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R Rizzoli

Publications and source records attributed to R Rizzoli.

At least 253 records · Page 14Linked to original sources
PubMed1986

Fibronectin distribution during lymph node development in guinea pig: an immunohistochemical study.

We carried out an immunohistochemical study on mesenteric guinea pig lymph nodes, from the 10th day prepartum till the 26th day postpartum, to assess the role of fibronectin in their organization during development. This glycoprotein is diffusely distributed in embryonic lymph nodes, suggesting a primer function during organogenesis. After birth, in fact, it is less widespread and is mainly localized around sinuses and vessels. Our data, supporting the important role of this glycoprotein during lymph node organization, are in agreement with the results obtained in other tissues and organs.

Animals↗
PubMed1986

Normalization of hypercalcemia associated with a decrease in renal calcium reabsorption in Leydig cell tumor-bearing rats treated with WR-2721.

The Rice-500 Leydig cell tumor (LCT) in Fischer rats is a model of humoral hypercalcemia of malignancy (HHM). In this model, the elevation of plasma calcium (Ca) does not result merely from an increased bone resorption, but also from an enhanced tubular Ca reabsorption (TRCa). We investigated the hypocalcemic response to WR-2721 [S-2,2-(3-aminopropylamino)-, ethylphosphorothioic acid] in LCT-bearing Fischer rats. WR-2721 is a potent inhibitor of normal and aberrant parathyroid hormone (PTH) secretion. Moreover, it exerts a PTH-independent inhibitory effect on TRCa. In hypercalcemic LCT-bearing rats WR-2721 induced a fall in plasma Ca from 3.24 +/- 0.12 to 2.66 +/- 0.23 mmol/liter within 2 h after one single injection of 0.7 mmol/kg body wt. The decrement in plasma Ca was associated with a marked increase in urinary Ca excretion, indicating an inhibition of TRCa. The elevated urine cyclic AMP of LCT-bearing rats, however, was not altered by WR-2721 treatment. These results suggest that in this HHM model, WR-2721 can normalize calcemia through its PTH-independent inhibitory effect on TRCa. WR-2721 could therefore be an effective drug to treat human hypercalcemia of malignancy, particularly in those tumors wherein a markedly enhanced renal Ca reabsorption contributes to the elevation of the plasma Ca level.

Absorption↗
PubMed1986

Parathyroid hormone-like changes in renal calcium and phosphate reabsorption induced by Leydig cell tumor in thyroparathyroidectomized rats.

The Leydig cell tumor Rice H-500 is a model of humoral hypercalcemia of malignancy. Hypercalcemia is considered to result mainly from increased bone resorption. However, a change in renal tubular reabsorption of calcium (Ca) as a contributing factor to the hypercalcemia has not yet been recognized. The purpose of this study was to examine whether the renal handling of Ca was altered in Leydig cell tumor-bearing rats. To avoid counterregulations by Ca-regulating hormones, the effect of the Leydig cell tumor on plasma Ca and phosphate (Pi), urinary Ca and Pi excretion, as well as Ca and Pi renal tubular reabsorptive capacity was investigated in thyroparathyroidectomized rats. Clearance experiments were conducted at a time of tumor development when the glomerular filtration rate was not compromised. Under these conditions, tubular reabsorption of Ca was stimulated, and the maximal tubular reabsorption of Pi was markedly reduced (2.69 +/- 0.27 vs. 4.57 +/- 0.21 mumol/min; P less than 0.001). These changes were accompanied by increased urinary cAMP excretion (77.1 +/- 6.3 vs. 34.7 +/- 2.8 pmol/ml glomerular filtrate; P less than 0.001). These results indicate that the Leydig cell tumor produces a factor with PTH-like activity on the renal tubular reabsorption of Ca and Pi. The increased tubular reabsorption of Ca may play an important role in the pathogenesis of Leydig cell tumor-induced hypercalcemia. This animal model appears to be particularly appropriate for studying the mechanisms of certain types of humoral hypercalcemia of malignancy, as some cancer patients display a change in the renal handling of Ca similar to that observed in primary hyperparathyroidism.

Absorption↗
PubMed1986

Detection of extracellular matrix antigens (fibronectin, laminin, type IV in collagen) in paraffin embedded sections by avidin-biotin-peroxidase complex labelling.

An avidin-biotin-peroxidase labelling method was applied to frozen sections and to routine-fixed, paraffin-embedded sections, and compared with immunohistochemical results of stromal antigen detection (type IV collagen, laminin and fibronectin) obtained in parallel on different neoplasias. Lung, breast and gastrointestinal tract tumors were studied. Superimposable sections were obtained from cryostat and formalin-fixed, paraffin-embedded specimens (previously digested by pepsin). The data demonstrate the potential use of immunohistochemical investigation of paraffin-embedded tissues for histological analyses of tumors.

Avidin↗
PubMed1985

[Pseudohypoparathyroidism, calcifying arteriopathy and ischemic skin necrosis].

