The sequence of events in haematogenous metastasis from colonic carcinoma was analysed, using 1541 necropsy reports from 16 centres. The findings are consistent with the cascade hypothesis that metastases develop in discrete steps, first in the liver, next in the lungs and finally, in other sites. Deviations of necropsy findings from the cascade model are largely explained on the basis of false negative reports. In only 216 of 1194 cases was there suggestive evidence that metastatic patterns (excluding lymph nodes) were causally related to lymphatic or non-haematogenous pathways. The incidence of metastatic involvement in 'other' (quaternary) sites correlated with target organ blood-flow (ml min-) per g, only when bone marrow and thyroid were excluded. In the thyroid the incidence was lower than expected on the basis of blood flow per g tissue; this may indicate that the thyroid is an unfavourable site for metastatic growth of colonic carcinoma. In the bone marrow it is higher; the latter may be due to delivery of cancer cells via both arterial blood and the vertebral venous plexus. Recognition of this pattern of metastases in the bone marrow could be important with respect of diagnosis and therapy, in patients with colonic carcinoma.

In animals with reduced renal mass increased glomerular filtration is associated with accelerated glomerular sclerosis. Whether hyperfiltration causes glomerular damage in humans is unknown. Since increased glomerular filtration occurs in obesity, the amount of glomerular sclerosis found in renal autopsy tissue from 46 patients with massive obesity was compared to that found in 46 normal body weight controls. Despite increased kidney weight and glomerular size, obese patients had the same proportion of completely sclerosed glomeruli as controls. In addition, no focal segmental glomerular sclerosis was seen in the obese group. It is concluded that patients with massive obesity have increased kidney weight and nephron size consistent with hyperfiltration. Nevertheless, massively obese patients do not appear to have increased glomerular sclerosis.

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The antihypertensive activity of terazosin, an investigational alpha 1-adrenergic-receptor blocker, and its effect on blood lipids were compared with placebo in a double-blind study. After a 3-week placebo baseline period, patients were randomized to receive terazosin (n = 22) or placebo (n = 16). The dose of terazosin was titrated over 2 weeks to a maintenance dosage of 10 mg once daily for 4 weeks. Antihypertensive efficacy was assessed: (1) at the end of the 24-hour dosing interval by comparing the average blood pressure (BP) after 3 and 4 weeks of maintenance therapy to the average BP after 2 and 3 weeks of placebo therapy, and (2) for 3 hours after drug ingestion at the final visit in comparison to the predose BP at that visit. At the end of the 24-hour dosing interval, 10 mg of terazosin reduced the mean supine systolic BP from 155.6 to 152.2 mm Hg and mean supine diastolic BP from 101.9 to 99.0 mm Hg (p less than 0.05). During the 3 hours after drug ingestion, mean supine systolic and diastolic pressures decreased maximally from 151.8 to 142.7 mm Hg (p less than 0.05) and from 99.5 to 91.0 mm Hg (p less than 0.05) respectively. No supine BP reduction differed significantly from the placebo response. During terazosin therapy there was a nonsignificant increase in mean body weight of 1.4 +/- 2.9 kg and no change in blood lipids. Thus the drug demonstrated greater antihypertensive activity 1-3 hours after ingestion than at the end of the 24-hour dosing interval.(ABSTRACT TRUNCATED AT 250 WORDS)