- Email: [email protected]
Epiploic appendagitis mimicking pelvic inflammatory disease (PID)
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Letter to the EditorLetters to the Editor / European Journal of Obstetrics & Gynecology and Reproductive Biology 140 (2008) 124–148
References [1] Melius FA, Julious TM, Nagel TC. Prolonged retention of intrauterine bones. Obstet Gynecol 1991;78:919–21. [2] Marcus SF, Bhattacharya J, Williams G, Brinaden P, Hamou J. Endometrial ossification: a cause of secondary infertility. Am J Obstet Gynecol 1994;170:1381–3. [3] Lewis V, Khan-Dawood F, King M, Beckmann C, Dawood MY. Retention of intrauterine fetal bone increases menstrual prostaglandins. Obstet Gynecol 1990;75:561. [4] Dawood MY, Jarret JC. Prolonged intrauterine retention of fetal bones after abortion causing infertility. Am J Obstet Gynecol 1982;143:715. [5] Cepni I, Kumbak B, Ocal P, Idil M, Aksu F. Infertility due to intrauterine residual fetal bone fragments. J Clin Ultrasound 2004;32:253–5.
Ebru Gurleyig Cem Celik* Firat Ersan Ozay Oral Zeynep Kamil Teaching Hospital, uskudar, Istanbul, Turkey *Corresponding author. Tel.: +90 216 3430608 E-mail address: [email protected] (C. Celik ) 16 April 2007 doi:10.1016/j.ejogrb.2007.09.011
Epiploic appendagitis mimicking pelvic inflammatory disease (PID) Dear Editor, We would like to report that epiploic appendagitis may mimic pelvic inflammatory disease (PID). Given the morbidity associated with PID, specifically its impact on fertility, the Centers for Disease Control and Prevention (CDC) have issued guidelines regarding its diagnosis and management [1]. Cervical motion tenderness or uterine tenderness is minimal diagnostic criteria. Inability to tolerate oral medications and inability to exclude a surgical etiology are amongst the criteria for inpatient treatment. A 27-year-old Hispanic multiparous woman presented to the emergency department reporting 1 week of worsening constant lower abdominal pain associated with nausea and vomiting, more marked on the left side. She had experienced similar less severe symptoms over the preceding year. She had exacerbations of the pain when driving over bumps on the road. She reported deep dyspareunia. Her appetite and food intake were decreased, with no change in bowel habits. The patient and her husband reported that they would welcome pregnancy, but had been told by a gynecologist in her home country that she was at high risk for ectopic gestation because of previously treated ‘‘pelvic
infections’’. Medical and surgical history was otherwise negative. On physical examination, the patient appeared very uncomfortable. She was afebrile with normal vital signs. Abdominal examination was significant for marked tenderness in both lower quadrants, more pronounced on the left side. On speculum examination white discharge from the cervical os was noted. The wet mount revealed moderate leukocytes, but no hyphae or clue cells. On bimanual examination there was significant marked cervical motion tenderness and bilateral adnexal tenderness. Rectal examination with Guaiac testing was negative. Laboratory testing revealed undetectable serum beta-HCG levels, a white cell count of 8.9 109 L1, hematocrit of 41.1%, and platelets of 361 109 L1. Electrolytes, liver function tests, amylase and lipase were all normal. On pelvic ultrasound, a homogenous endometrial stripe measuring 1.7 mm and no evidence of tubo-ovarian abscess (TOA) were seen. Assessment by the general surgery and gynecology services resulted in a clinical diagnosis of PID. Given her inability to tolerate oral medications, the patient was admitted for intravenous antibiotic therapy with levofloxacin and metronidazole, the alternative acceptable parenteral regimen per CDC criteria [1]. On hospital day 2, the patient continued to require opiate analgesia, with persistent marked tenderness on abdominal examination. Cervical probes sent at presentation were returned negative for Chlamydia trachomatis and Neisseria gonorrhoeae nucleic acid. A CT scan of the abdomen and pelvis was performed (Fig. 1). A diagnosis of epiploic appendagitis was made based on the classic findings of a solitary enhancing ovoid fatty lesion with surrounding soft tissue stranding [2]. The patient was treated with non-steroidal anti-inflammatory drugs, and antibiotics were discontinued. Her symptoms resolved within 1 week of presentation. The CDC recommends that ‘‘because of the difficulty of diagnosis and the potential for damage to the reproductive health of women, health-care providers should maintain a
Fig. 1. CT image demonstrating a solitary enhancing ovoid fatty lesion that abuts the anterior sigmoid colon wall, with surrounding soft tissue stranding (arrow). These findings are pathognomonic for a diagnosis of epiploic appendagitis [3].
