Cases reported "Pruritus"

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1/59. Bullous pemphigoid developing during systemic therapy with chloroquine.

    Bullous pemphigoid has been reported to be induced or precipitated by systemic therapy with several drugs, including penicillamine, captopril, frusemide and ampicillin. We report an African male patient with sarcoidosis who was prescribed chloroquine for progressive dyspnoea. After 3 months he developed generalized pruritus which evolved into a widespread bullous eruption with acral targetoid lesions resembling erythema multiforme. The histological and immunofluorescence findings were diagnostic of bullous pemphigoid. The atypical clinical features of this case resemble the phenotype that has been noted in previous reports of drug-induced bullous pemphigoid.
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2/59. A case report of olanzapine-induced hypersensitivity syndrome.

    hypersensitivity syndrome is defined as a drug-induced complex of symptoms consisting of fever, rash, and internal organ involvement. The hypersensitivity syndrome is well recognized as being caused by anticonvulsants. Olanzapine is an atypical antipsychotic agent whose side effects include sedation, weight gain, and increased creatinine kinase and transaminase levels. To date, there have been no reports of hypersensitivity syndrome related to this drug. A 34-year-old man developed a severe generalized pruritic skin eruption, fever, eosinophilia, and toxic hepatitis 60 days after ingestion of olanzapine. After termination of olanzapine treatment, the fever resolved, the skin rash was reduced, eosinophil count was reduced to normal, and the transaminase levels were markedly reduced. Clinical features and the results of skin and liver biopsies indicated that the patient developed hypersensitivity syndrome caused by olanzapine.
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3/59. fosinopril-induced prolonged cholestatic jaundice and pruritus: first case report.

    We report a case of fosinopril-induced prolonged cholestatic jaundice and pruritus in a 61-year-old man, with no previous hepatobiliary disease, who presented with asthenia, jaundice and itching 3 weeks after starting fosinopril therapy. Other drugs taken by the patient were not considered probable causes. The diagnostic evaluation showed no biliary obstruction and other possible causes of intra-hepatic cholestasis were excluded. liver biopsy showed cholestasis without bile duct damage. The disease ran a severe course during the 2 months of hospitalization, with prolonged itching for 6 months, eventually controlled with oral naltrexone. jaundice subsided after 4 months, with anicteric cholestasis persisting for more than 18 months. Similar occurrences have been reported with other inhibitors of angiotensin-converting enzyme (mostly captopril), but this is the first case of an important adverse reaction to fosinopril.
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4/59. Red man syndrome during administration of prophylactic antibiotic against infective endocarditis.

    Red man syndrome (RMS) is the occurrence flushing, pruritus, chest pain, muscle spasm or hypotension during vancomycin infusion. It usually happens as a result of rapid infusion of the drug but may also occur after slow administration. The frequency and severity of this phenomenon diminish with repeated administration of vancomycin. A case is presented whereby RMS occurred while prophylactic antibiotic against infective endocarditis was administered.
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5/59. Rapid improvement of icterus and pruritus by the oral administration of colestimide in two cases of drug-induced hepatitis.

    We report two cases of drug-induced hepatitis refractory to therapy of ursodeoxycholic acid and prednisolone, who were relieved of icterus and pruritus immediately by the oral administration of colestimide. Their liver dysfunction was not improved, by withdrawal of causative drugs or by treatment with prednisolone and ursodeoxycholic acid. Colestimide (3.0 g/day), a strong basic anion-exchange resin, was orally taken before breakfast and evening meal, leading to rapid and complete relief of icterus and pruritus. These cases suggested that colestimide would be useful for patients with cholestasis in drug-induced hepatitis, because this agent has few side effects and it is easy to take.
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6/59. Lymphocytic infiltrates as a presenting feature of Sweet's syndrome with myelodysplasia and response to cyclophosphamide.

    Sweet's syndrome has a well-recognized association with malignancies, around half of which have been acute myelogenous leukaemia. There are also numerous reports of Sweet's syndrome in association with myelodysplasia. We report two patients with Sweet's syndrome in whom the classical histological appearances were preceded by dermal lymphocytic infiltrates. A literature search using pubmed indicates that this phenomenon has not been previously reported. The cases demonstrate the chronicity of Sweet's lesions in association with haematological disease and the need for repeat biopsies to make the diagnosis. We also describe successful treatment with cyclophosphamide, which adds to the list of second-line drugs that may be used in Sweet's syndrome.
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7/59. Preliminary observation with dronabinol in patients with intractable pruritus secondary to cholestatic liver disease.

