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Biomedical subjects

G W Korting

Publications and source records attributed to G W Korting.

At least 19 recordsLinked to original sources
PubMed1988

A monoclonal Ro-antibody and the serum of a Ro-positive patient with subacute cutaneous lupus erythematosus (SCLE) react with basal layers of human epidermis.

Skin lesions, especially at areas exposed to sunlight, prove to be a major form of manifestation of diseases related to Ro-antibodies and neonatal-, 'ANA-negative-', and cutaneous types of lupus erythematosus. A monoclonal Ro-antibody established by our group reacts with a 60 kD polypeptide in extracts from human spleen, whereas in extracts from human epidermis the monoclonal Ro-antibody and a purified Ro-antibody from a monospecific serum of a patient with subacute cutaneous lupus erythematosus reacted with a 60 kD and a 48 kD protein. Performing immunofluorescence microscopy on HEp2-cells both antibodies showed a nuclear speckled staining pattern and a reaction with cytokeratin filaments. On skin biopsies obtained from the patient, predominantly the basal layers of the proliferative stratum germinativum demonstrated a high rate of immunofluorescence; antigen-expression seems to depend on sunlight exposure. From these data we assume that, especially in subacute cutaneous lupus erythematosus, cross-reaction of the Ro-antibody with one of the lower molecular keratins happens in that area of human epidermis which histologically shows cellular destruction.

Antibodies, Antinuclear↗
PubMed1979

[Zinc deficiency syndrome during long-term parenteral nutrition in a patient with Crohn's disease and cirrhosis of the liver. Casuistry and zinc-pharmacokinetic (author's transl)].

A 29 year old patient with Crohn's disease and posthepatitic HBsAg-positive cirrhosis developed zinc deficiency in the course of complete parenteral nutrition. Zinc deficiency was proven by a low plasma zinc level of 12 microgram/dl. The daily input of zinc was 0.5 mg as calculated from the zinc concentration of infusion solutions used in parenteral nutrition during 3 1/2 months of treatment. The clinical picutre was that of acrodermatitis enteropathica. Cirrhosis of the liver and Crohn's disease were contributory causes of zinc deficiency. 6 bolus injections of 12-36 mg of zinc (total amount 144 mg) were given during 13 days. The plasma zinc level increased to 60-80 microgram/dl. 52% of the total amount of zinc injected were excreted by urine. The plasma half-life times of zinc were independent from basic zinc concentrations and averaged 1.55 +/- 0.22 h. It is concluded that severe signs of zinc deficiency will develop during parenteral nutrition in the presence of conditions leading to a negative zinc balance. In the case of long-term complete parenteral nutrition zinc should be substituted from the beginning of the treatment on.

Acrodermatitis↗
PubMed1979

[Vasculitis racemosa hemoplegica].

The secondary symptomatic forms of livedo reticularis can follow cerebrovascular incidents with consecutive hemiplegia; this is rarely known. A further patient is described who developed an asymmetrical livedo reticularis on the hemiplegic half of the body. The reason of the hemiplegia was an intracerebral hemorrhage.

Adult↗
PubMed1978

[HLA antigen frequencies in patients with progressive systemic sclerosis and morphea (author's transl)].

Forty three patients with progressive systemic sclerosis and 24 patients with morphea are typed for 30 antigens of the HLA-A and B series. There is an increase of the frequency of HLA-B8 in patients with progressive systemic sclerosis (37% vs. 20% in controls: P less than 0.001, Pcorr. = n.s.). The increase of the HLA-B8 frequency seems to be most pronounced in patients with a diffuse form of progressive systemic sclerosis. 4 out of 5 patients are HLA-B8 positive (P = 0.00672). In patients with acrosclerosis is HLA-B8 only slightly increased (32%), but the increase is greater in male patients (44%) and in patients with an early onset of the disease (36%). With the exception of HLA-A1 there is no deviation of the frequencies of any other HLA antigen tested, especially not of HLA-Aw24. The number of patients with morphea is to small for statistical evaluation.

Adult↗
PubMed1978

Esophageal dysfunction and its pathogenesis in progressive systemic sclerosis.

In 25 patients with progressive systemic sclerosis esophageal involvement was studied prospectively by analysing subjective symptoms and radiological and manometric criteria. In all patients abnormal motility could be demonstrated by X-ray and/or manometry: radiologically in 18 (72%), manometrically in 22 (88%) cases. Dysphagia was present only in 11 patients (44%). Six patients (24%) had no subjective symptoms in spite of severe objective esophageal abnormalities. Therefore, the absence of esophageal symptoms does not exclude advanced affliction of the esophagus. To determine the pathogenesis of esophageal dysfunction the effects of 3.5 microgram/kg carbachol and of 0.6 microgram/kg pentagastrin i.m. on the lower esophageal sphincter pressure (LESP), on the amplitude and on the duration of peristaltic esophageal contractions were studied at random in 12 of the patients and 12 normal controls. The results suggest a primary myogenic genesis of the motor abnormalities by atrophy and sclerosis of esophageal smooth muscle.

Adult↗
PubMed1978

[Sclero-porphyria].

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Diagnosis, Differential↗