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wombat Views: 972
Published: 5 years ago
 
This is a reply to # 2,152,330

Re: overdiagnosis and liability



171.67.112.51/content/117/1/19.full.pdf


A story is told by Juan Rosai about an atypical
melanocytic lesion sent to him in consultation from a patholo-
gist friend in private practice.

After a long study, Dr Rosai
decided it was benign. His friend thanked him for his opinion,
but told him that he was still going to diagnose it as malignant
melanoma. He said that if he called it melanoma and it never
came back, everyone would be happy that the patient was
cured. If he called it benign and it came back, then he would
end up in court.

This is the dilemma that faces the practicing
pathologist every day. The tendency to “overdiagnose” seems
to be inevitable as long as there is a surfeit of aggressive,
unforgiving malpractice attorneys as well as pathology experts
and a limited risk to the “overdiagnosis.”

This tendency to overdiagnose clearly is accentuated in
private practice. Fueled by the perception that private practi-
tioners are not as good as their academic counterparts, cases in
growing numbers are being referred to the university setting
for a second opinion, sometimes years after the case originally
was signed out. If the diagnosis from this second opinion on a
thyroid nodule is malignant when the original diagnosis was
benign, the ramifications can be quite devastating. While there
certainly are benefits to second opinions,1and we are in no
way arguing against them, the unintended result of this prac-
tice is to render the private pathologist more vulnerable, more
prone to litigation, and more likely to overdiagnose. Defensive
pathology is now so ingrained in the psyche of most private
pathologists that it has become second nature.
The purely follicular variant of papillary thyroid carci-
noma (PTC) described by Lindsay in 19602and later popular-
ized by Chen and Rosai3and Rosai et al4is now well accepted.
The nuclear features have become tantamount to papillary
structures in the diagnosis of PTC. The nuclear features
include the following: (1) overlapping ground-glass, optically
clear, or “Orphan Annie” nuclei and (2) nuclear pseudoinclu-
sions and grooves, which represent cytoplasmic invaginations
into the nucleus. Despite the universal recognition of this
variant, it is not well characterized. The conventional PTC is
classically an invasive tumor even when the majority of it is
composed of follicles. The purely follicular variant of PTC on
the other hand is often well circumscribed and encapsulated.4
What clearly is lacking is a minimal histologic definition of the
follicular variant of PTC. Is an occasional grooved nucleus
with pale chromatin in a follicular neoplasm enough to warrant
a diagnosis of malignancy? Should the nuclear changes be
uniformly present throughout the nodule? Are the nuclear
changes that we are seeing significant or are they the “pseudo-
clear nuclei” described by Hapke and Dehner in the 1970s?5
At present, there are only a few long-term follow-up
studies (totaling only 107 patients, as nicely summarized by
Chan6) of the encapsulated follicular variant of PTC. While it
is true that only 1 of these 107 patients died of disease,7more
than 25% of these patients had regional lymph node metas-
tases. In addition, a recent study by Baloch and LiVolsi8
described 5 cases in which the encapsulated follicular variant
of PTC manifested as an occult primary with metastatic
disease, or in which bone metastases appeared many years
after resection, and invasion in the primary lesion was subtle
enough to be overlooked. Another study documented rare
clinical progression (lymph node metastases) in the macrofol-
licular variant of PTC despite the fact that the dominant
cytology and architecture of the primary tumor very closely
resembled goiter.9In summary, although the follicular variant
of PTC usually behaves in a very indolent fashion, it rarely
can cause distal metastasis. Furthermore, the follicular variant...

 

 
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