Search PubMedSearch

Biomedical subjects

R von Kries

Publications and source records attributed to R von Kries.

At least 19 recordsLinked to original sources

Des-gamma-carboxyprothrombin (PIVKA II) and plasma vitamin K1 in newborns and their mothers.

Assessments of the vitamin K status in newborns and their mothers by means of des-gamma-carboxy-prothrombin (PIVKA II) measurement have given equivocal results. Part of the variability could be attributed to differences in sensitivity (i.e. the ability to detect small concentrations) and validity (i.e. ability to detect vitamin K deficiency) of the methods applied. None of these methods have yet been validated with respect to plasma vitamin K1. In 22 healthy mother/infant pairs PIVKA II was determined using three different assays including ratio Xa/ecarin (Xa/ec), crossed immunoelectrophoresis (CIE), and an ELISA with a monoclonal antibody (MAB). The results were compared with conventional clotting tests and plasma vitamin K1. The following results were obtained: Cord blood: Clotting tests within age-related normal ranges; PIVKA II detection rates: 0/22 (Xa/ec), 1/22 (CIE), 4/22 (MAB); plasma vitamin K1: undetectable in 20/22. Mothers: Clotting tests all within normal range; PIVKA II detection rates: 1/22 (Xa/ec), 0/22 (CIE), 5/22 (MAB); plasma vitamin K1 (pg/ml) for all mothers (median; range): 186; 55-833; for PIVKA II positive mothers: 213; 59-699. PIVKA II detectability in newborns and mothers was not correlated. The results show an increase in sensitivity for PIVKA II detection in the order of MAB >> CIE > Xa/ec. Due to the very low plasma vitamin K1 at birth, no correlation was possible between cord PIVKA II detectability and plasma vitamin K1. However, in mothers at term PIVKA II MAB appears to be unrelated to the vitamin K status.

Adult

Vitamin K prophylaxis and vitamin K deficiency bleeding (VKDB) in early infancy.

The efficacy of vitamin K prophylaxis (1 mg im or sc, or 1-2 mg orally both given as a single dose at birth) in the prevention of vitamin K deficiency bleeding in early infancy was estimated in Germany during a 15-month period between 1988 and 1989. Cases were identified by a survey of all paediatric hospitals and population denominators by a survey of all obstetric hospitals. Response rates were 85% and 68%, respectively. Thirteen cases of vitamin K deficiency bleeding in early infancy with confirmed prophylactic states were confirmed, seven of whom had intracranial haemorrhage. The estimated efficacy of single parenteral administration of vitamin K versus no prophylaxis was 96.7% (95% confidence interval: 74-99.6%) and for single oral administration versus no prophylaxis 80.4% (9.1-95.6%). Single parenteral vitamin K prophylaxis gave substantial protection against vitamin K deficiency bleeding in early infancy. Single oral prophylaxis appeared to be less effective, although the difference was not significant, as indicated by the wide overlap of the respective 95% confidence intervals.

Administration, Oral

Left ventricular thrombus in a 2-year-old boy with cardiomyopathy: lysis with recombinant tissue-type plasminogen activator.

A 2-year-old boy with cardiomyopathy and clinical signs of cardiac failure presented with an echodense structure in the left ventricle. This structure was seen from different echocardiographic views adjacent to a hypokinetic area of the apex and lateral free wall. It was different in texture and motion from the underlying myocardium and thus met the diagnostic criteria of a left ventricular thrombus. This thrombus protruded into the cavum and was partly mobile. In view of a high embolic risk, thrombolytic therapy with recombinant tissue plasminogen activator was started. The thrombus resolved within 72 h without any embolic or bleeding complications. No recurrence of the thrombus was observed during a 3-month follow up period.

Cardiomyopathies

Renal handling of hydrogen ion excretion in relation to maturity indices in premature infants fed human milk.

In 40 premature infants fed human milk with an actual gestational age of 261 +/- 16 days and an actual body weight of 1.06-2.75 kg, 44 urine samples were collected, and blood acid-base status was measured on day 32 (+/- 16) of life. In the urine, the following results (mean +/- SD) were obtained: urine pH 6.05 +/- 0.65, titratable acidity 0.24 +/- 0.14 mmol/kg/day, ammonium 0.78 +/- 0.25 mmol/kg/day, net acid excretion 0.83 +/- 0.47 mmol/kg/day. There was no significant correlation between renal net acid or ammonium excretion and actual body weight. However, urine pH was positively correlated with body weight. Obviously, premature infants with an actual body weight below 1.5 kg need a higher stimulation of renal hydrogen ion secretion to excrete the same amount of ammonium than those with an actual body weight of about 2.5 kg. The limited renal acidification capacity of very low birth weight infants is a risk factor for the development of late metabolic acidosis.

Acid-Base Equilibrium

Biochemical evidence for the need of long-term mineral supplementation in an extremely low birth weight infant fed own mother's milk exclusively during the first 6 months of life.

In an extremely low birth weight infant fed expressed own mother's milk exclusively during the first 6 months of life, introduction of a human milk fortifier resulted in improvement of biochemical alterations consistent with metabolic bone disease of prematurity. Attempts to discontinue fortification at 9 weeks (discharge) and 21 weeks of age induced deterioration of biochemical parameters, demonstrating a persistent need for mineral supplementation during the whole period of breast-feeding. The effects of long-term human milk fortification are discussed.

Bone Diseases, Metabolic

Localized cicatricial pemphigoid (Brunsting-Perry): electron microscopic study.

