Reactive Mesothelial Hyperplasia

Rawa Muhsin
Serosal membranes
Layers
◦ Mesothelial cells
◦ Basement membrane
◦ Connective tissue

Meso (middle) + thele (nipple)

Histology
Small, flat to cuboidal cells
Well-defined cell borders
Single central nucleus
Homogeneous chromatin
No nucleolus
Cytology
Architecture
◦ Single cells, sheets, or small clusters with
scalloped periphery (<10-15 cells per group)
Cytology
◦ Foamy or dense cytoplasm ± vacuoles
◦ Peripheral clear outer rim
◦ Empty spaces between cells
◦ Binucleation is common
Immunohistochemistry
Positive markers Negative markers
◦ Keratins ◦ CK20
 Including AE1/AE3, ◦ MOC-31
CK7, CK 5/6, CK 8/18
◦ BER-EP4
◦ Calretinin
◦ CEA
◦ WT1
◦ CD15
◦ D2-40 (podoplanin)
◦ TTF-1

◦ HBME-1,
thrombomodulin
(CD141), N-cadherin
REACTIVE
MESOTHELIAL
HYPERPLASIA
Definition and etiogenesis
Proliferation of benign reactive
mesothelial cells
Reaction to injury, such as recurrent
effusions, inflammation, neoplasia, or
surgical procedures
Clinical
Asymptomatic
Incidental finding
Benign
Regresses when stimulus is removed
Macroscopy
None!
Macroscopy
Microscopy
Architecture
◦ Thickened mesothelial layer
◦ Papillae
◦ Psammoma bodies
◦ No invasion

Cytology
◦ Larger cells (than normal)
◦ Enlarged nucleus with open chromatin
◦ Prominent central nucleoli
◦ Variable mitotic activity and atypia
◦ Multinucleation
Differential diagnosis
Malignant mesothelioma (early stage)
Metastatic papillary carcinoma
◦ Clinical history
◦ Symptomatic
◦ IHC (TTF-1, ER/PR)
Müllerian rests
◦ Rare, in young women
◦ Glands without atypia or mitotic activity
◦ Dense spindle cell stroma
Reactive vs Mesothelioma
Definitive for mesothelioma
Stromal invasion with fibroblastic
response
◦ Sampling entire lesion is critical
◦ Highlight with keratin stains
Infiltrationof underlying fat, muscle, or
adjacent tissues
Favors reactive hyperplasia
Asymptomatic, incidental
Focal distribution with skip lesions
Absence of tumor cell necrosis
Inflammation common
Low Ki-67 (<9%)
Special studies
Special studies
Loss of BAP1 (by IHC)
◦ 40% in mesothelioma (more in epithelioid)
Loss of p16 (by FISH)
◦ 60% in mesothelioma (more in sarcomatoid)
◦ IHC doesn’t count; IHC for loss of MTAP
Each100% specific
Combined sensitivity 80%
Special studies
Mesothelioma
◦ p53, EMA, CD146, GLUT1, IMP-3
Reactive hyperplasia
◦ Desmin
Inconsistentresults
Not to be used in practice for now