Fat-free mass index: changes and race/ethnic differences in adulthood.

OBJECTIVE: Nutritional status is assessed by measuring BMI or percent body fat (%fat). BMI can misclassify persons who carry more weight as fat-free mass and %fat can be misleading in cases of malnutrition or in disease states characterized by wasting of lean tissue. The fat-free mass index (FFMI) is proposed to assess body composition in individuals who have a similar body composition but differ in height allowing identification of those suffering from malnutrition, wasting or those that possess a relatively high muscle mass. The purpose was to determine whether the FFMI differs in a group of racially/ethnically diverse adults. DESIGN: Cross-sectional. SUBJECTS: Subjects were a multi-ethnic sample (Caucasian, CA; African American, AA; Hispanic, HIS and Asian, AS) of 1339 healthy males (n = 480) and females (n = 859) ranging in age from 18-110 years. Total body fat, total fat-free mass and bone mineral density were estimated using dual energy X-ray absorptiometry. RESULTS: FFMI differed among the four ethnic groups (P ≤ 0.05) for both genders. A curvilinear relationship was found between age and FFMI for both genders although the coefficients in the quadratic model differed between genders (P ≤ 0.001) indicating the rate of change in FFMI differed between genders. The estimated turning point where FFMI started to decline was in the mid 20s for male and mid 40s for female participants. An age × gender interaction was found such that the rate of decline was greater in male than female participants (P ≤ 0.001). For both genders, FFMI was greatest in AA and the least in AS (P ≤ 0.001). There was no significant interaction between race and age or age(2) (P = 0.06). However, male participants consistently had a greater FFMI than female participants (P ≤ 0.001). CONCLUSIONS: These findings have clinical implications for identifying individuals who may not be recognized as being malnourished based on their BMI or %fat but whose fat-free mass corrected for height is relatively low.

Prevention of obliterative airway disease in HLA-A2-transgenic tracheal allografts by neutralization of tumor necrosis factor.

BACKGROUND: Inflammatory cytokines play an important role in the development of experimental obliterative airway disease (OAD) after transplantation. To further determine the immunologic mechanisms associated with OAD development, we used a murine tracheal transplant model in which a single mismatched HLA-A2-transgenic molecule is indirectly recognized by the recipient CD4+ T cells and then determined whether neutralization of several inflammatory cytokines affected the development of OAD. METHODS: Tracheas from HLA-A2+ C57BL/6 mice were heterotopically transplanted into C57BL/6 mice. Recipients were treated with neutralizing antibodies against tumor necrosis factor (TNF), interferon-gamma (IFN-gamma), or interleukin-1 (IL-1). Allograft histology as well as anti-HLA-A2 antibody development and T cell proliferative responses were determined at days +5, +15, +28, and +60. RESULTS: Allografts in untreated and anti-IFN-gamma-treated recipients demonstrated full development of OAD by day +28. Allografts in anti-TNF-treated recipients showed no evidence of OAD, even at day +60. Allografts in anti-IL-1-treated recipients showed airway epithelium changes by day +28 but minimal evidence of OAD by day +60. Spleen cells from untreated and anti-IFN-gamma-treated recipients showed significantly higher proliferative responses to HLA-A2+ cells, compared with syngeneic recipients (negative controls). In contrast, anti-TNF and anti-IL-1-treated recipients showed significantly lower proliferative responses to HLA-A2+ cells, compared with untreated recipients. Development of anti-HLA-A2 antibodies was detected in all recipients by day +15, with the exception of those treated with anti-TNF. CONCLUSION: Among the inflammatory cytokines, TNF seems to play a crucial role in the immunopathology of OAD developed after transplantation.

CD4+ T cell recognition of a single discordant HLA-A2-transgenic molecule through the indirect antigen presentation pathway induces acute rejection of murine cardiac allografts.

