DDSEP® 8 Quick Quiz

Q2. Correct answer: D. Glucose hydrogen breath test. 

Rationale  
The etiology of small intestinal bacterial overgrowth (SIBO) is complex but may include an issue with altered antibacterial defense mechanisms, such as achlorhydria from atrophic gastritis. SIBO can be diagnosed by a glucose hydrogen breath test, and therefore, it is the best next step in the management of this patient's symptoms given the history of atrophic gastritis. Chromogranin A testing and video capsule endoscopy are used in the diagnostic evaluation of suspected carcinoid syndrome and inflammatory bowel disease, respectively, and may be indicated in the subsequent evaluation of this patient's symptoms. In addition, both of these diagnoses are unlikely to cause intermittent diarrhea. Eluxadoline is an agent that combines a mu-opioid receptor agonist and a delta-opioid receptor antagonist and is indicated for the treatment of irritable bowel syndrome - diarrhea predominant (IBS-D). The diagnosis of IBS requires the presence of abdominal pain and is unlikely in an elderly patient with new onset of symptoms; therefore, this is not the diagnosis in this patient's case.  
 
Reference  
Jan Bures et al. World J Gastroenterol. 2010 Jun 28;16(24):2978-90.

Q2. Correct answer: D. Glucose hydrogen breath test. 

Rationale  
The etiology of small intestinal bacterial overgrowth (SIBO) is complex but may include an issue with altered antibacterial defense mechanisms, such as achlorhydria from atrophic gastritis. SIBO can be diagnosed by a glucose hydrogen breath test, and therefore, it is the best next step in the management of this patient's symptoms given the history of atrophic gastritis. Chromogranin A testing and video capsule endoscopy are used in the diagnostic evaluation of suspected carcinoid syndrome and inflammatory bowel disease, respectively, and may be indicated in the subsequent evaluation of this patient's symptoms. In addition, both of these diagnoses are unlikely to cause intermittent diarrhea. Eluxadoline is an agent that combines a mu-opioid receptor agonist and a delta-opioid receptor antagonist and is indicated for the treatment of irritable bowel syndrome - diarrhea predominant (IBS-D). The diagnosis of IBS requires the presence of abdominal pain and is unlikely in an elderly patient with new onset of symptoms; therefore, this is not the diagnosis in this patient's case.  
 
Reference  
Jan Bures et al. World J Gastroenterol. 2010 Jun 28;16(24):2978-90.

Q2. Correct answer: D. Glucose hydrogen breath test. 

Rationale  
The etiology of small intestinal bacterial overgrowth (SIBO) is complex but may include an issue with altered antibacterial defense mechanisms, such as achlorhydria from atrophic gastritis. SIBO can be diagnosed by a glucose hydrogen breath test, and therefore, it is the best next step in the management of this patient's symptoms given the history of atrophic gastritis. Chromogranin A testing and video capsule endoscopy are used in the diagnostic evaluation of suspected carcinoid syndrome and inflammatory bowel disease, respectively, and may be indicated in the subsequent evaluation of this patient's symptoms. In addition, both of these diagnoses are unlikely to cause intermittent diarrhea. Eluxadoline is an agent that combines a mu-opioid receptor agonist and a delta-opioid receptor antagonist and is indicated for the treatment of irritable bowel syndrome - diarrhea predominant (IBS-D). The diagnosis of IBS requires the presence of abdominal pain and is unlikely in an elderly patient with new onset of symptoms; therefore, this is not the diagnosis in this patient's case.  
 
Reference  
Jan Bures et al. World J Gastroenterol. 2010 Jun 28;16(24):2978-90.

Q1. Correct answer: B. Expulsion of water-filled balloon in 3 minutes.  

Rationale  
The balloon expulsion test is highly suggestive of dyssynergia. A balloon expulsion time of greater than 2 minutes is abnormal. An absent RAIR can be seen in Hirschsprung's disease or megarectum. Defecation index equals maximum rectal pressure during attempted defecation divided by minimum anal residual pressure during attempted defecation. A normal defecation index is greater than 1.5. Decreased anal sphincter pressure during simulated defecation is normal and therefore not consistent with dyssynergic defecation.  
 
References  
Wald A et al. Am J Gastroenterol. 2014 Aug;109(8):1141-57.  
Bharucha AE et al. Gastroenterology. 2013 Jan;144(1):218-38.