Letters to the Editor / European Journal of Obstetrics & Gynecology and Reproductive Biology 140 (2008) 124–148
low threshold for the diagnosis of PID.’’ [1] Therefore, gynecologists must recognize non-gynecologic conditions which fulfill minimal diagnostic criteria and mimic PID. Acute epiploic appendagitis is a self-limiting inflammation of the appendices epiploicae, known to mimic appendicitis and acute diverticulitis. CT scan findings of a 1.5–3.5 cm oval shaped, fat density lesion that abuts the anterior sigmoid colon wall, surrounded by inflammatory change, are thought to be pathognomonic for epiploic appendagitis [3]. Before the widespread advent of CT imaging, it was usually diagnosed at surgery. The etiology is thought to be torsion of epiploic appendages, with resultant vascular occlusion leading to ischemia. Treatment is conservative with oral anti-inflammatory medications, and antibiotics are not indicated. Surgery is not indicated and most patients recover with conservative management in less than 10 days. Misdiagnosis of acute epiploic appendagitis as PID may result in unnecessary hospital admissions and excessive use of broad-spectrum antibiotic therapy. This is the first report describing epiploic appendagitis as a mimic of PID.
References [1] Centers for Disease Control and Prevention, Workowski KA, Berman SM. Sexually transmitted diseases treatment guidelines, 2006. MMWR Recomm Rep 2006;55(RR-11):1–94. [2] Sandrasegaran K, Maglinte DD, Rajesh A, et al. Primary epiploic appendagitis: CT diagnosis. Emerg Radiol 2004;11(1):9–14. [3] Singh AK, Gervais DA, Hahn PF, et al. Acute epiploic appendagitis and its mimics. Radiographics 2005;25(6):1521–34.
Alexander M. Quaas* Department of Obstetrics and Gynecology, Massachusetts General Hospital, Boston, MA, United States Peter R. Mueller Department of Radiology, Massachusetts General Hospital, Boston, MA, United States Jennifer M. Kickham Department of Obstetrics and Gynecology, Massachusetts General Hospital, Boston, MA, United States *Corresponding author. Tel.: +1 617 7249030; fax: +1 617 7264267 E-mail address: [email protected] (A.M. Quaas) 21 April 2007 doi:10.1016/j.ejogrb.2007.09.002
135
Altered circulating neurokinin B (NKB) levels are not due to sequence variants in the encoding genes Dear Editor, The measurement of elevated levels of neurokinin B (NKB) in pregnancies complicated by pre-eclampsia has been confirmed in several studies [1]. To investigate whether DNA sequence variants could possibly underlie the alteration in circulating NKB levels or predispose to pre-eclampsia, we performed mutation screening of the TAC3 and TACR3 genes, which encode neurokinin B and its receptor (NK3), respectively, in 140 patients with early-onset severe pre-eclampsia [2] and 60 control individuals. Concurrently, NKB levels were measured by EIA in 52 of the patient samples. Genomic amplicons representing all the exons (with flanking intronic regions, some extending into the 50 and 30 untranslated regions) were subjected to Multiphor single stranded conformational polymorphism (SSCP)/heteroduplex analysis (HA). Conformational variants were further characterised by bidirectional automated sequencing and subsequently, genotyping was performed by restriction enzyme analysis, where appropriate. Five sequence variants were identified (Table 1) including three which had previously been documented. A novel intronic TAC3 base pair substitution (G-T) was identified 53 bp before the start of exon 4. There was no statistically significant association demonstrated in the comparison of genotype frequencies in patient and control groups ( p = 0.47). Despite the variant being localised beyond the consensus intron-exon splice boundary, and not within a recognized splice branch site, it could still create a splicing defect. This could result in an alteration in the level of the mature mRNA generated, and consequently contribute to disease, reported to be the case for 15% of all intronic polymorphisms [3]. The second novel variant was a T-C base pair substitution in the third nucleotide of TAC3 exon 5 (representing coding nucleotide position 295 of the gene). The variant was identified at similar frequencies in patients and controls (0.14 and 0.10, respectively) and no significant association was demonstrated in the comparison of the two groups ( p = 0.93). The effect of this sequence variant is a change from a hydrophilic serine to a hydrophobic proline amino acid residue. Application of the ESEfinder program (http://exon.cshl.edu/ESE) predicted that in the presence of the variant C allele, single SC35 and SRp40 binding sites are abolished, while a novel one is created. This provides in silica evidence for an increase in the potential of alternative splicing and needs to be addressed in functional studies. Of the previously documented sequence variants identified in this study, the TACR3 857A-G [dbSNP: rs2276973] is rare and TAC3-25 C-T [dbSNP:rs2291855] and TACR3 -103 T-C [dbSNP: rs3733632] are 50 untranslated region polymorphisms. A statistical significant difference, p = 0.02,
Letter to the EditorLetters to the Editor / European Journal of Obstetrics & Gynecology and Reproductive Biology 140 (2008) 124–148
References [1] Melius FA, Julious TM, Nagel TC. Prolonged retention of intrauterine bones. Obstet Gynecol 1991;78:919–21. [2] Marcus SF, Bhattacharya J, Williams G, Brinaden P, Hamou J. Endometrial ossification: a cause of secondary infertility. Am J Obstet Gynecol 1994;170:1381–3. [3] Lewis V, Khan-Dawood F, King M, Beckmann C, Dawood MY. Retention of intrauterine fetal bone increases menstrual prostaglandins. Obstet Gynecol 1990;75:561. [4] Dawood MY, Jarret JC. Prolonged intrauterine retention of fetal bones after abortion causing infertility. Am J Obstet Gynecol 1982;143:715. [5] Cepni I, Kumbak B, Ocal P, Idil M, Aksu F. Infertility due to intrauterine residual fetal bone fragments. J Clin Ultrasound 2004;32:253–5.
