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Electronomicroscopic investi gati ons
of a pancreati c neuroendocrine tumor:
an insulinoma case
G.-V. Mirancea 1 , S. Dima 2 , A.-M. Morosanu 3 ,
N. Mirancea 3 , I. Popescu 2 , S. Carniciu 4 ,
C. Ionescu-Tirgoviste 4
1 “Carol Davila” University of Medicine and Pharmacy,
Bucharest, Romania
2 Fundeni Clinical Insti tute, Bucharest, Romania
3 Insti tute of Biology Bucharest, Romanian Academy
4 Nati onal Insti tute of Diabetes, Nutriti on and Metabolic
Diseases “N.C. Paulescu”, Bucharest, Romania
Normal human endocrine pancreas is represented
by nearly one million of small islet cells of α, β,
δ, ε and PP (F) which can be identifi ed electron microscopically
(EM) by their specifi c granules. Each
above mentioned cell types of endocrine pancreas
secrets a specifi c hormone with important function
in the body homeostasia. In abnormal conditions,
dysfunction of β cells leads to two major diseases:
diabetis (type I or type II) and insulinoma. Insulinoma
is the most common form of endocrine pancreatic
tumor, usually benign, made up of specialized
β cells able to constantly secret insulin, causing
hyperinsulinemic hypoglycemia (less than 50 mg/
dL). Our investigated insulinoma case (male, 37
years old) were hospitalized with a presumptive diagnostic
of insulinoma. In order to perform a transmission
electron microscopic (TEM) investigation,
small tissue fragments from a normal pancreas (as
control) and a pancreatic tumor mass resulted by
surgery as curative therapeutic option (surgeon got
patients’ consent) were processed following the
routine TEM protocol (Mirancea et al., 2007). EM
investigated control pancreas has a normal architecture
as well as normal cell types composition of
islets. Desmosomal junctions connect adjacent
cells. EM examination revealed few interesting peculiar
aspects: the neoplastic lesions prevalently
represented by ß and α endocrine cells are extensive,
detrimental to pancreatic exocrine tissue areas.
Ultrastructurally, two β cells phenotypes are
detected: (1) cells with big and round in shape euchromatic
nuclei and (2) cells with polymorphic in
shape and heterocromatic nuclei. The nuclei of both
β cell types have 1 or 2 prominent nucleols. Inside
of the ß and α cells, cytoplasm is depleted or even
completely devoid of characteristic ß and α cell
granules. When compare cytoplasm of phenotype
(1) βcells with the cytoplasm of phenotype (2)
βcells, results that inside of the cytoplasm of phe-
REVISTA MEDICALÅ ROMÂNÅ – VOLUMUL LIX, NR. 2, An 2012
notype (2) βcells there are extensive and more frequently
areas devoid of cytomembranary organelles,
suggesting to be swollen (maybe oedematous),
which sometimes fuse with perinuclear cisternal
space.
The most important fi nding in this report for a
case of insulinoma is the high fragility of plasma
membrane of tumor cells. As a consequence of that
abnormality, plasma membrane of adjacent cells,
especially phenotype (2), tend to perform membranes
recombination and to form large syncytial
aspects.
There is a possible explanation for that. High
fragility of cytomembranes, including plasma
membrane is a hallmark for the malignant tumor
cells (Mirancea & Mirancea, 2010). On may speculate
that long exposure of endocrine cells to a lot of
paracrine factors (cytokines) and enzymes produced
by extravasated blood cells, including infl
ammatory cells, leads to the disorganization of
surface domains or even focally plasma membrane
destruction, already fragile by itself because of being
malignant tumor cells. Moreover, downregulation
of cell-cell and cell-extracellular matrix adhesions
might result in aberrant cell behavior,
including the promotion of cell migration and consequently
invasive growth, a pre-requisite for at
ectopic places secondary tumor formation (metastasis).
Here, we emphasise the power of the microenvironment:
as much as the stroma/cell vicinity is altered,
the adjacent epithelial tissue is affected in
their organization and function. The above mentioned
ultrastuctural abnormalities in our investigated
case suggest a possible evolution to a malignant
insulinoma.
1. Mirancea N., et al., 2007, J. Dermatol. Sci., 45: 175-185
2. Mirancea N. & Mirancea D. , 2010, Ultrastructura celulelor şi ţesuturilor,
703 pg., Ed. Ars Docendi, Univ. Bucureşti.
Dislipidemie mixtă cu debut precoce –
efecte imediate şi tardive.
Prezentare de caz
Mădălina Păunescu¹, Mihaela Mihu²
¹Insti tutul Naţional de Diabet, Nutriţie şi Boli
Metabolice „Prof. Dr. N. Paulescu“, Bucureşti
²Spitalul Clinic de Urgenţă pentru copii „Marie Curie“,
Bucureşti
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