[Diarrhea and peritonitis in infection caused by type A beta hemolytic streptococcus]. / Diarrhöe und Peritonitis bei Sepsis durch Streptococcus beta-haemolyticus Typ A.

During the last years the cases of severe group A streptococcus infection have increased. The clinical manifestation of this streptococcal toxic shock syndrome is similar to the better known toxic shock syndrome (TSS) provocated by staphylococcus. Shock, bacteremia and acute respiratory distress syndrome are common features, and death has been associated with this infection in 30% of patients. We present the case of a 46-year-old man who fell gravely ill with sepsis, diarrhoe, scarlatina rash, desquamation of hands and feet and acute abdomen caused by group A streptococcus infection. Finally we discussed the possible port of entry of this infection, the different clinical manifestation and the concepts of treatment.

[Hospital pharmacy: partner in the health care team]. / Pharmacie de l'hôptial: partenaire de l'équipe de soins.

The hospital pharmacy is responsible for providing each patient with the required drug treatment. This goal can be fulfilled by constant adaptation of the pharmaceutical services to the needs of the medical and nursing staff, hospital administration and other technical services. The goals and the functional relationship between the different activities of a hospital pharmacy are reviewed. The specific organisation of the Sierre-Loèche hospital pharmacy is presented. Centralisation of some services of the district hospital pharmacy within the central pharmacy of the "Institut Central des Hôpitaux Valaisans" provides the hospital with the required services. Pharmaceutical counseling based on a regular activity of the pharmacist within the health care team is a prerequisite to adapt organisation and services to the requirements of the clinical situation.

[Hyperphosphatemia and tetany following phosphate enema]. / Hyperphosphatémie et tétanie après clystère au phosphate.

Two patients with renal failure presented postoperatively with marked hyperphosphatemia and symptomatic hypocalcemia. This phosphate intoxication was due to a commonly used phosphate-containing enema. An increase in phosphatemia was also seen in two other patients prospectively followed after receiving the same product. The phosphate increase depends upon the retention duration of the enema. The use of phosphate-containing enemas in patients with renal failure is not entirely risk-free.

Vitamin D replacement therapy in patients with the nephrotic syndrome.

The possibility to achieve and maintain normal plasma levels of 25-hydroxyvitamin D3 (25OHD3), with long-term vitamin D replacement therapy, has been evaluated in 9 patients with nephrotic syndrome. Plasma levels of 25OHD3 rose from 10.8 +/- 5.0 (SD) nmol/l to 29.5 +/- 11.1 (p less than 0.001) with a daily dose of 25 micrograms of vitamin D3 per os. Plasma levels of 1,25-dihydroxyvitamin D3 were low before treatment (39.5 +/- 22.7 pmol/l) and returned to the normal range under therapy in the patients without renal failure. Low levels of vitamin D metabolites in nephrotic syndrome can be normalized with long-term oral vitamin D replacement therapy.

[Short-term effect of thiazides on magnesium and calcium metabolism and secondarily on that of phosphorus, uric acid, oxalate and cyclic AMP]. / Influence à court terme des thiazides sur le métabolisme du magnésium, du calcium et accessoirement sur celui du phosphore, de l'acide urique, de l'oxalate et de l'AMP cyclique.

Six healthy young volunteers were fed during two period of 9 days each by a strictly constantly liquid formula diet (Fresubin), on an ambulator basis. In a single blind cross-over randomized study, they were given either hydrochlorothiazide, 50 mg p.d., or a placebo during the first seven days of the two periods. The diuretic did not induce significant changes of either magnesemia or magnesiuria. In addition, the magnesium excretion after a challenging intravenous magnesium load remained unchanged. However, the thiazide normally increased the urinary excretion of sodium and potassium. It also induced hypocalciuria and hypercalcemia. The urinary excretion of cAMP and oxalic acid remained stable.

[Clinical importance of magnesium metabolism]. / Importance clinique du métabolisme du magnésium.

Magnesium is an important cation for the organism. In the cell, magnesium is a cofactor of numerous enzymatic processes, while in the extracellular compartment it is involved in neuromuscular excitation. Various clinical conditions lead to magnesium deficiency, the symptoms of which are highly protean. However, hypermagnesemia results almost exclusively from increased magnesium intake in patients with reduced glomerular filtration. The consequences of such magnesium intoxication are essentially neuromuscular.

[Primary hyperparathyroidism of the aged female: effect of estrogens on calcium metabolism]. / Hyperparathyroïdie primaire de la femme âgée: effet des oestrogènes sur le métabolisme calcique.

Serum calcium, urinary calcium and a calcium loading test were evaluated twice in 5 elderly women with primary hyperparathyroidism, once not under and once under estrogen therapy. The treatment produced a significant lowering of blood calcium and normalization of urinary calcium excretion in the fasting state, per 24 h and after calcium load. Estrogen therapy might be useful in conservative treatment of asymptomatic hyperparathyroidism and in symptomatic cases where surgery is impossible.

The duodenal mucosa in patients with renal failure: response to 1,25(OH)2D3.