Q1. Correct answer: B. Expulsion of water-filled balloon in 3 minutes.  

Rationale  
The balloon expulsion test is highly suggestive of dyssynergia. A balloon expulsion time of greater than 2 minutes is abnormal. An absent RAIR can be seen in Hirschsprung's disease or megarectum. Defecation index equals maximum rectal pressure during attempted defecation divided by minimum anal residual pressure during attempted defecation. A normal defecation index is greater than 1.5. Decreased anal sphincter pressure during simulated defecation is normal and therefore not consistent with dyssynergic defecation.  
 
References  
Wald A et al. Am J Gastroenterol. 2014 Aug;109(8):1141-57.  
Bharucha AE et al. Gastroenterology. 2013 Jan;144(1):218-38.

Q1. Correct answer: B. Expulsion of water-filled balloon in 3 minutes.  

Rationale  
The balloon expulsion test is highly suggestive of dyssynergia. A balloon expulsion time of greater than 2 minutes is abnormal. An absent RAIR can be seen in Hirschsprung's disease or megarectum. Defecation index equals maximum rectal pressure during attempted defecation divided by minimum anal residual pressure during attempted defecation. A normal defecation index is greater than 1.5. Decreased anal sphincter pressure during simulated defecation is normal and therefore not consistent with dyssynergic defecation.  
 
References  
Wald A et al. Am J Gastroenterol. 2014 Aug;109(8):1141-57.  
Bharucha AE et al. Gastroenterology. 2013 Jan;144(1):218-38.

Correct answer: B. Prednisone  

Rationale  
This is a case of Henoch-Schönlein purpura, which is a self-limited, systemic, nongranulomatous, autoimmune complex, small-vessel vasculitis with multiorgan involvement. It is characterized by a classic tetrad of nonthrombocytopenic palpable purpura, arthritis or arthralgias, gastrointestinal involvement, and renal involvement. GI involvement may mimic Crohn's disease, although the biopsies are usually diagnostic. Most cases are self-limiting, but oral steroids are indicated in patients with severe colicky abdominal pain; usually they're started as prednisone or methylprednisolone at 1-2 mg/kg per day for 1-2 weeks and then tapering to a stop in the next 1-2 weeks. Steroids may prevent major complications such as gastrointestinal bleeding or intussusception. Immunosuppressive drugs (cyclophosphamide, azathioprine, cyclosporine A, and mycophenolate mofetil) in combination with high-dose IV pulse steroids are recommended if there is no benefit from steroids alone.  
 
Reference  
Sohagia AB et al. Gastroenterol Res Pract. 2010. doi: 10.1155/2010/59764. 
 

Correct answer: B. Prednisone  

Rationale  
This is a case of Henoch-Schönlein purpura, which is a self-limited, systemic, nongranulomatous, autoimmune complex, small-vessel vasculitis with multiorgan involvement. It is characterized by a classic tetrad of nonthrombocytopenic palpable purpura, arthritis or arthralgias, gastrointestinal involvement, and renal involvement. GI involvement may mimic Crohn's disease, although the biopsies are usually diagnostic. Most cases are self-limiting, but oral steroids are indicated in patients with severe colicky abdominal pain; usually they're started as prednisone or methylprednisolone at 1-2 mg/kg per day for 1-2 weeks and then tapering to a stop in the next 1-2 weeks. Steroids may prevent major complications such as gastrointestinal bleeding or intussusception. Immunosuppressive drugs (cyclophosphamide, azathioprine, cyclosporine A, and mycophenolate mofetil) in combination with high-dose IV pulse steroids are recommended if there is no benefit from steroids alone.  
 
Reference  
Sohagia AB et al. Gastroenterol Res Pract. 2010. doi: 10.1155/2010/59764. 
 

Correct answer: B. Prednisone  

Rationale  
This is a case of Henoch-Schönlein purpura, which is a self-limited, systemic, nongranulomatous, autoimmune complex, small-vessel vasculitis with multiorgan involvement. It is characterized by a classic tetrad of nonthrombocytopenic palpable purpura, arthritis or arthralgias, gastrointestinal involvement, and renal involvement. GI involvement may mimic Crohn's disease, although the biopsies are usually diagnostic. Most cases are self-limiting, but oral steroids are indicated in patients with severe colicky abdominal pain; usually they're started as prednisone or methylprednisolone at 1-2 mg/kg per day for 1-2 weeks and then tapering to a stop in the next 1-2 weeks. Steroids may prevent major complications such as gastrointestinal bleeding or intussusception. Immunosuppressive drugs (cyclophosphamide, azathioprine, cyclosporine A, and mycophenolate mofetil) in combination with high-dose IV pulse steroids are recommended if there is no benefit from steroids alone.  
 
