HYPOTHYROIDISM WITH ASCITES

Primary hypothyroidism is a common clinical condition. Ascites caused by hypothyroidism is rare. So its diagnosis is often delayed and patients frequently receive unnecessary procedures such as liver biopsies and exploratory laparotomies. We report a male person of 58 years with hypothyroidism with ascites who responded well with thyroid hormone replacement therapy with complete resolution of ascites. Analyses of ascites from patients in this condition usually shows exudative ascites with high protein (>2.5 g/dL) and SAAG < 1.1 gm/dl. High index of suspicion is required to reach at such diagnosis. Though it is a rare but prognosis is excellent with replacement therapy.

TB or TB contact.On examination, he was mildly anaemic with mild ankle edema, coarse skin, sparse body hair, and loss of lateral third of both eye brows.Alimentary system reveled ascites with no other abnormality.Nervous system examination revealed delayed relaxation of ankle jerk.
On basis of the above findings we drew the conclusion this is a case of hypothyroidism.Then we performed USG of thyroid gland, thyroid scan and Thyro peroxidase Ab.All were found normal.
Thyroid hormone replacement therapy was started with gradually increasing doses of levothyroxine, from 25 microgram to 150 microgram daily.On 8 weeks later he had a good general wellbeing and was found euthyroid with abatement of ascites.So the maintenance dose of levothyroxin (150 microgram daily ) has been continued.

Discussion:
Hypothyroidism is a relatively rare cause of ascites.This is a potentially curable condition with thyroid hormone replacement therapy unlike chronic liver and renal disease where little can be offered to the patient.In evaluation of new cases of ascites, ascitic fluid study and SAAG may cut short the spectrum of different expensive and invasive investigations.SAAG demonstrates the transudative and exudative ascites.SAAG more than 11 gm/l (1.1 gm/dl) indicates transudative ascites. 3Chronic liver disease, portal hypertension, congestive cardiac failure, chronic kidney disease, nephrotic syndrome, malnutrition and hypoalbuminaemia of any cause, all produce transudative ascites.Whereas SAAG less than 11 gm/ l (1.1 gm/dl) indicates exudative ascites. 3Of the various causes, peritoneal malignancies, tuberculous peritonitis, pyogenic peritonitis and pancreatic ascites can all lead to high-protein ascites.Here hypothyroidism ascites is rare possibility but it should be kept in mind during evaluation of a exudative ascites There has been a suggestion that the SAAG may exceed 1.1 in patients with myxedema ascites, based on a review of eight patients 1 .Because so few cases have been studied and portal hypertension or heart failure do not seem to be the mechanisms causing ascites in patients with myxedema, we cannot conclude that a high SAAG is a typical feature in this disease 4 .Moreover, the patient reported here showed a low SAAG.Portal hypertension secondary to liver cirrhosis is the leading cause of ascites (more than 80% of cases) and peritoneal involvement in patients with malignant diseases is the second at about 10% 5 .
In case of malignancy demonstration of malignant cell and /or peritoneal biopsy should be considered. 6f there is any evidence of portal hypertension clinically with transudative ascitic fluid, ultrasonography and endoscopy of upper GIT should be done to detect portal hypertension, splenomegaly and oesophagial varices or congestive gastropathy respectively.As in this case ascitic fluid was exudative we performed thyroid function tests which proved decisive.
The mechanism of ascites fluid formation in patients with myxedema is unclear.There are two main hypotheses.The first is that low levels of circulating thyroid hormones cause increased extravasation of plasma proteins because of abnormal capillary permeability and the lack of a compensatory increase in lymph flow and protein return rate 20 .The second hypothesis is that hyaluronic acid accumulates in the skin and produces edema by a direct hygroscopic effect.However, hyaluronic acid has only been found in minute quantities in patients with myxedema ascitesnot large enough to exert a direct hygroscopic effect.However, it could interact with albumin to form complexes that prevent the lymphatic drainage of extravasated albumin 21 .
The cause of pseudo-obstruction is also poorly understood.The most commonly proposed mechanism is that hypothyroidism causes an alteration in impulse transmission at myoneural junctions by deposition of myxedematous infiltrate between the muscular fibers and plexus.Wells et al 22 proposed that intestinal poor function was related to autonomic polyneuropathy.
In conclusion hypothyroidism with ascites is rare but easy to treat.Treatment with thyroid hormone replacement therapy leads to complete regression of the ascites.High index of clinical suspicion is required to diagnose such cases.On rutine evaluation of ascites investigations should be done to find the common causes such as chronic liver disease, peritoneal malignancy and infection, congestive heart failure, chronic kidney disease, pancreatic ascites and along with thyroid function tests specially on patients with exudative ascites.

Table - I
Characteristics of reported patients with myxedema ascites