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Fig 1.

Late peri-implant breast seroma and total capsulectomy specimen of a patient with BI-ALCL.

A. Ultrasound-guided fine-needle aspiration of 100mL of left-sided breast peri-implant fluid collection. The color of the seroma ranged from cloudy yellow to blood-stained. B. Grossly normal-appearing peri-prosthetic capsule with no evidence of solid or infiltrating masses.

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Table 1.

Clinical and pathological features of BI-ALCL samples.

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Table 1 Expand

Table 2.

Clinical, microbiological and pathological features of reactive late seromas.

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Table 2 Expand

Fig 2.

Aspirate smear of five cases of BI-ALCL.

A. Case 1. B. Case 2. C. Relapse of case 2. D. Case 3. E. Case 4. F. Case 5. Smears showed large to medium-size atypical cells with irregularly shaped nuclei, conspicuous nucleoli and abundant clear cytoplasm in a fibrinous background. Morphologic features of BI-ALCL included hallmark cells with kidney-shaped nuclei (A arrows), binucleated Reed-Stenberg-like cells (B and E), cells with multiple nuclei (D) and mononucleated cells with prominent single or multiple nucleoli (D, E, F) (Papanicolaou smear, original magnification x400).

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Fig 3.

Immunophenotypic characterization of BI-ALCL cell blocks.

Representative cases are shown to underline the variability of CD3 expression in contrast to the consistent, intense and diffuse positivity for CD30 in BI-ALCL. In A CD3 was negative in almost all the tumor cells. In B CD3 staining was heterogeneous with the lymphomatous cells being CD3-negative, CD3-weakly positive and CD3-strongly positive. In C the majority of the neoplastic cells showed a faint CD3 expression (all original magnification x400).

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Fig 4.

Algorithm for the cytological diagnosis of late peri-implant breast seromas based on morphology, cellular composition and CD30 immunostaining.

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Table 3.

Immunophenotype of reactive late-onset breast peri-implant effusions.

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Table 3 Expand

Fig 5.

Cell block and immunohistochemistry of late onset breast peri-implant seromas.

A. Acute-type reactive effusion with numerous polymorphonucleates admixed with CD68+ macrophages and scattered CD3+ T-cells. B. Chronic-type reactive effusion with predominance of foamy macrophages C. Chronic-type reactive effusion with predominance of T cells. In all the reactive effusions CD30+ cells were very rare or absent. Scant PAX5+ B-cells were detected in all types of seroma (H&E and immunohistochemistry original magnification x400).

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Fig 6.

Morphological and molecular features of a CD30-rich reactive effusion.

The seroma was composed mainly by CD3+ T cells associated with scattered CD68+ macrophages and polymorphonucleates. Immunohistochemistry for CD30 stained a fraction of medium-large proliferating cells equal to 5% of the total cellularity (H&E, original magnification x200; mitotic figures in the inserts x400). TRG (Vg 9/11—Jg) clonality by Genescan fragment analysis showed a prominent peak (red arrows) within a polyclonal background in both the reference size ranges given by the BIOMED2 protocol (black arrows).

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Fig 7.

Histology of the 5 cases of BI-ALCL.

In all the cases CD30-positive neoplastic cells were confined within the peri-prosthesis fibrous capsule. In case 3 and 5 tumor cells were smaller with a darker nuclei than case 1, 2, and 4. Small lymphocytes and histiocytes were sparse within the capsule. Arrows indicate polyurethane crystals in the fibrinous/necrotic material adherent to the luminal side of the capsule. (original magnification x 100, insert x400).

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Fig 8.

TRG (Vγ If/10—Jγ) clonality by Genescan fragment analysis in BI-ALCL cases.

An oligoclonal and a polyclonal pattern were observed in the capsule (A) and in the involved axillary lymph node (B) of case 1 respectively. Monoclonal rearrangement identified by a single high peak was found in case 2 (C), case 3 (D), and case 4 (E). Case 5 (F) showed a monoclonal biallelic rearrangement.

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Fig 9.

Histology of breast peri-implant fibrous capsules in patients with late-onset non-neoplastic seroma.

A. Synovial metaplasia of the luminal side of the capsule associated with mild lymphocitic infiltrate. B. Intense chronic inflammation with numerous lymphocytes and plasmacells. C. Acute inflammation with neutrophils, edema and ectatic vessels. D. Sclerotic and acellular capsule with luminal aggregates of CD68+ CD30- histiocytes. E. Diffuse histiocytic reaction with foamy macrophages and pseudo-cystic spaces containing gel-like refractile and color-less material compatible with silicone (asterisk). F and G. Silicone and polyurethan crystals within phagocyte vacuoles of multinucleated giant cells (original magnification H&E, CD30 and CD68 staining x200; F and G x400).

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