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Biomedical subjects

A Pruna

Publications and source records attributed to A Pruna.

At least 73 records · Page 4Linked to original sources
PubMed1990

Granzyme B-gene expression: a marker of human lymphocytes "activated" in vitro or in renal allografts.

Human killer cells contain cytoplasmic granules in which serine esterases, or granzymes, and perforin have been identified. We have studied the induction of granzyme B-gene expression in peripheral blood lymphocytes and large granular lymphocytes activated by various stimuli in vitro as well as in cellular infiltrates at the site of renal allografts in patients with and without rejection. Using in situ hybridization, kinetic experiments have shown that granzyme B mRNA is an early marker of in vitro cell activation. Data obtained in vivo also indicate the presence of granzyme B mRNA-bearing cells, which argues in favor of the induction of granzyme B gene in cells activated in vivo.

Gene Expression Regulation, Enzymologic↗
PubMed1990

[Emphysematous pyelonephritis. Apropos of a case].

Emphysematous pyelonephritis is a rare form of pyelonephritis that carries a very poor prognosis. This article reports a review of the literature on this condition and describes the clinical and roentgenographic criteria for diagnosis. Diagnosis rests on the presence of clinical manifestations of pyelonephritis with intrarenal air-filled images on the roentgenograms. Both the author's personal experience and the data from the literature confirm the need for urgent treatment combining antimicrobial agents effective against Escherichia coli, the most common causative agent, and surgery, which usually consists in a nephrectomy.

Emphysema↗
PubMed1989

[Hypercalcemia in blood diseases and cancers].

The clinical classification of malignant hypercalcaemias according to the presence or absence of bone lesions no longer corresponds to the physiopathology of these hypercalcaemias as it is known today. Both focal osteolysis and humoral hypercalcaemia involve a number of substances, such as prostaglandins, cytokines, growth factors, PTH-rp and calcitriol, the action of which is neither specific nor single. A knowledge of their role in the pathogenesis of hypercalcaemia should lead to the development of antagonists for therapeutic purpose and to a better understanding of their individual physiological effects, since some of these mediators are present in non-tumoral tissues. In humoral hypercalcaemia, PTH-rp seems to play a major role on kidneys and bones.

Humans↗
PubMed1985

Critical role of oxalate restriction in association with calcium restriction to decrease the probability of being a stone former: insufficient effect in idiopathic hypercalciuria.

The probability of being a stone former (PSF) was calculated in 3 groups of idiopathic calcium stone formers [with normocalciuria (NC), dietary hypercalciuria (DH) and idiopathic hypercalciuria (IH)] in 4 conditions: while on a free diet; on a calcium- and oxalate-restricted diet during 4 days; after an oxalate load, while on a 1.5-gram calcium diet, and after an oxalate load while on a calcium-restricted diet. Combined calcium and oxalate restriction significantly decreased PSF only in NC and DH whereas the decrease was not significant in IH because of a concomitant significant increase in oxalate excretion. Increase of PSF with the oxalate load was significantly greater during a calcium-restricted diet than during the 1.5-gram calcium diet in all groups of patients (4, 6 and 12 times greater in NC, DH and IH, respectively). These data show the critical role of oxalate restriction when calcium is restricted in order to decrease the PSF. This combined restriction is however not sufficient in idiopathic hypercalciuric patients to decrease their PSF.

Calcium↗
PubMed1985

[Hypercalcemia with elevation of parathormone in lymphocytic lymphoma. Efficacy of ethanehydroxydiphosphonate by mouth].

Acute hypercalcaemia was observed in a 54 year old woman followed up over a five year period for a lymphocytic non-Hodgkin lymphoma, a complication which is rare in chronic lymphoproliferative disorders except multiple myeloma. This case is of interest from 3 points of view: haematological: the simultaneous occurrence of hypercalcaemia (4.80 mmol/l) and of a leukaemic phase (19,300 lymphocytes/mm3) with no signs of "transformation" of the haemopathy; physiopathological: increased osteoclastic bone resorption and a rise in serum parathormone (0.21 to 4.82 ng/ml); therapeutic: efficacy of oral ethane 1, hydroxy 1, 1 diphosphonate (20 mg/kg/day) in treating the hypercalcaemia.

