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The malabsorption syndrome, Treatment, Diagnosis, Evolution

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Definition of the malabsorption syndrome
The malabsorption syndrome represents a pathological situation characterized by a disorder of absorption, at small bowel level, of different nutritive compounds.
Malabsorption may be of pancreatic, hepatic or intestinal origin. Malabsorption syndrome may be caused by digestion disorder, with the secondary disorder of absorption(by hepatic, pancreatic causes) or may by ower directly to absorption disorder at the enteral level (in intestinal diseases).
In malabsorption, the most typical sign is steatorrhea, defined as a more than 5g fats/24 hours loss by stool.

The etiopathogenesis of the malabsorption syndrome
Different disease of the digestive tract may provoke disorders of digestion of alimentary principles and/ or disorders of absorption.
The protein digestion is modified in the pancreatic failure (decreasing of trypsin and chymotrypsin), in accelerated transit speed (enzymatic contact time reduced). The deficitary absorption of aminoacids appears in different intestinal diseases.
Glucide malabsorption is generated by maldigestion , especially in the disaccharidase deficit (lactase, maltase, sucrase) or in the chronic pancreatic insufficiency (deficit of pancreatic amylase). The chronic intestinal sufferance will generate disorders in the monosaccharide absorption.
Lipid malabsorption is generated by lipid maldigestion (gastric resection with Billroth II anastomosis), where billiary salts and lipase get into contact with food nonphysiologically; the Zollinger-Ellison syndrome, where excessive gastric acidity inactivates the pancreatic lipase; the insufficiency of pancreatic lipase in the chronic pancreatitis; the lack of lipid mycellisation by decreasing the billiary acids-pool in chronic hepatic diseases; intestinal bacterial overpopulation or reabsorption failure in the terminal ileon inflammation).
Etiology of the malabsorption syndrome
Causes of maldigestion:
a. Gastric causes:
  • gastrectomia Billroth II
  • gastroenteroanastomosis
  • Zollinger - Ellison syndrome;
b. Billiary causes:
  • chronic hepatic diseases
  • chronic billiary obstruction
c. Pancreatic causes:
  • chronic pancreatitis
  • pancreatic cystic fibrosis
d. Intestinal causes:
  • disaccharidases deficit (lactase, maltase, sucrase, trehalase)
  • afferent loop syndrome (by bacterial overpopulation).
Causes of intestinal malabsorption
a. Abnormal intestinal epithelium absorption:
  • celiac disease
  • Whipple disease
  • intestinal amiloidosis
  • chronic intestinal ischemia
  • Crohn’s disease of the intestine
  • tropical sprue
  • intestinal tuberculosis
B. Syndrome of short intestine
  • after surgery
  • enterocolic fistulas
  • surgical intestinal by-pass
c. Abnormal intestinal transport:
  • intestinal lymphoma
  • idiopathic intestinal lymphangectasia
  • congenital cystic pneumatosis
d. Increased intestinal transit speed:
  • hypertiroidia
  • chronic diarrhea
Clinical forms of malabsorption syndrome
  • malabsorption syndrome  maldigestion
  • malabsorption syndrome by disorders of intestinal absorption (malabsorption)
  • mixt malabsorption syndrome- when digestive disorders sre associated with those of absorption.
Clinical features
  • chronic diarrhea weight loss up to generalized malnutrition
  • steatorrhea (soft stools, light colored, smelling, adherent)
  • the abdominal distension
  • bloating
  • flatulence
  • abdominal discomfort
  • weight loss
  • the Bichat-bulk disappears
  • muscle atrophy
  • tegument changing
  • together with paleness, rough and dried skin,sometimes with pelagroid pigmentation
  • the tongue mucosa is red; lacking its small glands (glossitis), cheilosis
  • the nails decolorize and break easily
  • axilar and pubian hair reduces, in the latest stages, alopecia
  • the disorders in calcium absorption may generate osteomalacia bones pain and tetania
  • the deficiency of K vitamin generates tendency to bleeding
  • ascites
  • anemia
  • endocrine disorders: hypofisary failure (with troubles in children growth), corticosuprarenalian failure (Addison disease), gonadic failure (impotence and sterility).
Diagnosis of malabsorption syndrome
  • steatorrhea is a cardinal sign. Represent the elimination of more than 5g lipids/24 hours.
  • the coloring of a stool probe with Sudan III and numbering of fat corpuscles
  • creatorrhea = the proteic loss by stool
The etiology of malabsorption syndrome requires the evaluation:
a. Gastric:
  • barium examination, for the diagnosis of  gastrocolic fistula, gastroenteroanastomosis, gastrectomy with Billroth II anastomoses
  • gastroscopy: multiple ulcers in Zollinger Ellison syndrome
  • dosing gastrinemia possibly gastric chemism  stimulated with Pentagastrine
b. Billiar:
  • the biologic diagnosis of billiary obstruction, possibly completed with pancreatic computed tomography and endoscopic retrograde colangiopancreatography (ERCP)
c. Pancreatic:
  • pancreatic enzymes (amylase, lipase) may be increased
  • the imagistic modified aspect of pancreas or evalution by ERCP of pancreatic ductal aspect
  • altered pancreartic functional tests (PABA or Fluorescein diluarat)
  • more recently, determination of  I (first) faecal elastase mey demonstrate incipient stages of  pancreatic failure
  • determining VIP level (vasoactive intestinal polypeptide) may establish the diagnosis of VIP-oma or pancreatic cholera (severe, watery diarrhea), with hypokaliemia
d. Intestinal:
  • barium examination,with intestinal following up or enema-may evaluate the intestinal aspect and motility
  • duodenoscopy with duodenal biopsy ( celiac disease) or endoscopy may visualize the mucosal aspect (biopsy).
  • D-xilosis test
  • Schilling test-evaluates the absorption of B12 vitamin
  • small bowel biopsy of jejunal area may show the villous atrophies in celiac disease
  • colonoscopy  may show changing of rectocolitis, Crohn’s disease may be diagnosed
  • the lactose tolerance test (LTT) which may show a lactase deficit
Differential diagnosis
  • The malabsorption syndrome differential diagnosis may be done with different causes of chronic diarrhea, which have not attained malabsorption. In these cases, the weight loss and the modifying of biologic sanguine parameters (proteinemia, albuminemia) do not appear.
  • The colon neoplasm is accompanied by weight loss, diarrhea, iron-deficiency anemia and it must be differentiated from malabsorption syndrome.
  • In case of hepatic metastase, jaundice may be signaled and a tumoral liver may be palpated.
  • The neoplasm syndromes of different causes evolve with excessive weight loss, hypoproteinemia and hypoalbuminemia, but without diarrhea.
Evolution
  • malabsorption syndrome evolution is chronic, progressive, when the etiology is not discovered and treated. Denutrition evolves to excessive weight loss, and the uncorrected biological disorders aggravate.
Complication
  • hypoalbuminemia with edema and sever ascites
  • the decrease of  protrombin index with multiple bleedings
  • anemia
  • the sever decrease of serum electrolytes: K, Na, Ca, Mg
  • the decrease of vitamins
Treatment
The therapeutic attitude in malabsorption syndrome is mostly related to its etiology.
The alimentary diet : in celiac disease( where wheat, barley, oat and rye will be compulsory avoided, but replaced with rice and flour,potatoes) or the lactase defocot(where milk and dairy products will be completely avoided).
In chronic pancreatitis , the diet will completely avoid the alcohol intake and will drastically reduce fats.
On chronic diarrheas, the food rich in hard vegetal fibers will be avoided(radish, cabbage).