The structure of the duodenal mucosa was evaluated in duodenal biopsy samples obtained from patients with moderate renal failure (MRF) and in dialysis patients (HD) in an effort to examine the possibility that changes in duodenal mucosa may contribute to the impaired calcium absorption in renal failure (RF). The effect of therapy with 1,25(OH)2D3 on the duodenal mucosa in the HD patients was also studied. The results show that both MRF and HD patients have reduction in calcium reabsorption and in the length of their intestinal villi and crypts of Lieberkuhn. In the HD patients, these structural changes were more severe. Treatment with 1,25(OH)2D3 produced significant improvement in calcium reabsorption (P less than 0.01) as well as in length of villus and crypt (P less than 0.02) and increased mitotic activity in the crypts (P 0.02). Electron microscopy revealed the microvilli to be shorter, irregularly distributed, moth-eaten, and grainy, with these abnormalities disappearing after treatment. The data show that duodenal mucosa in RF exhibits structural abnormalities, which were normalized after 1,25(OH)2D3 therapy, and suggest that these derangements may play a role in the defective calcium reabsorption in RF.

[Therapy with vitamin D and D-metabolites]. / Therapie mit Vitamin D und D-Metaboliten.

Elucidation of the vitamin D endocrine system and the availability of potent metabolites have led to new approaches to vitamin D therapy. The traditional management of exogenous (sunlight) or endogenous (malabsorption) vitamin D deficiency without evidence of disordered vitamin D metabolism has not changed, since it consists of treatment with vitamin D itself--a therapy which preserves the normal intrinsic mechanisms for regulating the rate of production of 1,25-dihydroxycholecalciferol. 1,25-DHCC and the analogue compound 1 alpha-CC should be reserved for treatment of hypocalcemia consequent on chronic renal failure or hypoparathyroidism, where 1-hydroxylation is lacking or impaired. Hypophosphatemic rickets has been treated with 1-hydroxylated compounds, with promising results; this use of the latter metabolites warrants further investigation. The use of vitamin D metabolites and of pharmacological doses of vitamin D itself must be regarded as substitution of a hormone or hormone precursors. Therefore, careful monitoring of serum and urine calcium is required in every patient receiving these compounds, in order to avoid excessive dosage. Special attention must be paid to patients with sarcoidosis since they often develop hypercalcemia after vitamin D or UV-light exposure, as a result of an intrinsic regulation defect in 1,25-DHCC synthesis.

[Disturbances of the calcium-phosphorus metabolism and skeletal diseases following kidney transplantation]. / Störungen des Calcium-Phosphor-Stoffwechsels und Erkrankungen des Skeletts nach Nierentransplantation.

53 patients were followed up for an average of 3 years after renal transplantation for evaluation of disturbances in calcium-phosphorus metabolism and skeletal diseases. Postoperative hypercalcemia and hypophosphatemia can be related to persistence of hyperparathyroidism when kidney function is restored. Hypercalcemia was observed in 43% of the patients and lasted less than one year in 80% of cases. Transient hypophosphatemia was present in 15%. These abnormalities did not cause clinical symptoms or deterioration of renal function. However, the skeletal diseases are more impressive and in the first place osteopenia. Bone densitometry revealed decreased bone mineral content in two thirds of the females and one fifth of the males. In females the bone density decreased 3.3% during an average observation period of 7 months, but remained constant in males. Renal osteodystrophy is the main cause of the initial osteopenia. The absence of remineralization or the progression of bone losses is related to the initial persistence of hyperparathyroidism and to corticosteroid treatment. According, 12.5% of the patients presented pathological fractures (spine, hip). In 3 patients (5.7%) with reduced transplant function, osteomalacia without hypophosphatemia was observed. 4 patients (7.5%) had osteonecrosis of the femoral head. There was little progression and surgery was not necessary.

Vitamin D metabolites and calcium metabolism in patients with nephrotic syndrome and normal renal function.

Patients with nephrotic syndrome (NS) lose 25-hydroxyvitamin D3 (25OHD3) in the urine and have low blood levels of this metabolite. This abnormality may be responsible for the hypocalcemia, i.e. low ionized calcium. The mechanism of the hypocalcemia is not evident. It is possible that the low value of 25OHD results in low blood levels of other vitamin D metabolites, such as 1,25-dihydroxyvitamin D [1,25-(OH)2D] and 24,25-(OH)2D3; a deficiency of these compounds may cause defective intestinal absorption of calcium (alpha) and resistance to the calcemic action of parathyroid hormone (PTH), resulting in hypocalcemia. Studies were performed in 12 patients with NS and normal renal function to evaluate these questions. Blood levels of 25OHD, 1,25-(OH)2D, and 24,25-(OH)2D were all significantly (P < 0.01) lower in NS (4.0 +/- 0.8 ng/ml, 7.0 +/- 2.3 pg/ml, 1.8 +/- 0.2 ng/ml, respectively) compared to normal subjects (37.0 +/- 1.5 ng/ml, 37.0 +/- 1.2 pg/ml, and 3.4 +/- 0.2 ng/ml). Both alpha (0.21 +/- 0.2 vs. 0.27 +/- 0.1; P < 0.05) and the calcemic response to PTH (0.50 +/- 0.1 vs. 1.35 +/- 0.16 mg/dl; P < 0.01) in NS subjects were significantly lower than normal. The data indicate that 1) a deficient state of all of these vitamin D metabolites exists in patients with NS and normal renal function, 2) this abnormality underlies the defect in alpha and the resistance to the calcemic response to PTH, and all participate in the genesis of the hypocalcemia, 3) secondary hyperparathyroidism develops, and 4) both vitamin D deficiency and elevated blood levels of PTH are responsible for the bone lesions in these patients.