Bone Resorption↗
PubMed1985

Magnesium renal wasting in calcium stone formers with idiopathic hypercalciuria contrasting with lower magnesium:calcium urinary ratio.

Plasma magnesium (PMg) and urinary calcium (UCaV) and magnesium (UMgV) were measured after four days of calcium-restricted diet in 60 controls and 82 patients classified according to their calcium excretion in three groups: normo-calciuric (NCa), dietary hypercalciuria (DH) and idiopathic hypercalciuria (IH). When compared to controls, higher UMgV (4.26 +/- 0.28 mmol/d versus 3.4 +/- 0.16, p less than 0.01), lower PMg (0.79 +/- 0.01 mmol/d versus 0.84 +/- 0.01, p less than 0.05) and lower UMg/UCa ratio (0.6 +/- 0.04 versus 1.68 +/- 0.15, p less than 0.001) were observed only in IH. A significant correlation between UMgV and UCaV was found in controls, in NCa and in DH but not in IH. In conclusion, (1) the coexistence of a higher UMgV and of a lower PMg in IH suggests that there is a magnesium depletion in this group of patients; (2) since the lower UMg/UCa ratio may favour a higher propensity for calcium crystallisation and is seen only in IH, magnesium supplements may be specially indicated in this group.

Calcium↗
PubMed1984

[Primary hyperparathyroidism. Lack of effect of cimetidine on plasma levels of parathyroid hormone and calcium].

Because of the contradictory results formerly published as regards the effect of cimetidine in primary hyperparathyroidism, we have studied the effect of cimetidine at the daily dose of 1200 mg in 14 cases of primary hyperparathyroidism. The diagnosis was ascertained in all cases by the coexistence of an otherwise unexplained hypercalcemia and of a concomitantly elevated plasma concentration of immunoreactive parathyroid hormone (PiPTH) measured by 2 different antibodies and confirmed in 10 cases by surgical neck exploration. In 5 cases with severe hypercalcemia (greater than 12.0 mg/l) cimetidine was discontinued after 5 days because of its lack of effect on both plasma concentrations of calcium and PiPTH, and the patients were successfully operated. In 8 cases with milder hypercalcemia, cimetidine was given for 1.5-6 months. There was no significant change in both plasma concentrations of calcium (PCa) and PiPTH but a regression analysis showed that PCa was negatively correlated to time with a correlation coefficient which would have become significant if the follow-up had been 9 months. In the last patient severe hypercalcemia was controlled by simultaneous administration of phosphate, indomethacin and cimetidine without concomitant decrease of PiPTH; and 6 weeks after cimetidine discontinuation no significant increase of PCa and PiPTH occurred. These data show that cimetidine has no clinically therapeutic value in primary hyperparathyroidism.

Adolescent↗
PubMed1983

Effect of calcium restriction on renal excretion of oxalate and the probability of stones in the various pathophysiological groups with calcium stones.

To evaluate the adequacy of simple calcium restriction for patients with idiopathic calcium stones the effect of 5 days of calcium restriction without oxalate restriction on renal excretion of calcium and oxalate, and the corresponding probability of stones were assessed in 50 controls and 48 patients. Renal excretion of calcium decreased and that of oxalate increased significantly in all groups but the importance of the changes was critically dependent upon the underlying pathophysiological condition. The probability of stones decreased only in patients with absorptive hypercalciuria type II owing to the usual excessive calcium intake and increased in those with absorptive hypercalciuria type I and renal hypercalciuria, which are associated with true hyperabsorption of calcium and represent the 2 forms of idiopathic hypercalciuria. We believe that simple calcium restriction is beneficial for patients with idiopathic calculi only when the hypercalciuria is caused by exaggerated intake of calcium, since it increases the probability of stones in patients with idiopathic hypercalciuria. Calcium restriction always is associated with an increase in oxalate excretion, suggesting that simultaneous oxalate restriction should be added in all cases to decrease the probability of stones.

Adult↗