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Biomedical subjects

M H Rustin

Publications and source records attributed to M H Rustin.

At least 19 recordsLinked to original sources
PubMed1992

Efficacy of traditional Chinese herbal therapy in adult atopic dermatitis.

There has been considerable interest in traditional Chinese herbal therapy (TCHT) as a new treatment for atopic dermatitis. To establish the efficacy and safety of this treatment, a daily decoction of a formula containing ten herbs that has been found to be beneficial in open studies was tested in a double-blind placebo-controlled study. 40 adult patients with longstanding, refractory, widespread, atopic dermatitis were randomised into two groups to receive 2 months' treatment of either the active formulation of herbs (TCHT) or placebo herbs, followed by a crossover to the other treatment after a 4-week washout period. The main outcome measures were extent and severity of erythema and surface damage as judged by standardised body scores. The patients' own assessments of the overall response to treatment were also sought. The geometric mean score for erythema at the end of active treatment was 12.6 (95% confidence interval [CI] 5.9 to 22.0) and at the end of the placebo phase was 113 (65 to 180). The geometric mean score for surface damage was 11.3 (5.8 to 21.8) and 111.0 (68 to 182), respectively. The 95% CI for the mean geometric ratio for the two values with active treatment was 0.04 to 0.22 for erythema (p less than 0.0005) and 0.04 to 0.27 for surface damage (p less than 0.0005). Of the 31 patients who completed the study and expressed a preference, 20 preferred that phase of the trial in which they received TCHT whereas 4 patients preferred placebo (p less than 0.02). There was a subjective improvement in itching (p less than 0.001) and sleep (p less than 0.078) during the TCHT treatment phase. No side-effects were reported by the patients although many commented on the unpalatability of the decoction. TCHT seems to benefit patients with atopic dermatitis. Palatability of the treatment needs to be improved and its safety assured.

Administration, Oral↗
PubMed1992

Fc epsilon R11/CD23 receptor distribution in patch test reactions to aeroallergens in atopic dermatitis.

There is increasing evidence that exposure to organic allergens may induce or exacerbate lesional skin in patients with atopic dermatitis. In this study, patients with atopic dermatitis were patch tested to 11 common organic allergens and to control chambers containing 0.4% phenol and 50% glycerin in 0.9% saline. In biopsies from positive patch test reactions, patch test control skin, lesional eczematous and non-lesional skin from atopic individuals, and normal skin from non-atopic volunteers, the presence and distribution of macrophages (RFD7+), dendritic cells (RFD1+), and Langerhans cells, and the expression of the low-affinity receptor for IgE (CD23) were investigated. In patch test reactions and lesional skin samples, inflammatory infiltrates of diffusely distributed macrophages (RFD7+), dendritic cells (RFD1+), T lymphocytes (RFTmix+), and Langerhans cells (CD1+) were seen, the latter being present in both the epidermis and the dermis. The numbers of Langerhans cells were reduced in the epidermis and increased in the dermis in patch test reactions and lesional skin compared to their controls. Double staining revealed a change in the distribution of CD23 antigen. In patch test control and non-lesional biopsies many macrophages and only a few Langerhans cells within the dermal infiltrates expressed this antigen. In patch test reaction and lesional skin samples, however, the proportion of CD23+ dermal Langerhans cells had increased compared to macrophages. Furthermore, in these latter samples an increased proportion of dermal CD1+ cells expressed the dendritic cell (RFD1+) marker. These results show that following antigen challenge there are marked similarities between the phenotype of the cellular infiltrate in patch test reaction and lesional skin biopsies, and also demonstrate a changing distribution of CD23 on antigen-presenting cells.

Adult↗
PubMed1992

Phenytoin-induced pseudolymphoma. A report of a case and review of the literature.

