Predictable tissue shrinkage during frozen section histopathologic processing for Mohs micrographic surgery.

BACKGROUND: When confronted with a histologic specimen that is appreciably smaller than the same tissue specimen immediately after acquisition, the Mohs surgeon is faced with two possibilities, namely that the tissue has either shrunken during laboratory processing or that the histologic specimen is incomplete due to the introduction of technical errors during embedding, cutting, or staining of the skin specimen. Because the entire objective of Mohs micrographic surgery is to precisely examine the entire surgical margin of skin specimens, the surgeon must be able to determine that any size discrepancies introduced during laboratory processing are not related to incomplete surgical specimens. Although there are anecdotal suggestions that skin, like other human tissues, undergoes some degree of shrinkage during routine frozen section processing, the exact nature and magnitude of this phenomenon has not been previously investigated. OBJECTIVE: To quantify the degree of tissue shrinkage in Mohs micrographic surgical specimens processed with routine frozen sections and subsequent hematoxylin and eosin staining. METHODS: A total of 117 Mohs surgery patients (135 cutaneous tumors) were prospectively enrolled. The dimensions of initial stage surgical specimens were determined after removal from the patient, after freezing in a mounting medium, after placement on a glass microscopic slide, and after hematoxylin and eosin staining. Statistical analyses were performed in order to determine the significance of any discrepancies in specimen sizes introduced during laboratory processing. RESULTS: Skin specimens processed by frozen section techniques during Mohs micrographic surgery undergo statistically significant alterations in length. On average the measurements of specimens at the conclusion of histologic processing were 11.6% shorter than the measurements of the same specimens obtained immediately after surgical excision. Tissue specimens obtained from the trunk or extremities showed a greater degree of tissue shrinkage (16.3%) than specimens obtained from the head and neck (10.2%). CONCLUSIONS: Our results support anecdotal suggestions that skin specimens do indeed shrink during frozen section processing. By realizing that frozen section specimens can be expected to show some slight degree of shrinkage, the Mohs surgeon can appreciate situations that might allow greater confidence that a smaller specimen is nonetheless representative of the entire lateral and deep surgical margins.

Follicular mucinosis as a presenting sign of acute myeloblastic leukemia.

Follicular mucinosis is often associated with mycosis fungoides and has been rarely observed to occur with other neoplastic and inflammatory conditions. We describe a 60-year-old patient with follicular mucinosis who later developed acute myelogenous leukemia. This is the first reported case of follicular mucinosis as a presenting sign of acute myeloblastic leukemia in the absence of mycosis fungoides or leukemia cutis.

Variability in platelet procoagulant activity in healthy volunteers.

Blood platelets provide the major surface for thrombin generation. When platelets are activated they expose phosphatidylserine (PS) on their outer membranes, providing the surface on which two procoagulant enzyme complexes, the Xase and prothrombinase complexes, assemble. We hypothesized that there is biological variability in platelet procoagulant activity. To test this hypothesis, we activated isolated platelets from seventeen volunteers, and added plasma concentrations of factors VIII, IXa, and X for the Xase complex assembly, and F.Xa and II for the prothrombinase complex. Xase and prothrombinase activity were assayed using a chromogenic substrate. We found a two- to three-fold variation in Xase and prothrombinase activity, respectively. The distribution of Xase activity in the population was symmetric, while the distribution of prothrombinase activity was positively skewed. The difference in distribution implies that simple expression of procoagulant lipid was not the only determinant of procoagulant activity. Variation in prothrombinase activity was not due to the amount of platelet-released F.V. Neither microparticle production nor F.X binding correlated with Xase or prothrombinase activity. Using fluorescein-conjugated annexin V, we also found no direct correlation between the level of PS exposure and Xase or prothrombinase activity. This indicates that platelets must make other contributions, in addition to PS, to the activity of the Xase and prothrombinase complexes. There is evidence that platelets possess specific receptors for some coagulation proteins, although these receptors have not been isolated. Biological variability in the expression of platelet receptors might explain the differences in Xase and prothrombinase activities in our study.