Medical therapy
- in  Zollinger - Ellison syndrome the resection of gastrinoma and intense blocking of acid secretion will be done, using H / K ATP-ase pump proton blockers
  • Omeprazole 40-160mg/day
  • Lansoprazole or Pantoprazole
  • Sandostatin 200mg/day subcutaneous
- in chronic pancreatitis – the enzyme substitution
  • Creon
  • Nutrizym
  • Cotazym
  • Panzytrat
  • Digestal forte
- in intestinal causes of malabsorption of malabsorption, the medical treatment has  to have two compounds the dismicrobism which is treated with intestinal eubiotics: Saprosan 3x1 tb/day
Antinal 4x1 tb/day
Intetrix 4x1 tb/day
and on  the other hand the intestinal protection with products like Smecta 3x1 packet/day
or reduction of transit speed in case of the acute diarrhea with Loperamid (Imodium) 1-2 tb when needed.
in cesa of excessive flatulence - Dimeticone
in Crohn’s disease - Mesalazina
- corticotherapy
- Azathioprine

- in the Verner - Morrison syndrome – octreotide (Sandostatin) 200-300 mg/day

- in the Whipple disease - antibiotics
  • Tetracycline 4x250mg/day
  • Ampicilline
  • Trimetoprim/ Biseptol,10-12 months
- the following deficits must be corrected :
  • hypoalbuminemia by administration plasma
  • iron- deficiency anemia by administrating iron
  • macrocytic anemia by administrating B12 vitamin /folic acid
  • the electrolytic deficits (Na, K) will be corrected parenterally and those of Ca  and  Mg usually by oral medication.
  • the vitamin deficits (B complex, D and K) will be corrected, as well as the hormonal ones, when they appear.

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