Case Report
Spontaneous Bacterial Peritonitis in Subclinical Hypothyroidism
Authors
Dalip Gupta, Professor,
Preyander Thakur, Junior Resident,
Vivek Chabra, Junior Resident,
Munish, Junior Resident,
Gaurav Kapur, Junior Resident,
Sachin Sondhi, Junior Resident,
Dept. of Medicine, Indira Gandhi Medical College, Shimla, India.
Address for Correspondence
Dr. Preyander Thakur
Room no. 70, RDH
Indira Gandhi Medical College,
Shimla-171001,
Himachal Pradeesh,
India.
E-mail:
preyander.thakur@gmail.com
Citation
Gupta D, Thakur P, Chabra V, Munish, Kapur G, Sondhi S. Spontaneous Bacterial Peritonitis in Subclinical Hypothyroidism. Online J Health Allied Scs.
2013;12(3):13. Available at URL:
http://www.ojhas.org/issue47/2013-3-13.html
Open Access Archives
http://cogprints.org/view/subjects/OJHAS.html
http://openmed.nic.in/view/subjects/ojhas.html
Submitted:Jul 21,
2013; Accepted: Oct 28, 2013; Published: Nov 15, 2013 |
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Introduction:
Spontaneous Bacterial Peritonitis (SBP) is commonly associated with alcoholic and non-alcoholic liver cirrhosis.
A literature search revealed only one other reported case of myxoedema ascites associated with SBP.[1] SBP typically presents with abdominal pain,
fever and raised inflammatory markers such a C reactive protein and white blood cell count.
The case reported here describes a patient with subclinical hypothyroidism with concomitant SBP.
This patient did not have other risk factors for developing ascites such as a previous history of alcohol excess and hepatitis B infection.
Moreover investigations also eliminated cirrhosis of the liver, portal hypertension, malignancy, heart failure and other common causes of
ascites. Subclinical Hypothyroidism was determined to be the most likely cause of her symptoms. Treatment with thyroid replacement therapy
led to complete regression of the ascites and antibiotic therapy successfully treated the SBP.
Case Report:
A 75 years old woman from Jatog, Himachal Pradesh presented with 8 month history of constipation on and off and a
2 month history of increasing abdominal distension and 5 day history of increasing abdominal pain. She was non smoker and non alcoholic, non
diabetic and non hypertensive.
Clinical examination revealed a moderately built well nourished lady. Pulse rate was 60/minute, regular, blood
pressure was 120/90 mmHg, and respiratory rate was 18/minute. Cardiopulmonary examination was within normal limits. Abdominal examination revealed
free fluid in the form of shifting dullness, diffuse tenderness and decreased bowel sounds. The white blood cell count was 7590/cumm,
haemoglobin 11.2gm%, MCV 80.6fl, and platelets 178000/cumm. The C-reactive protein was positive. Renal function tests were within normal limits.
The alkaline phosphatase level was 127U/L, the total bilirubin was 5umol/L, the alanine amino-transferase was 14U/L and the aspartate amino
transferase was 30 IU/L. The total serum protein level was 57g/L, the albumin was 30g/L and the international normalised ratio (INR) was 1.0.
Thyroid function studies revealed a thyroid stimulating hormone (TSH) of 10.92mIU/L and a T4 of 7.70micgram/L and T3 of 0.66ng/mL. Amylase
was 39 IU/L. ANA was negative by latex agglutination method. Chest X - ray was within normal limits and ECG revealed sinus bradycardia.
Ultrasound of the abdomen and pelvis revealed marked ascites but there was no suggestion of liver cirrhosis or
gyanecological pathology. Computer tomography of the abdomen and pelvis revealed a large volume of ascites with minimal bilateral pleural effusion
but no feature of liver cirrhosis. UGI endoscopy was also normal. Echocardiogram revealed good systolic function.
A diagnostic and therapeutic ascitic drain was conducted. The ascitic fluid had a total protein level of 32g/L. The
white cell count was 6400, 90% of which were polymorphs. ADA levels 9.1U/L. Gram staining of the fluid revealed gram positive diplococci.
