Digestive Diseases and Sciences, Vol. 37, No. 9 (September 1992), pp. 1454-1459
CASE REPORT
Phlegmonous Gastritis Associated with HIV-1 Seroconversion Endoscopic and Microscopic Evolution J E A N - F A B I E N ZAZZO, G I L L E S TROCHt~, B E R T A N D M I L L A T , A L A I N A U B E R T , P I E R R E B E D O S S A , and L I L I A N E K1EROS KEY WORDS: phlegmonous gastritis; peritonitis; beta-hemolytic group A streptococcus; AIDS; HIV-1 seroconversion; gastroduodenoscopy; surgery.
Phlegmonous gastritis is a rare and often lethal disease. Since 1945, 38 cases have been reported. Diagnosis is rarely made premortem without laparotomy. U p p e r gastrointestinal e n d o s c o p y m a y be of value in establishing the diagnosis in emergencies with culture of purulent gastric aspirate and biopsies (1, 2). Mortality is high, usually within a few days. Aggressive treatment b y antibiotics, however, m a y improve the outcome (2, 3). Preexisting disease, such as peptic ulcers, gastric carcinoma, alcoholic liver disease, diabetes mellitus, invasive gastroscopic manipulation, oral intoxication with caustic substances, m a y be a risk-factor. Phlegmonous gastritis associated with the acquired immunodeficiency syndrome has been reported recently (4). We report a case of phlegmonous gastritis associated with HIV-1 seroconversion and with an extensive endoscopic and microscopic follow-up during recovery. CASE REPORT
On June 6, 1990, because of severe epigastric pain of 6 hr duration, vomiting, sweating and dizziness, a 40-yearold-white man was admitted to the hospital. The patient was slightly confused, with temperature of 38.5 ~ C, blood pressure 160/90 mm Hg, and a pulse rate of 108/min. Physical examination disclosed a vultuous facies and a moderate abdominal tenderness. There was a past history of alcohol use, appendicectomy when he was 12 years Manuscript received October 23, 199i; accepted January 15, 1992. From the Departments of Anesthesiology, Surgery, Gastroenterology, Pathology and Immunology, H6pital Antoine B6cl6re, Universit6 Paris-Sud, Clamart, France. Address for reprint requests: Dr. Jean-Fabien Zazzo, Intensive Care Unit, H6pital Antoine B6cl6re, 92141 Clamart C6dex France. 1454
old, surgery for sinusitis in 1986 followed by one blood unit transfusion and, three weeks before admission a diagnosis of gastroenteritis without fever was made by the general practitioner. White blood cell count on admission was 13,200/mm 3, with 34% polymorphonuclear leukocytes, 3% lymphocytes, 2% monocytes, 46% metamyelocytes, and 15% myelocytes; hemoglobin was 15.1 g/100 ml. Blood urea nitrogen, transaminases, and amylase were normal. Abdominal x-ray showed no intraperitoneal free air but a dilated loop of small bowel. Esophagogastroduodenoscopy performed 1 hr after admission was normal. Patient was then admitted in the surgical unit with nothingper os and intravenous electrolytic infusions with vitamins. Blood and urine samples were collected for cultures. No antibiotics were administrated on the first day. On the second day, epigastric tenderness and persisting signs of sepsis lend to laparotomy with a diagnosis of peritonitis of unknown origin. A purulent intraperitoneal diffuse exudate was found (direct examination revealed numerous white blood cells and grampositive cocci). The gastric wail was edematous and thickened, returning to normal aspect near the pylorus. Liver biopsy showed steatosis. Antibiotic therapy with penicillin G (12 million units/day) was began. No gastric resection was performed, and the abdominal incision was closed without drainage. The patient was admitted in intensive care unit and ventilated for 15 days because of hypoxemia. Blood, peritoneal fluid, and gastric aspirate collected on the operating day grew beta-hemolytic streptococcus, group A, while blood cultures collected at admission were sterile. Intravenous penicillin G was replaced with ampicillin and netromycine according to the culture results. On June 15, a second endoscopy was performed and revealed, in the gastric fundus and the antrum, wide and deep ulcerations covered by a fibrinopurulent exudate (Figure 1A and B). Pathology revealed a necrotic mucosa with intramural microabscesses (Figure 2) without any viral inclusions or fungi. On June 22, temperature was 37~ C; a third endoscopy showed similar lesions up to the pylorus. Microscopy was unchanged. On June 29, a fourth endoscopy revealed only two superficial ulcerations in the fundus still covered by persisting puruDigestive Diseases and Sciences, Vol. 37, No. 9 (September 1992)
0163-2116/92/0900-1454506.50/0 9 1992 Plenum Publishing Corporation
P H L E G M O N O U S GASTRITIS WITH HIV-1
Fig 1. (A) Endoscopic view eight days after admission: wide and deep ulceration of fundus. (B) Endoscopic view eight days after admission: fibrinopurulent exudate of antrum. (C) Endoscopic view a month after admission: edema and superficial ulcerations in the antrum area without purulent exudate. (D) Endoscopic view after recovery: stenotic aspect of the antrum.
