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PubMed1951

The topical and systemic use of cortisone in dermatology.

Part I of this report deals with the topical use of cortisone in a variety of skin diseases. Fifteen patients with chronic discoid lupus erythematosus, four patients with necrobiosis lipoidica diabeticorum, four with psoriasis, one with lichen planus and one with granuloma annulare were treated with cortisone ointment. All the patients with chronic discoid lupus erythematosus had some degree of improvement. In two patients with chronic lupus erythematosus, complete clearing of the eruption occurred. In four patients with necrobiosis lipoidica diabeticorum remarkable involution resulted. Patients with psoriasis, lichen planus and granuloma annulare were not benefited. Part II deals with the systemic use of cortisone. Eight patients with severe serum sickness-like penicillin reaction responded dramatically to parenterally administered cortisone. In two cases of pemphigus vulgaris and one case of Sulzberger-Garbe disease, the disease was kept in remission with cortisone administered intramuscularly as well as orally. Partial improvement resulted in a case of localized myxedema associated with malignant exophthalmus. Two patients with exfoliative dermatitis due to therapy with heavy metals responded dramatically to cortisone. No beneficial effects were noted in patients with chronic urticaria and atopic dermatitis.The systemic use of ACTH and cortisone in dermatology at present should be confined to patients with known fatal or hopelessly incapacitating diseases and to patients with extreme hypersensitivity reactions which may be protracted or life-endangering, and which can be controlled or cured with a relatively small total dosage of the agents in a short time.

Administration, Topical↗
PubMed1992

Chloroquine therapy in psoriatic arthritis.

Our aim was to examine the efficacy of chloroquine in psoriatic arthritis (PsA) and to assess whether chloroquine therapy exacerbated psoriasis. Thirty-two patients had been given chloroquine therapy while attending the University of Toronto Psoriatic Arthritis Clinic. Twenty-four patients continued therapy for at least 6 months, and 18, or 75%, demonstrated > 30% reduction in the actively inflamed joint count. Moreover, there was a significant decrease in the number of actively inflamed joints. A control group, consisting of 24 patients taking no remittive agents, seen during the same period of time, was identified. Only 14, or 58%, of these patients had a > 30% reduction in inflamed joint count over a 6-month period. This pattern was not significantly different (p = 0.19) from the chloroquine treated group. Of the 32 patients who had been given chloroquine, a total of 6 had an exacerbation of psoriasis, only 1 discontinued therapy. There was no case of exfoliative dermatitis. Six of the 24 control patients had an exacerbation of psoriasis. Our experience suggests that chloroquine may be an effective treatment in PsA, and that it does not exacerbate psoriasis. A prospective, randomized, double blind, controlled trial of antimalarial therapy in PsA is warranted.

Administration, Oral↗
PubMed2004

[Interpretation of laboratory data during cryptic leishmaniasis in dog].

