ABSTRACT
PURPOSE: Clostridium difficile enteritis is a rare infection, with less than a dozen cases reported in the literature. We present a case of a patient with total proctocolectomy and ileostomy, developing Clostridium difficile infection of small bowel. We discuss the role of Clostridium difficile toxins and review previously reported cases of Clostridium difficile enteritis after total colectomy. METHODS: A 65-year-old male with a history of total proctocolectomy and ileostomy 30 years previously had purulent ileostomy drainage and septic shock. The patient was recently treated with intravenous piperacillin, tazobactam, and levofloxacin for aspiration pneumonia in the previous admission. Ileostomy stool cultures tested positive for Clostridium difficile toxin A, and the patient was promptly treated with intravenous metronidazole. RESULTS: The patient was aggressively resuscitated and treated, recovered from the enteritis and shock, but died of pulmonary complications after a prolonged hospitalization. CONCLUSIONS: Review of previously reported cases of Clostridium difficile enteritis showed a high mortality rate. We attribute this to delayed diagnosis secondary to rarity of this illness. Some patients were diagnosed only after pseudomembranes in small-bowel segments were found at autopsy. This rare disease entity is firmly established among the differential diagnosis to clinicians treating patients with total proctocolectomy.
Subject(s)
Clostridioides difficile/isolation & purification , Enteritis/microbiology , Enterocolitis, Pseudomembranous/diagnosis , Aged , Anti-Infective Agents/therapeutic use , Enteritis/drug therapy , Enterocolitis, Pseudomembranous/drug therapy , Fatal Outcome , Humans , Ileostomy , Infusions, Intravenous , Male , Metronidazole/therapeutic use , Postoperative Complications , Proctocolectomy, Restorative , Shock, Septic/drug therapy , Shock, Septic/microbiologyABSTRACT
Adiponectin is an adipocyte-derived plasma protein with insulin-sensitizing and antiatherosclerotic properties. Because adipose tissue depots differ in the strength of their association with the adverse metabolic consequences of obesity, we studied the secretion of adiponectin in vitro from paired samples of isolated human omental and sc adipocytes and its regulation by insulin and rosiglitazone. Cells were incubated for 12 or 24 h with and without treatment with 100 nM insulin, 8 micro M rosiglitazone, or both combined; adiponectin secreted into the culture medium was measured by a RIA with a human adiponectin standard and normalized for cellular DNA content. Secretion of adiponectin by omental cells was generally higher than sc cells and showed a strong negative correlation with body mass index (r = -0.78;P = 0.013). In contrast, secretion from the sc cells was unrelated to body mass index. Compared with sc-derived adipocytes, adiponectin secretion from omental cells was increased by insulin or rosiglitazone alone and was up to 2.3-fold higher following combined treatment with insulin and rosiglitazone, whereas secretion from sc adipose cells was unaffected by these treatments. These data suggest that reduced secretion from the omental adipose depot may account for the decline in plasma adiponectin observed in obesity. Furthermore, enhanced adiponectin secretion from fat cells derived from the visceral compartment in response to rosiglitazone alone or in combination with insulin may play a role in some of the systemic insulin-sensitizing and antiinflammatory properties of the thiazolidinediones.