lent exudate. On July 6, a fifth endoscopy (one month after admission) revealed superficial ulcerations in the antrum area without purulent exudate (Figure 1C); bacDigestive Diseases and Sciences, Vol. 37, No. 9 (September 1992)
teriology was negative. Antibiotic therapy was stopped and oral nutrition reintroduced without any trouble. On July 16, a sixth endoscopy revealed healing lesions and a
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Digestive Diseases a n d Sciences, Vol. 37, N o . 9 ( S e p t e m b e r 1992)
PHLEGMONOUS GASTRITIS WITH HIV-1 stenotic aspect of the antrum (Figure 1D). Two months later, on September 7, the last endoscopy revealed a normal fundus with a sequellar stenosis of the antrum without clinical features of slowed gastric emptying (Figure 3). On June 18, a serologic screening was performed for hepatitis B, non-A, non-B, and HIV. Anti-HIV antibodies were tested by two different enzyme immunoassays (Diagnostics Pasteur Elavia I, and Abbott EIA I+II). Western blot analysis was carried out using HIV Western blot kits (Diagnostics Pasteur New Lavblot I, France). The original serum sample was clearly positive with the Abbott kit and showed an atypical Western blot pattern with only a faint gp 160 band. The second sample (on June 27) was reactive with all the enzyme immunoassays and showed increased titers of HIV antibodies but continued to have indeterminate Western blot results (faint gp 160). The follow-up sample, on July 9, showed five Western blot bands specific for HIV-1 infection (gp 17, 24, 55, 120, 160), whereas titers of antibodies increased quickly. LymphogC~..es profile showed a total lymphocyte count of 3.9 x 10/liter. Only 24% of these cells were positive for CD4. The patient denied any drug addiction, but he mentioned unprotected heterosexual contacts with different partners in the preceding months (February, March, and May). DISCUSSION We report a case of nonlethal phlegmonous gastritis associated with HIV-1 seroconversion and assessed by an extensive endoscopic follow-up with bacteriological and histologic sampling. Recovery was obtained with antibiotic therapy. The clinical picture was similar to the other cases reported. Epigastric pain with tenderness is common but fever is absent in some cases (1, 5-9). Peritonitis is rarely noted at admission (3, 5, 10-12) but may become evident a few days later (1, 7, 13). In 50% of cases the diagnosis is determined only at autopsy. Radiographic findings are usually nonspecific. Phlegmonous gastritis has already been diagnosed by endoscopy, but this procedure was performed only four days after admission (2, 14) or at an unmentioned date (1). In the present case, endoscopy performed 1 hr after admission was normal. Diagnosis was made by laparotomy, which revealed diffuse fibrinopurulent exudate in the peritoneal cavity and a thickened gastric wall from the cardia to the pylorus. Infection in phlegmonous gastritis is usually caused by oropharyngeal organisms. In 70% of cases, alpha- or beta-hemolytic streptococcus are isolated from blood, peritoneal, or gastric suction cultures. These cultures were positive on the second day after admission. Chronic alcoholism with or without liver involvement is a known predisposDigestive Diseases and Sciences, Vol. 37, No. 9 (September 1992)
ing factor. Recently, a case of phlegmonous gastritis was reported in a patient with AIDS (4) and in a patient who was a heroin abuser (no HIV serologic tests available) (9). Our patient developed HIV-1 seroconversion during hospitalisation. These findings underline the role of immunosuppression. A 100% mortality rate is reported by Miller et al (3) in medically treated patients as compared to a 18% mortality rate when a gastric resection is combined with antibiotics. If diagnosis is established by upper gastrointestinal endoscopy and bacteriology, aggressive treatment with antibiotics, (penicillin G, ampicillin, or ureidopenicillin) may be the best choice. In fact, the common factors in all the survivors were the early recognition of the disease by laparotomy or endoscopy and the prompt institution of intensive supportive measures and antibiotics. While under medical treatment, the risk of transmural infection producing gangrenous nonviable gastric tissue is high. Repeated abdominal x-ray during the clinical course must look for free intraperitoneal air and/or gas within the gastric wall. Septic shock or multiple organ failure must lead to operation. Endoscopies and biopsies showed, in the present report, that wide ulcerations persisted during the first three weeks after admission. Prompt recognition of phlegmonous gastritis by endoscopic biopsies and bacteriological sampling may improve the prognosis of these patients, especially when underlying disease (alcohol liver disease, immunosuppression) is present. Even though surgical resection combined with antibiotics has been advocated in patients with peritonitis and diffuse gastric involvement, a conservative treatment may be the best choice. The last few years have seen a rising incidence of immunocompromised patients (AIDS, organ transplantations, neutropenic patients) and streptococcal infections. Physicians need to be aware of these complications.
