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Biomedical subjects

B Hoppe

Publications and source records attributed to B Hoppe.

11 recordsLinked to original sources

[Vitamin D poisoning in infants: a preventable cause of hypercalciuria and nephrocalcinosis].

The established prophylaxis for vitamin D-deficient rickets today is 400 IU vitamin D3 given daily during the first year of life. With this regimen, vitamin D intoxication is a rare event. Nevertheless, we have recently seen 4 infants with vitamin D intoxication after a so called "stoss" prophylaxis, i.e. twice 300,000 units (7.5 mg) vitamin D3 orally within 4 weeks. One patient presented with failure to thrive due to marked hypercalcemia (3.9 mmol/l) and nephrocalcinosis, 2 patients showed medullary nephrocalcinosis on ultrasonography and one patient had gross hematuria and spontaneous passage of a calculus. Three patients had massive hypercalciuria (calcium/creatinine ratio 1.8-4.8 mol/mol, normal less than 1). The 25 (OH) vitamin D3 plasma levels, measured only in 2 patients, were strikingly increased (270 and 158 nmol/l, respectively, normal 25-80). Urinary calcium excretion slowly decreased to normal values on a low calcium diet and high fluid intake. Nephrocalcinosis, however, persisted in 2 patients and showed a slight progression ultrasonographically in one patient. The short time interval between vitamin D administration and onset of symptoms and the subsequent clinical course provide strong evidence that hypercalciuria and nephrocalcinosis were due to vitamin D "stoss" prophylaxis in all four cases. In conclusion, there is no indication for vitamin D "stoss" prophylaxis for vitamin D-deficient rickets in infants. Vitamin D intoxication still has to be considered as a possible cause of hypercalciuria.

Calcifediol

[Cross-country and downhill skiing in patients with myocardial infarct. Can silent ischemia be prevented by drug therapy?].

The appearance of ST segment depression in the exercise ECG serves as a threshold criterion when it comes to determining the "loadability" of myocardial infarction patients carrying out sports activities. In 27 MI patients, the question was investigated as to the extent to which abnormalities taking the form of silent ischemic episodes could be found during cross-country skiing on plains or during downhill skiing at an altitude of 800 to 2,000 meters. Such silent ischemic attacks were found in 20 out of the 27 patients. Both the duration and incidence were higher during sports activities than during normal day-to-day activities. The heart rate at the time of the appearance of the ischemic episodes was lower in the 12-hour ECG than during ergometry. During sports activities, however, the heart rates were frequently higher than the given training pulse rates. Treatment with nitrates (Isoket retard 120 mg) reduced the incidence and duration of silent ischemias. On account of the spontaneous variability of the parameter, it needs to be interpreted with caution. The incidence of silent ischemic episodes during sports activities in patients with clinical anomalies should prompt a rigorous treatment with drugs, and careful supervision of training.

Coronary Disease

[Alpha fetoprotein and HbF cells in the maternal blood and their modification through amniocentesis].

In 101 patients of the Frauenklinik der Medizinischen Hochschule Hannover we have measured the concentrations of fetal cells and alpha-fetoprotein before and after amniocentesis. There was a significant increase in both parameters corresponding to an arbitrary fetomaternal haemorrhage of 0,05--0,4 ml. AFP seemed to be more reliable than the fetal cell count. The site of placentation was of no influence on the fetomaternal haemorrhage. As less than 0,1 ml rhesus-positive fetal blood is enough to cause isoimmunization in mothers at risk we highly recommend to give immunoglobulin-anti-D to all unsensitized rhesus-negative mothers after amniocentesis.

Amniocentesis

[Diagnostic difficulties in a case of visceral lupus with disseminated neurological signs].

The reported case was observed in a patient aged 54 years with disseminated lesions in the central nervous system. The history of the disease covered 18 years with periods of exacerbations and remissions. Seven years after the appearance of neurological signs involvement of the internal organs and skin was noted. In the serum antinuclear antibodies, LE cells and high gamma globulin level were demonstrated. The course of the disease and the observed immunological changes justify the diagnosis of the lupoid sclerosis form of visceral lupus erythematosus.

Antibodies, Antinuclear