Leishmaniasis is a zoonosis caused by an intracellular parasite belonging to the genus Leishmania. In Europe, Africa, South America and China, visceral leishmaniasis is caused by L. infantum. The vectors of leishmaniasis are phlebotomine sandflies belonging to the genera Phlebotomus. According to the World Health Organization there are 2 million new cases each year and 1/10 of the world's population is at risk of infection. Leishmaniasis is considered a zoonosis and human are generally accidental hosts. The animal reservoir includes rodents, dog and other mammals. Several studies have indicate that half of the dogs with antileishmanial antibodies have no signs of disease although, animal with subclinical infections are potentially infectious to sand flies. The factors determining susceptibility or resistence to visceral leishmaniasis remain unclear, but the genetics of the host may play a major role. Clinical signs are: intermittent fever, hepatosplenomegaly, skin lesions and ulcers, alopecia, onychogryphosis, anemia, thrombocytopenia and hypergammaglobulinemia. In mice, the outcome of infection depends on the polarized activation of one of two subsets of CD4+ T cells, Th1 or Th2, the subdivision into Th1 and Th2 cells is based on the pattern of cytokines that they produce. Th1 cells produce gamma interferon (IFN-gamma) and interleukin -2 (IL-2), whereas Th2 cells produce IL-4, IL-5, and IL-10. An important difference between susceptible and resistant mice is that the resistant mice are able to switch to a Th1 profile and control the disease. An important factor in the "decision" to form a Th1 or Th2 phenotype is the early cytokine environment, and IL-12 is one of the cytokines that contributes significantly to the establishment of the Th1 phenotype. Canine leishmaniosis is endemic in the Mediterranean basin and, in most cases is caused by the parasite Leishmania infantum. The main clinical findings are skin lesions, local or generalized lymphoadenopathy, loss of body weight, glomerulopathy, ocular lesions, epistaxis and lameness. Non pruritic skin lesions are the usual manifestation and several forms have been described, such as exfoliative dermatitis and alopecia, and ulcerative, nodular and pustular dermatitis. Seroepidemiological studies of canine leishmaniasis have revealed a large number of asymptomatic seropositive animals. Moreover in areas where leishmaniasis is highly endemic, high proportion of apparently healthy animals show low levels of anti-Leishmania antibodies. Others have regressive forms of the desease, and their antibody levels will decrease in the following months or years; still others maintain low levels of antibodies without developing the desease for many years. However, the total number of infected animals is unknown. Canine leishmaniasis is a major zoonosic parasitic disease, enzootic in the Mediterranean area, caused by the intracellular protozoan Leishmania infantum. The dog is the main reservoir host of the parasite. However, most infected dogs do not present any clinical signs, and there is evidence that Leishmania infection prevalence rates in areas of endemicity are higher than those ascertained by serological studies. Visceral leishmaniasis is becoming a real problem of public health because it is an opportunistic infection in immunocompromised patients and in human immunodeficiency virus-positive subjects. The detection of the extent of the infection, particularly among asymptomatic dogs, is of great importance for the control of leishmaniasis. PCR has been applied successfully in recent years to detect Leishmania spp. even in the cases with any of the clinical manifestation of leishmaniasis. Very recently, real-time PCR for Leishmania has been applied to evaluate the parasitic load of dog tissues both at the time of the diagnosis and during follow-up of the therapy and to measure cytokine mRNA levels in different clinical samples of infected and uninfected dogs.

Animals↗
PubMed1992

[A case of pulmonary tuberculosis associated with severe skin eruption, prominent eosinophilia, and liver dysfunction induced by streptomycin].

A 42-year-old woman was admitted because of cough, sputum, and fever. A chest roentgenogram revealed a nodular density in the left upper lung field with satellite lesions compatible with tuberculoma. Mycobacterium tuberculosis was detected from sputum. Five weeks after starting the treatment with 0.4 g/day of isoniazid, 0.45 g/day of rifampicin, and 0.75 g/day of streptomycin, she showed itching erythema in the trunk. The white blood cell count was 4,500/mm3 with 14% eosinophils, and serum transaminases were slightly increased (GOT 101 U/L, GPT 74 U/L). Although isoniazid and rifampicin were stopped, the erythema with exfoliation spread to her extremities, suggesting exfoliative dermatitis. The white blood cell count reached 15,990/mm3 with 68% eosinophils (10,810/mm3). Stimulation indices measured with the lymphocyte stimulation test (LST) were 109% with rifampicin, 140% with isoniazid, and 275% with streptomycin, suggesting streptomycin-induced allergy. After cessation of streptomycin, the symptoms gradually improved. After the reaction had subsided, the treatment with isoniazid, rifampicin, and ethambutol was resumed, but she showed no further adverse reactions. LST seems to be very useful to identify the drug or drugs responsible for the reactions occurred during the treatment by antituberculosis drugs.

Adult↗
PubMedDate not supplied

DRESS syndrome associated with carbamazepine and phenytoin.

Drug Rash with Eosinophilia and Systemic Symptoms (DRESS) syndrome reflects a serious hypersensitivity reaction to drugs. Its clinical manifestations include diffuse maculopapular rash, exfoliative dermatitis, facial edema, lymphadenopathy, fever, multivisceral involvement and it is associated with a high mortality rate. We report a 62-year-old patient suffering from epilepsia presenting erythroderma following carbamazepine intake. Blood tests revealed eosinophilia, leukocytosis, elevated liver enzymes and high levels of Eosinophil Cationic Protein (ECP). We applied systemic steroids and anticonvulsant therapy was switched to phenytoin, which had been taken previously without adverse reactions. The skin eruptions persisted and the patient developed fever. Anticonvulsant medication was discontinued and skin eruptions finally resolved under steroid application. This case report demonstrates that cross reactivity between carbamazepine and phenytoin may not only lead to the development but also to the worsening of DRESS syndrome. ECP blood levels may represent a sufficient parameter to monitor the development of DRESS syndrome.

