Journal of Experimental Biology and Agricultural Sciences, October - 2015; Volume – 3(V) Journal of Experimental Biology and Agricultural Sciences http://www.jebas.org ISSN No. 2320 – 8694 CYTOMEGALOVIRUS INFECTION AS A POSSIBLE CAUSE OF OGILVIE'S SYNDROME: A CASE REPORT AND REVIEW OF THE LITERATURE 1,* 2 Magdalena Fernández García and Marcos Noé Madrid 1Department of Internal Medicine, Hospital Marqués de Valdecilla, University of Cantabria, Santander, Spain 2Family Medicine, Centro de Salud General Dávila, Santander, Spain Received – September 02, 2015; Revision – September 19, 2015; Accepted – October 14, 2015 Available Online – October 20, 2015 DOI: http://dx.doi.org/10.18006/2015.3(5).471.478 KEYWORDS ABSTRACT Colonic pseudo-obstruction Ogilvie's syndrome is an uncommon condition with a heterogeneous etiology. The mechanism is poorly Ogilvie's syndrome understood and likely multifactorial. An imbalance between the parasympathetic and the sympathetic Cytomegalovirus infection innervations of the intestine as well as an abnormal response against gut commensal bacteria are thought to be the main causes. We present the case of an apparently immunocompetent female patient with an Myenteric plexus infection Ogilvie's syndrome associated with cytomegalovirus infection. Enterocolitis All the article published by (Journal of Experimental * Corresponding author Biology and Agricultural Sciences) / CC BY-NC 4.0 E-mail: [email protected] (Magdalena Fernández García) Peer review under responsibility of Journal of Experimental Biology and Agricultural Sciences. Production and Hosting by Horizon Publisher (www.my- vision.webs.com/horizon.html). All _________________________________________________________rights reserved. Journal of Experimental Biology and Agricultural Sciences http://www.jebas.org 472 Fernández-García and Madrid 1 Introduction Present study reports the case of an apparently immunocompetent female patient with an Ogilvie's syndrome Acute colonic pseudo-obstruction, or Ogilvie's syndrome, associated with cytomegalovirus (CMV) infection. Besides, a occurs when symptoms and signs of intestinal obstruction of brief review of the literature on Ogilvie's syndrome with CMV the small or large bowel appears in the absence of a involvement is also presented. mechanical cause. It is typically reported in hospitalized or institutionalized patients with underlying severe illness or after 2 Case Report surgery (Vanek & Al-Salti, 1986). Sometimes infections (Tanida et al., 2013; Charatcharoenwitthaya et al., 2014), A 71 year-old female was admitted in to the Department of metabolic imbalances (Sunnoqrot & Reilly, 2015) or different Internal Medicine, Hospital Marqués de Valdecilla, University medications are involved in its origin (Cappell, 2004). of Cantabria, Santander, Spain in October 2013 because of Potential severe consequences as colonic spontaneous abdominal pain. Her medical history included diabetes mellitus perforation, colonic ischemia or intestinal bleeding may appear type 2 with non-proliferative diabetic retinopathy, chronic liver in its evolution. disease, Child A, secondary to ethanol consumption, Table 1 Main biochemical laboratory results in the reported patient PARAMETER (units) Result Reference Range PERIPHERAL BLOOD White blood cell count (x 103) 4.8 4.8 - 10.8 Neutrophils (%) 46 42.0 - 75.0/ Lymphocytes (%) 5.0 20.0 - 51.0 Band cells (%). 27 _ Metamyelocytes (%) 2 _ Platelets (x 103) 120 150 - 450 x 103 ESR (mm/1sth) 40 1.0 - 15.0 CRP (mg/dl) 10 0.1 - 0.5 Procalcitonin (ng/mL) 4 < 0.5 BIOCHEMISTRY Amylase (U/L) 51 1 - 100 Albumin 3 3.2-5.3 Prothrombin time (%) 57 70 - 100 ALT (U/L) 33 2 - 40 AST (U/L) 58 1 - 37 GGT(U/L) 18 7 - 32 Alkaline phosphatase (U/L) 49 40 - 129 Total bilirubin (mg/dL) 0.7 0.1 - 1.2 HYDROSALINE METABOLISM STUDY Creatinine (mg/dl) 1.4 0.50 - 1.20 Urea (mg/dL) 86 5 - 50 Sodium (mEq / L) 128 135 - 145 Potassium (mEq / L) 2.2. 3.5 - 5.0 GFR (MDRD-4) ml/min/1,73 m2 42 >60.00 Serum aldosterone (pg/ml) 10 10 - 310 PHOSPHO-CALCIC METABOLISM STUDY Serum calcium (mg/dL) 6.5 8.1 - 10.4 Ionized calcium (mM) 1.12 1.16 - 1.30 Ionic normalized calcium (mM) 1.15 1.16 - 1.30 i PTH (pg/ml) 51 10 - 45 25-OH-vitamin D (ng/ml) 24 20 - 60 Phosphorus (mg/dL) 2.8 2.3 - 4.0 Magnesium (mg/dL) 2.1 1.7–2.4 [Abbreviations: ESR: Erythrocyte sedimentation rate; CRP: Chain reaction polymerase; GFR: Glomerular Filtration Rate; ALT; Alanine aminotransferase AST; aspartate aminotransferase; GGT: gamma glutamyl transpeptidase ; i PTH: intact parathyroid hormone] _________________________________________________________ Journal of Experimental Biology and Agricultural Sciences http://www.jebas.org Cytomegalovirus infection as a possible cause of Ogilvie's syndrome: A case report and review of the literature. 