Pulmonary alveolar microlithiasis is characterized by the presence of innumerable minute concrements lying free within the alveoli, throughout the lungs, unattached to the alveolar walls. The disease is extremely rare; not more than 50 cases have been reported in the literature. Since symptoms are usually absent, the diagnosis is almost always made during a routine examination of the chest, when the roentgenologist is surprised to discover the disease in an advanced stage in an apparently healthy person. These two features, namely, a characteristic roentgenogram showing the presence of innumerable minute intra-alveolar concrements, like grains of sand, and the complete absence of symptoms, make possible a radiologic diagnosis even without a confirmatory pathologic report. The first case of microlithiasis was reported by Harbitz (1) in 1918, and the second by Schildknecht (2) in 1932. Schildknecht described for the first time the roentgen features, but Puhr (3) gave the disease the name of pulmonary alveolar microlithiasis, by which it is now known. Five more cases were reported between 1947 and 1953 (4–8). The remainder were published subsequently (9–11, 15–21). An interesting feature of the disease, as reported in the literature, is that it has on several occasions been observed in members of a single family (9, 10, 11). The 4 cases of pulmonary alveolar microlithiasis to be reported in this article, occurring in 4 sisters, are the first to be discovered in Colombia. So far as can be determined from a thorough review of the literature at our disposal, they are the only cases of the disease ever reported from South America. One of the patients died, and the clinical diagnosis of pulmonary alveolar microlithiasis was confirmed at autopsy. In patients with pulmonary alveolar microlithiasis, death occurs as a result of cardiac insufficiency, which in its turn is due to chronic cor pulmonale developing after ten, twenty, or more years of apparently good health. The early symptoms are those of discrete pulmonary insufficiency, which manifests itself over a more or less prolonged period by dyspnea and cyanosis on extreme exertion. In regard to etiology, it can be stated that the disease is none of the following conditions: an infection, an inflammatory process, a tumoral lesion, a pneumonoconiosis, or the result of either an endocrine or a circulatory disorder. It is generally believed that, through the influence of certain unknown factors, there is a disturbance in the respiratory metabolism of carbon dioxide, which promotes alkalinity at the alveolar surface, with consequent precipitation of the microliths. The familial nature of the disease has been explained on the basis of hereditary congenital predisposition. We believe, however, that the causal role of environment, dietetic factors, and living conditions cannot be overlooked.