To further define the role of indirect allorecognition, cardiac allografts from HLA-A2-transgenic (HLA-A2+) C57BL/6 mice were heterotopically transplanted into normal C57BL/6, CD4 T cell-knockout (KO) C57BL/6 mice, CD8 T cell-KO C57BL/6 mice, fully MHC-discordant BALB/c mice (allogeneic control), and HLA-A2+ C57BL/6 mice (syngeneic control). HLA-A2+ grafts were acutely rejected when transplanted into BALB/c mice (mean survival time: 10+/-0.8 days), normal C57BL/6 mice (mean survival time: 16.5+/-2.1 days) as well as CD8-KO mice (mean survival time: 12.8+/-1.3 days). Histopathological analysis revealed classical acute cellular rejection with moderate to severe diffuse interstitial CD4+ and CD8+ cellular infiltrates and significant intra-graft deposition of IgG and complement. In contrast, HLA-A2+ grafts were not rejected when transplanted into CD4-KO mice or HLA-A2+ mice. CD8-KO recipients treated with an anti-CD4 monoclonal antibody, but not with an anti-NK monoclonal antibody, failed to reject their allografts with prolonged administration of antibody (30 days). Spleen cells from mice rejecting HLA-A2+ allografts failed to lyse HLA-A2+ target cells indicating a lack of involvement of CD8+ T cells in the rejection process. In contrast, spleen cells from rejecting animals proliferated significantly to both HLA-A2+ cells and to a peptide derived from the HLA-A2 molecule. Development of anti-HLA-A2 antibodies was observed in all animals rejecting HLA-A2+ allografts. These results suggest that indirect allorecognition of donor MHC class I molecules leads to rejection of cardiac allografts and development of alloantibodies in this unique transplant model in which there is a single MHC discordance between donor and recipient.

Diagnostic criteria for minimally differentiated acute myeloid leukemia (AML-M0). Evaluation and a proposal.

We studied immunophenotypic features of 30 cases of minimally differentiated acute myeloid leukemia (AML-M0) using multiparameter flow cytometry and immunohistochemistry and evaluated the immunophenotypic features of previously reported cases to facilitate correct identification of myeloid lineage. All but 1 of our 30 cases expressed CD13 and/or CD33; 2 expressed CD19; 1 expressed CD10; none expressed both CD10 and CD19. Eleven of 30 cases expressed T-cell-associated antigens. All but 2 cases expressed CD34 and/or HLA-DR. Twelve of 27 cases expressed terminal deoxynucleotidyl transferase. Myeloperoxidase (MPO) expression was seen in 22 of 22 cases by immunohistochemistry and 1 of 4 by flow cytometry. None of 27 cases expressed cyCD3 and cyCD79a. We propose following modified criteria for AML-M0: (1) standard criteria for acute leukemia; (2) undetectable or less than 3% MPO or Sudan black B staining in blasts; (3) lack of expression of lymphoid-specific antigens, cyCD3 for T lineage and cyCD79 and cyCD22 for B lineage; and (4) positivity for any of the myelomonocytic lineage antigens known not to be expressed on normal T or B lymphocytes or positivity for MPO as detected by ultrastructural cytochemistry, immunohistochemistry, or flow cytometry.

Aberrant expression of T-cell-associated antigens on B-cell non-Hodgkin lymphomas.

We describe 9 well-characterized cases of B-cell non-Hodgkin lymphoma (NHL) that showed aberrant expression of T-cell-associated antigens by 2-color flow cytometry. Cases were as follows: chronic lymphocytic leukemia/small lymphocytic lymphoma, 4; follicle center cell lymphoma, 2; mantle cell lymphoma, 1; and diffuse large B-cell lymphoma, 2. CD2 was the most commonly expressed antigen (5 cases). CD8 and CD7 were identified in 2 cases each, including 1 case that expressed both CD7 and CD4. The disease course and response to treatment were compatible with the type and stage of lymphoma. No unusually aggressive behavior was noted in any case. A control group of 59 cases of benign lymph nodes analyzed during the same period showed no aberrant expression of T-cell-associated antigens; thus, such expression is not a feature of benign lymphoid proliferations. Study of these B-cell lymphomas may prove invaluable to study aberrant activation of silent or repressed T-cell differentiation genes. CD2-expressing B-cell NHLs may represent clonal expansion of CD2+ B lymphocytes that normally constitute a small fraction of peripheral B lymphocytes and should not be confused with composite B- and T-cell lymphomas. Unless aggressive behavior is noted consistently, no aggressive treatment is justified.

Critical analysis and diagnostic usefulness of limited immunophenotyping of B-cell non-Hodgkin lymphomas by flow cytometry.

