Difference between revisions of "Protein Losing Enteropathy"

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*Disruption to the intestinal wall due to [[Inflammation - Pathology|inflammation]] or infiltrative disease
 
*Disruption to the intestinal wall due to [[Inflammation - Pathology|inflammation]] or infiltrative disease
 
*Venous congestion of the GI tract
 
*Venous congestion of the GI tract
*GI [[Haemorrhage - pathology|haemorrhage]]
+
*GI [[Haemorrhage - Pathology|haemorrhage]]
 +
 
 
Hence, there are numerous causes of PLE in cats and dogs , including:
 
Hence, there are numerous causes of PLE in cats and dogs , including:
 
*Inflammation
 
*Inflammation
Line 27: Line 28:
  
 
Inflammatory bowel disease and lymphoma are the most common causes of PLE in both cats and dogs, with lymphangiectasia occurring much more commonly in dogs than in cats.  Chronic intussuscepta (usually occurring secondary to acute enteritis) and endoparasite infection are the most common causes of PLE in juvenile cats and dogs.  
 
Inflammatory bowel disease and lymphoma are the most common causes of PLE in both cats and dogs, with lymphangiectasia occurring much more commonly in dogs than in cats.  Chronic intussuscepta (usually occurring secondary to acute enteritis) and endoparasite infection are the most common causes of PLE in juvenile cats and dogs.  
 +
 +
Rare causes of PLE include:
 +
** Small intestinal bacterial overgrowth
 +
** Hypoalbunimaemia causing intestinal mural oedema
 +
** Increased activation of tissue plasminogen activator
 +
** Systemic lupus erythematosis (SLE)
 +
** Chemotherapy/radiotherapy
  
 
==Signalment==
 
==Signalment==
Line 84: Line 92:
  
 
====Ultrasonography====
 
====Ultrasonography====
*This may reveal thickening of intestines, mesenteric lymphadenopathy or abdominal effusion.
+
*This may reveal:
 
+
**Changes to intestinal wall structure, including:
 +
***Thickening without loss of normal layers (as with inflammatory bowel disease)
 +
***Thickening with loss of layers (as with intestinal neoplasia)
 +
***'Tiger stripes', an unreliable indicator of lymphangiectasia
 +
**Ascites or pleural effusion
 +
**Mesenteric lymphadenopathy
  
 
===Histopathology===
 
===Histopathology===
*Endoscopically-guided multiple biopsies are useful.  Surgical biopsy may be required for a definitive diagnosis of lymphoma and [[Lymphangiectasia#Description|secondary lymphangiectasia]].  A small fatty meal could be given the night before biopsy to increase the chance of diagnosing [[Lymphangiectasia|lymphangiectasia]].
+
Endoscopy can be used to visualise the proximal intestinal luminal surface and to obtain grab biopsies.  Surgical biopsies may be obtained for definitive diagnosis of lymphoma and [[Lymphangiectasia#Description|secondary lymphangiectasia]].  A small fatty meal could be given the night before biopsy to increase the chance of diagnosing [[Lymphangiectasia|lymphangiectasia]].
*Animals with PLE have a greater risk of biopsy site dehiscence with the subsequent development of peritonitis.
+
Care should be taken with this procedure as animals with PLE have a greater risk of surgical wound dehiscence with the subsequent development of peritonitis.
  
 +
Lesions that may be observed on histopathological analysis of biopsy samples include:
 +
** Inflammatory bowel disease (of various types)
 +
** Dilated lymphatics
 +
** Lipogranulomatous lymphangitis, especially in Soft-coated Wheaten terriers
 +
* Intestinal crypts become dilated with mucus, sloughed epithelial cells with or without inflammatory cells.
 +
* PLE is also associated with protein losing nephropathy (PLN).
 +
** PLN may be a chronic sequelae to the PLE.
 +
** Follows immune complex deposition in the glomerulus, causing glomerulonephritis or glomerulosclerosis.
 +
** PLN causes hypoalbunaemian and hypercholesterolaemia.
 +
** Similar PLN and PLE lesions seen in young Besenjis with immunoproliferative enteropathy and glomerulosclerosis.
  
 
==Treatment==
 
==Treatment==
 
Treatment of the underlying cause of disease should be initiated, if possible.
 
Treatment of the underlying cause of disease should be initiated, if possible.
  
===Plasma transfusion===
+
====Plasma transfusion====
 
*This may be used to increase plasma volume.  However, much of the albumin is lost in the gut and a substantial amount fails to remain in the intravascular compartment.  Therefore, the extent of increase in serum albumin level is not great.
 
*This may be used to increase plasma volume.  However, much of the albumin is lost in the gut and a substantial amount fails to remain in the intravascular compartment.  Therefore, the extent of increase in serum albumin level is not great.
 
*Administration of [[Colloids|colloid]] may be more suitable if it is essential to increase the plasma oncotic pressure.
 
