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Changes of the Blood in Gout

acid, uric, serum, garrod, disease, crystals, threads and chronic


The existence of " peccant humors" in the blood was always sus pected to be the cause of gout, and the discovery of sodium urate in the tophi gave a great show of probability to this hypothesis. When in 1848 Sir A. Garrod demonstrated an excess of uric acid in the blood of the gouty, one of the most important advances in our knowledge of the disease was made. Garrod most ingeniously sub stituted for the tedious chemical research of the laboratories a simple method of examination that could be performed by any one at the bedside. Having drawn a small quantity of blood with a lan cet or a cupping-glass, the serum is separated after coagulation of the mass, and is placed in a watch-crystal or small porcelain capsule. Six drops of 28-per-cent. acetic acid are then added to every drachm of liquid, and a few threads of lint are immersed in it. All the water of the serum is allowed to evaporate, and at the end of twenty four hours, or more, microscopical examination of the dried threads finds them covered with rhombohedral crystals of uric acid. A con trol specimen procured from the serum of a healthy person shows nothing of the sort. A similar result will b^ obtained if the serosity of a blister be treated in the same way. It is important to evaporate the serum at a temperature that does not exceed 70° F., for if the process goes on too rapidly crystals will not form.

If fermentation take place in the liquid, it becomes covered with a pellicle of am monio-magnesi an phosphates that get entangled with the threads and conceal the uric acid crystals. The earthy precipi tates, however, readily dissolve in pure water, and by their disap pearance unmask the insoluble uric-acid deposit. Fermentation may cause decomposition of the acid crystals, resolving them into oxalic acid, urea, and allantoin.

It is necessary, when procuring blood or serosity for this experi ment, to avoid the neighborhood of an actively inflamed joint. Serum taken from an area of inflammation contains no uric acid, even though it be abundant in the blood from other parts of the body. The acid is either destroyed within, or is repelled from the region of inflam matory action.

By this method the presence of uric acid in the blood can be demonstrated in all cases of gout. It is usually more abundant dur ing acute attacks of the disease, but it can be also discovered during the intervals of apparent health, as well as in cases of chronic and irregular manifestations of arthritism. Nor is it in the blood alone that the acid is present. It can be found in all the liquids and tissues of the body_ It is demonstrable in the serous fluids, in the lymph, occasionally in the perspiration, in morbid exudations, and even in the serosity that moistens the surface of an eczematous patch.

An approximately quantitative estimate of the amount of uric acid in the serum was arrived at by Garrod, who found that crystals of the acid could hardly be rendered visible with the microscope unless they exceeded one part in sixty-five thousand; and in order to appear really numerous they must reach the proportion of one part in six or seven thousand parts of liquid.

The state of the red corpuscles of the blood is not always the same. Garrod and his successors found little change in their number, but in chronic forms of the disease the evident anmuia indicated a reduc tion in their number and in the amount of haemoglobin. This im poverishment of the blood is not usually so great as it often appears to be in chronic rheumatism, unless the occurrence of gout is asso ciated with lead poisoning. When that complication exists the sever est forms of anemia are developed, and there is great destruction of the red blood corpuscles, with corresponding debility and exhaustion of the patient. Comparatively little is known•about the modifications of the blood-plasma. There is an increase of the fibrin-forming ele ments in acute cases of the disease, so that the blood drawn from such patients rapidly coagulates into the small and contracting clot that is characteristic of active inflammation. Unless renal disease should coexist, the albumin exhibits no change of any appreciable character. Even then the albuminous loss through the kidneys is too small to exert any notable effect upon the composition of the plasma. The same thing is probably true of the alkalinity of the blood—we are not in a position to estimate accurately its changes. The presence of oxalic acid in the blood was frequently noted by Garrod, but this should not occasion surprise, since oxalic acid may be obtained by splitting up the molecule of uric acid, and under cer twin circumstances one of these acids could not be present without the coexistence of the other.

Despite the fact that uric acid is usually overabundant in the blood of gouty subjects, there are cases on record in which the most careful analysis has failed to demonstrate its presence, even though the joints were thickly incrusted with tophi. Per contra, in cases of cirrhosis of the liver, gravel, and leukemia the blood contains an excess of uric acid without any manifestation of gouty symptoms. According to Haig, those symptoms are developed not by the free circulation of uric acid in the blood current, but by its determination from the blood into the articular structures.