Q & A
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July 2001 Q. In assessing chronic gastritis on mucosal biopsies, the quantity of chronic inflammatory cells in the lamina propria is used to discriminate between gastritis and normal. I have learned from texts and lectures that the normal number of chronic inflammatory cells varies and can include zero, few, and less than five per HPF. Is there a consensus on the number of chronic inflammatory cells in normal patients? A. The question asks about the minimum number of mononuclear cells needed to call a gastric biopsy abnormal, but because of similar queries regarding minimal criteria for abnormality in other GI sites, this response is generalized. The issue of abnormal inflammation in glandular GI tract mucosa can be divided into a three-part algorithm based on qualitative and quantitative assessments:
The small bowel will essentially never be judged abnormal based only on the quantity of lamina propria mononuclear cells. The lamina propria is normally rich in lymphocytes and plasma cells with a few eosinophils. "Flat" mucosa is typically artifactual in the absence of intraepithelial lymphocytosis. The only conceivable abnormal situation based on too many lamina propria mononuclear cells is one where the small bowel crypts are widely separated to such a degree that lymphoma or mast cell disease is suspected. Normal colon mucosa normally contains lymphocytes and plasma cells but they are confined to the luminal half of the lamina propria (except in the cecum where they are present throughout the lamina propria). Abnormal lamina propria mononuclear inflammation should always be accompanied by either intraepithelial lymphocytosis (microscopic colitis) or architectural derangement (idiopathic inflammatory bowel disease). Lacking either of these associations, one should be very critical about calling the biopsy abnormal. Don’t hesitate to call those biopsies normal. Remember, there is no such thing as "nonspecific chronic gastroenterocolitis." Bibliogrpahy Jerry Dayharsh, MD Dr. Burgart is a member of the Surgical Pathology Committee. Q. Is there an established or accepted level for WBCs in peritoneal dialysate fluid at which point a differential is not indicated? We are trying to provide a 100-cell differential, regardless of the WBC count. A. The laboratory medicine literature on peritoneal dialysate fluid is almost nonexistent. Standard reference texts1-4 refer peripherally to dialysate fluids in the course of discussing ascitic fluid in general. They suggest that total leukocyte counts of greater than 300-500/µL in ascitic fluid are abnormal and that, if greater than 25 to 50 percent of these cells are neutrophils, the diagnosis of peritonitis should be considered. McBride indicates that an absolute neutrophil count of 240-500/µL has a sensitivity and specificity for bacterial peritonitis in excess of 90 percent.4 According to literature related specifically to nephrology and dialysis,5,6 normal peritoneal dialysis fluid should contain less than 50 WBC/µL,7 less than 15 percent of which should be neutrophils. If the percentage of neutrophils exceeds 35 percent, the fluid should be considered suspicious for bacterial infection. Common nonbacterial causes of neutrophilia in dialysate fluids include infectious diarrhea or active colitis, menstruation or ovulation, and pelvic inflammatory disease. One report even attributed neutrophilia to travel over bumpy mountain roads en route to a dialysis center. Bacterial peritonitis should be seriously considered when any two of the following three criteria are present:
This last criterion is considered to be a minor one for purposes of initiating treatment as the sensitivity is only about 50 percent and results may not be available in less than two hours. However, a positive Gram stain is predictive of culture results in 85 percent of cases and should always be performed when cultures are set up. None of the above information specifically addresses the question of when to perform a WBC differential count on dialysis fluid. Assuming that antibiotic administration is based on a combination of clinical and laboratory criteria, and that the specimen would not have been submitted to the laboratory unless there was clinical evidence suggestive of sepsis, a conservative approach would be to perform a differential count on all cloudy dialysates, regardless of the total leukocyte count. The problem with this approach is that there will be times when a differential WBC would be performed on fluids containing very few cells, definitely a laborious task. Other sets of criteria may be equally valid. Probably the best approach is to arrive at criteria for your institution in consultation with your medical staff. References David Blomberg, MD Hematology/Clinical Microscopy Q. What kind of sterilization procedure do you recommend and how long should the cycle be for Creutzfeldt-Jakob disease postmortem cases? What is your opinion about the real situation with iatrogenic CJD in the United States and the necessity to use specific decontamination procedures to prevent transmission of prions in real practice? A. Creutzfeldt-Jakob disease and other transmissible spongiform encephalopathies are caused by infectious agents that are not inactivated by standard sterilization methods. Thus, special procedures are required to treat contaminated instruments, glassware, and other hard surfaces. Any visible blood should be removed by soaking or washing. Surgical instruments and glassware may then be decontaminated chemically or by autoclaving. Chemical decontamination may be accomplished by soaking for one hour in either sodium hypochlorite (freshly opened Clorox or similar chlorine bleach) or 2N sodium hydroxide. Gravity-displacement autoclaving should be performed at 132°C for at least one hour.1-3 As an additional precaution, one may combine the chemical