A patient with longstanding pseudohypoparathyroidism undergoing substitution with dihydrotachysterin, with normal to low serum calcium and phosphorus levels, developed extensive calcification of the subcutaneous tissue and an obliterative and calcified arteriopathy of the small subcutaneous arteries with ischemic skin signs (livedo reticularis, skin infarction and ulcerative necrosis). After stimulation with exogenous parathyroid hormone there was no increase in urinary cyclic AMP and the G-unit was significantly decreased. It was concluded that the patient is suffering from pseudohypoparathyroidism type 1a. The likely pathophysiological mechanisms and the therapeutic implications are discussed.

Arteries↗
PubMed1985

[Tumoral hypercalcemia: physiopathology and treatment].

The regulation of plasma calcium involves many factors acting at the gut, bone and kidney levels. The mechanism leading to hypercalcemia in malignant neoplasm may well differ according to the type of tumor, the presence or otherwise of bone metastasis, the stage of the disease as well as additional factors such as the state of hydration. Increased bone resorption would certainly play an important role. However, increased tubular reabsorption of calcium could be the main hypercalcemic mechanism in some types of malignant tumor. Therapeutically, the approach has so far been to reduce the input of calcium from gut and bone and/or improve its renal clearance. Until now, the most efficient action appears to be the blockage of bone resorption. Among several bone resorption inhibitors, the diphosphonate compounds have been shown in several reports to be quite efficient in normalising calcemia.

Bone Neoplasms↗
PubMed1985

Primary hyperparathyroidism in familial multiple endocrine neoplasia type I. Long-term follow-up of serum calcium levels after parathyroidectomy.

Serum calcium levels were analyzed after one or more explorations for primary hyperparathyroidism in familial multiple endocrine neoplasia type I. These data covered all 85 operations (performed in many hospitals) on 61 of 62 members from 14 kindreds. After 61 initial operations, there were high rates of persistent or recurrent hypercalcemia (54 percent) and chronic hypocalcemia (10 percent). These rates contrast with lower postoperative rates of hypercalcemia (4 to 16 percent) or chronic hypocalcemia (1 to 8 percent) in large series of primary hyperparathyroidism. Persistent or recurrent hypercalcemia after initial exploration decreased only modestly in patients who underwent surgery after 1975 versus before 1975 (46 versus 63 percent). The rate for long-term remission of hypercalcemia after initial parathyroidectomy was higher after a diagnosis of parathyroid hyperplasia was made (as opposed to adenoma) (57 versus 30 percent, p less than 0.05) and after removal of three or more glands (as opposed to removal of two and a half or less) (70 versus 34 percent, p less than 0.01). Following 24 reoperations, there were also high rates of persistent or recurrent hypercalcemia (46 percent) and chronic hypocalcemia (25 percent). After surgery in unselected patients with primary hyperparathyroidism, recurrent hypercalcemia (as opposed to persistent hypercalcemia) is distinctly uncommon; however, it was frequent in familial multiple endocrine neoplasia type I, with total recurrences increasing from 21 percent at five years to 41 percent at 10 years in patients who showed a normocalcemic interval after surgery. The data indicate that the occurrence of persistent or recurrent hypercalcemia after parathyroidectomy in familial multiple endocrine neoplasia type I remains frequent. Although recurrent hypercalcemia may be characteristic of the response to any technique of parathyroidectomy in familial multiple endocrine neoplasia type I and not preventable, persistent hypercalcemia can be decreased by preoperative recognition of the specific familial cause, involvement of an experienced surgical team, and histologic confirmation of the identification of three or more parathyroid glands.

Actuarial Analysis↗
PubMed1981

Effect of hydrochlorothiazide on 1,25-dihydroxyvitamin D3-induced changes in calcium metabolism in experimental hypoparathyroidism in rats.

1. Chronic administration of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] can normalize plasma calcium in human hypoparathyroidism and in thyroparathyroidectomized animals. The effect of 1,25(OH)2D3 on plasma calcium is associated with an increase in urinary calcium excretion. In an attempt to prevent this increase thyroparathyroidectomized rats receiving 1,25(OH)2D3 were also treated with hydrochlorothiazide for 9-11 days. 2. Calcium clearance studies show that hydrochlorothiazide stimulated the tubular reabsorption of calcium in thyroparathyroidectomized rats treated with 1,25(OH)2D3. 3. Calcium balance and kinetic studies indicated that hydrochlorothiazide decreased 1,25(OH)2D3-induced hypercalciuria in thyroparathyroidectomized rats. Hydrochlorothiazide did not affect the 1,25(OH)2D3-induced increase in plasma calcium. The hypocalciuric effect of hydrochlorothiazide was not associated with significant changes in calcium deposition into or release from bone. 4. In thyroparathyroidectomized rats treated with 1,25(OH)2D3 the hypocalciuric effect of hydrochlorothiazide was associated with a fall in intestinal calcium absorption. Overall, the calcium balance was unaffected. 5. Thus it appears that hydrochlorothiazide reduces the 1,25(OH)2D3-induced hypercalciuria in parathyroid hormone-deficient animals by decreasing intestinal calcium absorption. Despite the decreased absorption, hydrochlorothiazide does not reduce the 1,25(OH)2D3-induced increase in plasma calcium.