    pruritus due to cholestatic liver disease can be particularly difficult to manage and frequently is intractable to a variety of medical therapies. The aim of our study is to evaluate the efficacy of delta-9-tetrahydrocannabinol (delta-9-THC) for intractable cholestatic related pruritus (ICRP) that has failed conventional (and unconventional) remedies. Three patients were evaluated for plasmapheresis because of ICRP. All 3 patients had previously been extensively treated with standard therapies for ICRP including: diphenhydramine, chlorpheniramine, cholestyramine, rifampicin, phenobarbital, doxepin, naltrexone, UV therapy, and topical lotions. Even multiple courses of plasmapheresis were performed without any benefit for the intractable pruritus. All patients reported significant decreases in their quality of life, including lack of sleep, depression, inability to work, and suicidal ideations. All patients were started on 5 mg of delta-9-THC (Marinol) at bedtime. All 3 patients reported a decrease in pruritus, marked improvement in sleep, and eventually were able to return to work. Resolution of depression occurred in two of three. Side effects related to the drug include one patient experiencing a disturbance in coordination. Marinol dosage was decreased to 2.5 mg in this patient with resolution of symptoms. The duration of antipruritic effect is approximately 4-6 hrs in all three patients suggesting the need for more frequent dosing. Delta-9-tetrahydrocannabinol may be an effective alternative in patients with intractable cholestatic pruritus.
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8/59. Uncommon vancomycin-induced side effects.

    vancomycin has been used with increased frequency during the past 15 years and the most common toxicity with this drug is the red man syndrome . Other adverse effects include neutropenia, fever, phlebitis, nephrotoxicity, ototoxicity, thrombocytopenia, interstitial nephritis, lacrimation, linear iga bullous dermatosis, necrotizing cutaneous vasculitis and toxic epidermal necrolysis. Only two cases of vancomycin-induced stevens-johnson syndrome and one case of pancytopenia have been reported in the medical literature. The treatment for both situations is based on cessation of the vancomycin therapy; in cases of stevens-johnson syndrome, antihistamine and/or steroid agents can be used. This article reports a case of pancytopenia and a case of erythema major associated with neutropenia.
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9/59. Chronic pruritic neutrophilic eccrine hidradenitis in a patient with Behcet's disease.

    Neutrophilic eccrine hidradenitis (NEH) is a rare distinct entity that usually presents as asymptomatic erythematous papules that disappear spontaneously in 1-3 weeks. However, its appearance may be polymorphic, pruritic, recurrent or even chronic as is described in this case. The histological combination of neutrophilic infiltration in and necrosis of the eccrine secretory gland epithelium is highly characteristic for NEH. It typically occurs in patients receiving chemotherapeutic drugs for malignancies, but other associations have also been reported. To our knowledge, we report the first case of NEH in a patient with Behcet's disease (BD). Cutaneous manifestations of BD, an inflammatory systemic disorder of unknown origin, include neutrophilic dermatoses such as Sweet's syndrome and pyoderma gangrenosum, although these are unusual in BD. NEH could be another neutrophilic dermatosis related to BD. This observation suggests that NEH is not strictly related to chemotherapeutic drugs and malignancies. It appears to be a reactive dermatosis associated with other factors as well, including BD. Treatment was successful with dapsone 100 mg daily.
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10/59. The antihistamine fexofenadine does not affect I(Kr) currents in a case report of drug-induced cardiac arrhythmia.

    1. The human HERG gene encodes the cardiac repolarizing K( ) current I(Kr) and is genetically inactivated in inherited long qt syndrome 2 (LQTS2). The antihistamine terfenadine blocks HERG channels, and can cause QT prolongation and torsades de pointes, whereas its carboxylate fexofenadine lacks HERG blocking activity. 2. In the present study the ability of fexofenadine to block the K897T HERG channel variant was investigated. The underlying single nucleotide polymorphism (SNP) A2960C was identified in a patient reported to develop fexofenadine-associated LQTS. 3. K897T HERG channels produced wild-type-like currents in xenopus oocytes. Even at a concentration of 100 micro M, fexofenadine did not inhibit wild-type or K897T HERG channels. Coexpression of wild-type and K897T HERG with the ss-subunit MiRP1, slightly changed current kinetics but did not change sensitivity to terfenadine and fexofenadine. 4. Western blot analysis and immunostaining of transiently transfected COS-7 cells demonstrated that overall expression level, glycosylation pattern and subcellular localization of K897T HERG is indistinguishable from wild-type HERG protein, and not altered in the presence of 1 micro M fexofenadine. 5. We provide the first functional characterization of the K897T HERG variant. We demonstrated that K897T HERG is similar to wild-type HERG, and is insensitive to fexofenadine. Although the polymorphism changes PKA and PKC phosphorylation sites, regulation of K897T HERG by these kinases is not altered. 6. Our results strongly indicate that QT lengthening and cardiac arrhythmia in the reported case of drug-induced LQT are not due to the K897T exchange or to an inhibitory effect of fexofenadine on cardiac I(Kr) currents. British Journal of
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