Intestinal calcium absorption in patients with hyperthyroidism.

Intestinal 47Ca absorption was measured at 2 and 24 h after isotope ingestion in six patients with hyperthyroidism and seven normal subjects. Although 47Ca absorption was not different at 2 h, it was significantly lower (P < 0.01) after 24 h in the patients with hyperthyroidism. Factors related to the effects of thyroid hormone on intestinal function, in addition to abnormalities of vitamin D metabolism, are probably responsible for the defect.

Effect of an oral dose of 25-hydroxyvitamin D3 on its blood levels in patients with the nephrotic syndrome.

Patients with the nephrotic syndrome have low blood levels of 25-hydroxyvitamin D3 (25OHD3) due to urinary losses of the sterol. It is not known whether supplementation of this metabolite could raise its blood levels in these patients. The changes in the plasma levels of 25OHD3 and its kinetic behavior were studied after an oral dose of the sterol (200 microgram) in patients with the nephrotic syndrome in an effort to evaluate the usefulness of oral therapy to achieve and maintain normal blood levels of 25OHD3. Normal subjects served as controls. The results showed that intestinal absorption of 25OHD3 is significantly delayed and its elimination rate is significantly enhanced in patients with the nephrotic syndrome compared to control subjects. Despite these abnormalities, the plasma levels of 25OHD3 were within normal values even 48 h after the ingestion of the sterol. These data indicate that oral therapy with 25OHD3 given in proper doses is adequate to maintain normal blood levels of the sterol in patients with the nephrotic syndrome. Therefore, a therapeutic approach could be designed to manage the target organ disease due to 25OHD3 deficiency seen in these patients.

[Piperazine intoxication in long-term hemodialysis]. / Piperazinintoxikation bei Langzeithämodialyse.

A 35-year-old patient with terminal renal failure who had received 30 mg piperazine hexahydrate/kg body weight daily for 10 days for oxyuriasis was subsequently admitted to hospital in precoma with severe clinical symptoms not unlike those observed in so-called dialysis dementia: loss of consciousness, dysarthria, apraxia, clonic spasms, tremor, muscular weakness, dropping of objects, inability to think clearly and/or hallucinations. The EEG showed disturbances with diffuse, multifocal delta waves. Under maintenance hemodialysis the patient became asymptomatic one week after discontinuation of the piperazine therapy. Piperazine is contraindicated in patients with renal failure.

Hepatic metabolism of aminopyrine in patients with chronic renal failure.

1. To evaluate potential alterations in hepatic metabolism of drugs occurring in patients with renal insufficiency the fate of aminopyrine was studied in 17 patients with chronic renal failure and in 27 normal subjects. 2. Although patients with chronic renal failure exhibited large variations, their aminopyrine plasma disappearance times (mean 0.62 +/- SD 0.24 h-1) were significantly higher than those found in normal subjects (0.30 +/- 0.07 h-1, P less than 0.002). 3. 14CO2 derived from [dimethylamine-14C]aminopyrine disappeared from breath more rapidly in patients with chronic renal failure and a history of analgesic abuse (0.40 +/- 0.04 h-1) than in control subjects (0.22 +/- 0.03 h-1, P less than 0.01) and in other patients with chronic renal failure (0.24 +/- 0.04 h-1). 4. Dialysis treatment and serum creatinine concentrations were not correlated with the rates of aminopyrine metabolism. Two additional patients, however, with combined renal and hepatic disease, exhibited markedly slowed rates of aminopyrine demethylation. 5. Although chronic renal failure by itself might not alter microsomal drug metabolism it is concluded that, in patients with a history of abuse of phenacetin-containing analgesics, marked acceleration in aminopyrine N-demethylation may be observed.

[Influenza vaccination in dialysis patients]. / Grippeimpfung bei Dialysepatienten.

50 stabilized long-term hemodialysis patients were randomly selected to receive one intramuscular injection of a new influenza subunit vaccine containing only the surface antigens hemagglutinin and neuraminidase, or of an adjuvant containing whole virus vaccine. Both vaccines contained strains A/Victoria/3/75 and B/Hongkong/8/73. Both vaccines were very well tolerated and caused significant rises in the antibody titers within 4 weeks against both strains. The subunit vaccine produced significantly higher antibody titers against strain A than the whole virus vaccine.