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)

4 patients with urticaria pigmentosa were treated with oral disodium cromoglycate (DSCG) for 2 months. During the treatment urine excretion of the main histamine metabolite, 1,4-methylimidazoleacetic acid (MIAA), was determined, and sequential skin biopsies were examined. DSCG was found to have beneficial effect on pruritus and whealing in 3 patients. The one treatment failure was in a patient without pruritus. The skin lesions remained unchanged. DSCG treatment had no effect on MIAA excretion or on the number of mast cells found in the skin biopsies.
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PMID:Urticaria pigmentosa treated with oral disodium cromoglycate. 643 96

Mastocytosis gives rise to clinical symptoms such as flushing, itching and diarrhoea. We report a patient with urticaria pigmentosa without evidence of systemic involvement but with recurrent episodes of diarrhoea. The patient had elevated circulating levels of calcitonin, which might have been a mediator of her diarrhoea. We suggest that serum calcitonin level should be checked in patients with mast cell disease and diarrhoea.
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PMID:Hypercalcitoninaemia in a patient with urticaria pigmentosa. A possible cause of diarrhoea. 673 Oct 41

Fifty-six children and adults with urticaria pigmentosa were examined and their symptoms evaluated. Thirteen patients with cutaneous and systemic symptoms consented to participate in a blind trial and were treated for 1 month with placebo and for another month with oral disodium cromoglycate (DSCG). More than 66% of the patients noted relief of pruritus and gastrointestinal symptoms with DSCG. Reduction of wealing was less prominent. Patients have been continued on 400-800 mg of DSCG daily for up to 15 months with continuous improvement of their symptoms and no adverse effects.
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PMID:Urticaria pigmentosa: clinical picture and response to oral disodium cromoglycate. 679 92

The urinary excretion of histamine and its main metabolite, 1-methyl-4-imidazoleacetic acid (MeImAA), was determined in 30 adult patients with the clinical diagnosis of urticaria pigmentosa (UP). Clinical and laboratory investigations including skin histology, bone marrow examination, and scintigraphy of the skeleton, liver, and spleen revealed systemic manifestations in 14 cases. Among the 16 cases with dermal proliferation of mast cells only 3 cases classified as telangiectasia macularis eruptiva perstans (TMEP). All patients with systemic mastocytosis and UP excreted increased amounts of MeImAA in the urine while normal amounts were found in 2 of the patients with TMEP. A significant correlation existed between MeImAA excretion and the extent of mast cell infiltration in skin and internal organs. No such correlation was found for urinary histamine. Urinary MeImAA but not histamine is therefore considered a useful indicator of systemic involvement by reflecting the size of the mast cell histamine pool. The main symptom of the patients was pruritus, which was moderate to severe in 17 and mild or absent in 13 cases. Gastrointestinal symptoms were present in 14 patients. However, there was no obvious correlation between the excretion of MeImAA and any of the symptoms recorded. Neither was the severity of pruritus correlated to the histamine content of the skin, which was measured in both lesional and unaffected skin in 23 of the patients. Thus, symptoms possibly caused by histamine in mastocytosis patients are not directly related to urinary histamine metabolite excretion or tissue histamine content.
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PMID:Studies on histamine metabolism in mastocytosis. 684 97

Eight patients received PUVA for mastocytosis. Five women had typical adult-onset urticaria pigmentosa, without evidence of systemic disease. Another woman had suspected hepatic involvement while the remaining female had early-onset familial urticaria pigmentosa with morphologically atypical mast cells. The only male patient had cirrhosis with hepatic deposits of mast cells in addition to polycythaemia rubra vera. In all patients, except the man with systemic disease, there was reduced pruritus and wealing and partial to almost complete fading of the macules. The manifestations of urticaria pigmentosa recurred after treatment was discontinued. In both lesional and uninvolved skin there was no significant change in either the mean mast cell counts or mast cell ultrastructure after an average of twenty-seven PUVA exposures. In addition, PUVA did not cause a significant alteration in the histamine content of the skin. The beneficial effect of PUVA in urticaria pigmentosa therefore does not appear to be directly related to a change in mast cell numbers or morphology, or to the histamine concentration in the skin.
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PMID:Photochemotherapy (PUVA) in the treatment of urticaria pigmentosa. 686 May 73

