Signs and symptoms
Symptoms of pouchitis include increased stool frequency, urgency, incontinence, nocturnal seepage, abdominal cramping, pelvic discomfort, and arthralgia.Symptom severity does not always correlate with severity of endoscopically or histologically evaluated pouch inflammation. Additionally, these symptoms are not necessarily specific for pouchitis, as they may arise from other inflammatory or functional pouch disorders such as Crohns disease of the pouch, cuffitis, pouch sinus, or irritable pouch syndrome. The most reliable tool for diagnosis is endoscopy combined with histologic features (derived from tissue biopsies obtained during endoscopy). Diagnosis
Classification
Once a diagnosis of pouchitis is made, the condition is further classified. The activity of pouchitis is stratified as:
Remission (no active pouchitis)
Mild to moderately active (increased stool frequency, urgency, infrequent incontinence)
Severely active (hospitalised for dehydration, frequent incontinence)The duration of pouchitis is defined as acute (less than or equal to four weeks) or chronic (four weeks or more) and the pattern classified as infrequent (1–2 acute episodes), relapsing (three or fewer episodes) or continuous. Finally, the response to medical treatment as labelled as treatment responsive or treatment refractory, with the medication for either case being specified. Treatment
First line treatment is usually with antibiotics, specifically with ciprofloxacin and metronidazole. Ampicillin or piperacillin can also be considered as alternatives to empiric ciprofloxacin and metronidazole. Administration of metronidazole at a high daily dose of 20 mg/kg can cause symptomatic peripheral neuropathology in up to 85% of patients.
In adults, Burkitt lymphoma is uncommon and has poor outcomes. Unsatisfactory initial response to the treatment of Burkitt lymphoma with cyclophosphamide, vincristine, and prednisolone indicates a negative prognosis. Furthermore, failed initial treatment and return of Burkitt lymphoma after a six-month stint of time serve as a poor prognostic indicator. The adequate utilization of therapeutic drugs during initial treatment limits additional treatment options following the return of the disease. Notably, in areas of the world where the initial treatment of Burkitt lymphoma is inadequate further treatment options may remain for cases when the disease returns. Laboratory studies such as lactate dehydrogenase (LDH), CD4 count, and other cytogenetic studies are also prognostic indicators. Unsatisfactory outcomes have been associated with an LDH that is found to be two times above the upper limit of normal. Specifically, there is a poor prognosis associated with a CD4 count that is decreased in the immunodeficiency-associated variant of Burkitt lymphoma. Genetic mutations extending beyond the previously described MYC translocation may also serve as negative prognostic indicators. Some notable genetic findings that may be associated with poor outcomes include: 13q deletion, 7q gain, ID3 and CCND3 double-hit mutations, and 18q21 CN-LOH mutations. The prognosis for Burkitt lymphoma can be better determined following staging utilizing imaging modalities such as positron emission tomography and computed tomography scans where tumor burden and invasion of the central nervous system have been found to indicate a poor prognosis.