We report the sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) of various immunophenotypes characteristic of each class of B-cell non-Hodgkin lymphoma (NHL) based on analysis of 352 morphologically well-characterized B-cell NHLs and 175 benign lymph nodes (LNs) using 2-color flow cytometry. All B-cell NHLs that exhibited a characteristic immunophenotype (except diffuse large B-cell lymphoma) had a high NPV. The immunophenotypes of small lymphocytic lymphoma and mantle cell lymphoma showed high specificity, but only small lymphocytic lymphoma also showed a high PPV. One third of follicular lymphomas coexpressed CD23 and CD10. Diffuse large B-cell NHL showed no consistent immunophenotype. About 90% of all benign LNs expressed no substantial amounts of CD5, CD10, or CD23. Most benign LNs also failed to express substantial amounts of immunoglobulin heavy chains. In contrast, about 90% of NHLs showed expression of 1 or 2 heavy chains. The expression pattern of immunoglobulin light chains was not found helpful in favoring one lymphoma type over another. The usefulness of each immunophenotype for each lymphoma group is of particular diagnostic importance in limited specimens, such as fine-needle aspiration biopsies, small core biopsies, body effusions, extranodal sites, and nodal tissues with various artifacts.

Solitary skeletal hemangioma of the extremities.

OBJECTIVE: To report the clinicopathologic features of solitary skeletal hemangioma of the extremities and to review previous cases in the English language medical literature. PATIENTS: In addition to five of our own cases, 34 literature cases with substantial and 75 with partial clinicopathologic information were found. RESULTS: Our patients, three men and two women, ranged in age from 37 to 83 years (mean 65.6 years). The lesion was an incidental radiologic finding in two patients, while three were symptomatic. In no case was a correct preoperative radiologic diagnosis made, a malignant process being considered as a possibility in all. The hemangiomas were medullary; two involved a metacarpal, two the fibula, and one the humerus. In contrast, previously reported patients were younger (mean age 32 years), predominantly female (60%), and symptomatic in over 90% of cases. The lesion is rare in those younger than age 10 years or older than age 60 years. As in our patients, the long bones are most frequently involved (75%), with the diaphysis or metadiaphysis, as in four of our patients, the most common locations. Although 20% of cases occur in the hands or feet, metacarpal involvement is rare. Medullary origin, as in all of our cases, is most frequent, but 45% of cases are either periosteal (33%) or intracortical (12%). In the literature, cavernous hemangioma is the most frequent type. Three of our hemangiomas were cavernous, one capillary, and one venous, the latter being rarely reported in extremity bones. CONCLUSIONS: Due to the diversity of radiologic patterns produced by skeletal hemangioma, a correct preoperative diagnosis is rarely made. Almost all patients do well, even those with less than complete removal of the lesion; local recurrence is rare. All of our patients were well following either therapeutic or simple diagnostic procedures. Due to the destructive nature of some biopsy procedures, the histologic diagnosis of hemangioma may at times also be problematic.

Composite prolymphocytoid and hodgkin transformation of chronic lymphocytic leukemia.

The indolent course of chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) is occasionally altered by transformation to a histologically distinct, rapidly progressive, and clinically unresponsive hematologic malignant neoplasm. We report a case of CLL that, after 3 years of slowly progressive disease and treatment with single-agent chemotherapy (fludarabine phosphate), underwent a composite prolymphocytoid and classic Hodgkin lymphoma transformation. The diagnosis of classic Hodgkin lymphoma was based on the presence of Reed-Sternberg cells with typical morphologic structure and immunophenotype (CD15(+), CD30(+), CD45(-), CD20(-)) associated with the characteristic polymorphous inflammatory background consisting of numerous eosinophils, plasma cells, and reactive T lymphocytes. The remainder of the lymph node and the peripheral blood showed increased numbers of prolymphocytes admixed with typical small CLL cells. Recognition of such a transformation is of the utmost importance, since histologically similar Reed-Sternberg-like cells may be seen in Richter transformation. In contrast to prolymphocytoid transformation of CLL, Richter syndrome is rapidly fatal, with a median survival of 4 to 5 months. The patient pursued a clinical course similar to pure prolymphocytoid transformation and died with disease after 30 months following treatment with combination chemotherapy.

Tissue factor expression and angiogenesis in human prostate carcinoma.

