Inflammatory Myofibroblastic Tumor in the Adrenal Gland: A Case Report.

Inflammatory myofibroblastic tumors (IMTs) were first described by Harold Brunn in 1939. IMTs are mainly found in the lungs and other sites of the body; hence, its occurrence in the adrenal gland is exceptional. In the literature, less than 10 cases of IMTs in the adrenal gland have been reported. The etiology of IMT remains unknown, with post-inflammatory changes and a neoplastic origin being proposed. We present a case of a 19-year-old woman and adrenal gland IMT. The patient presented with abdominal pain and low cardiac output without hypovolemic shock. Computed tomography revealed a tumor in the adrenal gland measuring 11.4 cm with extravasation of contrast medium within the tumor. Treatment included conservative management with selective embolization due to minimal invasion of the inferior artery of the adrenal gland. The patient was then discharged with possibility of future elective surgery. Four months later, the size of the tumor decreased to 6.3 cm, and her Eastern Cooperative Oncology Group physical status was 0. The Multidisciplinary Tumor Board suggested surgical management. The final histopathology report was compatible with an IMT of the adrenal gland, with the immunohistochemical report showing positivity for anti-actin muscle-specific and anti-actin smooth muscle and negativity for anaplastic lymphoma kinase. IMTs of the adrenal gland may be treated electively through multidisciplinary management together with interventional radiology and surgery, achieving a favorable outcome for the patient.

Acute mesenteric thrombosis in two patients with COVID-19. Two cases report and literature review.

INTRODUCTION: The coronavirus disease 2019 (COVID-19) affects mainly the respiratory system, other organs may be involved, usually due to coagulation disturbances that lead to a high rate of thrombotic complications. CASE PRESENTATION: The first patient is 45 years-old who has been exposed to SARS CoV-2. Upon admission due to acute abdomen evidence surgery is performed in which an intestinal resection with an adequate post-surgical evolution takes place so the patient is discharged after 4 days with a prescription for oral anticoagulants. The second one is 42 years-old and has comorbidities. The patient is admitted upon evidence of COVID-19, after showing signs of vein mesenteric ischemia in a CT scan surgery is performed, however the patient dies 24 h after the intervention. DISCUSSION: Within severe cases of patients with COVID-19 the incidence of a symptomatology or gastrointestinal complications is high (39-73.8%). Thromboprophylaxis is recommended to all patients admitted for COVID-19, starting with heparin of low molecular weight as prophylaxis, as well as continuing with oral anticoagulants after being discharged. CONCLUSION: Despite the fact that knowledge of the disease is rapidly advancing, all available treatments are still nonspecific to SARS-CoV-2 and the optimal management of COVID-19 remains unclear. An unexplained clinical picture should raise the suspicion for rare conditions such as mesenteric thrombosis. Adequate prophylactic measures should be implemented both during hospitalization and after discharge.

Splenic PGE2-releasing macrophages regulate Th1 and Th2 immune responses in mice treated with heat-killed BCG.

Hosts infected with low doses of mycobacteria develop T helper cell type 1 (Th1) immunity, but at relatively higher doses, a switch to Th2 immunity occurs. Prostaglandin E2 (PGE2) is a proposed mediator of the Th1-to-Th2 shift of immune responses, and mycobacterial products induce PGE2-releasing macrophages (PGE2-MØ) in the mouse spleen in a dose-dependent manner. Splenic PGE2-M Ø from Balb/c mice, given 0.01 or 1 mg heat-killed (HK) Mycobacterium bovis bacillus Calmette-Guerin (BCG) intraperitoneally (i.p.), were characterized by the ex vivo release of PGE2 (>10 ng/10(6) cells), cytokine production, and expression of PGG/H synthase (PGHS)-1, PGHS-2, cytosolic PGE synthase (PGES), and microsomal PGES-1. At Day 14 after the treatment, mice treated with 1 mg, but not 0.01 mg, BCG had increased levels of PGHS-2+ PGE2-MØ, total serum immunoglobulin E (IgE), and serum IgG1 antibodies (Th2 responses) against heat shock protein 65 and purified protein derivative. Cultures of spleen cells isolated from these mice expressed interleukin (IL)-4 and IL-10 in recall responses. Treatment of mice receiving 1 mg BCG with NS-398 (a PGHS-2 inhibitor, 10 mg/kg i.p., daily) resulted in enhanced interferon-gamma (IFN-gamma) production with reduced IL-4 and IL-10 production in recall responses. This treatment also resulted in decreased total serum IgE levels. Treatment of C57Bl/6 mice with HK-BCG (0.5 mg dose) also induced a mixture of Th1 and Th2 responses, although IFN-gamma production was markedly increased, and IL-4 was decreased compared with Balb/c mice. Thus, our results indicate that by 14 days following treatment of mice with high doses of HK-BCG, splenic PGE2-MØ formation is associated with a PGHS-2-dependent shift from Th1-to-Th2 immune responses.