SUMMARY A 40-year-old man presented with peritonitis. Diagnosis of phlegmonous gastritis was made b y laparotomy. Conservative treatment combined with antibiotics was successful. Multiple endoscopies with biopsies illustrate the natural history of this disease. The patient developed HIV-1 seroconversion during hospital stay. Prompt diagnosis and treatment may improve the prognosis of this often lethal disease.
1457
ZAZZO ET A L
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Digestive Diseases and Sciences, VoL 37, No. 9 (September 1992)
P H L E G M O N O U S GASTRITIS W I T H HIV-1 REFERENCES 1. Avil~s JF, Fernandez-Serra J, Barcena R, Domiinguez F, Fernandez C, Ledo L: Localized phlegmonous gastritis: Endoscopic view. Endoscopy 20:38-39, 1988 2. Girodet J, Ren6 E, St6rin P, Vissuraire C, Bonfils S: Gastrite phlegmoneuse. Int6r6t pour un diagnostic pr6coce de l'endoscopie et de l'6tude bact6riologique du liquide d'aspiration gastrique. Gastroenterol Clin Biol 3:37-41, 1979 3. Miller AL, Smith B, Rogers AL: Phlegrnonous gastritis. Gastroenterology 68:231-238, 1975 4. Mittleman RE, Suarez RV! Phlegmonous gastritis associated with the acquired immunodeficiency syndrome/pre-acquired immunodeficiency syndrome. Arch Pathol Lab Med 109: 765-767, 1985 5. Stein LB, Greenberg RE, Ilardi CF, Kurtz L, Bank S: Acute necrotizing gastritis in a patient with peptic ulcer disease. Am J Gastroenterol 84:1552-1554, 1989 6. O'Toole PA, Morris JA: Acute phlegmonous gastritis. Postgrad Med J64:315-316, 1988 7. Bracco E, Sategna-Guidetti C, Durando R, Palestini N:
Digestive Diseases and Sciences, Vol. 3Z No. 9 (September 1992)
8.
9.
10.
11. 12. 13. 14.
Phlegmonous gastritis associated with a very high serum CPK level. J Clin Gastroenterol 9:364-366, 1987 Tierney LM, Gooding G, Bottles K, Montgomery CK, Fitzgerald FT: Phlegmonous gastritis and hemophilus influenzae peritonitis in a patient with alcohol liver disease. Dig Dis Sci 32:97-101, 1987 Blei ED, Abrahams C: Diffuse phlegrnonous gastroenterocolitis in a patient with an infected peritoneo-jugular venous shunt. Gastroenterology 84:636-639, 1983 Strauss ILl, Friedman M, Platt N, Gassner W, Wise L: Gangrene of the stomach: A case of necrotizing gastritis. Am J Surg 135:253-257, 1978 Williams BL, Becby DI: Acute diffuse phlegmonous gastritis. Br J Surg 60:498-500, 1973 Nevin NC, Eakins D, Clarke SD, Carson JL: Acute phlegmonous gastritis. Br J Surg 56:268-270, 1969 Lifton LJ, Schlossberg D: Phlegmonous gastritis after endoscopic polypectomy. Ann Intern Med 97:373-374, 1982 Bron BA, Deyhle P, Pelloni S, Krejs GJ, Siebenmann RE, Blum AL: Phlegmonous gastritis diagnosed by endoscopic snare biopsy. Am J Dig Dis 22:729-733, 1977
1459
CASE REPORT
Phlegmonous Gastritis Associated with HIV-1 Seroconversion Endoscopic and Microscopic Evolution J E A N - F A B I E N ZAZZO, G I L L E S TROCHt~, B E R T A N D M I L L A T , A L A I N A U B E R T , P I E R R E B E D O S S A , and L I L I A N E K1EROS KEY WORDS: phlegmonous gastritis; peritonitis; beta-hemolytic group A streptococcus; AIDS; HIV-1 seroconversion; gastroduodenoscopy; surgery.