Electron microscopic findings are presented in a patient with localized cicatricial pemphigoid (Brunsting-Perry). These findings revealed subepidermal separation below the basal lamina. The basal lamina and anchoring fibrils were well preserved and attached to the intact epidermis to form the roof of the blister. These findings support the concept that localized cicatricial pemphigoid, cicatricial pemphigoid, and disseminated cicatricial pemphigoid are closely related diseases and may explain the occurrence of scar formation in localized cicatricial pemphigoid. A review of 42 cases reported in the world literature is included, with emphasis on clinical, histologic, and immunofluorescence microscopic findings.

Aged

Hemorrhagic bullous amyloidosis. A histologic, immunocytochemical, and ultrastructural study of two patients.

In patients with bullous hemorrhagic amyloidosis of the skin, the skin lesions were the first manifestations of a plasma cell dyscrasia. Both cases were characterized by similar clinical, histologic, and ultrastructural findings showing an intradermal blister within deposits of amyloid substances. Immunohistologic investigations with a panel of antibodies directed against amyloid fibril proteins showed reactivity of the amyloid deposits with an anti-A lambda serum in both patients.

Aged

Vitamin K in infancy.

Vitamin K has regained paediatric interest due to a recurrence of bleeding caused by deficiency of the vitamin in newborns and young infants. Increasing awareness of these clinical problems, the development of new methods for the detection of vitamin K deficiency and the direct measurement of vitamin K in tissues have stimulated research. Much new data obtained from these studies has proved helpful to the understanding of vitamin K deficiency in infancy. For example low concentrations of vitamin K have been found in fetal and neonatal livers. The implications of these findings with respect to manifest vitamin K deficiency and to new methods for detection of subclinical vitamin K deficiency are discussed. Breast-feeding is a major risk factor for classical haemorrhagic disease of the newborn and for late onset bleeding due to vitamin K deficiency in young infants. The interdependencies between breast-feeding and vitamin K deficiency are discussed on the basis of new data obtained from direct measurement of vitamin K in maternal milk. The review further focuses on pathophysiological concepts of bleeding due to vitamin K deficiency in infancy and current concepts of vitamin K prophylaxis.

Breast Feeding

Solar urticaria induced by visible light and inhibited by UVA.

A 17-year-old male with solar urticaria is described. The action spectrum ranged from 400 to 520 nm. Wheals induced by visible light were inhibited by simultaneous or subsequent irradiation of the skin with UVA radiation. UVA irradiation prior to exposure to eliciting wavelengths revealed no inhibitory effect, nor was an inhibitory effect found by pre- or postirradiation of test sites with visible light longer than 530 nm. In vitro activation of the patient's serum by exposure to visible light induced wheal formation at the injection site. The wheal formed by in vitro-activated serum was suppressed only when the serum was exposed to UVA after, but not before irradiation with wavelengths of the action spectrum. This suggests that the inactivation of a photoallergen rather than of its precursor is the mechanism by which UVA exerts an inhibitory effect.

Adolescent

Vitamin K in the newborn: influence of nutritional factors on acarboxy-prothrombin detectability and factor II and VII clotting activity.

The incidence of acarboxy-prothrombin and the clotting activity of factors II and VII were evaluated on the fifth day of life in 183 healthy newborns, who had received no vitamin K prophylaxis. Acarboxy-prothrombin was detected in 93/183 newborns. All acarboxy-prothrombin-negative babies had factors II and VII clotting activities above 25% whereas a great variability was observed in acarboxy-prothrombin-positive babies: 21/93 had factor II and 14/93 had factor VII activities below 25%. Seventy-two of the acarboxy-prothrombin-positive babies had normal factor II and VII clotting times on the fifth day of life. These babies must be suspected to have had vitamin K deficiency on one of the first 4 days, as acarboxy-prothrombin has a 50% disappearance rate of 50 h. Acarboxy-prothrombin was mainly observed in breast-fed infants (84/122) and only rarely detectable in infants receiving supplementary (7/44) or exclusive formula feeding (2/17). The type of milk feeding however might be less important for the babies' vitamin K supply than the actual milk intake. All acarboxy-prothrombin-positive babies had received small amounts of milk on the first 4 days of life. In those with low factor II and VII clotting activities the milk intake was low throughout the first 4 days of life, whereas babies with acarboxy-prothrombin and and normal clotting activities had increased their milk intake to more than 100 ml on the third and fourth day of life. Recommendations for vitamin K prophylaxis in newborns should be given with regard to the feeding on the first days of life.

Biomarkers

Neurological manifestations in three German children with AIDS.

We report the neurological findings in two children with AIDS and one child with lesser AIDS. The first patient developed acute encephalopathy 37 months after having received a blood transfusion from a HTLV-III positive donor. CCT showed ring-enhancement and hypodense lesions with homogenous enhancement. Autopsy revealed CNS toxoplasmosis. The second child with AIDS, born to an iv drug-addicted mother, had one seizure at four months of age, but other neurologic signs were absent. She died of pneumonia due to Pneumocystis carinii at seven months of age. Postmortem examination of the brain revealed extensive nerve cell damage in the cerebral cortex and cerebellum, probably due to terminal hypoxemia and not AIDS-related. In both children clinical features of childhood AIDS like failure to thrive, lymphadenopathy, oral thrush and chronic pulmonary infiltrates were absent. The hallmark of the third child's clinical course was a progressive loss of psychomotor abilities with onset of the neurological symptoms nine months before other signs of AIDS occurred. AIDS should be suspected or excluded in children at increased risk for AIDS presenting with either acquired atypical CNS infection or unexplained developmental regression, even in the absence of other clinical symptoms of pediatric AIDS.

Acquired Immunodeficiency Syndrome