[Medical treatment of idiopathic calcium lithiasis (II)].
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Biomedical subjects
Publications and source records attributed to A Fournier.
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Plasma renin activity and aldosterone concentrations were measured simultaneously with urinary excretion of kallikrein and four prostaglandins (PGE2, PGF2 alpha, 6 keto PFG1 alpha and TXB2) in 23 patients with pregnancy induced hypertension (17 with permanent PIH and six with labile PIH, since in these latter their hypertension was controlled only by home bed rest) and in 16 normotensive pregnant women at the same stage of gestation (31 +/- 3 weeks). PRA was lower in permanent PIH than in controls and in labile PIH. No difference between the three groups was observed for plasma aldosterone and the urinary excretion of kallikrein and of the prostaglandins except that TXB2 was higher in labile PIH than in permanent PIH. Correlation studies of kallikrein disclosed correlations with most prostaglandin excretions, explained by the physiological stimulation of phospholipase A2 by kallidin. Correlation studies of PRA disclosed unexpected negative correlation with PGE2 and 6 keto PGF1 alpha in the permanent PIH group. In conclusion, labile PIH has a different biological profile than permanent PIH since they have higher PRA and higher TXB2 excretion, an association which suggests a more pronounced ureteral compression by the gravid uterus in this group. Permanent PIH has a disregulation of the renin angiotensin-prostacyclin loop since PRA and 6 keto PGF1 are negatively correlated. This suggests the role of an independent vasopressive substance which would stimulate PGI2 and suppress renin secretion.
After confirming hypercalcemia by 3 successive measurements of the total plasma calcium corrected for a plasma protein concentration of 72 g/l, which excludes spurious hypercalcemia due to dehydration, the physician orientates the aetiological diagnosis bearing in mind that primary hyperparathyroidism PHPT is the cause of 85 p. 100 of all asymptomatic forms of hypercalcaemia whilst overt or occult malignancy is the main cause (60 p. 100) of symptomatic forms of hypercalcaemia with PHPT responsible for 20 p. 100 of cases. Other causes, including drug toxicity with Vit D, calcium, Vit A, lithium, thiazide and aluminium hydroxide, sarcoidosis, hyperthyroidism, Addison's disease, pheochromocytoma and familial endocrine disorders are much rarer. Nevertheless, these rarer causes must be excluded on the clinical history and examination followed by radiological (chest X ray, plain abdomen X ray, bone X rays) and simple biological tests. The latter and/or scans tests should also help in a rapid diagnosis of metastatic carcinoma and multiple myeloma, so that the major diagnostic problem is to distinguish primary HPT from occult malignancy. This problem is greatly facilitated by reliable assays of C terminal or medium PTH rather than renal CAMP which is increased in 80 p. 100 of occult malignancies. When PTH assays is unavailable or unreliable Dent's hydrocortisone suppression test may be useful as a fall in'serum calcium is associated with occult malignancy in 70 p. 100 of cases and non-suppression is associated with PHPT in 91 p. 100 of cases. Discriminant analysis of the usual biochemical parameters may be helpful in this differential diagnosis and is accurate in about 90 p. 100 of cases. However, the association of PHPT and malignancy is also possible and not fortuitous.
Calcium stones is responsible for 80 per cent of the stones in the upper track. It is a frequent and particularly recurrent disease and for this reason it is important to prevent its recurrence by medical treatment, dissolution of calcium stones being impossible. In the first part of this review, we have presented the theoretical basis and the clinical studies concerning conservative therapy involving high fluid intake and dietary advice on calcium and oxalate intake. Then, for the various drugs proposed for recurrence prevention we have reviewed their mechanisms of action and the controlled clinical trials concerning these drugs. Finally, the practical therapeutical choices for the management of these patients are presented according to the results of the previous metabolic evaluation.
One hundred and six patients fulfilling accepted diagnostic criteria for Kawasaki disease (90 p. 100 of French-Canadian origin) were evaluated with serial electrocardiograms and echocardiograms (M mode and two-dimensional). Half of the patients (53) had cardiovascular manifestations at one time during their illness. Thirty-one had abnormal electrocardiograms: non specific ST and T wave changes inferiorly (27), prolonged QT intervals (6), first degree AV block (3). M mode echo was abnormal in 31 cases showing: slight pericardial effusion (17), flat septal movement (11), left ventricular dilatation (4), decrease of shortening fraction (2). Seven patients (6.4 p. 100) presented fusiform coronary aneurysm detected in 6 by two-dimensional echography (with angiographic confirmation) and at autopsy in another. M mode echo and electrocardiogram abnormalities were transient in the great majority of patients disappearing during an average follow-up period of 10 months. Coronary aneurysm had disappeared at the end of follow-up in two patients, regressed in three and remained identical in another. There were no relations between severity of clinical symptoms, electrocardiographic or echocardiographic (M mode) abnormalities and the development of coronary aneurysm. Serial studies with two-dimensional echo should be done in every patient with this disease for early detection and follow-up of coronary aneurysm.
The length of calcifications on the aorta and on the iliac and femoral arteries have been measured in hemodialyzed patients who did not take Vit D derivates but variable amount of calcium carbonate just before beginning hemodialysis then once a year for 3 years. The extension of these calcifications was exponential. The most important factors of arterial calcification extension are the male sex, the age only in the male sex, diastolic blood pressure, triglyceridemia, glycemia and calcemia. The treatment by calcium carbonate is however not by itself responsible of arterial calcification since no correlation was found between calcification extension and the doses of CaCO3.
