Pathologica 4-07.pdf - Pacini Editore

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Methods. We retrieved 259 consecutive cases (from February
1994 to March 2007) of spinal lesions from the files of
the Department of Pathology at the University of Bari. There
were 143 men (mean age 55.6) and 126 women (mean age
54.2). All patients underwent MRI of the spine and subsequent
biopsy of the lesion; tissue samples were formalinfixed
and routinely processed in order to obtain hematoxylineosin
slides, which were observed at light microscopy by a
dedicated pathologist. In 23 cases a frozen section examination
was performed; in 167 cases further immunohistochemical
investigations were performed.
Results. All cases in which a diagnosis was made by the
pathologist were subsequently reviewed and divided into 3
groups:
1. no MRI diagnosis was obtained (27 cases, 10.4%), most of
them (22,2%) being either a non-Hodgkin lymphoma or a
metastasis;
2. MRI and histological diagnosis did not match (47 cases,
18.1%), most of them (17%) being a mieloma;
3. MRI diagnosis (in many cases strongly supported by a proper
anamnesis) was confirmed by histopathology (158 cases,
61%), most of them (25.9%) being metastases.
Conclusions. We present a large series of 259 spinal lesions
and compare preoperative MRI with surgical pathology results;
since signs and symptoms are not specific to a single
neoplastic or non-neoplastic entity, diagnostic assessment is
largely based upon imaging and pathology.
Our results show that MRI displays great diagnostic accuracy
for metastatic lesions and neurinomas, while other neoplastic
lesions such as non-Hodgkin lymphomas are less likely
to be preoperatively identified by such technique. We believe
that the pathologist should be aware of this, especially
when evaluating such lesions on frozen sections.
Ruolo della biopsia muscolare nella
diagnostica delle miopatie da farmaci:
correlazioni clinico-patologiche
L. Maiarù, V. Tarantino, L. Badiali De Giorgi, M. Zavatta
* , R. D’Alessandro ** , R. Rinaldi *** , V. Carelli ** , G.N.
Martinelli, G. Cenacchi
Dipartimento Clinico Scienze Radiologiche e Istocitopatologiche,
e ** Dipartimento di Scienze Neurologiche, Università
di Bologna; * U.O. Ortopedia e *** U.O. Neurologia, Azienda
Ospedaliera-Universitaria Policlinico “S. Orsola-Malpighi”
Introduzione. Numerosi farmaci, tra cui statine, acido valproico,
propofol, zidovudina, clorochina e steroidi possono
provocare miopatia sia direttamente che con meccanismi
patogenetici indiretti. Scopo del nostro studio è stato quello
di verificare la possibilità di definire un quadro clinico-patologico
patognomonico delle miopatie iatrogene da farmaci,
ad oggi non riportato in letteratura.
Materiali e metodi. Abbiamo valutato casi di miopatia giunti
alla nostra osservazione nel periodo 01-05/04-07 (152
casi). I parametri clinico-laboratoristici considerati sono
stati: sintomatologia, esame obiettivo, terapia farmacologica
(correlazione temporale tra somministrazione dei farmaci e
insorgenza dei sintomi), CPKemia, EMG; sono stati quindi
valutati la biopsia muscolare e l’analisi molecolare del DNA
mitocondriale (1 caso) mediante long-PCR e sequenziamento
genico. La biopsia muscolare è stata studiata dopo congelamento
in N2 liquido. Le sezioni criostatate sono state trat-
tate di routine con colorazioni istologiche ed istochimiche
quali E-Eo, tricromica di Gomori, PAS, fosfatasi acida, fosfatasi
alcalina e istoenzimatiche per l’evidenziazione dell’attività
di NADH, Cox/SDH, ATPasi (4,35; 10,4). È stata infine
effettuata valutazione morfometrica per definire coefficiente
di variabilità diametrica e indici di atrofia e ipertrofia.
Risultati. Delle 152 biopsie studiate, 9 (circa il 5,9%) presentavano
alterazioni soprattutto a livello mitocondriale. Erano
spesso presenti oltre a fibre tipo ragged red, anche fibre
Cox-negative e alterazioni ultrastrutturali, quali iperplasia,
degenerazione, polimorfismo e rari megamitocondri. In un
caso la genetica molecolare ha evidenziato delezioni multiple
a carico del DNA mitocondriale.
Conclusioni. Dai risultati emerge che i parametri clinico-laboratoristici
rivelano un quadro miopatico aspecifico, quindi
la biopsia muscolare risulta fondamentale per la diagnosi. I
nostri dati mostrano alterazioni preferenzialmente a carico
dei mitocondri che escludendo una possibile causa di primitività
mitocondriale, identificano questi organuli quali target
principale coinvolto nel meccanismo etiopatogenetico della
miopatia da farmaci. In un caso l’azione del farmaco si è
sovrapposta ad una preesistente mutazione del DNA mitocondriale
(miopatia da propofol), slatentizzando il quadro
clinico.
Bibliografia
1 Guis S. Best Pract Res Clin Rheumatol 2003;17:877-908.
2 Sieb JP. Muscle Nerve 2002;27:142-56.
FREE PAPERS
Oxidative stress in livertransplantation: the
pathologist’s search for predictive tools
C. Avellini, G. Trevisan, G. Tell, U. Baccarani, C. Vascotto,
G.L. Adani, L. Cesaratto, C.A. Beltrami
Department of Medical and Morphological Sciences, Dept.
Surgery and Transplation, Department of Biomedical Sciences
and Technologies, Azienda Ospedaliero-Universitaria Udine
Introduction. Oxidative stress is a major pathogenetic event
occurring in several liver disorders and is a major cause of
liver damage due to ischaemia/reperfusion (I/R) during liver
transplantation. In order to identify early protein targets of
oxidative injury, we used a multiple approach, by morphological,
immunohistochemical and proteomic methods.
Methods. HepG2 human liver cells were treated for 10 minutes
with 500 mM H2O2 and studied by differential proteomic
analysis (two-dimensional gel electrophoresis and
MALDI TOF mass spectrometry). The same methods have
been applied on liver needle biopsy before vascular ligation
(T0), after cold (T1) and after warm (T2) ischaemia: these
specimen underwent to histological analysis (Suzuki score)
and immunohistochemical evaluation of APE1/Ref1 expression,
also on frozen sections.
Results. Post-translational changes of native polypeptides
are associated with H2O2 treatment sensitivity of 3 members
of Peroxiredoxin family of hydroperoxide scavengers (Prx I,
II, VI), that showed changes in their pI as result of overoxidation,
by modification of active site thiol into sulphinic
and/or sulphonic acid. The oxidation kinetic of all peroxiredoxin
was extremely rapid and sensitive, occurring at H2O2
doses unable to affect the common markers of cellular oxidative
stress. Similar results have been obtained on liver
biopsy specimen: significant higher value of Suzuki score