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Biomedical subjects

H Merk

Publications and source records attributed to H Merk.

At least 109 records · Page 6Linked to original sources
PubMed1984

[Skin changes in paraproteinemias (monoclonal gammopathies)].

Numerous skin disorders or skin lesions are associated with a monoclonal gammopathy (formerly: paraproteinemia). These skin diseases can be differentiated in the following way: specific skin lesions caused by monoclonal immunoglobulin producing cells in the skin, in generalized plasmocytoma or morbus Waldenström. In another group of disorders the monoclonal immunoglobulins induce functional disturbances, e.g. Raynaud syndrome (if the monoclonal immunoglobulins are cryoglobulins), xanthomatosis through interactions between these immunoglobulins and lipoproteins, purpura in immunoglobulin induced stasis and hyperviscosity. The unlimited spreading of the plasmocytoma cells replaces normal immunoglobulin producing plasma cells followed by a disturbance of the humoral immune response, which is frequently accompanied by atypical infections of skin or other organs. Furthermore, an almost obligatory association with monoclonal gammopathies has been demonstrated in a few skin diseases, e.g. scleromyxedema. However, the role of the immunoglobulins in these disorders is unknown. In some other skin diseases, such as pyoderma gangrenosum, acrodermatitis atrophicans Herxheimer, scleredema Buschke etc., a monoclonal gammopathy is only detectable in some patients.

Amyloidosis↗
PubMed1983

[Biochemical aspects of the inflammatory reaction - with special reference to oxygen].

This article gives a synopsis of the inflammatory reactions as well as its mediators under special consideration of the efferent part of the reaction. There is no doubt that histamine, complement, and the kinin system play an essential role; arachidonic acid (eicosatetraenic acid) and its metabolites, however, have gained comparable significance: prostaglandines, prostacyclines, and thromboxanes as metabolites of the cyclo-oxygenase, the leucotrienes SRS-A (slow reacting substances of anaphylaxis) and ECF (eosinophilic chemotactic factor) mediated via lipoxygenase. Moreover, oxygen and its metabolites hydrogen peroxide (H2O2), peroxide radicals (O-2), and hydroxyl radicals (.OH) as well as activated oxygen (singulett oxygen (1O2) play an important part with all aerobic living organisms. Inborn enzyme deficiency of the oxygen metabolism such as NADPH oxidase or cytochrome b-245 deficiency lead to chronic septic granulomatosis. The disease is characterized by reduced resistence against infections, decreased phagocytosis, insufficient killing of bacteria by leucocytes, and diminished oxygen burst. Thus the underlying enzyme deficiency leads to reduced formation of peroxide radicals frequently causing infections with septic complications. On the other hand, increased formation or reduced degradation of peroxide radicals may result in pathological reactions like chromosomal alterations, lipidperoxidation or oxidation of sulph-hydryl groups. The fact that increased peroxide radical formation may cause inflammation or chromosomal aberration is of importance with regard to the pathogenesis of several chronic inflammatory diseases of unknown etiology, such as systemic scleroderma or lupus erythematodes. The enzyme superoxide dismutase (SOD) converts peroxide radicals (O-2) into hydrogen peroxide (H2O2) which can be inactivated by catalase or peroxidase. Consequently, treatment with SOD may have an effective influence on chronic inflammatory dermatoses of unknown pathogenesis.

Dermatitis↗
PubMed1983

Influence of chronic UV-light exposure on hepatic and cutaneous monooxygenases.

Hairless female Ng/-mice were irradiated by UV-light for 16 h daily over a period of 24 weeks. Monooxygenase activities were measured in liver and skin, and an induction of the aryl-hydrocarbon hydroxylase was detected in liver by both fluorometric and radiochemical methods, whereas no induction of this enzyme could be demonstrated in the skin.

Animals↗
PubMed1983

[Analgetic drug intolerance].

Reactions as intolerance to aspirin and food additives were diagnosed in 41 cases during November 1979 -- March 1982. Allergy to pyrazolone-drugs were observed in 20 cases during the same period. 24% of the patients with intolerance to aspirin had also an intolerance to tartrazine. There were no familial occurrence of aspirin intolerance. Four patients had mainly asthma, 37 patients urticaria. New aspects of the pathogenesis of aspirin intolerance -- modulation of arachidonate metabolism and complement activation -- are discussed.

Analgesics↗
PubMed1983

Cimetidine and chlorpheniramine in the treatment of psoriasis.

We examined the efficacy of cimetidine and chlorpheniramine alone and in combination in the treatment of psoriasis under the conditions of a randomised controlled double-blind study. Analysis of data from 52 patients revealed that none of the treatment regimes showed a demonstrable beneficial effect on the course of the psoriasis.

Chlorpheniramine↗
PubMed1983

[Tar treatment in dermatology].

There is a controversial discussion of the carcinogenic action of coal tar used as a therapeutic agent in dermatologic practice. The carcinogen benzo(a)pyrene is present in most coal tar preparations, and it is a potent inducer of the aryl hydrocarbon hydroxylase activity in liver and skin after topical application. The formation of the most reactive metabolite of benzo(a)pyrene is catalyzed by aryl hydrocarbon hydroxylase hydroxylase. Topically used coal tar alters the mutagenicity of the urine indicating a systemic effect. These experimental data recommend to be very cautious in using coal tar as a therapeutic agent although there are only a few case reports on tumors after treatment with coal tar.

Administration, Topical↗
PubMed1982

[Progress in dermatology: new biochemical aspects].

