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Answer to the image of the month question (page 599):
870
CORRESPONDENCE
anism must have been operative in our patients. Coselection by HIV does not explain why we observed increased HCV viral loads in our CCR5-⌬32 homozygote patients. The explanation of a chance association proposed by Zhang et al. is not quite satisfactory considering our observations that (1) viral levels were on average approximately 1 log higher in our CCR5-⌬32 carriers than the wild-type patients; (2) a similar, albeit statistically nonsignificant, trend of increased viral loads was also seen in our heterozyogous CCR5-⌬32 HCV and HCV/HIV coinfected patients; and (3) the fact that we found lower frequencies of anti-HCV positive patients with undetectable viremia or viral loads below the detection level of the quantitative assay in our CCR5-⌬32 positive subgroups than in the wild-type patients. Finally, in a French cohort of HIV-positive patients the CCR5-⌬32 mutation was found to be highly associated with persistent viremia of the GB-C virus, a member of the Flaviviridae family closely related to HCV.3 Taken together, the comments provided by Mangia et al. and Zhang et al. seem to indicate that the sole starting hypothesis to our study, which was based on the putative reduced interferon-␥ producing T lymphocytes efficiency in patients with CCR5-⌬32 mutation needs to be modified. Nevertheless, there clearly exist patient groups that suggest an association between the CCR5-⌬32 mutation and persistent viremia that cannot be explained by selection due to protection against HIV infection or other proposed mechanisms. Nevertheless, the comments by Mangia et al. and Zhang et al. clarify the urgent need to better understand the potential role of CCR5⌬32 in non-HIV infections. Two types of studies may be helpful in this situation: Epidemiological analysis of other subgroups with close exposure to blood-borne infections, e.g., patients with high-risk drug using behavior, and functional studies at the cellular level of T lymphocytes. Epidemiological analysis of host genetics and infectious diseases poses a complex problem due to the possibility of multiple infections.
GASTROENTEROLOGY Vol. 124, No. 3
On one hand, this complexity carries the risk to find “spurious associations”; on the other hand, especially in such a situation, negative findings could also be “spurious” since selection bias can operate in either direction.
RAINER P. WOITAS GOHO AHLENSTIEL TILMAN SAUERBRUCH ULRICH SPENGLER Medizinische Klinik u. Poliklinik I Allgemeine Innere Medizin Universita¨ tsklinikum Bonn Bonn, Germany 1. Lechner F, Wong DK, Dunbar PR, Chapman R, Chung RT, Dohrenwend P, Robbins G, Phillips R, Klenerman P, Walker BD. Analysis of successful immune responses in persons infected with hepatitis C virus. J Exp Med 2000;191:1499 –1512. 2. Woitas RP, Ahlenstiel G, Iwan A, Rockstroh JK, Brackmann HH, Kupfer B, Matz B, Offergeld R, Sauerbruch T, Spengler U. The frequency of the HIV-protective CC chemokine receptor 5-⌬32/ ⌬32 genotype is increased in hepatitis C antibody positive patients. Gastroenterology 2002;122:1721–1728. 3. Vallet S, Dorval Y, Perfezou P, Correze P, Pasquier E, De Saint Martin L. A link between GB virus C infection and CCR5 genotype among the HIV infected patients. 42nd ICAAC Abstracts, American Society for Microbiology; September 27–30, 2002; San Diego, CA, 2002:281. doi:10.1053/gast.2003.50133
Answer to the Image of the Month Question (page 599): Gastric Wall Abscess The patient had a gastric wall abscess. Enhanced CT scan showed a low-density tumor with ring enhancement in the anterior wall of the stomach. A diagnosis of gastric wall abscess was made based on the CT appearance and aspiration needle biopsy after the endoscopic ultrasonography (EUS). The needle aspiration of the abscess yielded white pus and Streptococcus intermedius was identified by culture. He was treated by endoscopic drainage, antibiotics, and abstinence from food. During the second week of hospitalization, fever, leukocytosis, and upper abdominal pain disappeared. Then, he left the hospital without any symptoms, and his clinical course after discharge was uneventful. Abscess in the gastric wall, caused by bacterial infection, is extremely rare and the diagnosis is usually made late. It has been generally regarded as a secondary phenomenon to hematogenous spread complicating the infection of the other organs or local invasion of the gastric mucosa with bacteria. In the present case, because there was no evidence of other infectious foci, bacterial entry may have occurred from local invasion of the gastric wall at a site of minor mucosal injury caused by a foreign body, such as fish bones. In fact, this patient has the habit of eating whole small fish. Although we could not recognize fish bones in the stomach, we speculate that a fish bone stuck in the gastric wall might cause infection leading to abscess. Diagnosis of primary gastric wall abscess is not difficult but requires a high degree of suspicion because of its gravity. The endoscopic features of gastric abscess are nonspecific findings of a submucosal mass with thickened and reddened mucosal folds. Appropriate diagnostic imaging procedures such as abdominal ultrasonography, EUS, and CT scan can suggest a correct diagnosis. Early diagnosis and endoscopic internal drainage with appropriate antibiotic therapy are alternatives to aggressive surgery. Early diagnosis may allow cure of this disease with antibiotics alone.
References 1. Will U, Masri R, Bosseckert H, Knopke A, Schonlebe J, Justus J. Gastric wall abscess, a rare endosonographic differential diagnosis of intramural tumors: successful endoscopic treatment. Endoscopy 1998;30:432– 435. 2. Briggs TP, Tyler XE, Dowling BL. Gastric abscess-an unusual presentation. Case report. Eur J Surg. 1991;157:365–366. For submission instructions, please see the Gastroenterology website (http://www.gastrojournal.org).