The urinary excretion of histamine and its main metabolite, methylimidazoleacetic acid (MelmAA), was determined in 25 adult patients with the clinical diagnosis of urticaria pigmentosa (UP). Extensive clinical and laboratory investigation, including skin histology, bone marrow examination and scintigraphy of skeleton, liver and spleen, implied systemic manifestations in 16 cases. All patients with systemic mastocytosis (SM) excreted abnormal amounts of MelmAA (greater than 4.1 mg/24 h) and most of them 8.0 mg or more per day, while histamine excretion was increased in only nine (greater than 40 microgram/24 h). Thus, the urine content of MelmAA, but not histamine, could differentiate between UP and SM. Severe pruritus was found concomitant with increased urinary MelmAA and indicated systemic mastocytosis.
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PMID:Increased urinary methylimidazoleacetic acid (MelmAA) as an indicator of systemic mastocytosis. 708 Sep 64

One patient with urticaria pigmentosa was treated with PUVA. This treatment resulted in generalized tanning, decrease of Darier's sign and improvement of pruritus. However, the hyperpigmented macules overlying the mast cell infiltrates showed some persistence. This patient was subjected to biopsy of lesional skin before, during and at the end of oral photochemotherapy. During and after PUVA-therapy, histological examination revealed an increased number of free granules and a progressive decrease in the number of dermal mastocytes. Ultrastructurally necrotic cellular changes in the dermal mastocytes were observed. This suggests that PUVA-therapy may exercise its beneficial effect in urticaria pigmentosa by direct destruction of these cells. In addition, PUVA stimulates mast cell degranulation. Histaminaemia was estimated in this patient, before and after several irradiations. No significant changes were observed. Furthermore, histaminaemia was assayed in 15 patients with various dermatoses undergoing PUVA-therapy. No significant changes were observed. It is concluded that histaminaemia assayed using the fluorometric method of Shore et al. remains unchanged during oral photochemotherapy.
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PMID:[Dermal mastocytes, histaminaemia, and oral photochemotherapy (author's transl)]. 725 77

The effect of PUVA therapy on pruritus, the skin mast cell population and histamine metabolism has been studied in 3 patients with urticaria pigmentosa and manifestations of systemic mastocytosis. Relief of itch was found concomitant with a significant decrease of the major histamine metabolite 1-methyl-4-imidazoleacetic acid in the urine. The decrease occurred during the first 2 mo after starting PUVA therapy and was sustained during an observation period of 3 mo after discontinuation of the treatment. At this time a reduction of the number of mast cells was found in skin biopsy specimens. No evidence of acute histamine release in association with PUVA treatment was obtained. These results suggest that this effective new treatment for urticaria pigmentosa reduces the histamine turnover in the skin by inhibiting mast cell proliferation.
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PMID:Decreased urinary histamine metabolite after successful PUVA treatment of urticaria pigmentosa. 746 62

Long-term treatment with interferon alpha (IFN-alpha) has recently been shown to reduce the bone marrow infiltrate and cutaneous lesions in systemic mast cell disease. We therefore administered this cytokine to six patients with urticaria pigmentosa for up to 12 months, using subcutaneous injections of 5 x 10(6) U, initially five times, and subsequently three times a week. The generally well-tolerated therapy resulted in marked improvement of the cutaneous symptoms, especially in three of the patients who suffered from very severe pruritus. Two of the patients with bone marrow infiltration showed normal findings after treatment. However, in none of the patients was there any change in the skin lesions, or decrease in the degree of cutaneous mast cell infiltration, as evidenced by light and electron microscopic examination. These findings indicate that IFN-alpha is highly effective in the control of symptoms, but otherwise does not influence the cutaneous lesions of urticaria pigmentosa.
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PMID:Treatment of urticaria pigmentosa using interferon alpha. 876 58

We present an unusual case of adult-onset systemic mastocytosis with biopsy-proven skin and bone manifestations with the rare presentation of lumbar fracture and osteopenia. The normal 24-hour urine histamine is surprising in this patient, but it does not rule out mastocytosis. It is a sensitive assay that can give false negative results if stored before the assay is performed. Also histamine and PGD2 metabolites are more sensitive and specific. It is surprising that our patient did not have gastrointestinal symptoms. In one prospective study of 16 patients with systemic mastocytosis in which 75% had bone marrow involvement as the most common extracutaneous site, 80% were found to have gastrointestinal symptomatology, indicating such symptoms to be more common than previously thought. The lack of pruritus is also surprising, as most cutaneous lesions of urticaria pigmentosa are pruritic. Symptoms of systemic mastocytosis, particularly pruritus may respond to antihistamines and the bone disease may not respond to calcium and hormone manipulation. The main role of the latter is to prevent further bone loss. We may consider the use of cromolyn or ketotifen if she does not respond. Close follow-up will be needed to check for progression, however she appears to have a good prognosis with skin involvement and no hematologic abnormalities.
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PMID:Systemic mastocytosis: a diagnostic challenge. 774 67


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