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Editorials

What’s in a name? Eponyms, acronyms and POI

(EDITOR-IN-CHIEF)

Fuller Albright (1900–1969), whilst not the father of endocrinology, was certainly a founder of modern endocrinology. Albright first described or contributed to 14 major clinical syndromes, had several named after him and named a few himself, amongst them Primary ovarian insufficiency (POI), in 1942.

Albright was born in Buffalo, NY, in 1900, studied and trained at Harvard before spending time at Johns Hopkins in Baltimore and later in Vienna, where he worked for the pathologist Jacob Erdheim (who first described the relationship between the parathyroid gland and calcium metabolism). Erdheim was to have a profound influence on Albright, who described the former as ‘the greatest living pathologist’, so much so that the study of calcium metabolism became a major part of Albright’s professional life. He returned to Massachusetts General Hospital in 1929 and worked there for the rest of his career.

Seemingly both blessed and gifted, Albright’s professional career was impeded and then cut short by the progression of Parkinson’s disease, which he contracted at age 36. At the age of 56, when his speech and movement were severely impaired, he persuaded a leading New York neurosurgeon to attempt experimental surgery on his brain to allow him to continue working. Despite advice to the contrary from the surgeon and many colleagues, his will prevailed and the surgery proceeded. He suffered a major cerebral hemorrhage and he lived his remaining 13 years in a vegetative state. So much for informed consent.

Albright was first and foremost a clinician and researcher; he conducted three clinics each week – one in general endocrinology, one called the ‘stone’ clinic or ‘the quarry’, and a third on ovarian dysfunction. An Associate Professor, he declined further promotion on the grounds that he would become involved in too much administrative work.

Albright’s work on serum calcium and phosphorus regulation, primary hyperparathyroidism and renal excretion of calcium and phosphorus form the foundation of our understanding of mineral metabolism. Whilst mineral metabolism was the main thrust of his early career, research into the pituitary, adrenal and gonadal axis became more important over time and dominated his later career. He was amongst the first to describe and define the disorders associated with Cushing syndrome. He first described the link between postmenopausal osteoporosis and estrogen deficiency and went on to demonstrate that the condition could be treated with estrogen replacement. He described Klinefelter syndrome in 1942 (naming it after one of his students at the time), after studying male Draft Board recruits noted to have enlarged breasts and small testes.

In the same year, he demonstrated that Turner syndrome was not of pituitary origin but rather due to an ovarian disorder: primary ovarian insufficiencyCitation1. Albright chose the term primary ovarian insufficiency to emphasize that it was ovarian function that was the primary defect rather than some other defect such as a central defect in gonadotropin secretion (secondary ovarian insufficiency). However, controversy remains over nomenclature and many other terms have been used to describe this condition including gonadal dysgenesis, hypogonadotropic hypogonadism, ovarian dysgenesis, premature menopause, and premature ovarian failure.

The International Menopause Society (IMS) marks World Menopause Day each year with the release of a scientific White Paper on a topic considered to be of significant interest to women, to clinicians and to researchers. This White Paper is complemented with press and media releases relevant to the topic in all nations affiliated with the IMS via the Council of Affiliated Menopause Societies (CAMS). This year, our topic is premature ovarian insufficiency and the White Paper is published in this issue of ClimactericCitation2.

The term premature ovarian insufficiency has been chosen, by the IMS and others, because it encompasses spontaneous and iatrogenic causes of ovarian insufficiency and allows that some intermittent ovarian activity may still occur in a small percentage of women following the diagnosis.

POI is not rare. Traditionally, it has been estimated that the condition may affect 1% of women before age 40, but recent studies have demonstrated higher rates in some countries. The key diagnostic criteria are the presence of menopausal-level serum gonadotropins in association with irregular or absent menses in adolescent girls or women younger than 40 years of ageCitation2. Whilst the menopause for most women is a ‘normal’ physiological event (even if the sequelae are far from normal), the same is not true for women diagnosed with POI. The syndrome is associated with the symptoms and metabolic effects of sex steroid deficiency as well as the emotional sequelae associated with the diagnosis, in particular the sudden loss of fertility.

The lack of certainty regarding terminology and diagnostic criteria accompanied by the relative infrequency of the condition have led to typically long delays in diagnosis and misdiagnosis, poor patient counseling and support and inappropriate treatment, particularly when so-called risks of menopausal hormone therapy associated with older women are applied to this much younger group of women suffering from a true estrogen deficiency condition. This delay in diagnosis has been shown to be a significant factor in the reduced bone density commonly seen in this group of young women.

Studies have shown that many women have expressed dissatisfaction with their medical care, citing diagnostic delays, poor provision of information, confusion about treatment and an uncoordinated process as examplesCitation3.

The White Paper on Premature ovarian insufficiency is not a ‘bedtime’ read. It is, however, a distillation of all that is known regarding this important disorder, presented by a group of international experts. I commend it to you strongly; I hope you will read it, pass it on to your colleagues, and use it to guide your diagnostic and management practices. Above all, please remember this condition whenever you see a young woman who has had 3–4 months of irregular, let alone absent, menses. Most of the time she will have an ovulatory disorder brought on by hypothalamic dysfunction, polycystic ovaries, hyperprolactinemia, pregnancy and so on but, more often than you expect, she will be a young woman with POI.

Change is certainly needed in the areas of POI research, education and patient care. We need a coordinated and integrated approach to this problem. There have already been moves taken to populate an international database of POI patientsCitation4, but more must be done.

Perhaps POI may be an example of where the Internet of ThingsCitation5 could be used to establish a coordinated global response to diagnosis, management, treatment and long-term care.

References

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