Reference  
Sohagia AB et al. Gastroenterol Res Pract. 2010. doi: 10.1155/2010/59764. 
 

Correct answer: D. Antienterocyte antibodies 

Rationale  
Autoimmune enteropathy (AIE) is characterized by a severe malabsorption and secretory diarrhea, and is differentiated from celiac disease on small-bowel biopsy by the decreased numbers or absence of surface intraepithelial lymphocytes, apoptotic bodies present in the intestinal crypts, and absent goblet and Paneth cells. Patients with AIE may also carry other autoimmune conditions such as rheumatoid arthritis and multiple sclerosis. A group at the Mayo Clinic has published a set of diagnostic criteria based on their case series of adult AIE that requires ruling out other causes of chronic diarrhea in adults, specific histology supportive of AIE, and presence of malabsorption and ruling out other causes of villous atrophy. The presence of antienterocyte or antigoblet cell antibodies are supportive of a diagnosis of AIE, but their absence does not exclude the diagnosis.  
 
References  
Akram S et al. Clin Gastroenterol Hepatol. 2007;5(11):1282-90.  
Montalto M et al. Scan J Gastroenterol. 2009;44(9):1029-36.

Correct answer: D. Antienterocyte antibodies 

Rationale  
Autoimmune enteropathy (AIE) is characterized by a severe malabsorption and secretory diarrhea, and is differentiated from celiac disease on small-bowel biopsy by the decreased numbers or absence of surface intraepithelial lymphocytes, apoptotic bodies present in the intestinal crypts, and absent goblet and Paneth cells. Patients with AIE may also carry other autoimmune conditions such as rheumatoid arthritis and multiple sclerosis. A group at the Mayo Clinic has published a set of diagnostic criteria based on their case series of adult AIE that requires ruling out other causes of chronic diarrhea in adults, specific histology supportive of AIE, and presence of malabsorption and ruling out other causes of villous atrophy. The presence of antienterocyte or antigoblet cell antibodies are supportive of a diagnosis of AIE, but their absence does not exclude the diagnosis.  
 
References  
Akram S et al. Clin Gastroenterol Hepatol. 2007;5(11):1282-90.  
Montalto M et al. Scan J Gastroenterol. 2009;44(9):1029-36.

Correct answer: D. Antienterocyte antibodies 

Rationale  
Autoimmune enteropathy (AIE) is characterized by a severe malabsorption and secretory diarrhea, and is differentiated from celiac disease on small-bowel biopsy by the decreased numbers or absence of surface intraepithelial lymphocytes, apoptotic bodies present in the intestinal crypts, and absent goblet and Paneth cells. Patients with AIE may also carry other autoimmune conditions such as rheumatoid arthritis and multiple sclerosis. A group at the Mayo Clinic has published a set of diagnostic criteria based on their case series of adult AIE that requires ruling out other causes of chronic diarrhea in adults, specific histology supportive of AIE, and presence of malabsorption and ruling out other causes of villous atrophy. The presence of antienterocyte or antigoblet cell antibodies are supportive of a diagnosis of AIE, but their absence does not exclude the diagnosis.  
 
References  
Akram S et al. Clin Gastroenterol Hepatol. 2007;5(11):1282-90.  
Montalto M et al. Scan J Gastroenterol. 2009;44(9):1029-36.

Q2. Correct answer: E  

Rationale  
This patient has nausea and vomiting of pregnancy (NVP), and has tried conservative management. Doxylamine and vitamin B6 have been found to be safe and effective for NVP and are considered first-line therapy. Further testing with gastric-emptying study is not necessary because NVP has a high prevalence at weeks 4-6 of gestation and peaks at week 9-16. A nuclear test such as gastric emptying is not appropriate during pregnancy, though decreased gastric emptying due to estrogen and progesterone is thought to be related to NVP. Upper endoscopy would be considered if the nausea and vomiting is refractory. Ondansetron can be considered, but there have been some questions raised regarding safety and it is not considered first line. Meals high in protein have been found to decrease nausea more that carbohydrate-rich meals.  
 