Phlegmonous gastritis is a rare and often lethal disease. Since 1945, 38 cases have been reported. Diagnosis is rarely made premortem without laparotomy. U p p e r gastrointestinal e n d o s c o p y m a y be of value in establishing the diagnosis in emergencies with culture of purulent gastric aspirate and biopsies (1, 2). Mortality is high, usually within a few days. Aggressive treatment b y antibiotics, however, m a y improve the outcome (2, 3). Preexisting disease, such as peptic ulcers, gastric carcinoma, alcoholic liver disease, diabetes mellitus, invasive gastroscopic manipulation, oral intoxication with caustic substances, m a y be a risk-factor. Phlegmonous gastritis associated with the acquired immunodeficiency syndrome has been reported recently (4). We report a case of phlegmonous gastritis associated with HIV-1 seroconversion and with an extensive endoscopic and microscopic follow-up during recovery. CASE REPORT
On June 6, 1990, because of severe epigastric pain of 6 hr duration, vomiting, sweating and dizziness, a 40-yearold-white man was admitted to the hospital. The patient was slightly confused, with temperature of 38.5 ~ C, blood pressure 160/90 mm Hg, and a pulse rate of 108/min. Physical examination disclosed a vultuous facies and a moderate abdominal tenderness. There was a past history of alcohol use, appendicectomy when he was 12 years Manuscript received October 23, 199i; accepted January 15, 1992. From the Departments of Anesthesiology, Surgery, Gastroenterology, Pathology and Immunology, H6pital Antoine B6cl6re, Universit6 Paris-Sud, Clamart, France. Address for reprint requests: Dr. Jean-Fabien Zazzo, Intensive Care Unit, H6pital Antoine B6cl6re, 92141 Clamart C6dex France. 1454
old, surgery for sinusitis in 1986 followed by one blood unit transfusion and, three weeks before admission a diagnosis of gastroenteritis without fever was made by the general practitioner. White blood cell count on admission was 13,200/mm 3, with 34% polymorphonuclear leukocytes, 3% lymphocytes, 2% monocytes, 46% metamyelocytes, and 15% myelocytes; hemoglobin was 15.1 g/100 ml. Blood urea nitrogen, transaminases, and amylase were normal. Abdominal x-ray showed no intraperitoneal free air but a dilated loop of small bowel. Esophagogastroduodenoscopy performed 1 hr after admission was normal. Patient was then admitted in the surgical unit with nothingper os and intravenous electrolytic infusions with vitamins. Blood and urine samples were collected for cultures. No antibiotics were administrated on the first day. On the second day, epigastric tenderness and persisting signs of sepsis lend to laparotomy with a diagnosis of peritonitis of unknown origin. A purulent intraperitoneal diffuse exudate was found (direct examination revealed numerous white blood cells and grampositive cocci). The gastric wail was edematous and thickened, returning to normal aspect near the pylorus. Liver biopsy showed steatosis. Antibiotic therapy with penicillin G (12 million units/day) was began. No gastric resection was performed, and the abdominal incision was closed without drainage. The patient was admitted in intensive care unit and ventilated for 15 days because of hypoxemia. Blood, peritoneal fluid, and gastric aspirate collected on the operating day grew beta-hemolytic streptococcus, group A, while blood cultures collected at admission were sterile. Intravenous penicillin G was replaced with ampicillin and netromycine according to the culture results. On June 15, a second endoscopy was performed and revealed, in the gastric fundus and the antrum, wide and deep ulcerations covered by a fibrinopurulent exudate (Figure 1A and B). Pathology revealed a necrotic mucosa with intramural microabscesses (Figure 2) without any viral inclusions or fungi. On June 22, temperature was 37~ C; a third endoscopy showed similar lesions up to the pylorus. Microscopy was unchanged. On June 29, a fourth endoscopy revealed only two superficial ulcerations in the fundus still covered by persisting puruDigestive Diseases and Sciences, Vol. 37, No. 9 (September 1992)
0163-2116/92/0900-1454506.50/0 9 1992 Plenum Publishing Corporation
P H L E G M O N O U S GASTRITIS WITH HIV-1
Fig 1. (A) Endoscopic view eight days after admission: wide and deep ulceration of fundus. (B) Endoscopic view eight days after admission: fibrinopurulent exudate of antrum. (C) Endoscopic view a month after admission: edema and superficial ulcerations in the antrum area without purulent exudate. (D) Endoscopic view after recovery: stenotic aspect of the antrum.