Recent biochemical advances have contributed to clarification of certain skin diseases and metabolic disturbances with predominantly cutaneous symptoms. This is illustrated by the various forms of porphyria. Today we differentiate four hepatic forms: acute intermittent porphyria, variegate porphyria, hereditary coproporphyria and porphyria cutanea tarda, and two erythropoietic forms: congenital erythropoietic porphyria and erythropoietic protoporphyria, all of which are due to an inborn enzymatic deficiency of the heme biosynthesis. From the different forms of ichthyosis, the X-recessive ichthyosis has an underlying enzymatic deficiency of the steroid sulfatase, which seems of significance in the disturbance of keratinization. In epidermolysis bullosa dystrophica type Hallopeau-Siemens an increased collagenase activity was detected. Inhibition of this enzyme by phenytoin results in improvement of the blistering in this genodermatosis. The etiology and pathogenesis of psoriasis are unclear despite extensive efforts. The recently detected deficiency of the arylhydrocarbon-hydroxylase and its inducibility must be confirmed, additionally its significance in the pathogenesis of this disease is yet to be evaluated.

Arylsulfatases↗
PubMed1981

[Medicamental immunosuppression in dermatology (author's transl)].

The pharmacology of the most important immunosuppressive agents in dermatology: glucocorticoids, azathioprine, cyclophosphamide, methotrexate and chlorambucil are reviewed. Our own results of treatment with these drugs (102 patients, diagnosis: lupus erythematosus, dermatomyositis, scleroderma, overlap-syndrome, pemphigus vulgaris, bullous pemphigoid, cryoglobulinaemic purpura, and pyoderma gangraenosum) are presented.

Autoimmune Diseases↗
PubMed1981

[Cervical dysphagia in scleroedema adultorum Buschke (author's transl)].

Scleroedema adultorum Buschke is characterized by progressive hardening of the skin. In contrast to scleroderma the hardening occurs in the skin of the trunk while extremities remain largely free. Internal organs are said not to be involved in scleroedema adultorum Buschke. The full picture of the persistent form of scleroedema adultorum Buschke was observed in two patients. One patient complained of increasing dysphagia with regurgitation and aspiration. Manometry and X-ray cinematographic investigation showed inappropriate relaxation of the upper oesophageal sphincter. In the other patient who had not previously had swallowed difficulties manometry showed achalasia of the upper oesophageal sphincter. The functional disturbances of the upper oesophagus indicate the possibility of an involvement of internal organs in scleroedema adultorum Buschke. However, proof of an aetiological connection between disturbances of oesophageal motility and skin disease requires systematic investigations in a larger group of patients.

Adult↗
PubMed1981

Monoclonal gammopathy in scleredema. Observations in three cases.

A monoclonal gammopathy was observed in three patients with long-term and widespread scleredema (Buschke's disease). There was no evidence of multiple myeloma in any patient. Deposition of monoclonal immunoglobulins in the skin was not detected by direct immunofluorescence microscopy. In contrast to scleromyxedema (lichen myxedematosus), from which scleredema can be distinguished clinically and histologically, the monoclonal immunoglobulins in two cases were of IgG2-kappa and IgG3-kappa type. Only one of the three patients had IgG1-lambda paraproteinemia, which is frequently seen in scleromyxedema. Our findings suggest that diffuse scleredema may be characterized by paraproteinemia but that the possible role of monoclonal immunoglobulins in the pathogenesis of this disease has yet to be resolved.

Adult↗
PubMed1981

[Non allergic skin reactions of drugs (author's transl)].

Non allergic skin reactions are differentiated in the following way: overdose, idiosyncrasy, intolerance and side effects. An intoxication caused by an overdose of a drug may be initiated by an increased resorption through the skin (e. g. salicylic acid or the obsolete boric acid). An overdose of a drug often leads to coma and in many cases, if the patients are lying unattended (e. g. at home). ischemic skin reactions, such as blisters or necrosis occur at pressure areas. Intolerance is an undesirable reaction, produced by a normal therapeutic dose of the drug. Reactions of special interest are those imitating an anaphylactic reaction (type I), such as histamine liberation, complement activation or intolerance to analgetics, dyes or preserving agents. Idiosyncrasy summarizes reactions, which differs both qualitatively and quantitatively from the normal response to therapeutic dose of a drug. Additionaly these reactions are characterized by an underlying biochemical disturbance: drug-induced porphyric crisis in porphyria acuta intermittens, INH induced pellagra or drug-induced lupus erythematosus are discussed in this context in greater detail. Side effects of a drug is a misnomen, but this term cannot be done without. These undesired effects can be differentiated into obligatory effects as seen after cytostatic treatment in the form of alopecia; and possible reactions such as chloasmas after treatment with oral hormonal contraceptives. We assume that some of these side effects would belong to the category of idiosyncrasy or intolerance, if their pathogenesis were known.

Anaphylaxis↗
PubMed1980

[Non-allergic drug exanthemas].

Drug reactions similar to allergic reactions according to the differentiation by Coombs and Gell--type I to type V--can be triggered by drugs without the interaction of antibodies and lymphocytes. The immediate hypersensitivity reaction (type I) is imitated in three ways: 1. Histamine release from mast cells or basophiles by drugs without regines (IgE, IgG4), 2. complement activation by a drug via the classic or alternative pathway without reaction with an antibody. 2. intolerance reaction, that means a chronic urticaria triggered by an inhibitor of the prostaglandin synthesis (Aspirin, other analgesics, food additives and dyes). In contrast to the above reactions, non-immune mechanisms mimicking type II to type V reactions are of inferior clinical importance.

Complement Activation↗