A 30-year-old patient with a history of facial paralysis eleven years ago, habitual smoker, non-ulcer dyspepsia, anxious-depressive syndrome, irregular menstruations, and without toxic habits or risky sexual relations.
She came to the emergency room several times due to pain in the right hypochondrium and lumbar region radiating to genitals and voiding syndrome, being diagnosed several times with nephritic colic.
Since two months she has fever, increased abdominal diameter, dyspareunia, leucorrhea, dysuria, dark urine and oral mugüet.
He also presented weight loss without anorexia, without bowel habit disorders.
The examination revealed a painful abdomen with positive renal percussion and ascitic smell.
between anamnesis and clinical examination was thought of in a series of differential diagnoses such as: peritoneal carcimomatosis, liver disease, ovarian neoplasia, celiac disease, intestinal tuberculosis and ILD with pathological gymdromy
Laboratory tests showed neutrophilia without leukocytosis, lymphopenia, hypochromic microcytic anemia, decreased platelets, increased ESR (111 mm/h, n < 10) and increased CRP (182 mg/l).
He also had hypoalbuminemia of 2 g/l, increased globulins, slight increase of bilirubin.
The patient was submitted to a gynecological study, which was normal.
The Mantoux test was negative, and serology for Brucella, Retrovirus, HCV and HBV was also negative.
ADA was high (25.8 U/l, n < 18.2) and the neoplasic antigen Ca-125 was very high (714 U/ml, n < 35).
A pharyngeal exudate was positive for S. aureus.
Antigliadin and antiendomysium antibodies were normal.
Urine analysis revealed a moderate bilirubin increase, regardless of gender, with negative urine cultures.
Stool analysis was negative with respect to Ziehl-Neelsen culture for AFB on two occasions, and negative for Lowenstein culture.
A paracentesis of ascitic fluid was performed in which a clear liquid was obtained in which a total of 1,476 cells/ml stood out, being 80% polymorphous nuclear protein (n < 20%), LDH very negative.
In the plain abdominal X-ray we can check a normal gas distribution although with a certain tendency to be located towards the center, not being able to be adequately assessed because the flanks cannot be visualized.
In the pelvis, signs indicating free fluid presentation are observed.
Abdominal ultrasound shows free peritoneal fluid, not significant abdominal findings in viscera.
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A barium gastroduodenal study was carried out in which there was no alteration of the intestinal transit.
Abominal CT scan showed abundant free fluid and peritoneal thickening as the most striking signs.
Without the clear suspicion of the main pathology that originated the picture and bearing in mind peritoneal carcinomatosis, a diffuse intraperitoneal infection and peritoneal tuberculosis itself, the patient was admitted to the hospital for a diagnostic laparoscopy.
On entering the cavity we found many adhesions and septa intraperitoneal and between different abdominal organs, highlighting liver adhesions.
In addition, there was a very extensive peritoneal sowing of tuberculomas.
Peritoneal biopsy of tuberculomas and liver was taken, and the most striking adhesions were released.
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The pathological anatomy results revealed a peritoneal granulomatosis of suggestive tuberculous etiology with liver granulomatosis and etiology suggestive of tuberculous inflammatory parenchymal alterations of reactive character.