Animals↗
PubMed1977

Effect of thyroparathyroidectomy of calcium metabolism in rats: role of 1,25-dihydroxyvitamin D3.

Thyroparathyroidectomy (TPTX) decreases plasma calcium, bone formation and resorption, and tubular reabsorption of calcium. It also reduces the production of 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] which very likely results in the decrease in the intestinal calcium absorption (Vna) observed after TPTX. We have examined whether the influence of TPTX on plasma calcium and bone calcium fluxes could be corrected by doses of 1,25-(OH)2D3 (2 X 13 pmol/day ip), which just normalize Vna. The study was made by calcium balance and 45Ca kinetics in rats receiving a normal supply of vitamin D3. The results show that in TPTX rats physiological doses of 1,25-(OH)2D3 increased plasma calcium and decreased plasma phosphate. Calcium retention was not fully corrected because 1,25-(OH)2D3 increased urinary calcium excretion. The deposition into and the release of calcium from bone were enhanced by 1,25-(OH)2D3 but remained lower than in pair-fed sham-operated animals. Thus, in as much as the diminished renal production of 1,25-(OH)2D3 in TPTX is entirely responsible for the reduced Vna, the decrease in 1,25-(OH)2D3 could only partly explain the effect of thyroparathyroidectomy on bone calcium fluxes.

Animals↗
PubMed1977

Role of 1,25-dihydroxyvitamin D3 on intestinal phosphate absorption in rats with a normal vitamin D supply.

In vitamin D-deficient rats, impaired intestinal phosphorus (P) absorption can be corrected by 1,25-dihydroxyvitamin D(3)[1,25-(OH)(2)D(3)]. In the present study, it was investigated whether changes in 1,25-(OH)(2)D(3) production can influence intestinal P transport also in animals with a normal supply of vitamin D. The intestinal P absorption was evaluated in rats using both the in situ duodenal loop technique and the determination of the overall gastrointestinal absorption under three conditions known to influence the production of 1,25-(OH)(2)D(3): (a) variation in dietary P, (b) thyroparathyroidectomy (TPTX) with or without administration of parathyroid hormone (PTH), and (c) treatment with disodium ethane-1-hydroxy-1,1-diphosphonate (EHDP). In all circumstances changes in duodenal absorption paralleled the changes in the overall fractional absorption. (a) Lowering dietary P stimulated P absorption. (b) TPTX decreased P absorption. This effect was corrected either by the administration of PTH or by the administration of 1,25-(OH)(2)D(3). (c) EHDP, when given at a dose known to inhibit 1,25-(OH)(2)D(3) formation, decreased the duodenal P absorption in both intact and TPTX animals. This effect was corrected by 1,25-(OH)(2)D(3). In the TPTX-EHDP-treated animals, the administration of PTH did not rectify the low duodenal P absorption. These results support the thesis that, in rats with normal vitamin D supply, variations in the endogenous production of 1,25-(OH)(2)D(3) change the rate of P absorption. However, these changes are in such magnitude that they are of relatively small importance when compared to the effect of variation in the dietary intake of P. These results also strongly suggest that the action of PTH on duodenal P transport is mediated by its effect on 1,25-(OH)(2)D(3) production, inasmuch as the effect of the hormone is abolished after blocking the renal 1-hydroxylation with EHDP.

Animals↗
PubMedDate not supplied

Hypercalcemia and hyperosteolysis in vitamin D intoxication: effects of clodronate therapy.

Vitamin D intoxication is a rare cause of hypercalcemia, which is associated with severe and prolonged morbidity. Hypercalcemia and/or hypercalciuria are the consequence of increases in both intestinal absorption and bone resorption. We report on 7 cases of vitamin D overdose (25-hydroxyvitamin D: 710 +/- 179 nmol/l; normal range: 20-90). The indications for vitamin therapy were osteoporosis (5), hypoparathyroidism (1), and osteomalacia (1). Enhanced bone resorption was demonstrated by increased fasting urinary calcium excretion (0.192 +/- 0.067 mmol/l GFR, normal < 0.045). Sequential biochemical measurements in the hypoparathyroid patient showed the persistence of abnormally elevated fasting urinary calcium and of serum 25-hydroxyvitamin D concentrations, even after normalization of plasma calcium, emphasizing that enhanced bone resorption is a prominent feature of vitamin D action. The intravenous administration of a single infusion of the bisphosphonate clodronate to 3 patients led to a correction of hypercalcemia/hypercalciuria, whereas prednisone therapy given to 2 other cases barely affected the abnormal biochemical values. These results indicate that enhanced bone resorption encountered in vitamin D intoxication could be favorably influenced by bisphosphonate treatment.

Adult↗