Chest radiographs of 11 patients with supero-inferior ventricles proven by echocardiography and angiocardiography are presented. The main feature is the modified configuration of the left heart contour. Even if not specific, this sign is encountered frequently (72%) and may suggest the diagnosis.
The low molecular weight heparin CY 222 (CHOAY) has been compared to unfractioned heparin (UFH) in patients on chronic haemodialysis and haemofiltration at various doses as regards it biological activity (measured by Activated Partial Thromboplastin Time and by anti-Xa activity) and its clinical effect on clot formation in the blood lines and bleeding at the puncture sites or recent wounds. Compared to UFH, CY 222 has a greater anti-Xa activity for a shorter APTT. This biological difference is of clinical advantage since clotting in lines is comparable or less than with UFH whereas compression time at puncture sites is shorter and recently bleeding wounds in 28 patients did not bleed again. The long half life of CY 222 allows its use as a single priming dose of 300 anti-Xa U/kg in haemodialysis and 450 anti-Xa U/kg in haemofiltration.
Desferrioxamine (DFO), a chelating agent of aluminium was administered to 27 uraemic patients on chronic haemodialysis or haemofiltration with a minimal parenteral exposure to aluminium but taking various amounts of A1(OH)3 for about two years. All these patients had a double bone biopsy for measurement of their aluminium content and histomorphometric evaluation. Bone aluminium of our patients were 10 times greater than in our uraemic controls. Plasma aluminium increase (delta A1) induced by DFO correlated better than basal plasma aluminium with bone aluminium and cumulative dose of A1(OH)3 correlated with bone aluminium and delta A1 DFO. None of the patients had florid osteomalacia and only two had traces of aluminium staining. However 16 had mild mineralisation defect as demonstrated by low mineral appositional rate. The aluminium parameters were not different between the two groups of patients with or without mild mineralisation defect. It is concluded that the DFO test predicts bone aluminium but not mild histological osteomalacia in uraemic patients moderately aluminium over-loaded with phosphate binders.
1 alpha OH vitamin D3 at the dose of 6 micrograms per week was given for four weeks to 16 stable patients on chronic haemodialysis with a low dialysate aluminium while taking a constant dose of Al(OH)3. A significant increase of their plasma aluminium was observed while on 1 alpha(OH)D3 therapy and during the six weeks following. This increase correlated with the cumulative dose of Al(OH)3 and duration on dialysis but not with the recent dose of Al(OH)3. The increase in plasma aluminium observed with 1 alpha(OH)D3 and after its discontinuation is more likely to be due to aluminium redistribution than to increased intestinal aluminium absorption. This effect indicates the need for close monitoring of plasma aluminium in uraemic patients treated with 1 alpha(OH)D3.
A multidimensional analysis was used to evaluate, the influence on bone histology of various biochemical and hormonal factors in 20 uraemic patients on chronic haemodialysis or haemofiltration. A positive relationship (p less than 0.1) was found between PTH and osteoclastic and osteoblastic surfaces but not with mineral apposition and bone formation rates. The mineral appositional rate which reflects the cellular activity of osteoblasts was positively related to D metabolites 25(OH)D3 and 1,25(OH)2D3 and to phosphate (p less than 0.1). Mineral appositional rate and bone formation rate were negatively related to bone aluminium (p less than 0.05). These data indicate that: 1) PTH simulates bone turnover but has no direct effect on the bone cellular activity of osteoblasts which is mainly dependent on D metabolites and phosphate; 2) mild aluminium overload not severe enough to cause osteomalacia decreases bone formation in uraemic patients. This study evaluates the role of various simultaneously measured biochemical and hormonal factors on bone histological parameters in uraemic patients.
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.
In 14 children aged 4 to 12 years in whom the anatomy of the coarctation did not allow for an end-to-end anastomosis, we have performed a subclavian flap angioplasty. To correct the inconvenience of ligating the subclavian artery and to avoid the use of synthetic material, we used the internal mammary artery to reestablish circulation from the aorta to the subclavian artery. All patients are well. At postoperative catheterization (18 to 42 months, average 24) in the first eight, the mammary artery was patent and the flow to the subclavian was good.
Nine VIP sequences have been tested for their ability to inhibit the specific binding of 125I-VIP and to stimulate adenylate cyclase activity in intestinal epithelial membranes from rat and man. They are VIP 2-28; VIP 1-14; VIP 2-14; VIP 14-28; VIP 15-28; VIP 20-28; VIP 21-28 and two sequences where the N-terminal VIP 1-6 or VIP 1-9 have been joined covalently with the C-terminal VIP 20-28 or VIP 21-28. It appears that only VIP 2-28, VIP 14-28 and VIP 15-18 are able to inhibit competitively the binding of 125I-VIP to human and rat membranes. These analogues are respectively 88, 8,300 and 25,000 times less potent than VIP 1-28 in rat; they are respectively 70, 7,900 and 13,000 times less potent than VIP 1-28 in man. With respect to adenylate cyclase activation, VIP 14-28 and VIP 15-28 are very weak stimulators in the membranes from both species. VIP 2-28 behaves as a full VIP agonist in man whereas it is a partial VIP agonist in rat. These results indicate the structural importance of the whole VIP sequence for interacting with human and rat VIP receptors and further argue for a different structural requirement of rat and human receptors.
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