In tumors, the switch to the angiogenic phenotype is thought to be controlled by a balance of positive and negative angiogenic factors. Tissue factor (TF) produced by tumor cells has been implicated in the regulation of this "angiogenic switch" through its ability to concurrently induce the expression of angiogenic molecules such as vascular endothelial cell growth factor (VEGF), while inhibiting the expression of anti-angiogenic molecules such as thrombospondin 2. We have examined TF expression and its relationship to angiogenesis and tumor progression in human prostate carcinomas. Most of the prostate carcinoma specimens examined (73%; n = 67) express high levels of TF. Immunohistochemical analysis localized TF expression to the epithelial cells of malignant glands. TF expression was significantly correlated with tumor angiogenesis as measured by the microvessel density (MVD). In addition, TF expression was correlated with the preoperative PSA level, a strong predictor of recurrence in prostate carcinomas. Our findings show that TF expression by the malignant glands in prostate cancer is common and suggest a role for this molecule in regulating prostate cancer progression and angiogenesis.

Concurrent Ki-67 and p53 immunolabeling in cutaneous melanocytic neoplasms: an adjunct for recognition of the vertical growth phase in malignant melanomas?

Ki-67 labeling of paraffin sections has been correlated with the number of cells in non-G(o) phases of the replicative cell cycle, and this immunohistochemical technique has been applied to the evaluation of a variety of human neoplasms. Similarly, immunolabeling for p53 protein has been used to detect mutations in the corresponding gene, as a reflection of possible cellular transformation in the same context. Both of these techniques were applied to 253 melanocytic tumors of the skin to assess their possible utility in the diagnosis and subcategorization of such lesions. They included 76 banal (common) nevi (CN), 39 Spitz nevi (SN), 62 superficial spreading malignant melanomas in radial growth (SSMMs), 32 nodular malignant melanomas (NMMs), 21 lentigo maligna melanomas in radial growth (LMMs), and 23 melanomas arising in association with preexisting compound nevi (MCN). One hundred cells were counted randomly in each tumor, and dark, exclusively nuclear reactivity was scored as positive labeling; results were recorded as percentages. Negligible Ki-67 and p53 labeling was seen in CN and SN, at a level that was similar to that obtained in cases of LMM and MCN. The largest proportion of Ki-67-positive and p53-positive cells was observed in NMMs, followed by SSMMs. Radial growth-phase SSMMs and LMMs demonstrated immunoprofiles that were similar to those of melanocytic nevi, and MCN did so as well. The prototypical malignant melanocytic tumor representing the vertical growth phase-nodular melanoma--demonstrated a statistically significant difference from all other lesions in this study with respect to Ki-67 index (P = .008, chi2) and p53 reactivity (P < .000001, chi2). Subsequent concurrent use of a Ki-67 threshold index of 10% and a p53 index of 5% correctly indicated the presence of vertical growth in 75% of NMMs, whereas only 8% of radial growth phase melanomas of other types were colabeled at the same levels of reactivity for the two markers (P < .00001, chi2). Thus, although the distinction between benign and malignant melanocytic tumors could and should not be based on immunohistology for Ki-67 and p53, these results suggest that the latter determinants may, in fact, be used as an adjunct to morphology in the recognition of the vertical growth phase in cutaneous malignant melanomas.

Lack of expression of surface immunoglobulin light chains in B-cell non-Hodgkin lymphomas.

We describe 10 cases of B-cell non-Hodgkin lymphoma (NHL) that did not express immunoglobulin kappa or lambda light chains by dual-color flow cytometry. Cases were identified from 298 consecutive cases of B-cell NHL and included follicular center cell lymphoma, diffuse large B-cell lymphoma, small noncleaved cell lymphoma, and small lymphocytic lymphoma. One case did not express any immunoglobulin heavy chain (IgH) as well; however, isolated expression of IgG heavy chain was seen in another case. Immunoglobulin heavy chains were not part of the lymphoma panel in other cases. All 3 cases in which gene rearrangement studies were performed showed rearrangement of IgH genes, including the case that did not express surface IgH chains. Immunoglobulin kappa light chain genes were rearranged in 2 of 3 cases and were in germline configuration in the third. All 147 cases of benign lymph nodes analyzed by flow cytometry showed polyclonal expression of immunoglobulin kappa and lambda light chains. Because of the absence of surface immunoglobulin light chains, these tumors must be distinguished from precursor B-cell acute lymphoblastic leukemia, plasma cell tumors, and rare cases of florid follicular hyperplasia that do not express surface immunoglobulins. The absence of immunoglobulin expression on malignant B cells can result from defects at any level from gene transcription to translocation of fully assembled proteins to the cell surface.

