[Bone metabolism in non-cholestatic chronic hepatopathy]. / Metabolismo óseo en la hepatopatía crónica no colestásica.

BACKGROUND: Osteoporosis may be associated with parenchymal hepatopathy and chronic alcoholism. Biochemical studies which are linked with bone metabolism and the bone densitometry may help to understand its physiopathology, before the symptoms appear and its consequences become inevitable. PATIENTS AND METHODS: The study of bone metabolism and densitometry has been carried out in a population of 86 males, distributed in 4 groups: group I, control (17 men), group II, patients with chronic hepatopathy without alcoholism (25 patients), group III, chronic alcoholic without hepatopathy (21 patients), and group IV, patients with chronic alcoholic hepatopathy (23 patients). The results of densitometry and biochemical parameters in relation with bone metabolism are cross checked among these 4 groups. RESULTS: We found out that patients with chronic alcoholic hepatopathy have bone mineral density (BMD), at femoral level, significatively lower than that of the other 3 groups (p < 0.05). In chronic hepatopathy, regardless of its etiology, significant alterations in biochemical parameters of bone metabolism found, consisting basically in shrinked plasmatic level of 25-hydroxivitamin-D (25-OH-D) (p < 0.05). The plasmatic levels of calcitriol, magnesium and intact parathyroid hormone (PTHi) were significantly lower in chronic alcoholic hepatopathy than in the others 3 groups (p < 0.001, p < 0.001 and p < 0.05, respectively). CONCLUSIONS: Chronic hepatopathy is associated with deficiency in vitamin D. Alcoholism added to chronic hepatopathy has a negative influence on the plasmatic levels of calcitriol, magnesium and PTHi as well as in the femur BMD. Alcoholism not associated with chronic hepatopathy is not sufficient to cause significant alterations in the studied parameters.

[Concentrations of 25-hydroxyvitamin D3 in Antarctica]. / Concentraciones de 25-hidroxivitamina D3 en la Antártida.

BACKGROUND: Ultraviolet B radiation decidedly influences the synthesis of vitamin D and therefore mineral and bone metabolism. It must also be taken into account that a normal unsupplemented diet is usually deficient in this vitamin. Two groups of subjects pertaining to the Spanish Antarctic Expedition 1988-1989 were studied to determine whether special conditions of irradiation and solar exposure found in Antarctica induce alterations in the abovementioned metabolism. METHODS: Each group consisted of 11 healthy males with ingestion of less than 500 mg/day of calcium. The second group was administered vitamin D3 supplements of 1,000 UI/day. Two blood samples were performed at an interval of 22 days during the Antarctic summer to determine calcium, phosphorus, magnesium, parathormone (PTH) and 25-hydroxycholecalciferol [25(OH)D]. RESULTS: Neither group varied in calcemia, phosphoremia or magnesemia. In the first group the 25(OH)D decreased markedly (p less than 0.01) with no variations being observed in PTH. In the supplemented group, and insignificant increase of 25(OH)D was observed which was significant enough to cause a marked decrease in PTH (p less than 0.01). CONCLUSIONS: Subjects passing periods of time in Antarctica should receive vitamin D3 supplementation at doses less than 1,000 UI/day.

[Alterations in calcium metabolism in patients with active tuberculosis]. / Alteraciones del metabolismo del calcio en pacientes con tuberculosis activa.

BACKGROUND: Abnormalities in phosphocalcic and vitamin D metabolism may develop in patients with active tuberculosis (TB). Their incidence and relationship with the disease is not well known, particularly in our area. We have prospectively evaluated 40 patients with TB [(30 with localized TB (LTB) and 10 with disseminated TB (DTB)]. METHODS: After stabilizing the diet during 4 days, the calcium, phosphorus, magnesium and creatinine balances, blood ionic calcium, plasma intact PTH, 25-hydroxy vitamin D [25(OH)D] and serum 1.25 dihydroxyvitamin D [1.25(OH)2D] were measured. RESULTS: Hypercalcemia was not found in any patient, but 25% had hypercalciuria (HC). The 24-hour urinary excretion of calcium was higher in patients than in controls (3.2 +/- 1.7 mg/kg or 0.10 +/- 0.06 mg/100 ml of GFR vs 2.3 +/- 0.7 mg/kg or 0.08 +/- 0.03 mg/100 ml of GFR, p less than 0.05), basically at the expense of patients with DTB (4.4 +/- 1.8 mg/kg or 0.14 +/- 0.06 mg/10 ml of GFR, p less than 0.005). These had a lower PTH than patients with LTB and controls (12.8 +/- 7.7 vs 18.5 +/- 6.9 vs 19.5 +/- 6.0 pg/ml, p less than 0.05). Independently from the extent of the disease, the patients with HC had a lower PTH (12.6 +/- 6.8 vs 18.5 +/- 6.9 pg/ml, p less than 0.01) and higher serum 1.25(OH)2D (34.5 +/- 10.1 vs 25.0 +/- 7.2 pg/ml, p less than 0.01) than patients without HC. The levels of 25(OH)D were lower in patients with TB than in controls (11.2 +/- 6.0 vs 20.0 +/- 7.0 ng/ml, p less than 0.05), independently from the extent of the disease and the presence or absence of HC. CONCLUSIONS: Patients with tuberculosis may have hypercalcinuria with inadequately high levels of 1.25(OH)2D and low intact PTH. This abnormality appears to be correlated with the extent of the disease.

Acute antihypertensive effect of nifedipine on high and low salt diet.

To examine the influence of sodium balance in the acute response to nifedipine, we studied 10 untreated essential hypertensive patients aged 29 to 43 years. Blood pressure was recorded with the patients fasting and lying in the supine position, and 10 mg nifedipine was administered sublingually. Blood pressure was recorded again 3 h after nifedipine. Patients were studied after 1 week on both their unrestricted usual diet (NaU 206 +/- 29 mmol/day) and a low salt diet (NaU 66 +/- 8 mmol/day). The maximum hypotensive effect of nifedipine was observed at 90 min. The decrease of blood pressure tended to be greater and longer on high salt than low salt diet. Our results suggest that the acute antihypertensive effect of nifedipine is enhanced by sodium administration.

[Study of the renal tubular function in alcoholic hepatic cirrhosis (author's transl)]. / Estudio de la función tubular renal en la cirrosis hepática alcohólica.

The renal plasma flow (RPF), glomerular filtrate (GF), renal concentration strength and urinary acidification capacity in eight patients with alcoholic cirrhosis and five control subjects was studied. The maximum urinary acidification capacity was tested by means or arginine monochloride. In two patients, renal tubular acidosis (RTA) was observed. One patient manifested a slight decrease in RPF, GF, hyposthenuria, hyperchloremic metabolic acidosis and bicarbonaturia. The test for maintained acidification and the overload of bicarbonate indicated a mixed RTA. The other patient manifested incomplete distal RTA, which was briefly corrected with the administration of furosemide. These tubular defects were not associated with the loss of proteins, phosphates, glucose, aminoacids or renal lithiasis. Neither were they related to the serum levels of copper, globulins, or predisposition to hepatic encephalopathy. The association between hepatic cirrhosis and distal tubular acidosis is known, but until the present work, the fact that this hepatopathy can simultaneously affect the proximal and distal tubules had not been described.