The first theory argued that haemochromatosis was secondary to diabetes, but this idea was gradually dropped as it became clear that most patients with diabetes did not suffer from iron overload.
However, patients suffering from haemochromatosis did have diabetes and haemosiderin deposits in the pancreas, which is why «bronze diabetes» came to signify late-stage haemochromatosis.
The prevalence in the ethnic Norwegian population of homozygous and heterozygous inheritance is 0.8 % and 12 – 15 % respectively, which makes haemochromatosis one of the most common hereditary diseases in Norway (2).Nevertheless, a link was not ruled out, and some predicted the true answer by maintaining that iron deposits in the liver could cause sclerosis, and that the iron stemmed from food.At the same time, the haemolysis theory was discarded – a theory on the origin of iron which had ruled supreme since the time of von Recklinghausen.In 1889 the German doctor von Recklinghausen demonstrated that the liver contains iron, and because bleeding was considered to be the cause, he called the pigment «haemochromatosis».The link between iron deposition, diabetes and liver cirrhosis was still unknown.
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In his opinion, small daily iron deposits of up to 2 mg would explain the clinical end stage with an iron overload of 30 – 40 g at the age of 45 – 50.The theory was clinically logical, but incorrect in terms of explaining the accumulation of iron in cells, and it shed no light on the origin of the excess iron.The answer to where the iron came from remained illusive, and the disease came to be known as «idiopathic haemochromatosis».In 1935 the English doctor Joseph Sheldon (1894 – 1972) published Haemochromatosis, a retrospective review of all patients in the medical literature who so far had been diagnosed with haemochromatosis (12).Iron was found in all organs apart from the central nervous system.
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The book came to be a standard work which to this day provides the most complete picture of iron deposition in the body in cases of late-stage haemochromatosis.
The first description of a patient with haemochromatosis has been attributed to a French physician, dr. At the time, it was not known that the pigment was in fact iron, and the disease was referred to as «pigment cirrhosis» until professor Victor Hanot (1844 – 96) introduced the name of «bronze diabetes» in 1886 (6).
Armand Trousseau (1801 – 67), who in 1865 gave a lecture on glycosuria and a new syndrome presenting with diabetes, liver cirrhosis with yellow-grey granules and brown skin pigmentation in a 36-year-old male (fig 3) (4). Rudolf Virchow (1821 – 1902), in his autopsies on organs with internal bleeding, had described a yellow-brown pigment referred to as haematin as early as in 1847 (7).
Perls’ staining reaction became the standard histological technique used to demonstrate iron pigment, which since 1888 has been called «haemosiderin» (10).
In 1889 the German doctor Friedrich von Recklinghausen (1833 – 1910) was the first to stain liver autopsies from patients with bronze diabetes, thus demonstrating that the yellowish brown pigment was caused by massive iron deposition (11).