The Pathogenesis of Idiopathic Hypercalciuria: Evidence for Parathyroid Hyperfunction

We studied the effect of calcium deprivation and loading in17 healthy subjects and 76 patients with renal calculi. Fivehad primary hyperparathyroidism with an elevated plasma ionisedcalcium and detectable plasma parathyroid hormone. Forty-ninehad idiopathic hypercalciuria, defined by a urine calcium greaterthan 7 mmol/day on a free diet. Twenty-two were normo-calciuric.Fasting plasma calcium, corrected for albumin, was higher inthe patients with idiopathic hypercalciuria (2.40±0.10mmol/1) than in controls (2.28 ±0.05 mmol/1, p < 0.005).Plasma calcium was intermediate in the normocalciuric stoneformers (2.35 ±0.08 mmol/1) and elevated in the patientswith primary hyperparathyroidism (2.62 ± 0.07 mmol/1).Nephrogenous cyclic adenosine monophosphate (cAMP) and parathyroidhormone levels were highest in the primary hyperparathyroidgroup and did not differ significantly within the other groups.Nephrogenous cAMP correlated positively with plasma calciumin the patients with primary hyperparathyroidism and negativelyin controls; there was no correlation in the idio-pathic hypercalciuriagroup. Following an oral calcium load, plasma calcium rose andnephro-genous cAMP fell similarly in all groups. Fasting urinarycalcium and its increase after load were greatest in the idiopathichypercalciuria and primary hyperparathyroid groups, with inter-mediateresults in the normocalciuric patients. Neither the initialmetabolic patterns nor the response to thiazide fitted withthe previously described patterns of absorptive and renal hypercalciuria.Increased parathyroid gland activity is the most probable causeof idiopathic hypercalciuria.     

Effects of eating on plasma hyaluronan in patients with cirrhosis: Its mechanism and influence on clinical interpretation

Circulating levels of hyaluronan (HA) may be a clinically useful non-invasive test in liver disease to evaluate, for example, the degree of fibrosis or cirrhosis. Healthy subjects exhibit a two-fold or greater postprandial elevation of plasma HA. We undertook this work to determine the effect of eating on plasma HA in patients with cirrhosis, to define mechanisms underlying the changes observed and to examine whether using fasting samples improves the discriminating value of plasma HA as a clinical test. Plasma HA was measured using a protein-binding assay in serial samples obtained over 2.5 h, during which a 2100 kJ meal and/or intravenous infusion of octreotide (25 μg stat, 25 μg stat, 25 μg/h) were given, or in paired random and fasting samples from patients with cirrhosis. In six patients with Pugh's A cirrhosis, plasma HA increased more than two-fold after food ingestion, peaking after 75–90 min. In four patients (one Pugh's A), no response was observed. Octreotide transiently increased plasma HA by a mean of 20%, but, in combination with eating, reduced the peak plasma HA by 80% in responding patients. In 30 patients with cirrhosis, random plasma HA was abnormal in only 70% compared with 93% of autologous fasting samples, using the respective normal ranges ( P =0.01). Ingestion of food markedly increased plasma HA in patients with compensated but not decompensated cirrhosis, most likely due to a postprandial increase in splanchnic blood flow. Fasting patients prior to taking blood improves the clinical discriminating value of plasma HA.     

Fate of [14C]warfarin in guinea-pigs: effect of a concomitant single dose of salicylate

When a single dose of sodium salicylate (177·8 mg kg^?1, by mouth) was given with [¹⁴C] warfarin (1 mg kg^?1, i.p.) to guinea-pigs, the salicylate depressed the blood concentrations of ¹⁴C for 6 h. At 1 h, salicylate increased the distribution of ¹⁴C in the liver and brain, but at 1 and 6 h it was decreased in the blood and kidney. A significant portion of the ¹⁴C was excreted into the bile, but was subject to enterohepatic circulation and then excreted by the kidney. There was an enhancement of the biliary elimination of ¹⁴C in the first 5 h after salicylate and a decrease in ¹⁴C concentration in blood; the proportion of warfarin to its metabolites excreted in the urine and bile was unchanged. Salicylate displaced serum protein bound [¹⁴C]warfarin in vitro. Salicylate increases the initial biliary elimination of warfarin by displacing some of that bound to plasma protein. This facilitated uptake of warfarin by the liver where it was metabolized. This effect of salicylate did not modify the hypoprothrombinaemia produced by warfarin.     

Symptom relief and survival after chemo-embolization with Adriamycin,Lipiodol and Gelfoam for hepatocellular carcinoma

This is a retrospective study to evaluate the ability of arterial chemo-embolization with Adriamycin, Lipiodol and Gelfoam to relieve symptoms, primarily abdominal pain, and to prolong survival in patients with hepato-cellular carcinoma. Twenty patients were referred from 1986 to 1991 and in 18 the chemo-embolization procedure was successful. In the follow-up period to March 1992, 17 patients had died. Their survival times were not found to be significantly different from the reported rates of survival in patients given no therapy. In only one of 10 patients followed with computed tomography was a reduction in tumour size seen. Nine of 11 patients with pain reported significant relief from pain following treatment. Six patients had repeat embolizations that successfully relieved recurrent pain. In the authors’experience chemo-embolization was helpful in relieving pain, but did not prolong life.     

The Effect of Hemorrhage on Plasma Iron Turnover

The plasma iron turnover rate in rats following a single hemorrhage reachesa maximum in about 48 hours and returns to normal between the seventh andtenth day. There is considerable variation in individual rats in both the maximum rate attained and the time required for recovery. No significant difference in response was observed due to the severity of hemorrhage uponremoval of 2.7 to 18 per cent of total red cells.

Submitted on June 20, 1960 Accepted on November 20, 1960