Anticonvulsants↗
PubMed2004

[Emerging parasitic zoonoses: leishmaniosis].

Leishmanioses are a group of parasitic diseases that affect man and other mammals. They are caused by different species of trypanosomatids of the genus Leishmania Ross, 1903 and have tegumentary and/or visceral manifestations. The distribution of this re-emerging disease, which is found throughout the world (except in Antarctica), is influenced by various factors linked to both human activity and climatic change. The heteroecious life cycle of the Leishmania includes an invertebrate host (sandflies of the Phlebotomidae family). The dog is the main reservoir for many of the Leishmania species, simultaneously presenting both cutaneous and visceral clinical signs. The most frequent signs are skin abnormalities (dry exfoliative dermatitis, ulcers, periorbital alopecia and onychogryphosis), but ocular signs (keratoconjunctivitis and uveitis) and lymphadenomegaly are also common. Clinical diagnosis is difficult because of the great variety of symptoms and should, therefore, be confirmed by parasitological, serological and molecular methods. Several strategies are used to control the disease, including the treatment of infected animals. However, treatment failure is common and there is a risk that drug resistance will develop.

Animals↗
PubMed2005

Allopurinol-induced DRESS syndrome.

Hyperuricemia is present in approximately 5% of the population, the vast majority of whom are asymptomatic and at no clinical risk. Complications, including renal calculi, uric acid nephropathy and gout, occur in a small proportion of patients. Allopurinol, an analog of hypoxanthine, has been widely used in clinical practice for over 30 years for the treatment of hyperuricemia and gout. Two percent of patients taking this medication develop a mild exanthema. A syndrome characterized by exfoliative dermatitis, hepatitis, interstitial nephritis and eosinophilia has been described previously. Termed allopurinol hypersensitivity syndrome, its etiology is related to the accumulation of one of the allopurinol metabolites, oxypurinol; clearance of oxypurinol is decreased in the setting of renal insufficiency and the use of thiazide diuretics. The term DRESS syndrome (Drug Rash with Eosinophilia and Systemic Symptoms) was recently introduced to describe a disorder associated with various drugs or viral infections and characterized by similar features. The pathophysiology of allopurinol-induced hypersensitivity, clinical presentation and treatment are reviewed.

Allopurinol↗
PubMed2006

Probable cutaneous allergic response to subcutaneous heparin--a case report.

Heparin is a heterogeneous mixture of sulfated mucopolysaccharides, commonly used injectable anticoagulant. It is known to cause cutaneous adverse reactions like eczema, erythematous plaques, exfoliative dermatitis and tissue necrosis. We report a case of probable cutaneous allergic response caused by injection of heparin with an established causality and severity. The reaction developed after stopping the drug therapy and after the patient had already been discharged. Since heparin is a widely used drug and this reaction can manifest even after the drug therapy has ceased, thorough counseling of the patient is mandatory.

Adult↗
PubMed1991

[Pharmacologic effects of biotin on epidermal cells].

Biotin deficiency in animals causes pathological changes of the skin and its appendages including, for example, exfoliative dermatitis, depigmentation, and alopecia. The hooves of biotin-deficient swine are weak, brittle, and often necrotic. These changes disappear after dietary biotin supplementation. Biotin supplementation also noticeably improves the hoof quality of horses, cattle and swine having no apparent biotin deficiency. In order to elucidate the molecular basis of these effects, the influence of biotin on cytokeratin expression in a keratinocyte cell line (Ha-CaT) was investigated using electrophoretic and immunological techniques. Pharmacological biotin concentrations of 1 microM, and 100 microM in the culture medium caused a specific increase in cytokeratins, which are normally induced upon terminal differentiation of epidermal cells in vivo. The expression of cytokeratins occurring in stratified epithelia independent of differentiation were not affected. These findings show that biotin directly stimulates the differentiation of epidermal cells. Such a molecular mechanism revealed in cell culture could provide an explanation for the therapeutic effects of pharmacological doses of biotin on hoof quality in farm animals.