and autoclaving procedures, either by using chemical treatment followed by autoclaving or, best of all, by autoclaving in sodium hydroxide.1,3 After chemical or combined autoclaving/chemical treatment, the instruments and glassware must be rinsed thoroughly with water. Unless this rinse is sterile, surgical instruments will then require standard autoclaving prior to reuse. Instruments used in neurosurgery or ophthalmologic surgery on known or suspected cases of CJD are frequently discarded. Any tissue samples should be fixed in formalin, exposed to 96 to 100 percent formic acid for one hour, and then returned to formalin for additional fixation prior to processing.1 While the preceding procedures should be used whenever prion disease is suspected in a specific patient, there is no need for their routine use. At least 98 percent of all CJD cases are sporadic or familial; only one to two percent are iatrogenic. To date, all iatrogenic cases have involved exposure to CNS or closely related tissues. Most have been in recipients of cadaveric human growth hormone or dural grafts; a few cases due to corneal transplants, depth electrodes, and contaminated surgical instruments have also occurred.4 No cases have been documented of iatrogenically transmitted CJD following surgery at other body sites, presumably because prions are found less often and at lower titers outside the CNS.4-6 However, prudence would suggest using CJD precautions for any invasive procedure in an affected patient. Issues of transmissibility from exposure to non-neural tissue may be somewhat different for the new variant CJD, or vCJD, the form related to bovine spongiform encephalopathy. In vCJD, the agent is frequently present in lymphoid tissues, including lymphoid tissues associated with the gastrointestinal tract.7 One British patient with vCJD had an appendectomy within a year prior to the onset of neurologic symptoms. On review, prions were detected in the paraffin block of his appendix.8 Subsequently, over 3,000 tonsil and appendectomy specimens were re-examined. None contained prions, however,9 and CJD precautions have not been instituted in routine medical practice in the United Kingdom. No cases of vCJD have been reported in the United States; the most recent data on this topic are available on the Web site of the National Prion Disease Pathology Surveillance Center (www.cjdsurveillance.com). References Barbara J. Crain, MD, PhD Chair, Neuropathology Committee Q. Are there any methods that increase the chances of seeing positive crystals in synovial fluids (for example, placing a sample in the refrigerator prior to observation)? A. To my knowledge, there is no described method for enhancing the detection of monosodium urate crystals in joint fluid. Several authors have described the appearance of MSU crystals in refrigerated samples that were not present on initial examination.1,2 However, the significance of this finding is unknown. Furthermore, other authors have not observed this phenomenon.3-5 Calcium pyrophosphate crystals normally decrease in number over a period of several days, and refrigeration does not prevent this phenomenon. Alizarin red S staining of wet mounts or fixed preparations has been advocated to enhance detection of CPP crystals.6,7 This method stains a variety of calcium-containing compounds in synovial fluid, thus limiting its specificity.7,8 However, the method described by Lazcano et al, in which fixed cytology preparations are stained, permits evaluation of morphology and intra- versus extra-cellular localization of alizarin red S-staining material, thus improving specificity.7 References Steven H. Kroft, MD Hematology/Clinical Microscopy Resource Committee Q. What is the best diagnostic test for Crohn’s disease? A. No definitive diagnostic test for Crohn’s disease—other than bowel biopsy showing typical histopathology—exists. A serological test called anti-Saccharomyces cerevisiae antibody, or ASCA, which suggests Crohn’s disease over irritable bowel syndrome and ulcerative colitis, is available from at least one reference laboratory (Prometheus, San Diego). Reagents are available from Inova Diagnostics (San Diego). The maximum test sensitivity for Crohn’s disease is obtained when IgG and IgA class ASCA tests are performed. This yields a combined sensitivity of approximately 52 percent. The low sensitivity of the test implies it will not be useful in screening unselected patients for that diagnosis. Patients with Crohn’s limited to the large bowel (Crohn’s colitis) are generally not positive for ASCA but instead are often positive for a form of antineutrophil cytoplasmic antibody, which is called atypical P-ANCA to distinguish it from typical P-ANCA that is associated with some systemic vasculitides. I would recommend that both ASCA and ANCA be ordered if one is attempting to find a test to increase the probability of Crohn’s disease in the differential diagnosis. For a review of current medical opinion concerning these tests, please see "Shades of gray in gastrointestinal testing" by William Check, PhD, in CAP TODAY (August 2000). Another recommendation in evaluating a patient with the differential diagnosis of irritable bowel syndrome versus inflammatory bowel disease is that the patient also be tested for celiac disease. Celiac disease (gluten-sensitive enteropathy) causes intestinal cramping and urgency similar to IBS and IBD. It occurs at a frequency of about three to four per 1,000 people in the U.S. population, but only 30 to 40 percent of patients have typical clinical symptoms. I recommend IgA antiendomysial antibody and antitissue transglutaminase ELISA for screening. Many gastroenterologists also screen using antigliadin antibody; however, in my experience, this test is neither specific nor sensitive for celiac disease. James A. Goeken, MD Diagnostic Immunology |
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