Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033774 (pruritus)
 14,546 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Scombroid poisoning has become an almost world-wide medical problem. It is probably the most common cause of fish poisoning, although frequently misdiagnosed as "Salmonella infection'. While there remains some question as to the definitive etiology, there is little doubt that the poisoning is caused by the ingestion of certain mackerel-like fishes whose tissues have undergone a number of changes provoked by bacteria, and involving the conversion of histidine to histamine, potentiated by diamines. Improper storage of the fishes, usually at temperatures above 20 degrees C, appears to be the most important predisposing factor. The organisms most commonly involved are Proteus sp., Clostridium sp., Escherichia sp., Salmonella sp. and Shigella sp. Twenty-five cases of scombroid poisoning are presented. The clinical manifestations were very similar in most cases, consisting of: alterations in taste; anxiety; hyperemia, particularly of the face and neck; nausea; pruritus; headache; certain other symptoms and signs. Most patients responded to antihistamitics, and all cases were self-limiting.
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PMID:Scombroid poisoning: mini-review with case histories. 382 4

Lattice corneal dystrophy type II associated with familial amyloid polyneuropathy type IV (Finish type, FAP-IV) has not yet been reported in Japan. We report 7 cases in a Japanese family. The proband, a 64-year-old man, suffering from itching in his limbs, impaired lip movement, and dysarthria, consulted the Department of Neurology, University of Tokyo. Neurological examination revealed bilateral facial, glossopharyngeal, vagal, and hypoglossal nerve palsy, and impaired distal vibratory perception. His vision was 1.2 and he had fine lattice corneal dystrophy in both eyes. Short glassy lines were randomly scattered in the lattice dystrophy. Corneal sensation was normal and there was no evidence of recurrent corneal erosion. Immunohistological and biochemical studies confirmed the diagnosis of FAP-IV. Six siblings were neurologically suspected to be FAP-IV patients with similar lattice corneal dystrophy. The family pedigree suggested an autosomal dominant trait of inheritance.
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PMID:[Lattice corneal dystrophy type II with familial amyloid polyneuropathy type IV]. 828 56

The case of a 36-year-old man with a villous adenoma of the duodenum is presented. His history included jaundice, pruritus, and weight loss. Physical examination was otherwise unremarkable. Laboratory data included anemia, guaiac-positive stool, hyperamylasemia, and abnormal liver function tests. Biliary ductile dilation was seen on ultrasonography; a filling defect in the duodenum was seen on CT scan, and endoscopic biopsy revealed villous adenoma with dysplasia. Pancreatoduodenectomy was performed and recovery was uneventful. Histopathology confirmed moderate dysplasia. Review of the literature reveals this to be a rare lesion (less than 1% of duodenal neoplasms). Local excision has been advocated for small, histologically proven benign, lesions. Where doubt of benignity exists, however, and in the case of "giant" tumors (>3.0 cm greatest dimension), pancreatoduodenectomy is indicated.
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PMID:Pancreatoduodenectomy for giant benign villous adenoma of the ampulla of Vater. 912 23

We report a patient who developed significant liver dysfunction following therapy with terbinafine. At the end of a 3 1/2-wk course of terbinafine, he developed progressive jaundice and pruritus. His serum bilirubin peaked at 30.9 mg/dl 3 wk after discontinuing terbinafine. A liver biopsy revealed mild to moderate mixed cellular infiltrate in the portal tracts, and hepatocellular and canicular cholestasis. His liver tests normalized 100 days after stopping terbinafine.
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PMID:Terbinafine hepatotoxicity: case report and review of the literature. 951 58

We observed a case of linear lichen planus extending from the right cheek to the jaw, which was accompanied by itching and an unusual sensation in the mouth. The eruption was located along the mandible and aligned with the mandibular nerve. The right molars of the patient contained metal compounds and these were considered to be the cause of his disease. Patch testing with various dental metals showed positive reactions to palladium and platinum. A biopsy specimen showed a lichenoid reaction in the lesional tissue, and dermal contact dermatitis was noted at the palladium patch test site. His dentist reported that palladium-silver-gold or nickel-chrome alloys without platinum had been used in the crown and bridge of his molars. After removal of the dental alloys, the skin eruption resolved with some residual hyperpigmentation. In addition, the peculiar mouth sensation disappeared dramatically within 2 months.
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PMID:Linear lichen planus in the region of the mandibular nerve caused by an allergy to palladium in dental metals. 956 24