Acute lymphoblastic leukemia with an unusual t(8;14)(q11.2;q32): a Pediatric Oncology Group Study.

We present the clinicopathologic findings and survival data on 10 patients with acute lymphoblastic leukemia (ALL) and a rare t(8;14)(q11.2;q32). There were five male and five female patients, nine Caucasians and one Black, aged 4-17 (median 10.9) years. Three had Down syndrome. Eight (80%) patients had a white blood cell (WBC) count <50 x 109/l at presentation. No patient had central nervous system involvement or a mediastinal mass. Two patients had concurrent splenomegaly and hepatomegaly. Adenopathy was absent in four, minimal in three, moderate in one and prominent in two patients. All eight cases where immunophenotyping was performed by flow cytometry showed a B-precursor phenotype with expression of CD10 (CALLA). Only one case exhibited t(8;14)(q11.2;q32) as the sole karyotypic abnormality. Three patients were classified as standard-risk and seven high-risk by NCI (National Cancer Institute) consensus risk group categories. All patients achieved complete remission and seven patients were in complete continuous remission (CCR) after chemotherapy designed for B-precursor ALL. Three patients relapsed after 23.5, 31.3 and 32.1 months of EFS; the first patient also had t(9;22)(q34;q11), the second had a WBC count of 126 x 109/l at presentation while the third patient had no high risk features except for age 10 years. Thus, from our data, the t(8;14)(q11.2;q32) does not appear to confer an increased risk of relapse. Further observations are needed to confirm this conclusion.

Brief cyclosporine treatment prevents intrathymic (IT) tolerance induction and precipitates acute rejection in an IT rat cardiac allograft model.

BACKGROUND: Intrathymic (IT) alloantigen combined with administration of rabbit anti-rat anti-lymphocyte serum (ALS) intraperitoneally induces donor-specific tolerance to rat cardiac transplants. The purpose of this study was to examine the effect of a brief course (4 days) of cyclosporine (CsA) on the development of IT tolerance. METHODS: Buffalo (BUF) (RT1b) rats were given 25x10(6) fully MHC-mismatched Lewis (LEW) (RT1l) splenocytes by IT injection plus 1.0 ml of ALS intraperitoneally. Twenty-one days later, IT donor-specific LEW (group 1) or third-party (ACI, RT1a) (group 2) hearts were heterotopically transplanted to the abdominal aorta A third group of BUF (group 3) were given daily CsA (10 mg/kg) by oral gavage for 4 days before administration of IT LEW cells and ALS. Rejection as defined by the cessation of a palpable heartbeat was confirmed by histology. Cytokine profiles of allografts from all groups were then analyzed using a multi-probe RNase protection assay. RESULTS: Sixty-seven percent of IT/ALS-treated BUF recipients not pretreated with CsA accepted LEW heart grafts for greater than 90 days. However, 86% of animals treated with CsA for 4 days before IT injection and ALS rejected allografts at 10.7+/-3.2 days. Third-party allografts (ACI) were uniformly rejected (7.0+/-0.0 days). Histology confirmed cellular rejection in CsA-treated allografts and cytokine analysis detected increased interleukin (IL)-3, IL-5, and tumor necrosis factor-alpha when compared to increased IL-2 and interferon-gamma in rejecting untreated controls. CONCLUSIONS: CsA can prevent the induction of intrathymic alloantigen tolerance. These results support the development of a CsA-sensitive, but IL-2-independent, active regulatory mechanism after intrathymic exposure to donor-specific alloantigen and depletion of mature peripheral T cells.

Genetic analysis of prostatic atypical adenomatous hyperplasia (adenosis).

Atypical adenomatous hyperplasia (AAH) of the prostate, a small glandular proliferation, is a putative precursor lesion to prostate cancer, in particular to the subset of well-differentiated carcinomas that arise in the transition zone, the same region where AAH lesions most often occur. Several morphological characteristics of AAH suggest a relationship to cancer; however, no definitive evidence has been reported. In this study, we analyzed DNA from 25 microdissected AAH lesions for allelic imbalance as compared to matched normal DNA, using one marker each from chromosome arms 1q, 6q, 7q, 10q, 13q, 16q, 17p, 17q, and 18q, and 19 markers from chromosome 8p. We observed 12% allelic imbalance, with loss only within chromosome 8p11-12. These results suggest that genetic alterations in transition zone AAH lesions may be infrequent. This genotypic profile of AAH will allow for comparisons with well-differentiated carcinomas in the transition zone of the prostate.

