide,  Octreotide.
Ear Nose Throat	No underlying causes
Endocrine	Graves’ disease,  Hyperthyroidism,
Environmental	No underlying causes
Gastroenterologic	Angiodysplasia, Bacterial overgrowth, Celiac disease, Cholecystectomy, Choledocholithiasis, Chronic atrophic gastritis, Chronic pancreatitis, Diverticulosis, Inflammatory bowel disease, Mesenteric ischemia, Post-gastrectomy, Post-vagotomy, Primary bile acid malabsorption  , Primary sclerosing cholangitis, Radiation enteropathy, Short bowel syndrome, Strictures.
Genetic	Abetalipoproteinemia, Cystic fibrosis  , Diacylglycerol acyltransferase 1 deficiency, Johanson-blizzard syndrome  , Pancreatic lipase deficiency, Pearson syndrome, Shwachman-Diamond syndrome.
Hematologic	No underlying causes
Iatrogenic	No underlying causes
Infectious Disease	Fish tape worm, Giardiasis  , HIV related malabsorption, Hookworm, Round worm, Tropical sprue, Whipple’s disease
Musculoskeletal/Orthopedic	No underlying causes
Neurologic	No underlying causes
Nutritional/Metabolic	No underlying causes
Obstetric/Gynecologic	No underlying causes
Oncologic	Colorectal cancer, Pancreatic cancer, Zollinger-Ellison syndrome.
Ophthalmologic	No underlying causes
Overdose/Toxicity	No underlying causes
Psychiatric	No underlying causes
Pulmonary	No underlying causes
Renal/Electrolyte	No underlying causes
Rheumatology/Immunology/Allergy	Systemic sclerosis
Sexual	No underlying causes
Trauma	No underlying causes
Urologic	No underlying causes
Miscellaneous	Natural fats (Butterfish, Escolar, Oilfish), Artificial fats (Olestra).

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Vindhya BellamKonda, M.B.B.S [2] Aravind Reddy Kothagadi M.B.B.S[3]

Steatorrhea must be differentiated from other causes of mal-absorption such as cystic fibrosis, Hartnup’sdisease, Whipple’s disease, Zollinger Ellison syndrome, acrodermatitis enteropathica, intestinal lymphangiectasia.

The following table outlines the major differential diagnoses of malabsorption.^{[1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30]}

