Неплохая идея
‘What’s in a name? That which we call a rose/By any other name would smell as sweet’ (Juliet,
from Romeo and Juliet by William Shakespeare). Shakespeare’s implication is that a name
is nothing but a word, and it therefore represents a convention with no intrinsic meaning.
While this may be relevant to romantic literature, disease names do have real meanings,
and consequences, in medicine. Hence, there must be a very good rationale for changing
the name of a disease that has a centuries-old historical context. A working group of
representatives from national and international endocrinology, and pediatric endocrine
societies now proposes changing the name of ‘diabetes insipidus’ to ‘arginine vasopressin
deficiency (AVP-D)’ for central etiologies, and ‘arginine vasopressin resistance (AVP-R)’ for
nephrogenic etiologies. This article provides both the historical context and the rationale
for this proposed name changing
Endocrine Connections
(2022) 11, e220378
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H Arima et al. e220378
11:11
Reasons for changing a disease name
Understanding of disease processes is a dynamic field,
with rapidly evolving concepts of pathophysiology based
on emerging molecular and genetic data. Consequently,
newer understanding of pathophysiology is one of the
major reasons for renaming diseases. In endocrinology,
appreciation of hyperprolactinemia as the common
pathophysiology underlying many different clinical
situations causing galactorrhea and amenorrhea led to
the effective abandonment of many previous eponymous
names for these conditions, such as Chiari–Frommel
syndrome, Forbes–Albright syndrome and Ahumada–
del Castillo syndrome (1). A second reason is based on
historical discoveries that a previous eponymous name for
a syndrome was inappropriately attributed to an individual
who was not the first or even the most significant person
involved in the description of the syndrome (2). A
third reason is later appreciation of medically unethical
behaviors of individuals with diseases eponymously
named for them, as characterized by the renaming of
Reiter’s syndrome to ‘reactive arthritis’ and Wegener’s
granulomatosis to ‘granulomatosis with polyangiitis’,
because of the association of the eponymous physicians
with Nazi antihumanitarian crimes (3, 4). The first three
of these reasons for changing disease names make a
strong case for detaching eponyms from disease processes
whenever possible (5). However, endocrinologists would
be loathe to abandon the eponyms of Addison, Cushing,
Hashimoto and others for their unique and seminal
contributions to our understanding of endocrine disease
processes. However, yet a fourth reason for renaming
diseases is when traditional disease names lead to confusion
between pathophysiologically different processes, leading
to treatment errors and consequent adverse outcomes for
patients. This last reason represents the major impetus to
change the name of diabetes insipidus at this time.
Historical context
Before explaining the rationale for the name change, it is
instructive to review the historical context for the name of
diabetes insipidus. The polyuria and polydipsia of diabetes
were first described by Demetrius of Apameia (1st–2nd
century BC), who used the term ‘diabetes’, meaning
‘passing water like a siphon’ to describe the polyuria
characteristic of this condition. Araetus of Cappadocia
(81–138 AD) further defined the clinical characteristics of
this disease (6). Although observations that the urine was
sweet were alluded to in both Greek and Indian history, the
first documented report of the sweet character of diabetic
urine was published by the English physician Sir Thomas
Willis in 1674 (The Diabetes or Pissing Evil). However, the
differentiation between the saccharine urine of glucosuria
and the non-saccharine urine of other forms of polyuria is
attributed to the Scottish physician William Cullen, who
appended the Latin word ‘mellitus’ (sweet) to the Greek
term ‘diabetes’ to distinguish between these two types of
polyuria (7). In 1794, Johann Peter Frank first introduced
the term ‘diabetes insipidus’ to differentiate these patients
from those with diabetes mellitus (7). These terms
persisted as valid clinical descriptions without known
pathophysiology until the vasopressor and antidiuretic
actions of posterior pituitary extracts were discovered in
the late 19th and early 20th centuries, including the use
of posterior pituitary extracts to treat diabetes insipidus.
In the mid-20th century, arginine vasopressin (AVP) was
synthesized and identified as the antidiuretic hormone,
and the distinct central and nephrogenic etiologies of
diabetes insipidus were recognized and characterized (8).
Despite new knowledge of the underlying pathophysiology
of the different etiologies of diabetes insipidus by the late
20th century, no attempts were made to rename diabetes
insipidus according to the known causes of the disorder,
namely, deficiency of AVP or resistance to the receptormediated actions of AVP.
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