Acute promyelocytic leukemia with additional chromosomal abnormalities and absence of Auer rods.

We report 4 acute promyelocytic leukemia cases that demonstrated karyotypic abnormalities in addition to the classic t(15;17) translocation and did not contain any Auer rods in leukemic blasts and dysplastic promyelocytes, either in the peripheral blood or in the bone marrow. Morphologically, 2 cases were characterized as the common or hypergranular type, and 2 were otherwise typical of the microgranular variant. Three patients had typical clinical and laboratory signs of disseminated intravascular coagulation. Immunophenotypic analysis of the blasts and dysplastic promyelocytes by dual-color flow cytometry revealed an immunoprofile consistent with acute promyelocytic leukemia. Cytogenetic analysis of the bone marrow revealed the following karyotypes: case 1, [47,XY,t(15;17)(q22;q12),+21]; case 2, [47,XY,t(15;17)(q22;q12),-16,+2 mar]; case 3, [47,XX,t(15;17)(q22;q12)ider(17)(q10),+8]; and case 4, [47,XY,der(5)t(5;?9)(p15;q12).t(15;17)(q22;q12]. Review of an additional 7 cases with t(15;17) as the sole cytogenetic abnormality revealed Auer rods in all cases. Our findings emphasize the importance of cytogenetics in evaluating acute myeloid leukemias. Acute promyelocytic leukemia without Auer rods, which may be morphologically confused with other types of leukemia (in particular, acute myeloblastic leukemia, type M2 or M5) or agranulocytosis with maturation arrest, appears to be associated with additional chromosomal abnormalities and possibly a poorer prognosis.

Prostatic adenocarcinoma with atrophic features: a study of 202 consecutive completely embedded radical prostatectomy specimens.

Prostatic adenocarcinoma may manifest with morphologic features that may be mistaken for benign glandular atrophy. The incidence, morphometric extent, and diagnostic attributes of atrophic prostatic adenocarcinoma have not been defined in radical prostatectomy cases. The size, grade, and stage at which prostatic carcinomas manifest atrophic change and whether these atrophic appearing adenocarcinomatous glands are proliferative, quiescent, or dying (apoptotic) also have not been established. To characterize prostatic adenocarcinoma with atrophic features, we studied 202 consecutive completely embedded radical prostatectomy specimens from previously untreated patients. The histomorphologic attributes of atrophic carcinoma were compiled and compared with benign atrophy and usual prostatic adenocarcinoma without atrophic features. The atrophic carcinoma volume was quantitated by image analysis, the proliferation index was determined by Ki-67 immunolabeling, and the apoptosis index was assessed by TdT [terminal deoxynucleotidyl transferase]-mediated dUTP [deoxyuridine triphosphate]-biotin nick end labeling (TUNEL). Of 202 prostatic adenocarcinoma cases, 32 (15.8%) demonstrated atrophic features. The malignant glands resembled benign atrophic glands by showing profound cytoplasmic volume loss, yet these glands almost always (96.4%) exhibited an infiltrative growth pattern, always lacked basal cells (confirmed by 34betaE12 immunostaining), and exhibited nuclear atypia with nucleomegaly and nucleolomegaly. The atrophic carcinoma foci had a mean volume of 0.3 cc (range, 0.01-2 cc), representing a mean of 16% of total carcinoma volume. The mean proliferation index for atrophic prostatic carcinoma was 4% compared with 1.2% for benign atrophy and 5.3% for usual nonatrophic carcinoma. Apoptosis was identified in only 1 of 32 atrophic prostatic carcinomas. Carcinomas with and without atrophic features did not differ in histologic grade, tumor volume, or pathologic stage. Most atrophic carcinomas were moderately differentiated, of Gleason grade 3. We conclude that the atrophic pattern of prostatic carcinoma is a distinctive morphologic presentation of proliferating, intermediate-grade, prostatic adenocarcinoma that has significant diagnostic rather than prognostic implications.