Categories		Cause		Clinical manifestation									Lab findings
				Symptoms								Findings
				Duration		Diarrhea			Fever	Abdominal pain	Weight loss
													Stool exam	CBC
				Acute	Chronic	Watery	Bloody	Fatty						WBC	Hgb	Plt
Gastrointestinal		Crohn’s disease		–	+	+	+	+	±	+	+	Abdominal tenderness Oral mucosal lesions Uveitis Arthritis Erythema nodosum Pyoderma gangrenosum	WBC + RBC +	↑	↓	↑
		Ulcerative colitis		–	+	+	+	+	±	+	+	Abdominal tenderness Blood on rectal examination Skin rash Iritis Uveitis Seronegative arthritis	WBC + RBC +	↑	↓	↑
		Celiac disease		–	+	±	–	±	–	+	+	Abdominal distention Increased bowel sounds Oral mucosal lesions Hepatosplenomegaly Ascites Dementia Dermatitis herpetiformis	Fat droplets on sudan stain	Nl	↓	Nl
		Cause		Duration		Diarrhea			Fever	Abdominal pain	Weight loss	Findings	Stool exam	CBC
				Acute	Chronic	Watery	Bloody	Fatty						WBC	Hgb	Plt
		Cystic fibrosis		–	+	–	–	+	±	+	+	Abdominal distention Hepatosplenomegaly Rectal prolapse Recurrent respiratory tract infection Bronchiectasis	Fat droplets on sudan stain	Nl	↓	Nl
		Chronic pancreatitis		–	+	+	–	+	–	+	+	Abdominal tenderness Pancreatic pseudocyst Diabetes mellitus	Fat droplets on sudan stain Fecal elastase +	Nl	Nl	Nl
		Bile acid malabsorption		–	+	+	–	+	–	–	+	Malabsorption Hypotension Tachycardia	Fat droplets on sudan stain	Nl	Nl	Nl
		Lactose intolerance		+	+	+	–	–	–	+	–	Abdominal tenderness Abdominal distention Headache Vertigo Memory impairment Lethargy	–	Nl	Nl	Nl
Infection	Bacterial	Cause		Duration		Diarrhea			Fever	Abdominal pain	Weight loss	Findings	Stool exam	CBC
				Acute	Chronic	Watery	Bloody	Fatty						WBC	Hgb	Plt
		Whipple’s disease		–	+	+	–	+	±	+	+	Hepatosplenomegaly Ascites Abnormal extraocular movement Lymphadenopathy Hyperpigmentation Uveitis Endocarditis Encephalitis Dementia	Fecal fat +	↓	↓	↓/↑
		Tropical sprue		+	+	+	–	+	+	+	+	Angular stomatitis Oral mucosal lesion Myalgia Neuropathy Edema	WBC + Stool culture +	Nl	↓	Nl
		Small bowel bacterial overgrowth		–	+	+	–	+	–	+	+	Abdominal distention Rosacea	WBC + Stool culture + Fecal fat +	Nl	↓	Nl
		Cause		Duration		Diarrhea			Fever	Abdominal pain	Weight loss	Findings	Stool exam	CBC
				Acute	Chronic	Watery	Bloody	Fatty						WBC	Hgb	Plt
	Virus	HIV		–	+	+	–	–	+	+	+	Abdominal distention Diffuse abdominal tenderness Lymphadenopathy Disseminated infection	WBC +	↓	↓	Nl
	Parasite	Giardia		–	+	+	–	+	–	+	+	Abdominal distention Diffuse abdominal tenderness Urticaria Depression	Ova +	Nl	Nl	Nl
		Isospora		+	+	+	–	+	+	+	+	Abdominal distention Diffuse abdominal tenderness	WBC + RBC + Ova + Fecal fat +	↑	Nl	Nl
Tumors		VIPoma		+	+	+	–	+	–	+	+	Abdominal distention Abdominal RUQ tenderness Nausea Vomiting Rash Facial flushing Dehydration Lethargy Muscle weakness	–	Nl	Nl	Nl
		Zollinger–Ellison syndrome		–	+	+	+	+	–	+	+	Epigastric tenderness Jaundice	–	Nl	↓	Nl
		Cause		Duration		Diarrhea			Fever	Abdominal pain	Weight loss	Findings	Stool exam	CBC
				Acute	Chronic	Watery	Bloody	Fatty						WBC	Hgb	Plt
		Lymphoma		–	+	+	+	–	+	+	+	Diffuse abdominal tenderness Hepatosplenomegaly Ascites	RBC +	Nl	↓	Nl
Medication/Toxicity		ACE inhibitors Digoxin Cephalosporins Statins Thiazide diuretics Triptans Lactulose Anti retroviral agents Chemotherapeutic agents Antifungals Magnesium		+	+	+	–	±	±	+	+	Abdominal distention Dehydration	–	↑	Nl	Nl
Iatrogenic		Short bowel syndrome		+	+	+	–	+	–	–	+	Abdominal distention Abdominal tenderness Prior intestinal surgery Peripheral edema Muscle atrophy	Fecal fat +	Nl	↓	↑
		Radiation enteritis		+	+	+	+	+	–	+	+	Abdominal tenderness Prior history of malignancy and radiation therapy Telangiectasias	WBC + RBC + Fecal fat +	Nl	↓	Nl
Others		Cause		Duration		Diarrhea			Fever	Abdominal pain	Weight loss	Findings	Stool exam	CBC
				Acute	Chronic	Watery	Bloody	Fatty						WBC	Hgb	Plt
		Abetalipoproteinemia		–	+	+	–	+	–	+	+	Abdominal distension Ataxia Visual field defect Dysarthria	–	Nl	Nl	Nl
		Hyperthyroidism		–	+	+	–	–	±	+	+	Lump in the neck Lid lag Sweating Hyperpigmentation Proptosis Tremor Increased DTR	Fecal fat +	Nl	Nl	Nl
		Diabetic neuropathy		–	+	+	–	+	–	+	+	Fecal incontinence	Fecal fat +	Nl	↓	Nl
		Systemic sclerosis		–	+	+	±	+	–	+	+	Epigastric tenderness Fecal incontinence Raynaud phenomenon Pulmonary hypertension Arthritis Telangiectasia Chronic renal failure	RBC + Fecal fat +	Nl	↓	Nl

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sunny Kumar MD [2]

The demographic measures of steatorrhea can be explained by independent causes of steatorrhea.

Following are common causes and their independent demographic variables.