*Administration of [[Colloids|colloid]] may be more suitable if it is essential to increase the plasma oncotic pressure.
  
===[[The Effects of Diuretics on the Kidneys - Anatomy & Physiology|Diuretics]]===
+
====[[The Effects of Diuretics on the Kidneys - Anatomy & Physiology|Diuretics]]====
 
*These can be used to reduce any ascites or pleural effusion.
 
*These can be used to reduce any ascites or pleural effusion.
 
*[[Heart Failure, Treatment#C. Pharmacological |Spironolactone]] may be more effective than [[Heart Failure, Treatment#C. Pharmacological|frusemide]].
 
*[[Heart Failure, Treatment#C. Pharmacological |Spironolactone]] may be more effective than [[Heart Failure, Treatment#C. Pharmacological|frusemide]].
  
===Antithrombotic therapy===
+
====Antithrombotic therapy====
 
*Treatment may be initiated with low dose aspirin to prevent the development of thrombo-embolism.
 
*Treatment may be initiated with low dose aspirin to prevent the development of thrombo-embolism.
  
===Dietary Supplementation with Calcium===
+
====Dietary Supplementation with Calcium====
 
*Calcium carbonate may be added to the diet if a low serum concentration of ionised calcium is documented.
 
*Calcium carbonate may be added to the diet if a low serum concentration of ionised calcium is documented.
  
 
==Prognosis==
 
==Prognosis==
This depends on the underlying cause.
+
This depends on the underlying cause but Soft-coated Wheaten terriers are known to have a median survival time of five months after diagnosis of PLE and of two months if they suffer from concurrent protein-losing nephropathy.
  
 
=From Pathology=
 
=From Pathology=
===Causes of PLE===
 
  
* Severe inflammatory disease.
 
** Protein is lost in exudate.
 
* [[Lymphangiectasia|Lymphangiectasia]].
 
** Loss of protein-rich lymph due to obstruction of gut lymphatics.
 
* Increased mucosal permeability.
 
** E.g. erosions, loss of tight junctions, lymphosarcoma.
 
* Increased loss of enterocytes (less important).
 
* Also:
 
** Immunoproliferative enteropathy
 
** Lymphocytic plasmacytic enteritis
 
** Eosinophilic enteritis
 
** GI ulceration/erosion
 
** Giardiasis
 
** Chronic intussusception
 
** Small intestinal bacterial overgrowth
 
** Neoplasia
 
** Hypoalbunimaemia causing mural oedema
 
** Increased activation of tissue plasminogen activator
 
** Systemic lupus erythematosis (SLE)
 
** Vascular lesion in the GI mucosa
 
** Chemotherapy/radiotherapy.
 
  
 
===Pathology===
 
===Pathology===
  
* Lesions include:
+
* L
** Inflammatory bowel disease
 
** Dilated lymphatics
 
** Lipogranulomatous lymphangitis.
 
* Intestinal crypts become dilated with mucus, sloughed epithelial cells with or without inflammatory cells.
 
* PLE is also associated with protein losing nephropathy (PLN).
 
** PLN may be a chronic sequelae to the PLE.
 
** Follows immune complex deposition in the glomerulus, causing glomerulonephritis or glomerulosclerosis.
 
** PLN causes hypoalbunaemian and hypercholesterolaemia.
 
** Similar PLN and PLE lesions seen in young Besenjis with immunoproliferative enteropathy and glomerulosclerosis.
 
  
  

Revision as of 16:26, 5 July 2010




Description

Protein-losing enteropathy (PLE) refers to the loss of plasma proteins into the gastro-intestinal (GI) tract, exceeding the absorptive capacity of the intestines. PLE can be caused by:

  • Disruption to the intestinal wall due to inflammation or infiltrative disease
  • Venous congestion of the GI tract
  • GI haemorrhage

Hence, there are numerous causes of PLE in cats and dogs , including:

  • Inflammation
  • Infiltrative disase
    • Alimentary lymphoma
  • Congestion
  • GI haemorrhage
    • e.g., hypoadrenocorticism, ischaemia

Inflammatory bowel disease and lymphoma are the most common causes of PLE in both cats and dogs, with lymphangiectasia occurring much more commonly in dogs than in cats. Chronic intussuscepta (usually occurring secondary to acute enteritis) and endoparasite infection are the most common causes of PLE in juvenile cats and dogs.