Reference  
ACOG Committee on Practice Bulletins-Obstetrics. Obstet Gynecol. 2018 Jan;131(1):e15-e30.

Q2. Correct answer: E  

Rationale  
This patient has nausea and vomiting of pregnancy (NVP), and has tried conservative management. Doxylamine and vitamin B6 have been found to be safe and effective for NVP and are considered first-line therapy. Further testing with gastric-emptying study is not necessary because NVP has a high prevalence at weeks 4-6 of gestation and peaks at week 9-16. A nuclear test such as gastric emptying is not appropriate during pregnancy, though decreased gastric emptying due to estrogen and progesterone is thought to be related to NVP. Upper endoscopy would be considered if the nausea and vomiting is refractory. Ondansetron can be considered, but there have been some questions raised regarding safety and it is not considered first line. Meals high in protein have been found to decrease nausea more that carbohydrate-rich meals.  
 
Reference  
ACOG Committee on Practice Bulletins-Obstetrics. Obstet Gynecol. 2018 Jan;131(1):e15-e30.

Q2. Correct answer: E  

Rationale  
This patient has nausea and vomiting of pregnancy (NVP), and has tried conservative management. Doxylamine and vitamin B6 have been found to be safe and effective for NVP and are considered first-line therapy. Further testing with gastric-emptying study is not necessary because NVP has a high prevalence at weeks 4-6 of gestation and peaks at week 9-16. A nuclear test such as gastric emptying is not appropriate during pregnancy, though decreased gastric emptying due to estrogen and progesterone is thought to be related to NVP. Upper endoscopy would be considered if the nausea and vomiting is refractory. Ondansetron can be considered, but there have been some questions raised regarding safety and it is not considered first line. Meals high in protein have been found to decrease nausea more that carbohydrate-rich meals.  
 
Reference  
ACOG Committee on Practice Bulletins-Obstetrics. Obstet Gynecol. 2018 Jan;131(1):e15-e30.

Q1. Correct answer: E 

Rationale  
Transient lower esophageal sphincter relaxation (TLESR) is a physiologic phenomenon that allows venting of swallowed air from the stomach in response to distension of the proximal stomach. Patients with GERD typically reflux gastric content through a compliant esophagogastric junction into the esophagus during a TLESR; the frequency of TLESRs may also be higher in patients with GERD. TLESRs are suppressed during deep sleep, and are less frequent when LES relaxation is abnormal (e.g., esophageal outflow obstruction). Baclofen, a GABAB receptor agonist, can reduce TLESR frequency, and can reduce reflux episodes in patients with reflux. Obese patients and those with obstructive sleep apnea can have increased frequency of TLESRs. The frequency of TLESR is not related to degree of gastric acid secretion in the stomach.  
 
References  
Kuribayashi S et al. Neurogastroenterol Motil. 2010 Jun;22(6):611-e172.  
Hershcovici T et al. Neurogastroenterol Motil. 2011 Sep;23(9):819-30.

Q1. Correct answer: E 

Rationale  
Transient lower esophageal sphincter relaxation (TLESR) is a physiologic phenomenon that allows venting of swallowed air from the stomach in response to distension of the proximal stomach. Patients with GERD typically reflux gastric content through a compliant esophagogastric junction into the esophagus during a TLESR; the frequency of TLESRs may also be higher in patients with GERD. TLESRs are suppressed during deep sleep, and are less frequent when LES relaxation is abnormal (e.g., esophageal outflow obstruction). Baclofen, a GABAB receptor agonist, can reduce TLESR frequency, and can reduce reflux episodes in patients with reflux. Obese patients and those with obstructive sleep apnea can have increased frequency of TLESRs. The frequency of TLESR is not related to degree of gastric acid secretion in the stomach.  
 
References  
Kuribayashi S et al. Neurogastroenterol Motil. 2010 Jun;22(6):611-e172.  
Hershcovici T et al. Neurogastroenterol Motil. 2011 Sep;23(9):819-30.

