This is a serious condition of the small intestine which results in a protein-losing enteropathy. Although rare in the dog it is said to be seen more commonly in Yorkshire Terriers () and as a hereditary disease in the Norwegian Lundehunds (). The aetiology is not known although a congenital (primary) or acquired (secondary) obstruction to the intestinal lymphatic drainage is implicated. Secondary cases may include right-sided heart failure, constrictive pericarditis, neoplastic or inflammatory obstructions to the lymphatics or granuloma formation of mesentric lymph nodes (). Most cases are frequently found to be secondary to chronic inflammatory bowel disease (). Gross dilation of the lacteals and deeper lymph vessels occurs and there is said to be reduced immunoglobulin A (IgA) levels and consequently more chance of secondary infection occurring (). Chyle leaks out of the dilated lacteals leading to a serious loss of plasma protein and thus hypoproteinaemia ().
The main symptoms observed are chronic diarrhoea associated with weight-loss and frequently subcutaneous oedema, ascites and hydrothorax due to hypoproteinaemia. The appetite may initially be intact but as the condition advances anorexia develops.
Diagnosis is based on the observation of hypoproteinaemia (both albumin and globulin fall), lymphopenia, poor fat and xylose absorption tests, and reduced serum folate and B12 levels. A microcytic anaemia may occasionally occur. Confirmation of protein loss into the intestine can be made using radiolabelled albumin given intravenously, and the faeces monitored for 3 days for radioactivity ().
In the Norwegian Lundehund there is inflammation associated with lymphangiectasia but there is no leucopenia nor obvious site of lymphatic obstruction. Lymph nodes are usually small and unreactive. No dietary basis has been found for the condition and there is thought to be an immunodeficiency or hypoplasia of the lymphatic system.
Laparotomy and biopsy of the small intestine is required to obtain a definitive diagnosis. Gross examination of the mesentery will reveal dilated lymphatic vessels and lymphadenopathy. Histologically there are dilated lacteals and other lymphatic vessels and some evidence of inflammation (). Partial villus atrophy and crypt hyperplasia may also be seen ().
The prognosis is very ditficult to predict as some dogs respond very well to treatment while others totally fail to respond. The cases which are diagnosed early appear to have a greater chance of being successfully treated than advanced cases. There is no way of determining which outcome will occur before treatment is initiated. Where there is evidence of heart disease or obstruction, this should be treated. In idiopathic forms prednisolone at 2mg/kg/day together with tylosin 10mg/kg bid should be given. Long-chain triglyceride (LCT) is formed into chylomicrons and released into the lacteals. In lymphangiectasia this results in lymphatic hypertension and so further protein loss. So in addition a low fat diet such as Hills i/d or Waltham low fat diet should be fed. If additional fat is required for energy this can be given as medium-chain triglyceride (MCT) which is absorbed into the portal blood and not the lymphatic system. An adequate vitamin/ mineral supplement should be added because fat absorption is impaired.
Incoming search terms:
- lymphangiectasia b12