SUPPURATIVE GASTRITIS IN AN HIV PATIENT: A CASE REPORT. SUPURATIVNI GASTRITIS KOD HIV POZITIVNOG BOLESNIKA: PRIKAZ

Introduction. Suppurative gastritis (SG) is a rare disease characterized by a bacterial infection of the stomach wall. This condition has high mortality rate, especially in patients with predisposing factors such as alcoholism, immunodeficiency and previous endoscopic gastric procedures.Case report. A 41 year old male was hospitalized with epigastric pain, fever and vomiting. The symptoms started a few days after esophagogastroduodenoscopy (EGD). His personal medical history included periodical excessive alcohol consumption. Based on initial blood tests the patient was diagnosed with sepsis and was promptly started a treatment with antibiotics. In the first few days of hospitalization there was an improvement in inflammation marker levels, but the patient was still febrile and with the referred epigastric pain. A computed tomography scan showed marked thickening of the gastric wall and EGD revealed deep ulcers in the stomach with fibrinopurulent exudate. Histological examination of gastric biopsies showed necrosis and abscesses. Blood cultures were positive for Stenotrophomonas maltophilia and Pseudomonas aeruginosa with subsequent change in antibiotics. The repeated blood tests showed leucopenia and the


Introduction
Suppurative gastritis (SG) also known as phlegmonous gastritis, is a rare disease characterized by a bacterial infection of the stomach wall. 1,2,3It is usually related to Strepotococcus infection. 4This condition has high mortality rate, around 27%, especially in patients with predisposing factors such as alcoholism, immunodeficiency and previous endoscopic gastric procedures. 1,5Early diagnosis and rapid antibiotic treatment, with or without surgery, are pivotal for the survival of patients with SG. 1,3 Herein, we report the first case, to our knowledge, of SG caused by Enterococcus spp. in a human immunodeficiency virus (HIV) patient.

Case report
A 41 year old male presented at the Emergency Department of Clinical Center of Vojvodina -Novi Sad (Serbia), with a two days history of severe epigastric pain, fever and vomiting.These symptoms started a few days after the execution of esophagogastroduodenoscopy (EGD) following the eradication treatment for Helicobacter pylori gastritis.His personal medical history included periodical excessive alcohol consumption and multiple fractures after a car accident.
Laboratory test results on hospital admission revealed increased inflammatory markers -C reactive protein 285.9 mg/L, procalcitonin 40.76 ng/ml, increased levels of blood urea nitrogen (14.2 mmol/L) and serum creatinin (323 μmol/L) and thrombocytopenia (119x10 9 /ml).Based on these results the patient was initially diagnosed with sepsis and was promptly started a treatment with ceftriaxone, ciprofloxacin and metronidazole.An abdominal CT scan showed marked thickening of the gastric wall, splenomegaly and enlarged mesenteric lymph nodes.In the first few days of hospitalization, we registered an improvement in inflammation marker levels, but the patient was still febrile and with the referred epigastric pain.However, the blood cultures were negative.
Due to the CT finding, a EGD was performed and it revealed multiple deep ulcers (diameter 3.5 cm) in the gastric corpus with fibrinopurulent exudate (Fig. 1).Consequently the patient was switched to total parental nutrition.New blood cultures were positive for Stenotrophomonas maltophilia and Pseudomonas aeruginosa, with subsequent change in antibiotic treatment with amoxicillin and gentamycin.Histological examination of gastric biopsies showed necrotic detritus on the surface of gastric mucosa with coagulation necrosis and abscesses (Fig. 2).
The blood tests repeated in the third week after admission showed leucopenia, and in suspicion of immunodeficiency the patient was screened for HIV and the test came back positive.In the fifth week of illness, a second EGD was performed and showed signs of inflammation and pus in the stomach (Fig. 3), with a gastric aspirate culture positive for Enterococcus spp.In accordance with antibiotic resistance, the treatment was modified with vancomycin, and after two weeks a third EGD showed healed gastric mucosa confirmed by pathohistological evaluation (Fig. 4).

Discussion
SG is an exceedingly rare diagnosis. 6It is more common in patients with gastrointestinal comorbidities that cause mucosal injury such as chronic gastritis, gastric cancer or ulcer. 5Medical history might reveal esophagectomy, gastric biopsies and other invasive procedures performed in weeks preceding the initiation of symptoms. 1Around half of the patients diagnosed with purulent gastritis have immunosuppression factors. 1 It is also closely related to septicemia. 5 Gastric ulcers in patients with HIV infection are most commonly associated with opportunistic infections (Mycobacterium avium, cytomegalovirus or herpes simplex virus) or opportunistic tumors.So far the only known case of purulent gastritis in an HIV patient was related to a patient with Kaposi sarcoma. 7Pathogens causing SG can be identified from gastric tissue and fluid cultures. 2The most frequent pathogen is Streptococcus spp.(especially S. pyogenes) in about 57-70% of cases. 1,3,4Other identified pathogens include Staphylococcus spp, Escherichia coli, Haemophilus influenzae, as well as Proteus and Clostridium spp. 1,3,4Polymicrobial infection is described in around 17% of cases. 1 In our case two bacteria were identified in the blood cultures and Enterococcus spp. was isolated from the gastric aspirate.
The usual clinical presentation of SG consists of severe and acute epigastric pain, fever and vomiting. 5As these symptoms are nonspecific, SG is often misdiagnosed as more common conditions such as perforated peptic ulcer and other causes of acute abdomen. 5G can be initially diagnosed by EGD, abdominal CT or endoscopic ultrasound (EUS), while the deffinitive diagnosis is acquired by histological examination and culture of the gastric biopsies. 5Typical signs of SG during EGD include erythema and edema of the gastric folds with fibrinopurulent exudate. 1 CT scan and EUS may show thickening of the gastric wall. 1,3lthough SG predominantly involves the submucosa of the stomach, the inflammation may progress and involve all layers. 3Histopathologically, the submucosa is thickened due to infiltration by neutrophil granulocytes and plasma cells. 3,5In advanced cases, possible histological findings include necrosis, abscess formation, intramural hemorrhage and thrombosis of the submucosal blood vessels. 5Differential diagnosis of SG commonly includes superinfected malignancy, gastric lymphoma, gastrointestinal stromal tumor, tuberculosis. 1,6ptimal treatment for SG consists of antibiotics, with surgery reserved for refractory and complicated cases. 1 The histological description was a key factor in our case because it provided prompt diagnosis and early treatment.

Conclusion
Taking in consideration the high mortality rate of SG, it is necessary to make an early diagnosis and start the treatment against specific pathogens, since it can be crucial for a better outcome of this clinical condition.