Abstract:We here document two cases of von Recklinghausen's disease with both pheochromocytomas and gastrointestinal stromal tumors (GIST). It is very rare that these three disorders are found to occur simultaneously, although the fact that preoperative detection of GIST is difficult except with large tumors may be important in this respect. In the present cases, GIST were not evident on preoperative computed tomography and magnetic resonance imaging, and were identified unexpectedly during surgery. Our findings indicate that investigation of the intraperitoneal space should be performed during adrenalectomy for pheochromocytomas with von Recklinghausen's disease.
The prevalence of hypertension was studied in 374 patients with non-insulin dependent diabetes mellitus (NIDDM) and in 1197 non-diabetic controls. The diagnosis of hypertension was made when the mean systolic pressure of three measurements on different occasions was 151 mmHg or greater, or the mean diastolic pressure was 91 mmHg or greater. The prevalence was 42.8% in the diabetics and 17.8% in the controls. It showed a significant difference over age 31 (p <0.05). Proteinuria (p <0.001), abnormal ECG (p <0.01), hyperlipidemia (p <0.05) and hypertensive or sclerotic changes of the retina (p <0.001) were more frequently observed in the diabetics than in the controls. Hypertension was found in 71% of those with proteinuria, 48% with diabetic retinopathy, 61% with abnormal ECG and 54% with hyperlipidemia in the diabetics. The incidence of proteinuria was 22.8% in the diabetic hypertensives and was 8.3% in the nondiabetic hypertensives (p <0.001). 24 subjects out of 119 diabetics, who were normotensive at their initial visits, became hypertensive within 10 years (N-H), and 95 remained normotensive (N-N). 38% of N-H showed proteinuria already on their initial examinations and 3% of N-N did. 73% of those who showed proteinuria on their initial examination became hypertensive and 13% of those who were free from proteinuria did (p <0.001). The results suggest that diabetic nephropathy plays an important role in developing hypertension in diabetics. diabetes mellitus ; hypertension ; diabetic nephropathyIt has been reported that the prevalence of hypertension in diabetic patients is greater than in non-diabetic controls (Moss 1962; D'Alonzo 1967, 1971). The results of the Framingham Study (Kannel et al. 1970(Kannel et al. , 1971 indicated that hypertension has an adverse effect on the progression of coronary heart diseases, cerebrovascular diseases and other peripheral vascular disorders in
We studied the renal effects of nicardipine, a calcium entry blocker, in eight patients with essential hypertension (group A, WHO I or II), six hypertensive type II diabetics with mild-to-moderate nephropathy (group B, urinary albumin 200-789 mg/day), and six hypertensive type II diabetics with severe or advanced nephropathy (group C, urinary albumin 1,596-4,300 mg/day). The patients received an intravenous dose of nicardipine hydrochloride (0.5 mg) or saline placebo in a random order. Glomerular filtration rate (GFR) and renal blood flow (RBF) were measured by means of thiosulfate sodium and p-aminohippurate, respectively, during the 30 min after the nicardipine or saline injection. Blood pressures were serially monitored during the study. Nicardipine reduced both systolic and diastolic blood pressures significantly (P less than .05 to .01) at all measurement periods in all study groups compared with the respective placebo. Nicardipine increased RBF (P less than .01), GFR (P less than .05), and urinary Na+ excretion (P less than .01) and decreased total renal vascular resistance (P less than .01) in groups A and B, but these parameters remain unchanged in group C. The filtration fraction remained unaltered in all groups. The results indicate that nicardipine has several favorable renal effects with a concomitant hypotensive action in hypertensive type II diabetics with mild-to-moderate nephropathy, as observed in patients with uncomplicated essential hypertension, and the renal pharmacological responsiveness appears to be related to the severity of nephropathy.(ABSTRACT TRUNCATED AT 250 WORDS)
We measured the 24-h excretion of urinary kallikrein in 27 patients with Type 2 (non-insulin-dependent) diabetes and in 10 normal control subjects. Mean (+/- SD) kallikrein excretion in diabetic patients with nephropathy (6.2 +/- 2.4 naphthyl units (NU)/day, n = 13) was significantly lower than in control subjects (12.8 +/- 3.4 NU/day, p less than 0.01) and in diabetic patients without nephropathy (9.4 +/- 3.4 NU/day, n = 14, p less than 0.05). Kallikrein excretion in hypertensive diabetic patients with nephropathy (5.1 +/- 1.6 NU/day, n = 8) was significantly lower (p less than 0.05) than in normotensive patients with nephropathy (8.3 +/- 2.1 NU/day, n = 5). There were no significant differences in kallikrein excretion rate (24-h excretion of urinary kallikrein/24-h creatinine clearance) among control subjects (9.9 +/- 4.3 NU/ml), diabetic patients with (9.0 +/- 3.2 NU/ml) and without (9.3 +/- 3.5 NU/ml) nephropathy. However, kallikrein excretion rate in hypertensive diabetic patients with nephropathy (7.7 +/- 3.3 NU/ml) was significantly lower (p less than 0.05) than in normotensive diabetic patients with nephropathy (11.8 +/- 2.0 NU/ml, n = 10). Respective basal and post-stimulated (with intravenous furosemide 40 mg plus 60 min ambulation) plasma aldosterone concentrations measured in control subjects and in hypertensive diabetic patients with nephropathy were similar and increased to the same extent in the 2 groups (5.5 +/- 3.2 versus 5.3 +/- 3.2 and 9.3 +/- 2.6 versus 10.5 +/- 3.4 ng/ml), although the respective plasma renin activity tended to be lower in diabetic patients than in control subjects (0.7 +/- 0.6 versus 1.3 +/- 0.9 and 1.8 +/- 1.8 versus 3.0 +/- 2.6 ng-1 . ml-1 . h-1).(ABSTRACT TRUNCATED AT 250 WORDS)
Fetal rat pancreatic cells were isolated from pancreatic primordia on days 12-14 of pregnancy and cultured for 48 h in the presence of 5 mmol/l glucose. Insulin accumulation in the medium over the next 24 h was measured. Cultured cells from day 12 fetuses secreted about 1 fmol insulin per pancreas in response to 5 or 15 mmol/l glucose irrespective of whether 1 mmol/l tolbutamide, 400 µmol/l diazoxide, 5 mmol/l theophylline or 10 mmol/l mannoheptulose was present. In contrast, insulin released from day 13 cultured cells increased significantly from 3·0 0·6 to 6·2 2·2 fmol per pancreas, when the glucose concentration was raised. Tolbutamide increased, diazoxide and mannoheptulose decreased and theophylline had no effect on insulin release. Even more pronounced effects were found on insulin release from day 14 cultured cells, in which theophylline also increased the release. In addition, insulin release from cells from pregnancy day 14 was 75 16 amol/min per pancreas when the cells were perifused for 15-20 min in the presence of 5 mmol/l glucose within 3 h of isolation. Increasing the glucose concentration to 15 mmol/l or adding tolbutamide increased, whereas diazoxide decreased, insulin release in the freshly isolated cells. The insulin content of rat pancreata from pregnancy day 13 was 0·06 0·01 pmol per pancreas and increased approximately 10-fold every second day up to 6·7 0·9 pmol on day 17 of pregnancy. Between day 17 and 19 the pancreatic insulin content increased about fivefold to 39 2 pmol. The present data suggest that critical components of the insulin-secretory machinery, including ATP-regulated K + channels, glucokinase and adenylate cyclase activities, are present in the developing -cell earlier than hitherto thought.
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