Biomedical subjects

H Rickmann

Publications and source records attributed to H Rickmann.

6 recordsLinked to original sources

PubMed2003

Cerebral haemodynamic pathologies in HELLP syndrome.

The syndrome of haemolysis, elevated liver enzymes and low platelets (HELLP syndrome) is understood as a unique variant of severe preeclampsia. This disorder complicates between 2 and 7% of gestations and is associated with a high perinatal morbidity and a maternal morbidity ranging between 1 and 4%. Intracerebral complications only rarely occur, especially intracerebral haemorrhage was described only in single cases, often correlated with fatal maternal outcome. The analysis of patients with HELLP syndrome treated at our hospital revealed three cases with severe neurological deterioration. Possible pathogenetic factors are discussed.

Adult↗

PubMed2003

Prothrombin G20210A mutation, but not factor V Leiden, is a risk factor in patients with persistent foramen ovale and otherwise unexplained cerebral ischemia.

BACKGROUND: Paradoxical embolism via persistent foramen ovale (PFO) is suspected to be a frequent cause of stroke in younger patients. We investigated whether the prevalence of the risk factors for venous thrombosis factor V Leiden (FVL) and prothrombin G20210A mutation (PT G20210A) is increased in this group of patients. METHODS: We examined FVL and PT G20210A mutation in 220 patients (group 1) with cerebral ischemia associated with a PFO and without other etiology, in 196 patients with cerebral ischemia of an etiology other than PFO (group 2), and in 362 healthy subjects (group 3) from the same region in Germany. RESULTS: Heterozygosity for the PT G20210A mutation was more common in group 1 (5.0%) than in group 3 (1.4%; sex- and age-adjusted odds ratio 3.66; 95% CI 1.25-10.75; p = 0.01). By contrast, the mutation was not more common in group 2 (2.6%; odds ratio 1.50; 95% CI 0.42-5.41; p = 0.5). Prevalences of FVL were not different between groups. CONCLUSIONS: We identified PT G20210A but not FVL - the strongest genetic risk factor for deep venous thrombosis - to be significantly associated with stroke attributed to PFO. These findings rise doubts about the concept of paradoxical brain embolism as the dominating mechanism in stroke associated with PFO.

Adult↗

PubMed1998

Prothrombin gene G20210-->A transition is a risk factor for cerebral venous thrombosis.

BACKGROUND AND PURPOSE: It has been recently reported that a G-->A transition at nucleotide position 20210 in the 3'-untranslated region of the prothrombin gene is associated with elevated plasma prothrombin levels and an increased risk of deep venous thrombosis. To date, it is unknown whether this polymorphism also represents a risk factor for cerebral venous thrombosis (CVT). METHODS: Venous blood samples were collected from 45 patients with CVT and from 354 healthy blood donors as controls. A second control group consisted of 131 subjects with acute ischemic stroke or transient ischemic attack (TIA). Genomic DNA was isolated from peripheral blood leukocytes. Amplification of DNA was performed by polymerase chain reaction (PCR). The G-->A transition at nucleotide position 20210 of the prothrombin gene was detected by allele-specific restriction digestion. RESULTS: The G20210-->A transition in the prothrombin gene was found in a heterozygous form in 4 of 45 patients with CVT (8.9%) and in 8 of 354 healthy control subjects (2.3%). This difference was statistically significant (P=0.010). The G20210-->A transition increased the relative risk for CVT approximately 5-fold (age-adjusted odds ratio 5.7; 95% CI 1.5 to 21.5). In contrast, in the group of patients with acute cerebral ischemia, only 3 of 131 subjects (2.3%) were heterozygous for the G20210-->A transition, which corresponded to the prevalence in the group of healthy blood donors. CONCLUSIONS: The recently described G20210-->A transition in the 3'-untranslated region of the prothrombin gene is an inherited risk factor for CVT but obviously not for acute ischemic stroke or TIA.

Adolescent↗

PubMed1994

[Rhombencephalitis caused by Listeria monocytogenes].

We report the case of a 57-year-old man with Listeria rhombencephalitis. This had been ascertained by means of Listeria isolation from the cerebrospinal fluid. After an nonspecific prodromial period with nausea and headache, he developed fever, meningism, brain stem dysfunction and an organic psychosis. With early antibiotic therapy (ampicillin/gentamycin), it was possible to bring about a restitio ad integrum. Different brain-imaging methods (computed tomography, MRI, brain SPECT) in the acute and follow-up stages are discussed.

Ampicillin↗

PubMed1990

[Data processing the the RAST laboratory].

We describe a clinical laboratory information system for the RAST laboratory based on personal computers. In developing this system, we paid special attention to easy handling which does not require any computer experience on the user's side. Data storage and retrieval are managed by a relational database system with fast data access. Aside from the usual functions of a laboratory information system, the laboratory work is facilitated by a clear distribution of samples, the possible on-line connection to various analyzers, as well as the provision of cumulative results and a fast access to archive data.

Allergens↗

PubMed1989

Subsensitivity of presynaptic adenosine A1-receptors in caudal arteries of spontaneously hypertensive rats.

(-)-N6-(R-phenylisopropyl)-adenosine (R-PIA) depressed tritium overflow and vasoconstriction evoked by electrical stimulation to a similar extent in isolated tail arteries of Wistar rats (WR) preincubated with [3H]noradrenaline. The inhibitory effects of adenosine, 5'-N-ethylcarboxamidoadenosine (NECA) and R-PIA were determined on the constrictor responses of tail arteries obtained from WR, as well as spontaneously hypertensive (SHR) and Wistar Kyoto rats (WKY). In WR and WKY, the rank order of agonist potency (R-PIA greater than NECA greater than adenosine) was compatible with the presence of adenosine A1-receptors. Whereas adenosine, NECA and R-PIA were equiactive in WR and WKY, they produced no or only slight changes in SHR. The left renal arteries of some WR were partially occluded to induce hypertension. R-PIA had the same effect in the tail arteries of these animals as in preparations obtained from sham-operated WR. The above results suggest that the subsensitivity of presynaptic A1-receptors in the blood vessels of SHR is genetically determined. This could contribute in vivo to enhanced transmitter release from terminals of perivascular nerves and subsequent increases in vascular resistance.

Adenosine↗