Ebru Gurleyig Cem Celik* Firat Ersan Ozay Oral Zeynep Kamil Teaching Hospital, uskudar, Istanbul, Turkey *Corresponding author. Tel.: +90 216 3430608 E-mail address: [email protected] (C. Celik ) 16 April 2007 doi:10.1016/j.ejogrb.2007.09.011
Epiploic appendagitis mimicking pelvic inflammatory disease (PID) Dear Editor, We would like to report that epiploic appendagitis may mimic pelvic inflammatory disease (PID). Given the morbidity associated with PID, specifically its impact on fertility, the Centers for Disease Control and Prevention (CDC) have issued guidelines regarding its diagnosis and management [1]. Cervical motion tenderness or uterine tenderness is minimal diagnostic criteria. Inability to tolerate oral medications and inability to exclude a surgical etiology are amongst the criteria for inpatient treatment. A 27-year-old Hispanic multiparous woman presented to the emergency department reporting 1 week of worsening constant lower abdominal pain associated with nausea and vomiting, more marked on the left side. She had experienced similar less severe symptoms over the preceding year. She had exacerbations of the pain when driving over bumps on the road. She reported deep dyspareunia. Her appetite and food intake were decreased, with no change in bowel habits. The patient and her husband reported that they would welcome pregnancy, but had been told by a gynecologist in her home country that she was at high risk for ectopic gestation because of previously treated ‘‘pelvic
infections’’. Medical and surgical history was otherwise negative. On physical examination, the patient appeared very uncomfortable. She was afebrile with normal vital signs. Abdominal examination was significant for marked tenderness in both lower quadrants, more pronounced on the left side. On speculum examination white discharge from the cervical os was noted. The wet mount revealed moderate leukocytes, but no hyphae or clue cells. On bimanual examination there was significant marked cervical motion tenderness and bilateral adnexal tenderness. Rectal examination with Guaiac testing was negative. Laboratory testing revealed undetectable serum beta-HCG levels, a white cell count of 8.9 109 L1, hematocrit of 41.1%, and platelets of 361 109 L1. Electrolytes, liver function tests, amylase and lipase were all normal. On pelvic ultrasound, a homogenous endometrial stripe measuring 1.7 mm and no evidence of tubo-ovarian abscess (TOA) were seen. Assessment by the general surgery and gynecology services resulted in a clinical diagnosis of PID. Given her inability to tolerate oral medications, the patient was admitted for intravenous antibiotic therapy with levofloxacin and metronidazole, the alternative acceptable parenteral regimen per CDC criteria [1]. On hospital day 2, the patient continued to require opiate analgesia, with persistent marked tenderness on abdominal examination. Cervical probes sent at presentation were returned negative for Chlamydia trachomatis and Neisseria gonorrhoeae nucleic acid. A CT scan of the abdomen and pelvis was performed (Fig. 1). A diagnosis of epiploic appendagitis was made based on the classic findings of a solitary enhancing ovoid fatty lesion with surrounding soft tissue stranding [2]. The patient was treated with non-steroidal anti-inflammatory drugs, and antibiotics were discontinued. Her symptoms resolved within 1 week of presentation. The CDC recommends that ‘‘because of the difficulty of diagnosis and the potential for damage to the reproductive health of women, health-care providers should maintain a
Fig. 1. CT image demonstrating a solitary enhancing ovoid fatty lesion that abuts the anterior sigmoid colon wall, with surrounding soft tissue stranding (arrow). These findings are pathognomonic for a diagnosis of epiploic appendagitis [3].
