A previously healthy 30-year-old woman presented with progressive abdominal pain and disorientation in October 2012.
Emergency abdominal ultrasound showed fatty liver and abundant ascites.
Haemoglobin 42%, 13 g/dl hemoglobin, 13,600 leukocytes and 582,000 platelets.
C-reactive protein 112 mg/L (VR: up to 5 mg/L), biochemical profile, liver profile, renal function and normal plasma electrolytes.
Abdominal computed axial tomography showed a mild left pleural effusion, with increased diffuse density of mesoperitoneal adipose tissue associated with the presence of metastatic peritoneal implants and abundant ascites.
The ascitic fluid study showed: Adenosindeaminase: 7.35 (VR: up to 32 IU/L), glucose 115 mg/dl, proteins 6 g/dl, leukocyte count of 91% mononuclear cells/mm3.
Negative results for smear microscopy, Koch culture and current culture.
Given these findings, we also requested a carboxyl antigen which was lower than 0.5 ng/ml, alpha-fetoproteins lower than 1.3 ng/mL and chorionic gonadotropin lower than 2 mIU/M.
Due to the absence of etiologic diagnosis it was decided to perform exploratory laparotomy, which showed multiple nodules in the peritoneum, abundant ascitic fluid of turbid aspect, highlighting ovaries and uterus of normal macroscopic aspect.
Anatomopathological analysis of three peritoneal lesions was performed, highlighting the presence of adipose tissue extensively compromised with chronic lymphocytic and cellular inflammatory infiltrate neutrophils and hyaline fibrosis.
A lesion composed of myofibroblasts of elongated shape with pale chromatin and small punctiform nucleolus stands out.
1.
Immunohistochemistry was negative for ALK, calretinin, CD30, CK5-6 and desmin, and was positive.
The result was positive for smooth muscle actin and Ki67 (5-10%), compatible with a diagnosis of IMT.
Since surgical management in this context could be associated with high morbidity and mortality, by extension of peritoneal lesions medical therapy with prednisone 40 mg daily associated with celecoxib 400 mg daily, which received for 6 months is proposed.
The patient evolves unfavourably, because the pain and abdominal discomfort increase what makes her unable to perform her labor functions (Imagen 2).
A control tomography scan showed an increase in the size and number of peritoneal lesions associated with increased ascites, mild pleural effusion and new lesions in liver and pancreas.
Given the aggressive behavior, a new histological study is performed and a new exploratory laparotomy is performed.
Anatomopathological and immunohistochemical analyses showed the same results.
Given the absence of a high mitotic index in the histological analysis, management with chemotherapy is rejected.
After reviewing the literature, infliximab is proposed from a similar case with good results.
To discuss the case with the ethics committee of our center, in addition to obtaining the patient's consent, intravenous infliximab was started at 300 mg weekly 0, 2, 6 and then every 8 weeks.
Prior to the use of infliximab, a study was conducted for hepatitis B virus, hepatitis C and human immunodeficiency and a study for latent TB with QuantiFERON®, all with negative results.
The follow-up of the patient at 10 months showed a decrease in abdominal pain and dyspnoea, achieving reintegration into the activity.
The control tomography at 9 months showed stability of the tumor lesions, absence of new lesions and regression of ascites.