473 Figure 1 Abdominal X-ray on admission: Diffuse dilatation of intestines and thickened colonic wall. Figure 2 Abdominal computed tomography scan findings: Dilation of the whole colonic frame. Diffuse thickening of the wall of the rectum and sigmoid colon, without observing regional inflammatory changes, associated collections or masses. anxiety disorder, chronic L4-L5-S1 radiculopathy and a On admission, the patient was hemodynamically stable. Her kyphoplasty due to T12 vertebral fracture three years before temperature was 37ºC, blood pressure was 110/70 mmHg, admission. She denied any tobacco or illicit drug use. She was heart rate was 108 b.p.m and respiratory rate was 22 breaths on metformin, spironolactone, omeprazole, pregabalin, per minute. The patient complained about abdominal pain to clonazepam, alendronate and calcium carbonate plus palpation in the entire abdomen and in the auscultation, cholecalciferol treatment. She referred a history of chronic hypoactive bowel sounds were present. Abdominal X-ray on constipation exacerbated for the last two weeks with admission showed diffuse dilatation of intestines and thickened progressive increase in abdominal perimeter without emission colonic wall (Figure 1). Rectal examination was normal and of gas or feces. In the emergency ward, watery stools without the nasogastric aspirate was clear, without blood or fecaloid pathological products were objectified as well as profuse content. Discontinuation of oral intake, intravenous fluid episodes of nausea and emesis. replacement and piperacillin-tazobactam treatment were started. _________________________________________________________ Journal of Experimental Biology and Agricultural Sciences http://www.jebas.org 474 Fernández-García and Madrid Figure 3 Endoscopic findings: Extense area of edema, erythema and friable mucosa, with multiple lineal fibrinous-based ulcers. Table 1 summarizes the main laboratory studies conducted. gastrointestinal endoscopy was performed too, showing Despite the general condition of the patient was good, profuse esophageal varices grade I. watery diarrhea and vomiting persisted. A severe electrolyte imbalance, not present on admission lab-determinations Table 2 shows the microbiological and immunological studies appears. Arterial blood gases showed a pH of 7.28, pCO2 39.1 performed. Histopathological examination of the colonic mm Hg, bicarbonate of 17.1 mEq/l and a BE of -8.700, biopsy showed an intense acute and chronic inflammation in compatible with a simple metabolic acidosis. A significative the lamina propria and granulation tissue but no intranuclear hypokalemia (2.2 mEq / L) and hypocalcemia (6.6 mEq / L) inclusions were observed. A PCR method to detect human lead us to the infusion of potassium chloride and calcium herpesvirus and enterovirus (Clart Entherpex, Genomica SAU, gluconate, with serum potassium and calcium concentrations Madrid, Spain) was used in the specimen from the maintained in the 3.5 mEq /l and 7.8 mg/dL, respectively. colonoscopic biopsy. The molecular analysis was positive for CMV, and the diagnosis of CMV infection was established. An abdominal computed tomography scan objectified the presence of morphological changes related to liver cirrhosis On the twelfth hospital day intravenous ganciclovir was started and perihepatic ascites. Cholelithiasis, without parietal or at induction dose (5 mg/kg/12h) during the first week. Then, regional inflammatory signs and no dilatation of the bile ducts the patient completed 4 weeks of maintenance dose treatment were observed. (5/mg/kg/24h). The clinical outcome was favourable with the normalization of gastrointestinal transit and the resolution of A striking dilation of the whole colonic frame was present, the colonic pseudo-obstruction. Three months later, a new from the cecal area to the rectal ampulla, accompanied by a control ileo-colonoscopy was performed and biopsies were diffuse thickening of the wall of the rectum and sigmoid colon, taken again. In this case, the molecular analysis was negative without observing regional inflammatory changes, associated for CMV. collections or masses. No contrast defects were identified in the mesenteric artery or vein. There was no sign of intestinal Discussion pneumatosis which may suggest mesenteric ischemia. No significant dilatations of the small bowel loops were present Ogilvie (1948) first described this syndrome in association (Figure 2). The diagnosis of Ogilvie’s syndrome was with retroperitoneal malignancy infiltration of the celiac established and nasogastric and rectal tubes were placed, plexus. Today, its precise mechanism is still unknown but the improving both, abdominal distension and, partially, emesis so most plausible and accepted theory suggests an impairment