lent exudate. On July 6, a fifth endoscopy (one month after admission) revealed superficial ulcerations in the antrum area without purulent exudate (Figure 1C); bacDigestive Diseases and Sciences, Vol. 37, No. 9 (September 1992)
teriology was negative. Antibiotic therapy was stopped and oral nutrition reintroduced without any trouble. On July 16, a sixth endoscopy revealed healing lesions and a
1455
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Digestive Diseases a n d Sciences, Vol. 37, N o . 9 ( S e p t e m b e r 1992)
PHLEGMONOUS GASTRITIS WITH HIV-1 stenotic aspect of the antrum (Figure 1D). Two months later, on September 7, the last endoscopy revealed a normal fundus with a sequellar stenosis of the antrum without clinical features of slowed gastric emptying (Figure 3). On June 18, a serologic screening was performed for hepatitis B, non-A, non-B, and HIV. Anti-HIV antibodies were tested by two different enzyme immunoassays (Diagnostics Pasteur Elavia I, and Abbott EIA I+II). Western blot analysis was carried out using HIV Western blot kits (Diagnostics Pasteur New Lavblot I, France). The original serum sample was clearly positive with the Abbott kit and showed an atypical Western blot pattern with only a faint gp 160 band. The second sample (on June 27) was reactive with all the enzyme immunoassays and showed increased titers of HIV antibodies but continued to have indeterminate Western blot results (faint gp 160). The follow-up sample, on July 9, showed five Western blot bands specific for HIV-1 infection (gp 17, 24, 55, 120, 160), whereas titers of antibodies increased quickly. LymphogC~..es profile showed a total lymphocyte count of 3.9 x 10/liter. Only 24% of these cells were positive for CD4. The patient denied any drug addiction, but he mentioned unprotected heterosexual contacts with different partners in the preceding months (February, March, and May). DISCUSSION We report a case of nonlethal phlegmonous gastritis associated with HIV-1 seroconversion and assessed by an extensive endoscopic follow-up with bacteriological and histologic sampling. Recovery was obtained with antibiotic therapy. The clinical picture was similar to the other cases reported. Epigastric pain with tenderness is common but fever is absent in some cases (1, 5-9). Peritonitis is rarely noted at admission (3, 5, 10-12) but may become evident a few days later (1, 7, 13). In 50% of cases the diagnosis is determined only at autopsy. Radiographic findings are usually nonspecific. Phlegmonous gastritis has already been diagnosed by endoscopy, but this procedure was performed only four days after admission (2, 14) or at an unmentioned date (1). In the present case, endoscopy performed 1 hr after admission was normal. Diagnosis was made by laparotomy, which revealed diffuse fibrinopurulent exudate in the peritoneal cavity and a thickened gastric wall from the cardia to the pylorus. Infection in phlegmonous gastritis is usually caused by oropharyngeal organisms. In 70% of cases, alpha- or beta-hemolytic streptococcus are isolated from blood, peritoneal, or gastric suction cultures. These cultures were positive on the second day after admission. Chronic alcoholism with or without liver involvement is a known predisposDigestive Diseases and Sciences, Vol. 37, No. 9 (September 1992)
ing factor. Recently, a case of phlegmonous gastritis was reported in a patient with AIDS (4) and in a patient who was a heroin abuser (no HIV serologic tests available) (9). Our patient developed HIV-1 seroconversion during hospitalisation. These findings underline the role of immunosuppression. A 100% mortality rate is reported by Miller et al (3) in medically treated patients as compared to a 18% mortality rate when a gastric resection is combined with antibiotics. If diagnosis is established by upper gastrointestinal endoscopy and bacteriology, aggressive treatment with antibiotics, (penicillin G, ampicillin, or ureidopenicillin) may be the best choice. In fact, the common factors in all the survivors were the early recognition of the disease by laparotomy or endoscopy and the prompt institution of intensive supportive measures and antibiotics. While under medical treatment, the risk of transmural infection producing gangrenous nonviable gastric tissue is high. Repeated abdominal x-ray during the clinical course must look for free intraperitoneal air and/or gas within the gastric wall. Septic shock or multiple organ failure must lead to operation. Endoscopies and biopsies showed, in the present report, that wide ulcerations persisted during the first three weeks after admission. Prompt recognition of phlegmonous gastritis by endoscopic biopsies and bacteriological sampling may improve the prognosis of these patients, especially when underlying disease (alcohol liver disease, immunosuppression) is present. Even though surgical resection combined with antibiotics has been advocated in patients with peritonitis and diffuse gastric involvement, a conservative treatment may be the best choice. The last few years have seen a rising incidence of immunocompromised patients (AIDS, organ transplantations, neutropenic patients) and streptococcal infections. Physicians need to be aware of these complications.