Animals↗
PubMed1991

Iron deficiency: structural and microchemical changes in hair, nails, and skin.

Deficiency of nutritional iron represents a public health problem recognized throughout much of the world. The overall prevalence rate of patients with iron deficiency (ID) who need supplementary iron therapy ranges markedly from less than 10% to as high as 70% among various ethnic and socioeconomic groups. Dermatologically, the iron-deficit state can be a secondary condition or trigger a wide range of mucocutaneous alterations. Early appreciation of adverse cutaneous manifestations of ID seems to have commensurate significance not only in predicting the presence of undiagnosed ID, but also for providing specified avenues for rational therapeutic approaches to patients with ID. Dermatopathic anemia has attracted the attention of clinicians because ID was found to be a metabolic consequence of skin diseases such as erythroderma, exfoliative dermatitis, psoriasis, eczema, and many others. Previous studies had suggested that iron may be lost in accelerated turnover of the keratinocyte from scaling; currently, malabsorption of iron is accepted implication accounting for dermatopathic anemia. However, mucocutaneous affections adversely manifested by ID have not been extensively reviewed and published in the current dermatologic literature because of the potentially benign course of the adverse conditions and the limited degree of clinical expression. Therefore, changes in hair, nails, mucosa and tongue, pruritus, chronically sustained inflammation, dermatitis herpetiformis, and photodermatitis are among the adverse cutaneous sequelae whose relation to ID are highlighted and discussed in the present review. Because of their clinical and diagnostic importance, other extracutaneous physical signs of ID, such as blue sclerae and pica, are also included in this review.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

[A case of rheumatoid arthritis complicated with auranofin-induced acute interstitial pneumonitis].

A case of auranofin(AF)-induced acute interstitial pneumonitis in a patient with rheumatoid arthritis (RA) is reported and possible mechanism of the incidence is discussed. A 57 year-old woman with a history of RA starting in early April 1989, had been prescribed AF for seven days prior to her referral to this hospital. Because of the severity of her polyarthritis, AF was discontinued; therapy with gold sodium thiomalate (GST) instead was started on 23 June 1989. The patient responded quite favorably. At a total cumulative dose of 160mg of GST, however, she developed generalized exfoliative dermatitis and the drug was discontinued. On 29 Sept. 1989 when her skin lesions cleared up completely, she was put on AF again. Six days after resumption of AF therapy, she developed fever. Nonproductive cough and dyspnea on exertion was observed within the following three days. The chest X-ray film revealed diffuse reticular-linear infiltrates more prominently in both upper lobes. Arterial blood gas studies showed hypoxemia and a restrictive ventilatory defect was demonstrated by pulmonary function studies. AF was stopped. High dose pulse iv corticosteroid(CS) therapy combined with oral CS was instituted. Immediate improvement of both subjective and objective findings was observed. By using the patient's peripheral blood lymphocytes, delayed lymphocyte stimulation test(DLST) against the probable causative agents was performed before the bolus CS therapy. Stimulation Index(shown in percentage) was markedly elevated in AF(724%) as compared with GST(163%). The fiberoptic bronchoscopy with bronchoalveolar lavage(BAL) was performed. Analysis of BAL fluid revealed increased cellularity (9 x 10(5)/ml) with marked lymphocytosis of 79%.(ABSTRACT TRUNCATED AT 250 WORDS)

Arthritis, Rheumatoid↗
PubMed1988

Eruptive seborrheic keratoses associated with erythrodermic pityriasis rubra pilaris. Possible role of retinoid therapy.

A 74-year-old female patient with an erythrodermic pityriasis rubra pilaris developed multiple seborrheic keratoses during the early stage of the skin disorder. There was no evidence of an underlying internal malignancy. Initially, the patient was treated with etretinate. The seborrheic keratoses all faded away during the next 3-4 months without any specific treatment. The possible role of retinoid treatment in the resolution of seborrheic keratoses is discussed.

Aged↗