[Follow-up of chronic inflammatory bowel disease. A 10-year material]. / Oppfølging av kronisk inflammatorisk tarmsykdom. Et ti års materiale.

During a ten year period, all patients (N = 641) with chronic inflammatory bowel disease were systematically followed, clinically and endoscopically by means of mucosal biopsies. The complexity of these disorders was obvious, and in 103 patients it was impossible to establish a diagnosis of either ulcerative colitis or Crohn's disease. Fulminant colitis occurred in 9.8% of the ulcerative colitis patients and only four of these had to have surgery. Total colectomy was necessary in only 58 patients. Twenty-one patients died, four from causes related to the inflammatory bowel disease. Six patients with ulcerative colitis were treated for adenocarcinoma of the colon. No malignancies were found in the patients with Crohn's disease. The biopsies showed only two patients with high grade dysplasia.

Complications of fiberoptic gastrointestinal endoscopy--five years' experience in a central hospital.

Complications in relation to fiberoptic gastrointestinal endoscopy were recorded prospectively during the five-year period 1980-1984. Diagnostic esophago-gastroduodenoscopy (EGD) had non-fatal complications in ten out of 7,314 procedures (0.14%) and three deaths (0.04%). Therapeutic EGD had non-fatal complications in eight out of 440 procedures (1.8%) and two deaths (0.5%). Diagnostic endoscopic retrograde cholangiopancreatography (ERCP) had non-fatal complications in 15 out of 1,930 procedures (0.8%) and one death (0.05%). Therapeutic ERCP had non-fatal complications in 14 out of 554 procedures (2.5%) and six deaths (1.1%). Diagnostic colonoscopy had non-fatal complications in five out of 3,538 procedures (0.14%) and therapeutic colonoscopy in 21 out of 1,055 procedures (2.0%). There were no deaths in connection with diagnostic or therapeutic colonoscopy. The recommendations based on this series are: Put greater emphasis on a proper evaluation of indications and contraindications. Avoid sedation of patients with respiratory failure. If possible, postpone procedures which may cause bleeding in patients with impaired hemostasis until proper correction has been achieved.

Aging and urinary vasopressin excretion in healthy men.

The influence of age on urinary excretion of arginine vasopressin (antidiuretic hormone) was examined in three groups of healthy men, 25 +/- 1 (n = 12), 40 (n = 44) and 50 years of age (n = 28) respectively. Despite increasing plasma vasopressin with progressive age (2.5 +/- 0.6 vs. 3.5 +/- 0.4 vs. 7.4 +/- 1.0 ng/l, respectively) (means +/- SE), urinary excretion of vasopressin turned out similar (6.7 +/- 1.0 vs. 6.8 +/- 0.8 vs. 6.9 +/- 0.6 ng/h). No differences in sodium excretion, serum osmolality and creatinine clearance appeared that could explain these findings. The present results suggest that age-related impairment of renal concentrating capacity is compensated for by increasing circulating plasma vasopressin. Furthermore, differences in tubular handling of the hormone with age may explain the present findings, and may be another compensatory mechanism for decreased urinary concentrating ability.

Increased plasma vasopressin in low renin essential hypertension.

Baseline plasma vasopressin concentrations were measured in 48 men (all 50 years old) with decreased plasma renin concentration and untreated, sustained essential hypertension and in 29 healthy normotensive men. Mean hypertensive plasma vasopressin concentration was more than twice as high as the corresponding normotensive level (15.7 +/- 2.2 [SE] vs 7.5 +/- 1.0 pg/ml; p less than 0.001). Plasma renin concentration in the hypertensive group was reduced compared with that in the normotensive group (0.28 +/- 0.04 vs 0.46 +/- 0.06 Goldblatt units X 10(-4)/ml). These differences appeared despite virtually identical serum osmolality, creatinine clearance, and urinary sodium excretion in the two groups. In the first 38 hypertensive subjects, arterial plasma epinephrine concentrations were significantly increased over those of the first 28 control subjects (99 +/- 12 vs 68 +/- 6 pg/ml; p less than 0.025). In contrast to those with low renin essential hypertension, 35 men with normal renin essential hypertension (all 40 years old) had normal plasma vasopressin levels that were not significantly different from those in a comparable normotensive control group (3.7 +/- 0.8 vs 3.5 +/- 0.4 pg/ml). Arterial epinephrine concentrations were not significantly different between normal renin subjects and the control group. After 6 weeks of treatment with the nonselective beta-adrenergic receptor blocker oxprenolol in 11 subjects with low renin hypertension, blood pressure was reduced and the plasma vasopressin concentration fell from 27.6 +/- 6.4 to 13.5 +/- 4.2 pg/ml (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Dietary sodium intake increases vasopressin secretion in man.

Plasma vasopressin concentration and urinary vasopressin excretion were measured in a control situation, during sodium depletion and on days 1, 2, and 7 during high sodium intake in twelve 23-26-year-old men on a free-water intake. Urinary vasopressin excretion decreased from 6.7 +/- 1.0 ng/hr (control) to 3.9 +/- 0.3 ng/hr (p less than 0.01) when sodium excretion decreased from 188 +/ 18 to 16 +/- 2 mmol/24 hr. During the first day of high sodium intake, the urinary vasopressin excretion increased to 10.0 +/- 1.2 ng/hr (p less than 0.01) compared with control and remained high throughout the sodium repletion. Through all collection periods at low, normal, and high sodium intake, vasopressin excretion increased concomitantly with serum sodium concentration and osmolality. After low sodium intake for 7 days, the serum vasopressin concentration averaged 2.7 +/- 0.6 ng/l, and this level was maintained throughout the sodium repletion period. These results are compatible with a stimulatory effect of dietary sodium intake on pituitary vasopressin secretion in man. Dietary sodium may stimulate vasopressin secretion through extracellular osmolality or even by a direct effect of extracellular sodium on periventricular receptors. Plasma renin concentrations or sympathetic nervous activity offered no further explanations. Urinary vasopressin excretion provides more useful information than do plasma concentrations, as the latter can fluctuate rapidly.

