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Biomedical subjects

V Voigtländer

Publications and source records attributed to V Voigtländer.

At least 19 recordsLinked to original sources
PubMed2002

[Multiple superficial basal cell carcinomas following chronic ingestion of sodium hydrogen carbonate containing arsenic].

Basal cell carcinomas (BCC) are caused by various factors such as ultraviolet light, ionizing radiation, possibly human papilloma viruses and chemical agents. Among the latter inorganic trivalent arsenic has long been recognized as an important cause of BCC. A 70-year-old woman developed multiple basal cell carcinomas mainly on the trunk after taking sodium hydrogen carbonate contaminated with arsenic for many years for chronic gastritis.

Aged↗
PubMed2001

[Recurrent nodular panniculitis in hereditary alpha-1-antitrypsin deficiency].

BACKGROUND: Hereditary alpha 1-antitrypsin deficiency may be very rarely associated with chronic panniculitis and is therefore often diagnosed only with delay. CASE REPORT: The typical clinical features of the disease are described in a 37-year-old woman. This case underlines the importance of determining alpha 1-antitrypsin levels in patients with chronic relapsing panniculitis. Therapeutic approaches are discussed.

Adult↗
PubMed2001

[Kidney involvement in hypocomplementemic urticaria-vasculitis syndrome--a simulated systemic lupus erythematosis].

We report a case of hypocomplementemic urticarial vasculitis (HUV). The clinical course was characterized by urticaria, angio-edema, pericarditis, joint pain and conjunctivitis. The laboratory findings revealed moderate proteinuria, erythrocyturia, normal renal function, normotension, reduction of C3, C4 and C1q complement with elevated C1q antibodies. Antinuclear antibodies were inconstantly positive. Renal biopsy showed a mild form of membranous glomerulonephritis. Despite intensive therapeutic measures (dapsone, immunosuppressives and immunoglobulins), relapses of urticaria occurred frequently. HUV is probably a minor form of systemic lupus erythematosus.

Adult↗
PubMed2000

[Hereditary prolidase deficiency. Contribution to differential therapy refractory leg ulcer diagnosis].

Leg ulcers may be caused by many different diseases. Most frequently, they are due to vasculopathies, to a lesser extent to metabolic, neuropathic or hematologic diseases. Neoplasms, connective tissue diseases, infections, trauma, and panniculitis should also be included in the differential diagnosis. A 38-year-old Caucasian female patient with hereditary prolidase deficiency developed progressive and very painful leg ulcers. The ulcers first appeared in childhood and did not respond to various treatments. Additional features of prolidase deficiency included mental retardation, short stature, extensive dental caries, and multiple malar teleangiectases. Hereditary prolidase deficiency is a very rare autosomal recessive disease. It is caused by heterogeneous mutations of the prolidase gene and affects many aspects of protein metabolism. Ion exchange chromatography and high voltage electrophoresis of urine can prove the suspected diagnosis. So far, there is no efficient therapy for hereditary prolidase deficiency. All reported treatment attempts have ended in failure.

Adult↗
PubMed2000

[From scabies room to modern specialty department. 90 years Ludwigshaven Dermatology Clinic].

The dermatology clinic Ludwigshafen was founded in 1910. Dr. Siegfried Fuss was head of the clinic for almost 40 years. The clinic's history reflects the rapid industrial growth of the city, the destruction of two world wars and the progress of dermatology during this century. Today, the clinic is an academic teaching hospital affiliated with the University of Mainz with 45 beds and offers a broad spectrum of modern dematological diagnostic procedures and therapies.

Dermatology↗
PubMed1997

Barraquer-Simons syndrome (with sensorineural deafness): a contribution to the differential diagnosis of lipodystrophy syndromes.

Among the lipodystrophies, the Barraquer-Simons syndrome is a rare condition. We describe a 27-year-old woman with progressive loss of subcutaneous fat after 15 years first affecting the face and spreading to the upper part of the body. She also suffered from deafness and had marked changes in cranial MRI. We discuss possible differential diagnosis such as the Cockayne, SHORT and Berardinelli-Seip syndrome.

Adult↗
PubMed1991

[Proteus syndrome].

Proteus syndrome is a rare congenital disorder in which the major clinical manifestations are skeletal deformities and hamartomatous tumors. The case of a 42-year-old woman with right hemihypertrophy, macrodactyly of the right hallux, extreme kyphoscoliosis and bilateral plantar connective tissue naevi is reported. Proteus syndrome is reviewed with reference to this patient.

Adult↗
PubMed1990

[Gardner-Diamond syndrome].

This paper presents a 26-year-old woman with the characteristic features of Gardner-Diamond syndrome: recurrent painful bruises reproducible by intradermal injection of autologous red blood cells, and a "hysterical" personality pattern together with nonspecific multisystem complaints.

Adult↗
PubMed1989

[Immune modulators in the treatment of malignant melanoma].