Letters to the Editor / European Journal of Obstetrics & Gynecology and Reproductive Biology 140 (2008) 124–148
low threshold for the diagnosis of PID.’’ [1] Therefore, gynecologists must recognize non-gynecologic conditions which fulfill minimal diagnostic criteria and mimic PID. Acute epiploic appendagitis is a self-limiting inflammation of the appendices epiploicae, known to mimic appendicitis and acute diverticulitis. CT scan findings of a 1.5–3.5 cm oval shaped, fat density lesion that abuts the anterior sigmoid colon wall, surrounded by inflammatory change, are thought to be pathognomonic for epiploic appendagitis [3]. Before the widespread advent of CT imaging, it was usually diagnosed at surgery. The etiology is thought to be torsion of epiploic appendages, with resultant vascular occlusion leading to ischemia. Treatment is conservative with oral anti-inflammatory medications, and antibiotics are not indicated. Surgery is not indicated and most patients recover with conservative management in less than 10 days. Misdiagnosis of acute epiploic appendagitis as PID may result in unnecessary hospital admissions and excessive use of broad-spectrum antibiotic therapy. This is the first report describing epiploic appendagitis as a mimic of PID.
References [1] Centers for Disease Control and Prevention, Workowski KA, Berman SM. Sexually transmitted diseases treatment guidelines, 2006. MMWR Recomm Rep 2006;55(RR-11):1–94. [2] Sandrasegaran K, Maglinte DD, Rajesh A, et al. Primary epiploic appendagitis: CT diagnosis. Emerg Radiol 2004;11(1):9–14. [3] Singh AK, Gervais DA, Hahn PF, et al. Acute epiploic appendagitis and its mimics. Radiographics 2005;25(6):1521–34.
Alexander M. Quaas* Department of Obstetrics and Gynecology, Massachusetts General Hospital, Boston, MA, United States Peter R. Mueller Department of Radiology, Massachusetts General Hospital, Boston, MA, United States Jennifer M. Kickham Department of Obstetrics and Gynecology, Massachusetts General Hospital, Boston, MA, United States *Corresponding author. Tel.: +1 617 7249030; fax: +1 617 7264267 E-mail address: [email protected] (A.M. Quaas) 21 April 2007 doi:10.1016/j.ejogrb.2007.09.002
135
Altered circulating neurokinin B (NKB) levels are not due to sequence variants in the encoding genes Dear Editor, The measurement of elevated levels of neurokinin B (NKB) in pregnancies complicated by pre-eclampsia has been confirmed in several studies [1]. To investigate whether DNA sequence variants could possibly underlie the alteration in circulating NKB levels or predispose to pre-eclampsia, we performed mutation screening of the TAC3 and TACR3 genes, which encode neurokinin B and its receptor (NK3), respectively, in 140 patients with early-onset severe pre-eclampsia [2] and 60 control individuals. Concurrently, NKB levels were measured by EIA in 52 of the patient samples. Genomic amplicons representing all the exons (with flanking intronic regions, some extending into the 50 and 30 untranslated regions) were subjected to Multiphor single stranded conformational polymorphism (SSCP)/heteroduplex analysis (HA). Conformational variants were further characterised by bidirectional automated sequencing and subsequently, genotyping was performed by restriction enzyme analysis, where appropriate. Five sequence variants were identified (Table 1) including three which had previously been documented. A novel intronic TAC3 base pair substitution (G-T) was identified 53 bp before the start of exon 4. There was no statistically significant association demonstrated in the comparison of genotype frequencies in patient and control groups ( p = 0.47). Despite the variant being localised beyond the consensus intron-exon splice boundary, and not within a recognized splice branch site, it could still create a splicing defect. This could result in an alteration in the level of the mature mRNA generated, and consequently contribute to disease, reported to be the case for 15% of all intronic polymorphisms [3]. The second novel variant was a T-C base pair substitution in the third nucleotide of TAC3 exon 5 (representing coding nucleotide position 295 of the gene). The variant was identified at similar frequencies in patients and controls (0.14 and 0.10, respectively) and no significant association was demonstrated in the comparison of the two groups ( p = 0.93). The effect of this sequence variant is a change from a hydrophilic serine to a hydrophobic proline amino acid residue. Application of the ESEfinder program (http://exon.cshl.edu/ESE) predicted that in the presence of the variant C allele, single SC35 and SRp40 binding sites are abolished, while a novel one is created. This provides in silica evidence for an increase in the potential of alternative splicing and needs to be addressed in functional studies. Of the previously documented sequence variants identified in this study, the TACR3 857A-G [dbSNP: rs2276973] is rare and TAC3-25 C-T [dbSNP:rs2291855] and TACR3 -103 T-C [dbSNP: rs3733632] are 50 untranslated region polymorphisms. A statistical significant difference, p = 0.02,