Etiology and Treatment

Developments in laboratory medicine brought physicians to something approaching consensus regarding the pathophysiology of chlorosis. By the mid-nineteenth century, reasonably accurate methods were available to determine the number of red blood cells and their hemoglobin content. With this it became apparent that the sine qua non of chlorosis was an iron deficiency anemia. In the minds of many physicians, chlorosis could now be separated from earlier mimics such as love-sickness, hypochondriasis, and neurasthenia.

The natural history of chlorosis, whether treated with iron or not, remained a matter of dispute. In part, this undoubtedly related to frequent misdiagnoses. Using iron, some physicians reported that a single cure was lasting (Thomson 1886; Faber and Gram 1924). For others the disease progressed to phthisis, many cases of which probably were tuberculosis as such, rather than chlorosis. After iron be came a standard treatment, there was general agreement that the disease recurred when treatment was stopped, but responded when iron was reinstituted and continued.

Ralph Stockman wrote the most comprehensive and effective accounts of the nature and treatment of chlorosis (Stockman 1893, 1895a, 1895b). In his series of 63 cases, 27 were suffering their first attack, 11 their second, and 22 several attacks. Of the last group, some were chronically anemic. If patients remained on the prescribed iron long enough, the chronic cases responded as well as the newly diagnosed (Stockman 1895c). From what we now know of iron deficiency anemia, those receiving proper doses of iron should have done well, whereas the improperly or untreated cases would have ended badly, even fatally.

Some observers might look on the use of iron in treating chlorosis before an iron deficiency had been demonstrated as sheer luck, and one more example in the history of medicine where physicians did the right thing for the wrong reason. Yet although there are many examples of right thing—wrong reason in medicine's past, iron for chlorosis probably is not one of them. For when physicians employed proper iron compounds in correct doses, the clinical results were dramatic and altogether convincing. The failures, when iron was used, might more properly be thought of as doing the right thing with the wrong regimen.

Even if it was correct that the central feature of chlorosis was an iron deficiency anemia, a good deal of confusion remained. Still to be elucidated were a host of diseases marked by pallor, wasting, and lassitude, some of which had anemia as a secondary manifestation. These included nephritis, hypothyroidism, subacute bacterial endocarditis, mitral stenosis, and tuberculosis. What did subside was the focus on many factors once thought of as central, but which were now relegated to a contributory role at most. These included lack of fresh air and exercise, corsets, love sickness with its related sexual frustration, Rudolph Virchow's notion of hypoplasia of the arterial system, and a variety of uterine disorders.

Chlorosis reminds us of the complex interaction between physiology and social elements in the genesis of human disease. This interplay is better understood in light of our current notions of iron metabolism. To protect the body against the destructive effects of excessive iron, intestinal absorption is fixed at a rate that barely replaces the small amount lost normally. This balance is so exquisite that the prolonged loss of 2 teaspoons of blood daily will ex ceed the body's ability to absorb iron from a normal diet, and anemia follows. Iron deficiency anemia can result from a decrease in dietary iron, an increase in bodily demand for iron, or a loss of blood.

In chlorosis the decrease in iron intake came about either from poverty that precluded the intake of iron-rich foods or from cultural influences that led young women to avoid meat, eggs, and even milk because of the belief that animal foods increased the sexual drive, a very undesirable state of affairs in Victorian times. The increase in bodily demands for iron, for our purposes, resulted simply from the rapid growth associated with adolescence. For the historian of disease seeking physiological explanations for chlorosis, these factors would combine to produce an iron deficiency anemia.

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