We report a patient with phenytoin-induced pseudolymphoma mimicking cutaneous T-cell lymphoma (CTCL). Despite withdrawal of phenytoin, there was persistence of the cutaneous eruption and lymphadenopathy. Southern blot analysis of immunoglobulin and T-cell receptor genes was therefore used to assess whether there was a clonal lymphoid expansion. However, no rearrangement of the beta T-cell receptor gene or immunoglobulin heavy-chain gene was detected in tissue DNA from skin and lymph nodes. One year later the patient became asymptomatic, although he is still at risk of developing a true malignant lymphoma in the future, a condition known as pseudo-pseudolymphoma. It is suggested that genotypic studies may help in the initial diagnosis and the subsequent management of such patients.

Adult↗
PubMed1992

Eosinophilic pustular folliculitis in an HIV-positive man: response to cetirizine.

Eosinophilic pustular folliculitis is a rare condition which is being increasingly reported in HIV-positive patients. Many therapies have been used to treat this condition. We report the first successful use of the H1 antihistamine cetirizine to treat the condition and postulate that the specific antieosinophilic action of this drug may explain the beneficial clinical effect seen in our patient.

Cetirizine↗
PubMed1992

Cutaneous granulocytic sarcoma (chloroma) presenting as the first sign of relapse following autologous bone marrow transplantation for acute myeloid leukaemia.

A 25-year-old man suffering from acute myeloid leukaemia developed a solitary lesion on the upper abdominal wall 6 months after receiving an autologous bone marrow transplant. The lesion was a chloroma and proved to be the only evidence of clinical relapse. This is the first reported case of this rare condition occurring following bone marrow transplantation.

Acute Disease↗
PubMed1992

Characterization of histamine receptor sub-types regulating prostacyclin release from human endothelial cells.

1. The histamine receptor sub-types that are involved in the initiation and maintenance of prostacyclin (PGI2) release from human endothelial cells have been investigated. 2. Endothelial cells cultured from umbilical vein (HUVEC) were incubated with either histamine, the selective H1-receptor agonists, 2-methyl histamine (2-MeHA) or thiazolylethylamine (ThEA), the H1-agonist/H3-antagonist, beta-histidine (beta-His), the selective H2-agonist, dimaprit, the H2-agonist/H3-antagonist, impromidine, the selective H3-agonist, (R)alpha-methylhistamine ((R)alpha-MeHA) and the H3-antagonist, thioperamide. 3. The H1-agonists and the H3-agonist (R)alpha-MeHA induced a concentration (100 nM-1 mM) and time-dependent release of PGI2 as determined by radioimmunoassay for 6-keto-PGF1 alpha, but were less potent than histamine itself. The rank order of potency was the same following 30 min and 24 h incubation, i.e. histamine > ThEA > 2-MeHA >> beta-His > (R)alpha-MeHA. 4. Histamine and 2-MeHA (1 microM-1 mM), ThHEA (10 microM-1 mM) and (R)alpha-MeHA (1 mM), but not beta-His, induced a significantly greater increase in PGI2 release after 24 h incubation than after 30 min incubation (P < 0.05). 5. Neither the selective H2-agonist, dimaprit, nor the H2-agonist/H3-antagonist, impromidine alone induced release of PGI2. 6. The H1-antagonist, mepyramine (10 microM), abolished release of PGI2 induced by histamine, the H1-agonists and (R)alpha-MeHA but the H2-antagonist cimetidine (10 microM) and the H2/H3-antagonist, burimamide (10 microM) did not significantly modulate PGI2 release. 7. Although the H3-agonist (R)alphax-MeHA induced release of PGI2, it failed to modulate PGI2 release in the presence of histamine.8. Low concentrations of the H3-antagonist, thioperamide (100 nM) did not modulate histamine release of PGI2 at all but after 24 h incubation, thioperamide (10-4 M) partially reduced PGI2 release in the presence of histamine.9. These results indicate that PGI2 from HUVEC is initiated and maintained via histamine HI-receptor occupancy. There appears to be no involvement of either H2- or H3-receptors in this particular endothelial cell histaminergic response.

Cells, Cultured↗