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Biomedical subjects

G Goerz

Publications and source records attributed to G Goerz.

At least 217 records · Page 12Linked to original sources
PubMed1979

Laboratory investigations in patients with generalized psoriasis under oral retinoid treatment. A multicenter study of computerized data.

Numerous laboratory parameters were examined 235 patients with generalized psoriasis treated orally with retinoid and in 35 patients treated topically with anthralin as control. Computer evaluation of the obtained data revealed statistical trends to elevation of the total serum bilirubin level and increasing number of blood monocytes after long-term oral treatment. No other statistically significant changes of the laboratory data were found. Particularly, the liver function tests (transaminases, prothrombin and alkaline phosphatase) showed no significant alterations. Only in a few cases did the retinoid compound have an influence on the GPT and GOT levels. The reasons for this individual sensitivity to the drug remain unknown. No significant alterations were found in the control group treated topically with anthralin.

Administration, Oral↗
PubMed1979

Two primary malignant melanomas in a patient with plasmacytoma.

The occurrence of two primary malignant melanomas (superficial spreading melanoma, superficial spreading melanoma with nodular growth) in a patient with diffuse plasmacytoma treated with chemotherapy and radiation is described. Such an association does not appear to have been reported previously.

Female↗
PubMed1979

[Occurrence of HBs-antigen and anti-HBs in patients with porphyria cutanea tarda (author's transl)].

Serum 63 patients with porphyria cutanea tarda (PCT) was examined for the presence of HBs-antigen and anti-HBs by the CombRIA-Au method. HBs-antigen was not detected in any of the examined blood samples. In contrast to these findings in 12 of the 63 PCT-patients (= 28 per cent), anti HBs was detected in the serum. The results showed that a high percentage of our PCT patients had been afflicted with an inapparent hepatitis B and were producing HBs-antibodies.

Antibodies, Viral↗
PubMed1979

[Clinic and treatment of porphyria cutanea tarda (author's transl)].

Symptomatology and pathogenesis of porphyria cutanea tarda (PCT) are shortly reviewed. The different possibilities in the treatment of PCT are discussed with special reference to the phlebotomy according to Ippen and to the chloroquine administration according to the regimen described by Kordac and Semradova in 1974. 75 PCT patients were treated with chloroquine (Resochin, Nivaquine). After 9.3 +/- 3.4 months (means +/- SE) all patients excreted normal amounts of porphyrins, and the clinical symptoms disappeared. 14 of these patients relapsed after a mean period of 21 months after the withdrawal of chloroquine.

Bloodletting↗
PubMed1979

[Behaviour of the hepatic glutathione (GSH) in the rat in continuous administration of hexachlorobenzene (HCB) (author's transl)].

Adult male Wistar rats were fed with a diet containing 0.05% hexachlorobenzene (HCB) over a period of at least 90 days. At intervals group of 4 animals each were killed and the GSH- and cytochrom P-450-content, the 7-ethoxycoumarin-deethylation activity were measured in the liver. At the same time the urinary porphyrin excretion was determined. After ten days a massive induction of the microsomal mixed function monooxygenase system could be demonstrated, whereas the porphyria (e.g. an increased excretion of urinary porphyrins) became manifest after 56 days HCB-exposure. At the same time (56th day of experiment) the GSH content in the liver rapidly decreased. It is assumed that at the beginning of th HCB-feeding the microsomal mixed function monooxygenase are induced and the uroporphyrinogen decarboxylase is inhibited. This inhibition causes an accumulation of highly carboxylated porphyrins in the liver. Later on (around the 56th day of HCB exposure) a hepatic GSH decrease leads to an increase of heavy metal ions and to a disturbance of the heme biosynthesis that means the manifestation of the HCB-porphyria.

Animals↗
PubMed1978

[Hexachlorbenzene (HCB) induced porphyria in rats. Influence of HCB-metabolites on the biosynthesis of heme (author's transl)].

Female adult Wistar rats were fed with a diet containing 0.05% hexachlorobenzene (HCB) or its metabolites, pentachlorobenzene (PCB) and pentachlorphenole (PCP). These chlorinated aromatic hydrocarbons produced an increase in the liver cytochrome P-450 content in about the same degree, however, only the application of HCB showed an extremely high rise in the P-450 enzymatic activity expressed in terms of the O-dealkylation of 7-Ethoxycoumarine. No alteration was observed in the urinary porphyrin excretion in the PCB and PCP treated animals, whereas 60 days after the beginning of the HCB application a high level of porphyrins could be detected in the urine of the animals. It seems unlikely therefore that the HCB metabolites (PCB and PCP) are porphyrogenic agents. In addition, although induction of the liver cytochrome P-450 system was observed after PCP pretreatment of the rats over a period of 40 days, the consequent application of HCB did not influence the establishment of the experimental porphyria.

Animals↗
PubMed1978

[Porphyria cutanea tarda: possible treatment and its results (author's transl)].

In 4 of 12 patients with porphyria cutanea tarda (PCT) treatment with p-aminobenzoic acid (PABA) achieved normal porphyrin excretion and disappearance of the skin changes. But this result is far worse than that obtained with the venesection method of Ippen. PABA treatment should, therefore, be discontinued.--Among 56 patients (37 males, 19 females) given chloroquine treatment (twice 125 mg per week), normal porphyrin excretion and disappearance of the skin changes occurred in 32 after an average duration of treatment of 8 months, while in 21 (15 males and 6 females) an improvement set in after an average treatment duration of only 5 months so far. The treatment failed in three patients, but one of them lapsed his treatment and one died of an intercurrent disease, so that only one can be reckoned a true failure of chloroquine treatment.

4-Aminobenzoic Acid↗
PubMed1978

[Oral psoriasis treatment with a new aromatic retinoid (Ro 10-9359): a multi-centre controlled study of 291 patients (preliminary results) (author's transl)].

In a multi-centre study 291 patients with psoriasis were treated with (a) oral doses of the recently developed retinoid Ro 10-9359, (b) classical local dithranol application, and (c) both. In a preliminary evaluation of 203 patients treated orally excellent or good results were obtained in 120 (61%), no response in 31 (15.8%). The initial dose was 1.0 mg/kg body-weight daily, i.e. 50-75 mg, which was then reduced to 25-50 mg daily. A clinical response was noted after 2-3 weeks. Particularly, severe erythrodermic and pustular forms of the disease responded surprisingly well to the drug so that cytostatic agents were avoided. Under long-term administration, however, relapses were still seen. Most side-effects were reasonably well tolerated. But in 14% of patients the drug had to be discontinued because of hair loss, paronychia or slight elevation of transaminases (up to 40 U/I). This new drug is thus a potent antipsoriatic agent: it is effective, easily controlled and causes only moderate side-effects.

Administration, Oral↗
PubMed1978

[Lyell' syndrome: a review with special regard to the form caused by drugs (author's transl)].

The clinical evolution of Lyell' syndrome (LS), its complications, the histological findings, the nosological position and the differentiation from erythema exsudativum multiforme are dealt with. There are at least two etiological forms of LS: the LS caused by staphylococci, and the LS caused by drugs. The former mainly occurs in children, and is caused by staphylococci of the phagous group II, while the latter is mainly caused by sulfonamides, pyrazolones, penicillines, barbiturates and salicylates. The causative responsibility of a certain drug can be proved by three criteria: 1. Relapse of LS after exposure to the same drug. 2. Allergy to the drug taken before the onset of LS. 3. Positive allergy tests. The hypothesis concerning the pathogenesis of LS caused by drugs, the differential diagnosis and therapeutical guidelines are dealt with.

Acute Kidney Injury↗