The experience gained to date with immunomodulators used as therapeutical and adjuvant measures in the treatment of cutaneous malignant melanoma is reviewed. In large studies no therapeutic effect has been shown for levamisole, DNCB and BCG preparations. The effectiveness of monoclonal antibodies, histamine type 2 receptor antagonists, thymus factors and mistletoe extracts cannot yet be assessed due to a lack of clinical studies. The recent use of the lymphokines: tumor-necrosis factor, interleukin 2 and interferons, has shown that tumor therapy with immunomodulators is possible, but many questions still remain to be answered, so that their use, especially as an adjuvant measure, should be restricted to controlled studies.

Adjuvants, Immunologic↗
PubMed1989

Collagen biosynthesis anomalies in prolidase deficiency: effect of glycyl-L-proline on the degradation of newly synthesized collagen.

Prolidase deficiency is a rare hereditary disease characterized by an iminodipeptiduria especially composed by glycyl-L-proline which is not further degraded. The study of collagen metabolism in fibroblast cultures from three prolidase-deficient patients showed an increase in the rapidly degraded collagen and a decrease in the proline pool. In order to elucidate the mechanism of this metabolic disturbance, glycyl-L-proline was added to the cell cultures. In the control cultures, the addition of this dipeptide caused an increase in the rapidly degraded collagen and a decrease in the proline pool. The effects on the patient fibroblasts depended on the severity of the deficiency. The metabolic function of the dipeptide glycyl-L-proline was discussed in the light of these results.

Adult↗
PubMed1988

[The cytoskeleton in hereditary ichthyoses].

The hereditary forms of ichthyosis can be considered to be models of impaired terminal epidermal differentiation. Analysis of the cytokeratin polypeptide pattern represents a new attempt at elucidating the mechanisms of keratinization mechanisms which are still unclear. We therefore studied the cytokeratin expression of the following types of ichthyosis: autosomal dominant ichthyosis vulgaris (n = 4), X-linked recessive ichthyosis vulgaris (n = 4), recessive non-bullous congenital ichthyosiform erythroderma (n = 1), recessive classical lamellar ichthyosis (n = 2), autosomal dominant lamellar ichthyosis (n = 1), and Netherton syndrome (n = 1). After dissection of frozen sections of the interfollicular epidermis, two-dimensional gel electrophoresis was performed. For immunofluorescence microscopy a panel of monoclonal cytokeratin antibodies (KG8.13, KK8.60, KA5 and AE1) was used. Cytokeratin polypeptide expression was basically unchanged compared with normal epidermis. In contrast, however, the antibody AE1 did not stain the basal cell layer in most types of ichthyosis, regardless of their genetic type. The cytokeratin polypeptides nos. 6 and 16, which are generally considered markers of hyperproliferation, were not expressed in either type of ichthyosis vulgaris (XRI or ADI), but were detected in trace amounts in various types of congenital ichthyosis.

Antibodies, Monoclonal↗
PubMed1987

[Increased birth weight in psoriasis vulgaris--an evolutionary advantage?].

With regard to the frequent alterations of insulin secretion and glucose tolerance in psoriatic patients, the birth weights of children of 100 psoriatic mothers were compared with the birth weights of children of 100 carefully matched control mothers. The mean birth weight in the psoriatic group was 140 g higher than that of the control group. A birth weight of more than 4,000 g was observed in the children of 20.4% of the psoriatic mothers and in only 11.3% in the control group. The frequency of diabetes mellitus independent of insulin (type II) in psoriasis recalls the hypothesis of the "thrifty" genotype, which suggests an explanation for the high incidence of diabetes in modern societies. On the basis of our results, this hypothesis may also be applied to psoriasis. In addition, we studied the influence of pregnancy on the course of psoriasis. Improvement was noted in 27.8% (complete remission in 20%), exacerbation in 14.7%; in 46.6% the disease remained unchanged.

Biological Evolution↗
PubMed1987

[Tick bite fever].

Tick bite fever (boutonneuse fever) is endemic in India, Africa and especially the Mediterranean countries. It is occasionally "imported" into central European countries by tourists. The exanthematic disease is caused by infection with Rickettsia conori, which is usually transmitted by the brown dog tick. A typical primary lesion at the site of the tick's bite is an important diagnostic hint. The treatment of choice are tetracyclines.

Adult↗
PubMed1986

[Clinical and pathogenetic aspects of aspirin intolerance].

Aspirin intolerance has become increasingly important in clinical dermatology during the past decade, especially as a diagnostic aid in chronic urticaria. It is recommended, to distinguish clinically between the intolerance syndrome and an intolerance provocation (of preexistent asthma or urticaria). Pathogenetically, various antibody-independent mechanisms are discussed of which most authors favour a defective regulation of arachidonic acid metabolism.

Arachidonic Acid↗
PubMed1986

Adverse dermatological reactions to pyrazolones.

All analgesics can occasionally induce adverse skin reactions. Especially in the early period of pyrazolone therapy, a large variety of cutaneous manifestations were attributed to the use of these drugs. An updated analysis is attempted.

Angioedema↗