COURSE OF THE DISEASE - ADDISON'S DISEASE AND OTHER The onset is gradual. An impairment of general health is to be noted, and the patient complains of languor and debility. The order of symptomatic development is not uniform. Alelasma may, or may not, be an early indication. In dark people this hardly attracts attention. In fair persons the pigmentary altera tion is readily appreciable. Melasma may precede any marked change in general health for as long a period as from eight to sixteen months, and it is important to take note of this and seek for other in dications of the disease without delay. On the other hand, progres sive asthenia, together with indications of cardiac failure and gastric irritability, may long be the chief symptom noticeable, pigmentation setting in late. A fatal issue has been noted in cases where melasma was entirely absent, the disorder having run its course too rapidly, as it were, for this characteristic symptom to occur. The disease may prove fatal within six or twelve months of the earliest symptoms of failing health. It is rare for the leading symptoms of Addison's disease to continue beyond one year without the onset of more or less melasma.
It is important to know that in the course of the malady there may be remissions and exacerbations in respect of the chief symptoms. In following up cases, this fact has been strongly impressed on my observation, and it affords at least some encouragement in respect of treatment. The end may, however, come very suddenly.
Asthenia is the key-note of the malady. The patient finds it eas ier to walk about than to stand for any length of time. This is not uncommon in many cases of cardiac debility from any cause. Rest in bed is sometimes imperative, since sitting up may induce syncopal attacks. But even this serious condition may pass off, and the pow ers revive for weeks or months till a fresh exacerbation occurs.
The cardiac action is singularly feeble, the pulse small in volume and of low tension. Dilatation of the ventricular walls is, however, little, if at all, marked.
Anemia is present, but not to an extreme degree. There is a gen eral impoverishment of the blood, but no leukemia.
Dyspnom is, however, met with, as in anmnia and cardiac debil ity, also palpitation on exertion, sighing, and yawning.
Gastric irritability is commonly marked, indicated by nausea, hiccough, and vomiting. These symptoms may for a time be the most pronounced of all. The breath is sometimes very fetid.
Wasting is singularly absent iu respect of both muscle and fat. The temperature of the body is subnormal throughout the progress of the disease unless active tuberculosis sets in in the lungs, or other iutercurrent troubles arise. Addison's disease is apyretic.
Clinical observation fully confirms this fact. But some cases have been noted in which febrile paroxysms occurred. These were gener ally associated with marked nervous symptoms such as excitement, delirium, drowsiness, loss of consciousness, and convulsions before death.
Dr. questions the constant apyrexia of Addison's dis ease, but the great body of observed facts is against him. In the eases alluded to above, it is sought to explain the fact by supposing That some special toxine was present in the blood. MacMunn quotes the experiments of Foa and Pellacani, who injected aqueous and al coholic extracts of the adrenals into rabbits and found most toxic effects, due apparently to the action of some ptomaine, leading to si nal, bulbar, and respiratory central paralysis and pyrexia. He believes it may be the function of the adrenals to remove irom the circulation, and metabolize into a harmless product, this material arising from p•oteid disintegration, which, when the adrenals are diseased, accumulates in the blood and produces nervous symptoms and py rexia. Adrenal toxine is believed by to be a nitrogenous, non-crystallizable substance. We can only remark with respect to the cases just alluded to that they are exceptional and atypical. They must, however, be remembered by future observers.