As the patient was in an inverted position, it was thought that the prolapsing organs of the genital tract would be returned to their normal position by the force of gravity and the shaking motion. "Hippocrates had his own theories regarding the cause of prolapse. He thought that recent childbirth, wet feet, sexual excesses, exertion, and fatigue may have contributed to the condition. Polybus, Hippocratess son-in-law, wrote: "a prolapsed uterus was treated by using local astringent lotions, a natural sponge packed into the vagina, or placement of half a pomegranate in the vagina." In 350 A.D., another practitioner named Soranus described his treatments which stated that the pomegranate should be dipped into vinegar before insertion. Success could be enhanced if the woman was on bed rest and reduced intake of fluid and food. If the treatment was still not successful, the womans legs were tied together for three days.In 1521, Berengario da Carpi performed the first surgical treatment for prolapse. This was to tie a rope around the prolapse, tighten it for two days until it was no longer viable and cut it off. Wine, aloe, and honey were then applied to the stump.In the 1700s, a Swiss gynecologist, Peyer, published a description of a cystocele. He was able to describe and document both cystocele and uterine prolapse. In 1730, Halder associated cystocele with childbirth. During this same time, efforts began to standardize the terminology that is still familiar today.
Type 2A is caused by inheriting two mutated alleles, one from each parent, for the HJV (aka HFE2) gene, which encodes the protein hemojuvelin. Hemojuvelin is responsible for the maintaining correct levels of the protein hepcidin, which regulates iron absorption in the blood. Without functional hemojuvelin, hepcidin levels are reduced, and the amount of iron absorbed into the blood during digestion is unable to be halted. Type 2B is caused by inheriting two mutated alleles, one from each parent, for the HAMP gene, which encodes the protein hepcidin. Hepcidin is responsible for regulating absorption of iron from the small intestine to the blood during the digestion of food, such to prevent blood iron levels from becoming too high. A lack of functional hepcidin prevents the body from stopping iron absorption when it has already reached adequate levels.Type 2A is the most common form, accounting for roughly 9 out of every 10 cases of the disease. Diagnosis
An individual may be suspected to have this condition based on their medical history, physical exam findings, and blood tests, and confirmation of the diagnosis can be made with further testing, often with use of gene panels. Differential Diagnosis
Juvenile hemochromatosis shares signs and symptoms with many other conditions including:
Other types of hereditary hemochromatosis
Atransferrinemia
Aceruloplasminemia
African iron overload
Neonatal hemochromatosis
Transfusional iron overload and other forms of secondary hemochromatosis
Porphyria cutanea tarda

Blood Testing
The presence of hemochromatosis may be discovered incidentally on blood testing, or a diagnosis suspected based on symptoms may be supported or ruled out by blood testing.