In the past 2 years, a 4 year-old boy has had an anaphylactic reaction whenever he contacted food prepared with fish. The symptoms included intense itching in the throat and eyes, which progressed to generalized urticaria and facial angioedema. This was accompanied by cough, wheezing and dyspnea. Many fish preparations caused these episodes including several different kinds of fish (cod, tuna, salmon, trout, eel...), fish soup, chopsticks contaminated with fish preparations and canned fish. Elevated levels of total serum IgE (224 IU/ml) and specific IgE for cod (93.1 IU/ml), tuna (> 100 IU/ml), salmon (> 100 IU/ml), trout (64.4 IU/ml), mackerel (41.2 IU/ml) and eel (28.1 IU/ml) were found by the Pharmacia CAP system RAST FEIA in our allergy clinic. A skin prick test for mixed fish extracts (contain flounder, cod and halibut) was positive. A fish challenge test for cod, tuna, salmon, trout and eel all showed anaphylactic reactions. His allergic symptoms stabilized gradually after strictly avoiding ingestion of fish and using drug treatment. He also had a similar anaphylactic reaction to frogs. The best treatment for fish allergy is avoidance. Avoidance of fish may need to include both ingestion and inhalation of cooking vapors.
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PMID:Fish induced anaphylactic reaction: report of one case. 968 28

We report a child with an isolated complex III respiratory chain deficiency and global developmental delay who had severe pruritus with elevated plasma bile acid levels. A liver biopsy showed micronodular cirrhosis, and enzymologic evaluation demonstrated an isolated complex III deficiency in both liver and muscle. His pruritus improved and serum bile acid levels decreased after treatment with menadione and vitamin C.
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PMID:Respiratory chain complex III [correction of complex] in deficiency with pruritus: a novel vitamin responsive clinical feature. 1006 75

A 65-year-old man presented with recurrent generalized pruritus and excoriations of many years' duration. He had been treated with antihistamines, topical corticosteroids, and antibiotics for secondary wound infections, but improvement was only temporary. He had also been hospitalized for leg ulcers complicated by cellulitis. Examination revealed multiple oval and linear red papules and nodules measuring 0.5 to 2 cm in diameter. Some of the lesions were eroded and had a central crater and yellowish crust. The patient also had hypopigmented linear scars localized to the posterior scalp, neck, upper back, chest, abdomen, arms, and legs with sparing of the middle and lower back (figures 1 and 2). An ulcer measuring 1.5 x 2 cm that was surrounded by indurated skin was present on the medial aspect of his right ankle. The ulcer was partially covered by yellow exudate. There was no evidence of cellulitis. Liver enzyme, serum creatinine, and thyrotropin levels, as well as a chest roentgenogram, were normal. Wound cultures for bacteria and fungi were nonsignificant. A punch biopsy from a representative lesion showed an abrupt epidermal defect with sparse superficial lymphocytic infiltrate in the dermis. The patient was admitted to the hospital to isolate him from his home environment. He received a 10-day course of systemic cephalexin, topical clobetasol propionate ointment for the affected skin areas, and oral hydroxyzine for pruritus. Ultraviolet light therapy was instituted once daily and was to continue for 2 months. His lesions had improved moderately by the time he was discharged from the hospital. On follow-up 2 weeks later, his lesions were flat and had resulted in hypopigmented scars. Three months later, however, he had persistent, intense pruritus, and new excoriations had developed on his forearms and back. He improved after receiving treatment with oral doxepin hydrochloride.
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PMID:Generalized pruritus without primary lesions. Differential diagnosis and approach to treatment. 1068 6

The authors report a 5-year-old boy with Hodgkin disease and cholestatic jaundice that predated the start of treatment for his lymphoma. His clinical course was punctuated by relentless progression of jaundice, characterized by obstructive pattern liver function tests, severe pruritus, intermittent fever, and marked hypercholesterolemia with development of palmar xanthomata. The jaundice was found to be attributable to vanishing bile duct syndrome (VBDS). The extent of hepatic dysfunction precluded appropriate treatment of the lymphoma with chemotherapy, and the boy died of liver failure. In the differential diagnosis of jaundice in children with Hodgkin disease, VBDS should be considered.
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PMID:Jaundice caused by the vanishing bile duct syndrome in a child with Hodgkin lymphoma. 1077 30

A 48-year-old Caucasian man recounted the onset of keratotic papules on the trunk at the age of 8 years, with subsequent spread to the forearms, scalp, and forehead. His most severe disease was present on the legs. He complained of pain, itching, and noted exacerbations in the summer and with sweating. The family history was negative. On physical examination, the most striking finding was that of extensive, markedly hyperkeratotic plaques on the lower legs >(Fig. 1). His scalp, forehead, chest, and back exhibited mild involvement, with scattered brown keratotic papules, while his forearms showed mildly hyperkeratotic plaques. Flat-topped brown papules were present on the dorsum of the hands, with a few keratotic papules on the palms, and a few nails with distal notching and red longitudinal streaks. There were no palmar pits or oral mucosal lesions. A shave biopsy was performed of a plaque on the leg, and showed a papillomatous and markedly hyperkeratotic lesion >(Fig. 2). Suprabasal acantholysis in the elongated rete produced characteristic lacunae. The acantholysis was associated with dyskeratosis including corps ronds and grains >(Fig. 3). Together, these features were characteristic of Darier's disease. Treatment years earlier with topical retinoids, topical steroids, topical keratolytics, and multiple oral antimicrobials had been unsuccessful, and isotretinoin had been discontinued due to elevated triglycerides. Treatment was initiated with acitretin and, after 3 months, mild improvement was noted
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PMID:Cornifying Darier's disease. 1112 46


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