It has been known for long that the origin of endemic goitre may be closely associated with a particular water, and that the disease may disappear with the introduction of a fresh and pure supply; but all the attempts to bring it into relation with particular mineral constituents have so far failed, and the available evidence points strongly in favour of some infective agent.
Captain McCarrison's recent observations in Gilgit and Chitral have led him to this conclusion. The disease is endemic in these parts, and villages with the same water supply suffer comparatively from it, while others under similar circumstances, but with a different water supply may be wholly exempt. In a village where goitre was unknown, it became endemic shortly after the arrival of a goitrous family, all the other social conditions remaining unchanged; and its incidence along a common water supply became increased the further the village from the source, presumably as the result of continued contamination from affected communities upstream.
There is, however, evidence that infection may arise in other ways. The use of boiled water may in some cases be a sufficient protective, but in other instances wholly fails, and goitre may, as in an instance narrated by Dr. Mackenzie, be endemic in one village and not in another, though the water supply is common to both. Goitre too seems to attack in particular communities whose social circumstances are poor, and to disappear with the introduction of improved sanitation.
From the individual standpoint goitre is more prevalent among the poorer classes and among persons engaged in agricultural pursuits; and is, for example, practically unknown among the European residents in Gilgit and Chitral. There is there a distinct seasonal prevalence of the disease.
The evidence then is strongly in favour of an infective origin of endemic goitre, and points to the alimentary tract as the probable site of entrance of the parasite. But investigations have so far failed to isolate the active agent, though organisms have been found in the faeces of goitrous patients, and recovery in recent cases follows the administration of thymol.
It is at least possible that exophthalmic goitre may prove to be the result of a similar infection, though evidence is so far almost wholly wanting. Myxoedema and cretinism may also presumably be in some cases associated with an infective etiology, though other causes have been shown to produce functional destruction of the gland.
It seems reasonable, on the evidence available, to make certain that infective agents no longer gain access to the alimentary tract in cases of endemic goitre and Graves' disease; and even in the myxoedemas similar precautions should be observed, though in all probability the damage to the gland is already irretrievable. A pure water supply is the essential factor, and rain water or boiled water should be utilized, not only as a beverage but for culinary and domestic uses, until the infected supply can be replaced. Captain McCarrison's evidence of other possible methods of infection should lead to renewed precautions with regard to the possible contamination of other articles of diet. In all cases removal to non-affected areas is preferable, at any rate for a time.
The appetite in the thyroidal diseases is apt to be defective, and it may be, especially in cretins, perverted. A due supervision of the diet must be maintained in consequence. Alimentary symptoms are, as a rule, absent in cases of goitre and the myxoedemas, though constipation may require attention.
In exophthalmic goitre, however, both gastric and intestinal symptoms may be severe, and may even lead rapidly to death. Attacks of vomiting and diarrhoea occur, sometimes in conjunction, sometimes isolated. Nausea may be intense and vomiting persistent and violent, following the ingestion of everything, whether fluid or solid; epigastric pain is sometimes acute, or, on the other hand, may be absent. The diarrhoea is usually painless, but large loose stools may be passed frequently, and if continued, prostration becomes extreme. The tachycardia becomes exaggerated, the cardiac power fails, and death ensues from cardiac exhaustion. Death may occur within four or five days, but the duration of fatal attacks is usually longer.
In some instances the symptoms follow notable indiscretions in diet, but in others their origin is obscure. Acetonaemia often co-exists, and both acetone and diacetic acid may be recognized in the urine.
The diet in these cases then must be carefully regulated, and the ingestion of irritating food-stuffs prevented. The food should be bland and easily digested, and any minor digestive symptoms should be promptly attended to. Thirst is sometimes extreme, and the constant imbibition of fluids seems at times provocative of such attacks. In cases with acute gastric or intestinal symptoms treatment is rarely of much avail. It should be conducted on the lines already laid down.