Cigarette smoking: an independent risk factor for atherosclerosis in the hypogastric-cavernous arterial bed of men with arteriogenic impotence

We investigated the relationship between cigarette smoking and atherosclerosis of the hypogastric-cavernous arterial bed by evaluating arteriograms of young impotent men referred for selective pudendal angiography. Those patients with hemodynamically significant atherosclerosis had smoked more pack-years than had patients without arterial disease. These differences were statistically significant (p less than 0.05) for the common penile artery (32.8 pack-years, 40 patients versus 22.3 pack-years 57 patients) and the dorsal artery (31.3 pack-years, 48 patients versus 22.0 pack-years, 49 patients). The effect of cigarette smoking as an independent risk factor for atherosclerotic disease in the hypogastric-cavernous arterial bed was evaluated as well. When controlled for age, trauma history, hypertension and diabetes, cigarette smoking was independently associated with atherosclerosis in the internal pudendal artery (p less than 0.05). The relative risk (and 95% confidence interval) of developing internal pudendal artery atherosclerosis for each 10 pack-years smoked was 1.31 (1.05 to 1.64). A third analysis investigated the potential interactive effects of cigarette smoking and pelvic or perineal trauma. A significantly higher incidence (p less than 0.05) of cavernous artery atherosclerosis was found among smokers with a history of chronic perineal trauma (33 patients) compared to nonsmokers with a similar history (25 patients). The findings of this study indicate that cigarette smoking is an independent risk factor in the development of atherosclerotic lesions in the internal pudendal and common penile arteries of young impotent men. Cigarette smoking appears to predispose these patients to early atherosclerotic lesions in the cavernous artery following chronic perineal trauma.     

Effects of cyclophosphamide and of busulfan on spleen colony-forming units and on hematopoietic stroma.

The effects of cyclophosphamide (CY) and busulfan (BU) on the hematopoietic stromal function (HS-P) of mouse marrow were evaluated. Stromal function of femoral marrow was assessed by implanting the test femur s.c. into an isogeneic host and determining the number of CFU-S in the implant 6 weeks later. Since the CFU-S have been shown previously to be primarily of host origin, this presumably measures the abilit- of donor hematopoietic sites to harbor host CFU-S. After injection of CY, the number of CFU-S in the marrow fell but recovered to normal within 6 weeks. The HS-P function fell to half-normal after 10 mg of CY and did not regenerate detectably in 6 weeks. On the other hand, 2 mg of BU i.p. caused a lesser initial decline in the number of CFU-S, but recovery was still incomplete after 6 weeks. BU given p.o. had a more marked effect on CFU-S and caused a significant decline in the HS-P function. Doses of CY (5 mg/dose) given intermittently appear to cause cumulative damage to HS-P function. HS-P function did not, in any experiment, recover significantly in the 6 weeks following the last dose of CY. This result suggests that large doses of the alkylating agent CY causes prolonged and perhaps permanent HS-P damage. This damage to the HS-P is cumulative when the CY is given at weekly intervals. Despite lack of HS-P recovery, CFU-S regenerate rapidly after CY therapy is stopped. On the other hand, BU also causes damage to the HS-P. However, even when BU is given at a dosage that does not significantly affect the HS-P, CFU-S recovery is delayed, suggesting that BU affects the CFU-S in a manner that differs qualitatively from that of CY.     

Recurrent obstipation as a complication of partial pancreatectomy for non-beta cell adenoma of the pancreas.

Verner and Morrison, in 1958, reported non-insulin-secreting tumours of the pancreas that were associated with a syndrome of refractory diarrhea, achlorhydria and hypokalemia. Surgical resection of such tumours results in rebound acid hypersecretion and cessation of the watery diarrhea. The authors report the case of an 84-year-old man who had three of the four major criteria for diagnosis of the Verner Morrison syndrome. Hypokalemia was absent, but this was possibly due to the large doses of potassium chloride that he was taking in conjunction with diuretics. After resection of the tumour severe obstipation with resultant bowel obstruction developed in addition to rebound hypersecretion and relief of watery diarrhea. Treatment, consisting of bulk laxatives in appropriate amounts, alleviated the obstipation.     

Acalculous parotid sialadenopathy

Acalculous inflammation of the parotid gland has been regarded by some as a specific disorder that can be staged as to the severity of the disease process. A review of the literature, however, indicates a divergence of opinion. It is the purpose of this study to test this hypothesis by a retrospective double-blind analysis of clinical, sialographic and histopathologic findings. Forty-two patients who were seen by the Department of Otolaryngology, Washington University School of Medicine from 1961 to 1970 were evaluated by two separate teams. There were 20 sialograms and 30 pathologic specimens, and all were re-examined. Eleven patients had both sialographic studies and histopathologic examination. The clinical presentations and sialographic findings were reviewed. These findings were then compared to each other. Our results indicate that we could not evaluate the severity of the clinical disease by sialography or histopathology. There was no consistent method of staging the sialographic and pathologic findings. In addition, there was no correlation between these two parameters. They reflect neither the patient's clinical syndrome pattern nor the extent of disease. It appears that the parotid gland responds variably to inflammation. These observations are exemplified by case histories.