Evidence of age-related variation in plasma vasopressin of normotensive men.

The influence of age on plasma arginine vasopressin was examined in three groups of healthy men, 25 +/- 1 (n = 12), 40 (n = 23) and 50 years of age (n = 13), respectively. The three groups were comparable in body height, weight, blood pressure, heart rate, serum and urine osmolality, electrolytes and endogenous creatinine clearance. Compared to the 25-year olds, the 50-year old men had more than three times higher basal plasma vasopressin (7.8 +/- 1.4 vs. 2.5 +/- 0.6 ng/l, p less than 0.01), only one-third the plasma renin concentration (0.36 +/- 0.05 vs. 1.10 +/- 0.33 G.U. X 10(-4)/ml, p less than 0.01) and a significantly higher plasma noradrenaline (267 +/- 21 vs. 199 +/- 19 ng/l, p less than 0.05) while plasma adrenaline remained essentially unchanged. The 40-year olds had intermediate plasma vasopressin concentrations (4.2 +/- 0.6 ng/l). Thus, age is a variable with a substantial effect on plasma concentrations of vasopressin in addition to the well-known effect on renin and noradrenaline. Age must be taken into account in further clinical studies on vasopressin.

Dietary sodium intake and vasopressin excretion in man.

The present study was undertaken to examine the possible relationship between dietary sodium intake and arginine vasopressin (AVP). In 12 normotensive men (aged 23-26 years) urinary AVP excretion decreased from 6.7 +/- 1.0 to 3.9 +/- 0.3 ng/h (P less than 0.01) when sodium excretion by dietary intervention for one week was reduced from 188 +/- 18 to 16 +/- 2 mmol/24 h. At a high sodium intake (300 mmol/day), AVP excretion increased to 10.0 +/- 1.2 ng/h during the first day (P less than 0.01) and remained high throughout one week of sodium load. These results are compatible with a major physiological role of sodium in AVP secretion in man. A sodium-AVP relationship may play a role in the pathogenesis of essential hypertension since recent reports suggest elevated plasma AVP in essential hypertensive states.

Arteriovenous difference of plasma vasopressin in normal man and effect of posture.

In 13 normotensive 50-year-old men arterial plasma vasopressin (11.3 +/- 2.1 ng/l, mean +/- SE) was significantly increased over venous (7.8 +/- 1.4 ng/l) in the supine position with an arteriovenous difference of 3.5 +/- 1.2 ng/l (p less than 0.05). After 30 min in the upright position, an average increment of 45% to 11.3 +/- 1.8 ng/l was observed for venous vasopressin. Since a similar increase was not found for arterial vasopressin, the arteriovenous difference decreased with 29% to 2.5 +/- 2.1 ng/l and was no longer statistically significant. The correlation between supine and standing vasopressin was statistically significant both for arterial (p less than 0.001) and venous plasma (p less than 0.05). These data indicate a substantial removal of plasma vasopressin by receptors even in the peripheral vascular beds (forearm) and not only in the liver and the kidneys as previous literature claims. The arteriovenous difference decreases in the upright position, most likely because of reduced plasma vasopressin clearance.

Increased plasma vasopressin and serum uric acid in the low renin type of essential hypertension.

In 22 50-year-old men with long-standing, untreated essential hypertension of the low renin type, venous plasma vasopressin concentrations were about three times those of 15 matched normotensive control subjects (p less than 0.005). These patients also had increased arterial concentrations of noradrenaline and adrenaline (p less than 0.05) but there was no direct association between these two catecholamines and vasopressin. On the other hand, adrenergic beta-receptor blockade with oxprenolol reduced both blood pressure and plasma vasopressin (p less than 0.01) while venous plasma dopamine concentrations significantly increased. In addition, the hypertensives had highly significantly increased serum uric acid (p less than 0.001) that correlated positively with venous vasopressin concentrations (p less than 0.05). According to these data, patients with the volume-sustained low renin type of essential hypertension have increased plasma vasopressin concentrations that probably are inversely related to dopaminergic nervous activity. The data also indicate that increased plasma vasopressin correlates with serum uric acid, most probably through increased tubular reabsorption of this acid.

Hyperthermia and rhabdomyolysis in self-poisoning with paracetamol and salicylates. Report of a case.

A young women ingested large amounts of different analgesics, mainly salicylate and paracetamol. On admission about 17 hours later, clearly toxic serum levels of both drugs were demonstrated. She was comatose with respiratory failure for 5 days. During the first day there was a period of several hours of therapy-resistant hyperthermia. A severe bleeding tendency was probably related to profound coagulation defects. Persistingly elevated serum levels of ASAT and ALAT for two weeks were presumably caused by a toxic effect of paracetamol on the liver. When consciousness was regained, widespread pareses of skeletal muscles, predominantly of the lower limbs, were demonstrated. These were related to extensive rhabdomyolysis as evidenced by extremely elevated serums levels of CPK for 6 weeks, and by muscle necrosis in biopsy specimens. There was a gradual improvement, but walking disturbances were still present after one year. The hyperthermia was probably related to the cerebral effects of salicylates or the combination of multiple drugs. The rhabdomyolysis might be related to a deleterious effect of hyperthermia on the muscles or to an effect of paracetamol on the skeletal muscles similar to that which might occur in the myocardium, or to a combination of these mechanisms.