Rare causes of PLE include:

    • Small intestinal bacterial overgrowth
    • Hypoalbunimaemia causing intestinal mural oedema
    • Increased activation of tissue plasminogen activator
    • Systemic lupus erythematosis (SLE)
    • Chemotherapy/radiotherapy

Signalment

The following breeds of dog may be afflicted:

  • Basenji
  • Lundehund
  • Soft-Coated Wheaten Terrier
    • May have concurrent protein-losing nephropathy
    • Most affected animals have a common ancestor
    • Females are more commonly affected than males
  • Yorkshire Terrier
  • Shar Pei


Diagnosis

Clinical Signs

  • Weight loss is the most evident sign.
  • Diarrhoea occurs due to the loss of protein into the GI tract and subsequent osmotic movement of fluid. Melaena may occur with GI haemorrhage.
  • Oedema, ascites and pleural effusion due to reduced plasma oncotic pressure.
  • Thickened intestines may be detectable on abdominal palpation and this may be related to the primary pathological process.
  • Thromboembolic disease due to the loss of anticoagulants such as antithrombin III.
  • Hypocalcaemic tetany due to a reduced ability to absorb the fat soluble vitamin D.


Laboratory Tests

Haematology

  • Lymphopaenia occurs with lymphangiectasia due to the loss of lymph.

Biochemistry

  • Panhypoproteinaemia
    • Hypoglobulinaemia with hypoalbuminaemia is a pattern more suggestive of PLE.
    • Albumin is usually lost in excess of globulin in protein losing nephropathy.
  • Hypocholesterolaemia, especially in lymphangiectasia.
  • Hypocalcaemia
    • Ionised calcium concentration should be measured to determine the significance of this finding as serum calcium concentration is closely related to total protein level.

Other Tests

  • Measurement of faecal alpha1-protease inhibitor
    • This marker has a similar molecular weight to albumin and it is lost into the GI tract in PLE. Its concentration can be measured in faeces as it is not degraded by GI enzymes. Faecal samples must be frozen on collection before submission to a laboratory in the USA.
  • 51-Chromium labelled albumin
    • A radioactive marker (51-Chromium) is attached to recombinant albumin molecules before injection into animal. Faecal samples are collected to determine whether the labelled albumin is being lost into the GI tract. Although this test represents the 'gold standard' test, it is available only at a limited number of referral institutes.

Diagnostic Imaging

Radiography

  • Abdominal radiographs
    • The results are usually unremarkable but discrete mass lesions or ascites may be evident.
  • Thoracic radiographs

Ultrasonography

  • This may reveal:
    • Changes to intestinal wall structure, including:
      • Thickening without loss of normal layers (as with inflammatory bowel disease)
      • Thickening with loss of layers (as with intestinal neoplasia)
      • 'Tiger stripes', an unreliable indicator of lymphangiectasia
    • Ascites or pleural effusion
    • Mesenteric lymphadenopathy

Histopathology

Endoscopy can be used to visualise the proximal intestinal luminal surface and to obtain grab biopsies. Surgical biopsies may be obtained for definitive diagnosis of lymphoma and secondary lymphangiectasia. A small fatty meal could be given the night before biopsy to increase the chance of diagnosing lymphangiectasia. Care should be taken with this procedure as animals with PLE have a greater risk of surgical wound dehiscence with the subsequent development of peritonitis.

Lesions that may be observed on histopathological analysis of biopsy samples include:

    • Inflammatory bowel disease (of various types)
    • Dilated lymphatics
    • Lipogranulomatous lymphangitis, especially in Soft-coated Wheaten terriers
  • Intestinal crypts become dilated with mucus, sloughed epithelial cells with or without inflammatory cells.
  • PLE is also associated with protein losing nephropathy (PLN).
    • PLN may be a chronic sequelae to the PLE.
    • Follows immune complex deposition in the glomerulus, causing glomerulonephritis or glomerulosclerosis.
    • PLN causes hypoalbunaemian and hypercholesterolaemia.
    • Similar PLN and PLE lesions seen in young Besenjis with immunoproliferative enteropathy and glomerulosclerosis.

Treatment

Treatment of the underlying cause of disease should be initiated, if possible.

Plasma transfusion

  • This may be used to increase plasma volume. However, much of the albumin is lost in the gut and a substantial amount fails to remain in the intravascular compartment. Therefore, the extent of increase in serum albumin level is not great.
  • Administration of colloid may be more suitable if it is essential to increase the plasma oncotic pressure.

Diuretics

Antithrombotic therapy

  • Treatment may be initiated with low dose aspirin to prevent the development of thrombo-embolism.

Dietary Supplementation with Calcium

  • Calcium carbonate may be added to the diet if a low serum concentration of ionised calcium is documented.

Prognosis

This depends on the underlying cause but Soft-coated Wheaten terriers are known to have a median survival time of five months after diagnosis of PLE and of two months if they suffer from concurrent protein-losing nephropathy.

From Pathology

Pathology

  • L


References

  • Ettinger, S.J. and Feldman, E. C. (2000) Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat Volume 2 (Fifth Edition) W.B. Saunders Company.
  • Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition) BSAVA.
  • Nelson, R.W. and Couto, C.G. (2009) Small Animal Internal Medicine (Fourth Edition) Mosby Elsevier.
  • Willard, M. (2005) Protein-Losing Enteropathy in Dogs and Cats 30th World Congress of the WSAVA.