No malignant cell was found in three consecutive samples that were sent. The ascitic fluid culture grew streptococci. It was treated with a 5 day
course ofpipericillin and tazobactam and levothyroxine was also started. Patient improved and on discharge only minimal ascities was there on
ultrasonography.
On follow after 2 months, patient had no free fluid on USG and her TSH was 3.12mIU/L.
Discussion:
Hypothyroidism is a common clinical condition. Ascites caused by hypothyroidism is also rare accounting for less
than 1% of new onset ascites.[2] De Castro et al’s review of 18 reported cases of myxoedema ascites indicated that symptoms resolve with
thyroid replacement therapy.[3] Therefore myxoedema ascites is an easily treated and preventable condition with careful thyroid replacement therapy.
The mechanism by which a patient with hypothyroidism develops ascites is unknown. There have however been several
hypotheses proposed. The first hypothesis proposed that the oedema was produced by a direct hygroscopic effect due to hyaluronic acid accumulation
in the skin. However this is unlikely to be significant in myxoedema ascites as only minute quantities of hyaluronic acid are present. However albumin
hyaluronic acid complexes could form preventing drainage of extravasated albumin.[4] The second hypothesis proposed increased capillary
permeability in myxoedema that returns to normal with thyroid replacement therapy.[5] The third hypothesis proposed that in the hypothyroid state,
there is a reduced rate of albumin synthesis and catabolism, an increased rate in the transcapillary escape of albumin and an increase in the
extravascular mass of albumin.[6]
SBP is a common complication of alcoholic and non-alcoholic liver cirrhosis, however it is a rare complication of
myxoedema ascites. Literature search yielded one previous reported case of SBP in a patient with myxoedema ascites.[1]
It has been suggested that low protein concentrations in ascitic fluid predisposes to SBP.[7] De Castro et al’s
review of 18 reported cases of myxodemea ascites revealed that a feature of the condition is a high protein ascitic fluid content.[3] Therefore
high ascitic protein levels may partially account for low levels of SBP in patients with myxoedema ascites. In this case described above the
ascitic protein level was high, so other factors must have predisposed the patient to SBP. Hypothyroidism has been proposed to suppress cell
mediated immunity. Animal studies have also indicated that hypothyroidism depresses lymphocyte function and treatment with thyroid replacement
therapy reverses this effect.[8] These studies have not been verified in humans; however Schoenfeld et al suggest this as a cause for bacteraemia
in a male patient with severe hypothyroidism.[9]
References:
- Alberti LE, Lopez-Gomez A, Alberti-Flor JJ. Spontaneous bacterial peritonitis in a patient with myxoedema ascites. Digestion 2003;68:91-93.
- Watanakunakorn C, Hodges RE, Evans TC. Myxoedema. A study of 400 cases. Arch Intern Med 1965;116:183-189.
- De Castro F, Bonacini M, Walden JM, Schubert TT. Myxoedema Ascites Report of two cases and review of the literature. J Clin Gastroenterol 1991;13(4):411-414.
- Bonvalet JP, David R, Baglin A, Hatt PY. Myxoedema with inappropriate antidiuresis and hyperaldosteronism. Ann Med Interne 1970;121:949-955.
- Lange K: Capillary permeability in myxoedema. Am J Med Sci 1944;208:15.
- Parving HH, Hansen JM, Nielsen SL, Rossing N, Munck O, Lassen NA. Mechanisma of oedema formation in myxoedema-increased protein extravasation and relatively slow lymphatic drainage. N Engl J Med 1979;301:460-465.
- Runyon BA. Low-protein-concentrations in ascitic fluid is predisposed to spontaneous bacterial peritonitis. Gastroenterology 1986;91:1343-1346.
- Fabris N. Immunodepression in thyroid-deprived animals. Clin ExpImmunol 1973;12:601-611.
- Schoenfeld PS, Myers JW, La Rocque JC. Suppression of cell-mediated immunity in hypothyroidism. South Med J 1995;88:347-349.
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