• The incidence of celiac disease is approximately 10-13 per 100,000 individuals worldwide.
• In United States the incidence of celiac disease is approximately 10 per 100,000 individuals.
• The incidence of celiac disease has been increasing over the years. This can be attributed to increasing use of serologic screening, leading to more accurate results and early diagnosis in cases of mild disease. A general trend in incidence of celiac disease over the years is as under:
  • In 1950, the incidence of celiac disease was estimated to be 1 case per 100,000 individuals worldwide.
  • In 1960-1980, the incidence of celiac disease was estimated to be 2 cases per 100,000 individuals worldwide.
  • In 1990, the incidence of celiac disease was estimated to be 3-5 cases per 100,000 individuals worldwide.
  • In 2000, the incidence of celiac disease was estimated to be 9 cases per 100,000 individuals worldwide.

• Worldwide, the prevalence of celiac disease is estimated to be 500 to 1000 per 100,000 individuals.
• In United States, the prevalence of celiac disease is approximately 710 per 100,000 individuals.
• The overall prevalence of celiac disease has been increasing in United States from 170 per 100,000 individuals in 1988 to 440 per 100,000 individuals in 2012.
• In Europe the prevalence of celiac disease is estimated to be 1000 per 100,000 individuals. The Scandinavian countries, Ireland, and the United Kingdom population tended to show a higher prevalenceof celiac disease of approximately 1000 to 1500 per 100,000 individuals.
• In Australia the prevalence of celiac disease is estimated to be 400 per 100,000 individuals.
• In New Zealand the prevalence of celiac disease is estimated to be 1200 per 100,000 individuals.
• In India the prevalence of celiac disease is estimated to be 300 per 100,000 individuals.
• In North Africa, Algeria with its refugees in the Sahara desert have the highest prevalence of celiac disease at 5600 per 100,000 individuals.

• The risk for celiac disease is higher for people with diabetes, autoimmune disorder and relatives with celiac disease individuals because of shared HLA typing.

• Celiac disease affects children and adults alike.
• In children celiac disease peaks in early childhood.
• In adults celiac disease is usually diagnosed around fourth and fifth decades of life.

• Celiac disease usually affects individuals of the non-Hispanic white race (1000 per 100,000 individuals), Hispanics (300 per 100,000 individuals) and non-Hispanic blacks (200 per 100,000 individuals).
• HLA-DQ2 associated celiac disease is frequently found in white populations located in Western Europe.

• Women are more commonly affected by celiac disease than men.
• The female to male ratio is approximately 3:1.
• In contrast, patients over the age of 60 who are diagnosed with celiac disease are most commonly males.

• Tthe highest prevalence of celiac disease has been reported in Algerian refugees. These individuals have a high rate of consanguinity and high frequencies of HLA-DQ2.

Cystic fibrosis (CF) is an autosomal recessive disorder whose incidence has long been estimated as 1/2500 live births in Caucasians.

Epidemiology and demographics of small intestinal bacterial overgrowth is as follows: 

• Small intestinal bacterial overgrowth is more commonly observed among elderly patients.

• Small intestinal bacterial overgrowth (SIBO) affects men and women equally.

• There is no racial predilection for small intestinal bacterial overgrowth (SIBO).

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

Common risk factors in the development of steatorrhea include Celiac disease, cystic fibrosis, exocrine pancreatic insufficiency, inflammatory bowel disease, small intestinal bacterial overgrowth, hypolipidemic drugs

• Common risk factors in the development of Steatorrhea include:
  • Celiac disease
  • Cystic fibrosis^[1]
  • Exocrine pancreatic insufficieny
  • Inflammatory bowel disease
  • Small intestinal bacterial overgrowth
  • Hypolipidemic drugs

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

There is insufficient evidence to recommend routine screening for steatorrhea

There is insufficient evidence to recommend routine screening for steatorrhea

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Vindhya BellamKonda, M.B.B.S [2]Sunny Kumar MD [3]

If left untreated, steatorrhea can lead to severe malnutrition due to inability of gastrointestinal tract to absorb fat soluble vitamins and ultimately severe weight loss. Complication of steatorrhea include anemia, intestinal obstruction, weight loss. Prognosis of steatorrhea is generally good with appropriate treatment.

If left untreated, steatorrhea can lead to severe malnutrition due to inability of gastrointestinal tract to absorb fat soluble vitamins and ultimately severe weight loss.atorrhea:^[1][2][3]

Complication of steatorrhea include:^[4][5]

• Adults
  • Anemia
  • Intestinal obstruction
  • Weight loss

• Children
  • Failure to thrive
  • Anemia
  • Weight loss

Prognosis of steatorrhea is generally good with appropriate treatment.

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