Q1. Correct answer: E 

Rationale  
Transient lower esophageal sphincter relaxation (TLESR) is a physiologic phenomenon that allows venting of swallowed air from the stomach in response to distension of the proximal stomach. Patients with GERD typically reflux gastric content through a compliant esophagogastric junction into the esophagus during a TLESR; the frequency of TLESRs may also be higher in patients with GERD. TLESRs are suppressed during deep sleep, and are less frequent when LES relaxation is abnormal (e.g., esophageal outflow obstruction). Baclofen, a GABAB receptor agonist, can reduce TLESR frequency, and can reduce reflux episodes in patients with reflux. Obese patients and those with obstructive sleep apnea can have increased frequency of TLESRs. The frequency of TLESR is not related to degree of gastric acid secretion in the stomach.  
 
References  
Kuribayashi S et al. Neurogastroenterol Motil. 2010 Jun;22(6):611-e172.  
Hershcovici T et al. Neurogastroenterol Motil. 2011 Sep;23(9):819-30.

Q2. Correct answer: D  
 
Rationale  
Deficient intake of fiber and folate may originate in the food choice of the individual, whereas some deficiencies of intake, such as thiamine, appear to be celiac specific. The provider should encourage intake of nutrient-dense foods including wholegrain foods, enriched if possible, legumes, fruits, vegetables, lean meat, fish, chicken, and eggs. It is not necessary to prioritize micronutrient supplements over achieving nutritional adequacy through dietary intake. Iron deficiency is an effect of untreated celiac disease.  
 
Reference  
1. Shepherd SJ, Gibson PR. J Human Nutr Dietet. 2012;26:349-58. 
 

Q2. Correct answer: D  
 
Rationale  
Deficient intake of fiber and folate may originate in the food choice of the individual, whereas some deficiencies of intake, such as thiamine, appear to be celiac specific. The provider should encourage intake of nutrient-dense foods including wholegrain foods, enriched if possible, legumes, fruits, vegetables, lean meat, fish, chicken, and eggs. It is not necessary to prioritize micronutrient supplements over achieving nutritional adequacy through dietary intake. Iron deficiency is an effect of untreated celiac disease.  
 
Reference  
1. Shepherd SJ, Gibson PR. J Human Nutr Dietet. 2012;26:349-58. 
 

Q2. Correct answer: D  
 
Rationale  
Deficient intake of fiber and folate may originate in the food choice of the individual, whereas some deficiencies of intake, such as thiamine, appear to be celiac specific. The provider should encourage intake of nutrient-dense foods including wholegrain foods, enriched if possible, legumes, fruits, vegetables, lean meat, fish, chicken, and eggs. It is not necessary to prioritize micronutrient supplements over achieving nutritional adequacy through dietary intake. Iron deficiency is an effect of untreated celiac disease.  
 
Reference  
1. Shepherd SJ, Gibson PR. J Human Nutr Dietet. 2012;26:349-58. 
 

Correct answer: C  
 
Rationale  
According to the Multi-Society Task Force on Colorectal Cancer, colonoscopy should be performed 1 year after resection, and again 3 years later, in order to decrease the risk of metachronous colorectal cancer.  
 
Reference  
1. Kahi CJ, Boland CR, Dominitz JA. Gastroenterology. 2016. 150(3):758-68.e11.

Correct answer: C  
 
Rationale  
According to the Multi-Society Task Force on Colorectal Cancer, colonoscopy should be performed 1 year after resection, and again 3 years later, in order to decrease the risk of metachronous colorectal cancer.  
 
Reference  
1. Kahi CJ, Boland CR, Dominitz JA. Gastroenterology. 2016. 150(3):758-68.e11.

Correct answer: C  
 
Rationale  
According to the Multi-Society Task Force on Colorectal Cancer, colonoscopy should be performed 1 year after resection, and again 3 years later, in order to decrease the risk of metachronous colorectal cancer.  
 
Reference  
1. Kahi CJ, Boland CR, Dominitz JA. Gastroenterology. 2016. 150(3):758-68.e11.

Q2: Correct answer: D  
 
Rationale  
Episodic hepatic encephalopathy is usually precipitant induced in over 80% of cases and precipitants include dehydration, infections, over diuresis, gastrointestinal bleeding, constipation, and the use of narcotics and sedatives. The key is to identify and treat the precipitant. A diagnostic workup to rule out other disorders that can alter brain function and mimic hepatic encephalopathy should also be performed.  
 
Reference  
Viltstrup H et al. Hepatic encephalopathy in chronic liver disease: 2014 Practice Guideline by the American Association for the Study of Liver Diseases and the European Association for the Study of the Liver. Hepatology. 2014;60(2):715-35. 