SUMMARY A 40-year-old man presented with peritonitis. Diagnosis of phlegmonous gastritis was made b y laparotomy. Conservative treatment combined with antibiotics was successful. Multiple endoscopies with biopsies illustrate the natural history of this disease. The patient developed HIV-1 seroconversion during hospital stay. Prompt diagnosis and treatment may improve the prognosis of this often lethal disease.
1457
ZAZZO ET A L
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1458
Digestive Diseases and Sciences, VoL 37, No. 9 (September 1992)
P H L E G M O N O U S GASTRITIS W I T H HIV-1 REFERENCES 1. Avil~s JF, Fernandez-Serra J, Barcena R, Domiinguez F, Fernandez C, Ledo L: Localized phlegmonous gastritis: Endoscopic view. Endoscopy 20:38-39, 1988 2. Girodet J, Ren6 E, St6rin P, Vissuraire C, Bonfils S: Gastrite phlegmoneuse. Int6r6t pour un diagnostic pr6coce de l'endoscopie et de l'6tude bact6riologique du liquide d'aspiration gastrique. Gastroenterol Clin Biol 3:37-41, 1979 3. Miller AL, Smith B, Rogers AL: Phlegrnonous gastritis. Gastroenterology 68:231-238, 1975 4. Mittleman RE, Suarez RV! Phlegmonous gastritis associated with the acquired immunodeficiency syndrome/pre-acquired immunodeficiency syndrome. Arch Pathol Lab Med 109: 765-767, 1985 5. Stein LB, Greenberg RE, Ilardi CF, Kurtz L, Bank S: Acute necrotizing gastritis in a patient with peptic ulcer disease. Am J Gastroenterol 84:1552-1554, 1989 6. O'Toole PA, Morris JA: Acute phlegmonous gastritis. Postgrad Med J64:315-316, 1988 7. Bracco E, Sategna-Guidetti C, Durando R, Palestini N:
Digestive Diseases and Sciences, Vol. 3Z No. 9 (September 1992)
8.
9.
10.
11. 12. 13. 14.
Phlegmonous gastritis associated with a very high serum CPK level. J Clin Gastroenterol 9:364-366, 1987 Tierney LM, Gooding G, Bottles K, Montgomery CK, Fitzgerald FT: Phlegmonous gastritis and hemophilus influenzae peritonitis in a patient with alcohol liver disease. Dig Dis Sci 32:97-101, 1987 Blei ED, Abrahams C: Diffuse phlegrnonous gastroenterocolitis in a patient with an infected peritoneo-jugular venous shunt. Gastroenterology 84:636-639, 1983 Strauss ILl, Friedman M, Platt N, Gassner W, Wise L: Gangrene of the stomach: A case of necrotizing gastritis. Am J Surg 135:253-257, 1978 Williams BL, Becby DI: Acute diffuse phlegmonous gastritis. Br J Surg 60:498-500, 1973 Nevin NC, Eakins D, Clarke SD, Carson JL: Acute phlegmonous gastritis. Br J Surg 56:268-270, 1969 Lifton LJ, Schlossberg D: Phlegmonous gastritis after endoscopic polypectomy. Ann Intern Med 97:373-374, 1982 Bron BA, Deyhle P, Pelloni S, Krejs GJ, Siebenmann RE, Blum AL: Phlegmonous gastritis diagnosed by endoscopic snare biopsy. Am J Dig Dis 22:729-733, 1977
1459
