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<p>The 1950 colorimetric reaction of Porter-Silber for the measurement of 17-hydroxy-corticosteroids in the urine is a milestone in the diagnosis of hypercortisolism. Since the 17th century, “suprarenal” tumours had been associated with virilism and obesity, but it was only in 1932 that the eponym Cushing’s syndrome was coined for the association between “basophilic adenoma of the adenohypophysis” and <i>habitus</i> <i>pletoricus</i>, android and truncular-supraclavicular adiposity, moon face, red striae, hypertrichosis, myopathy, atrophy of the skin, acrocyanosis, amenorrhea, loss of libido/impotence, radiographic bone rarefaction, neutrophilic leukocytosis, lymphocytopoenia/eosinopoenia, hypernatraemia/hypokalaemia, hyperglycaemia/glucosuria, and arterial hypertension. Cushing, however, believed that this clinical picture was dependent on gonadotropic, neuropophyseal, and/or diencephalic function (so-called polyglandular syndrome). However, for the first time in 1933, Julius Bauer associated that symptomatology with a pituitary stimulation of the adrenals (so-called hyperadrenalism), an hypothesis confirmed in 1942–43 by Fuller Albright. In 1950, this led Bauer to introduce the distinction between Cushing’s disease and syndrome, still accepted today compared to the historical eponym Cushing-Bauer syndrome, which corresponds to endogenous hypercortisolism.</p>

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La Sindrome di Cushing-Bauer prima della reazione di Porter-Silber

  • 期刊论文

  • 发表日期：

    2026年1月20日

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  • Roberto Toni,
  • Fulvio Barbaro,
  • Giusy Di Conza,
  • Francesca Pia Quartulli,
  • Salvatore Mosca,
  • Silvio Caravelli,
  • Giammarco Gardini,
  • Massimiliano Mosca

摘要

The 1950 colorimetric reaction of Porter-Silber for the measurement of 17-hydroxy-corticosteroids in the urine is a milestone in the diagnosis of hypercortisolism. Since the 17th century, “suprarenal” tumours had been associated with virilism and obesity, but it was only in 1932 that the eponym Cushing’s syndrome was coined for the association between “basophilic adenoma of the adenohypophysis” and habitus pletoricus, android and truncular-supraclavicular adiposity, moon face, red striae, hypertrichosis, myopathy, atrophy of the skin, acrocyanosis, amenorrhea, loss of libido/impotence, radiographic bone rarefaction, neutrophilic leukocytosis, lymphocytopoenia/eosinopoenia, hypernatraemia/hypokalaemia, hyperglycaemia/glucosuria, and arterial hypertension. Cushing, however, believed that this clinical picture was dependent on gonadotropic, neuropophyseal, and/or diencephalic function (so-called polyglandular syndrome). However, for the first time in 1933, Julius Bauer associated that symptomatology with a pituitary stimulation of the adrenals (so-called hyperadrenalism), an hypothesis confirmed in 1942–43 by Fuller Albright. In 1950, this led Bauer to introduce the distinction between Cushing’s disease and syndrome, still accepted today compared to the historical eponym Cushing-Bauer syndrome, which corresponds to endogenous hypercortisolism.