Q2: Correct answer: D  
 
Rationale  
Episodic hepatic encephalopathy is usually precipitant induced in over 80% of cases and precipitants include dehydration, infections, over diuresis, gastrointestinal bleeding, constipation, and the use of narcotics and sedatives. The key is to identify and treat the precipitant. A diagnostic workup to rule out other disorders that can alter brain function and mimic hepatic encephalopathy should also be performed.  
 
Reference  
Viltstrup H et al. Hepatic encephalopathy in chronic liver disease: 2014 Practice Guideline by the American Association for the Study of Liver Diseases and the European Association for the Study of the Liver. Hepatology. 2014;60(2):715-35. 

Q2: Correct answer: D  
 
Rationale  
Episodic hepatic encephalopathy is usually precipitant induced in over 80% of cases and precipitants include dehydration, infections, over diuresis, gastrointestinal bleeding, constipation, and the use of narcotics and sedatives. The key is to identify and treat the precipitant. A diagnostic workup to rule out other disorders that can alter brain function and mimic hepatic encephalopathy should also be performed.  
 
Reference  
Viltstrup H et al. Hepatic encephalopathy in chronic liver disease: 2014 Practice Guideline by the American Association for the Study of Liver Diseases and the European Association for the Study of the Liver. Hepatology. 2014;60(2):715-35. 

Q1: Correct answer: B  
 
Rationale  
A serum ceruloplasmin less than 5 mg/L and a 24-hour urine copper excretion greater than 100 mcg/24 hours are both highly suggestive of Wilson's disease, a disorder of copper metabolism caused by a mutation in a P-type ATP-ase that mediates the excretion of copper into the bile. Treatment of Wilson's disease consists of copper chelation therapy. Commonly used therapies include D-penicillamine, trientine, and zinc. Patients on therapy should have 24-hour urine copper determination every 6-12 months. Patients on maintenance trientine or D-penicillamine should have urine copper excretion of 200-500 mcg/24 hours. Patients on zinc therapy should have much lower copper excretion, in the range of 75 mcg/24 hours.  
 
References  
1. European Association for the Study of the Liver. EASL clinical practice guidelines: Wilson's disease. J Hepatol. 2012;56:671-85.  
2. Roberts EA, Schilsky ML. Diagnosis and treatment of Wilson disease: An update. Hepatology. 2008;47:2089-111.

Q1: Correct answer: B  
 
Rationale  
A serum ceruloplasmin less than 5 mg/L and a 24-hour urine copper excretion greater than 100 mcg/24 hours are both highly suggestive of Wilson's disease, a disorder of copper metabolism caused by a mutation in a P-type ATP-ase that mediates the excretion of copper into the bile. Treatment of Wilson's disease consists of copper chelation therapy. Commonly used therapies include D-penicillamine, trientine, and zinc. Patients on therapy should have 24-hour urine copper determination every 6-12 months. Patients on maintenance trientine or D-penicillamine should have urine copper excretion of 200-500 mcg/24 hours. Patients on zinc therapy should have much lower copper excretion, in the range of 75 mcg/24 hours.  
 
References  
1. European Association for the Study of the Liver. EASL clinical practice guidelines: Wilson's disease. J Hepatol. 2012;56:671-85.  
2. Roberts EA, Schilsky ML. Diagnosis and treatment of Wilson disease: An update. Hepatology. 2008;47:2089-111.

Q1: Correct answer: B  
 
Rationale  
A serum ceruloplasmin less than 5 mg/L and a 24-hour urine copper excretion greater than 100 mcg/24 hours are both highly suggestive of Wilson's disease, a disorder of copper metabolism caused by a mutation in a P-type ATP-ase that mediates the excretion of copper into the bile. Treatment of Wilson's disease consists of copper chelation therapy. Commonly used therapies include D-penicillamine, trientine, and zinc. Patients on therapy should have 24-hour urine copper determination every 6-12 months. Patients on maintenance trientine or D-penicillamine should have urine copper excretion of 200-500 mcg/24 hours. Patients on zinc therapy should have much lower copper excretion, in the range of 75 mcg/24 hours.  
 
References  
1. European Association for the Study of the Liver. EASL clinical practice guidelines: Wilson's disease. J Hepatol. 2012;56:671-85.  
2. Roberts EA, Schilsky ML. Diagnosis and treatment of Wilson disease: An update. Hepatology. 2008;47:2089-111.