CORRESPONDENCE
anism must have been operative in our patients. Coselection by HIV does not explain why we observed increased HCV viral loads in our CCR5-⌬32 homozygote patients. The explanation of a chance association proposed by Zhang et al. is not quite satisfactory considering our observations that (1) viral levels were on average approximately 1 log higher in our CCR5-⌬32 carriers than the wild-type patients; (2) a similar, albeit statistically nonsignificant, trend of increased viral loads was also seen in our heterozyogous CCR5-⌬32 HCV and HCV/HIV coinfected patients; and (3) the fact that we found lower frequencies of anti-HCV positive patients with undetectable viremia or viral loads below the detection level of the quantitative assay in our CCR5-⌬32 positive subgroups than in the wild-type patients. Finally, in a French cohort of HIV-positive patients the CCR5-⌬32 mutation was found to be highly associated with persistent viremia of the GB-C virus, a member of the Flaviviridae family closely related to HCV.3 Taken together, the comments provided by Mangia et al. and Zhang et al. seem to indicate that the sole starting hypothesis to our study, which was based on the putative reduced interferon-␥ producing T lymphocytes efficiency in patients with CCR5-⌬32 mutation needs to be modified. Nevertheless, there clearly exist patient groups that suggest an association between the CCR5-⌬32 mutation and persistent viremia that cannot be explained by selection due to protection against HIV infection or other proposed mechanisms. Nevertheless, the comments by Mangia et al. and Zhang et al. clarify the urgent need to better understand the potential role of CCR5⌬32 in non-HIV infections. Two types of studies may be helpful in this situation: Epidemiological analysis of other subgroups with close exposure to blood-borne infections, e.g., patients with high-risk drug using behavior, and functional studies at the cellular level of T lymphocytes. Epidemiological analysis of host genetics and infectious diseases poses a complex problem due to the possibility of multiple infections.
GASTROENTEROLOGY Vol. 124, No. 3
On one hand, this complexity carries the risk to find “spurious associations”; on the other hand, especially in such a situation, negative findings could also be “spurious” since selection bias can operate in either direction.
RAINER P. WOITAS GOHO AHLENSTIEL TILMAN SAUERBRUCH ULRICH SPENGLER Medizinische Klinik u. Poliklinik I Allgemeine Innere Medizin Universita¨ tsklinikum Bonn Bonn, Germany 1. Lechner F, Wong DK, Dunbar PR, Chapman R, Chung RT, Dohrenwend P, Robbins G, Phillips R, Klenerman P, Walker BD. Analysis of successful immune responses in persons infected with hepatitis C virus. J Exp Med 2000;191:1499 –1512. 2. Woitas RP, Ahlenstiel G, Iwan A, Rockstroh JK, Brackmann HH, Kupfer B, Matz B, Offergeld R, Sauerbruch T, Spengler U. The frequency of the HIV-protective CC chemokine receptor 5-⌬32/ ⌬32 genotype is increased in hepatitis C antibody positive patients. Gastroenterology 2002;122:1721–1728. 3. Vallet S, Dorval Y, Perfezou P, Correze P, Pasquier E, De Saint Martin L. A link between GB virus C infection and CCR5 genotype among the HIV infected patients. 42nd ICAAC Abstracts, American Society for Microbiology; September 27–30, 2002; San Diego, CA, 2002:281. doi:10.1053/gast.2003.50133
Answer to the Image of the Month Question (page 599): Gastric Wall Abscess The patient had a gastric wall abscess. Enhanced CT scan showed a low-density tumor with ring enhancement in the anterior wall of the stomach. A diagnosis of gastric wall abscess was made based on the CT appearance and aspiration needle biopsy after the endoscopic ultrasonography (EUS). The needle aspiration of the abscess yielded white pus and Streptococcus intermedius was identified by culture. He was treated by endoscopic drainage, antibiotics, and abstinence from food. During the second week of hospitalization, fever, leukocytosis, and upper abdominal pain disappeared. Then, he left the hospital without any symptoms, and his clinical course after discharge was uneventful. Abscess in the gastric wall, caused by bacterial infection, is extremely rare and the diagnosis is usually made late. It has been generally regarded as a secondary phenomenon to hematogenous spread complicating the infection of the other organs or local invasion of the gastric mucosa with bacteria. In the present case, because there was no evidence of other infectious foci, bacterial entry may have occurred from local invasion of the gastric wall at a site of minor mucosal injury caused by a foreign body, such as fish bones. In fact, this patient has the habit of eating whole small fish. Although we could not recognize fish bones in the stomach, we speculate that a fish bone stuck in the gastric wall might cause infection leading to abscess. Diagnosis of primary gastric wall abscess is not difficult but requires a high degree of suspicion because of its gravity. The endoscopic features of gastric abscess are nonspecific findings of a submucosal mass with thickened and reddened mucosal folds. Appropriate diagnostic imaging procedures such as abdominal ultrasonography, EUS, and CT scan can suggest a correct diagnosis. Early diagnosis and endoscopic internal drainage with appropriate antibiotic therapy are alternatives to aggressive surgery. Early diagnosis may allow cure of this disease with antibiotics alone.
References 1. Will U, Masri R, Bosseckert H, Knopke A, Schonlebe J, Justus J. Gastric wall abscess, a rare endosonographic differential diagnosis of intramural tumors: successful endoscopic treatment. Endoscopy 1998;30:432– 435. 2. Briggs TP, Tyler XE, Dowling BL. Gastric abscess-an unusual presentation. Case report. Eur J Surg. 1991;157:365–366. For submission instructions, please see the Gastroenterology website (http://www.gastrojournal.org).