Cases reported "Mastocytosis"

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11/33. Massive histamine release in a patient with systemic mastocytosis.

    We have measured plasma histamine concentrations, systemic vascular resistance, cardiac output and arterial pressure during laparotomy in a patient with systemic mastocytosis. The patient developed vasodilation and hypotension during surgery, associated with a massive increase in plasma histamine concentration.
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12/33. Inhibition of mediator release in systemic mastocytosis is associated with reversal of bone changes.

    A 59-year-old male presented with systemic mastocytosis with extensive skeletal involvement resulting in vertebral compression fractures and bone pain. Histomorphometric analysis of bone revealed increased mast cells, elevated static parameters of bone resorption, and low bone formation. serum calcium, phosphorus, and alkaline phosphatase were normal; however, serum 1,25-dihydroxyvitamin D3 and osteocalcin levels were low. Histamine levels in plasma and urine were elevated. Following therapy with ketotifen, the patient had resolution of bone pain along with decreased flushing and pruritus. Elevated plasma and urine histamine levels normalized, as did 1,25-dihydroxyvitamin D3 and osteocalcin levels. Indices of low bone formation improved on therapy. Eroded surfaces improved but remained elevated. This case is the first demonstration that bone symptoms and histomorphometric change in systemic mastocytosis are reversed with inhibition of mast cell degranulation. The role of mast cells and their products in bone metabolism is poorly understood, but the therapy of bone disease in systemic mastocytosis should include inhibition of the release of mast cell products along with the use of histamine antagonist.
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13/33. The effect of disodium cromoglycate and ketotifen on the excretion of histamine and N tau-methylimidazole acetic acid in urine of patients with mastocytosis.

    Treatment of four mastocytosis patients with the mast cell stabilising drugs, disodium cromoglycate and ketotifen failed to alter significantly the urinary excretion levels of histamine or N tau-methylimidazole acetic acid. No clinical improvement was noted in any subject after treatment by either drug.
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14/33. osteoporosis associated with mastocytosis confined to bone: report of two cases.

    Two women, ages 53 and 46, presented with multiple spontaneous vertebral fractures. serum calcium, 25OHD, 1,25-(OH)2D, PTH, and 24-h urinary calcium were all normal. Bone mineral analysis (BMA) was performed at the junction of the distal third of the radius by single photon absorptiometry. BMA on Patient 1 was 0.68 g/cm2 and on Patient 2 was 0.58 g/cm2, with the normal being 0.70 g/cm2 and 0.77 g/cm2, respectively. In addition to vertebral fractures, x rays of Patient 2 revealed lytic lesions of the tibia and ulna. Bone biopsies revealed osteopenia associated with generalized eosinophilic fibromastocytosis and increased resorption without evidence of increased numbers of osteoclasts. There was no evidence of extraskeletal mast cell involvement. Our observations contribute to the increasing evidence that mast cells play a direct role in the etiology of osteoporosis in certain patients. Possible pathophysiologic mechanisms include mast cell release of heparin, histamine, prostaglandin d2 or other osteolytic substances.
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15/33. mastocytosis: one year's experience.

    The diagnosis of systemic mastocytosis without urticaria pigmentosa has been made with increasing frequency since modern methods of histamine assay have been used clinically. We examined the incidence of urticaria-angioedema and mastocytosis over a recent 12-month period. Of 490 new patients we saw, 52 had urticaria-angioedema, and ten had evidence of excess histamine /- PGD2, with at least ten mast cells per high-power field on skin biopsy. The average age was approximately 35 years; the male:female ratio was 1:4 for urticaria-angioedema and 1:2 for mastocytosis. Symptoms of mastocytosis included flushing, abdominal cramping/diarrhea, syncope, urticaria-angioedema, pruritus, and headache. Symptoms have typically been prevented by a combination of H1 and H2 antagonists, with addition of a cyclo-oxygenase inhibitor in syncopal cases. Acute hypotension has responded to epinephrine.
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16/33. Systemic mastocytosis: management of an unusual case with histamine (H1 and H2) antagonists and cyclooxygenase inhibition.

    A patient with urticaria pigmentosa and systemic mastocytosis developed hypotension following indomethacin administration. He then developed further episodes not related to indomethacin. Based upon the experience of others with the management of patients with systemic mastocytosis who showed exceptional reaction to cyclooxygenase inhibition, it was decided to treat him with H1 and H2 blockade followed by aspirin, another cyclooxygenase inhibitor. The procedure was carried out under careful observation with cardiac monitoring. After 160 mg of aspirin, he developed hypotension, tachycardia, and flushing accompanied by difficulty of breathing and headache. A vasoconstrictor drug (levarterenol) was administered. The patient's symptoms subsided, and after 1 hour aspirin was again administered, this time with no side effects. The dosage was increased to 975 mg every 6 hours, and he has had no further hypotensive episodes on this regime for 2 years. Cyclooxygenase inhibition, combined with H1 and H2 blockade, is an effective treatment for this condition, but for these patients initiation of aspirin therapy should be carried out with extreme care.
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17/33. Systemic mastocytosis, an unusual cause of osteoporosis.

    A 45-year-old patient is described presenting with severe axial osteoporosis. The presence of maculopapular skin lesions and the combination of osteolytic and osteoblastic bone lesions led to the tentative diagnosis of systemic mastocytosis. This diagnosis was confirmed by measurement of urinary histamine metabolites and by bone biopsy showing increased numbers of mast cells and fibroblast-like cells. The importance of these diagnostic procedures in this rare cause of osteoporosis is discussed.
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18/33. Painful orbital inflammatory lesions and mastocytosis.

    A 15-year-old female patient developed painful nodules in an anophthalmic socket that were exacerbated by treatment with steroids and narcotics. Although orbit biopsy showed chronic inflammation, the diagnosis of mastocytosis was confirmed with skin biopsy and urinary levels of histamine. The patient responded to excision of nodules and treatment for mastocytosis. Painful orbital lesions associated with mastocytosis have not been reported previously.
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19/33. Histamine levels and cardiovascular responses during splenectomy and splenorenal shunt formation in a patient with systemic mastocytosis.

    Systemic mastocytosis is a rare disorder characterised by the infiltration of many tissues by abnormal numbers of mast cells. life-threatening episodes of bronchospasm and hypotension are common in response to a variety of triggers which cause mast cell degranulation. We present the case history of a patient with severe mast cell disease who successfully underwent splenectomy and portocaval anastomosis. Peri-operative therapy was directed towards mast cell stabilisation, and histamine-releasing drugs were avoided. Cardiovascular data, together with blood histamine levels and thrombin times, indicated that mast cell degranulation did not occur. A review of the current literature concerning mast cell disease as it relates to anaesthesia is presented and suggestions for the safe management of such cases are given.
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20/33. mastocytosis with malabsorption, myelofibrosis, and massive ascites.

    mastocytosis is an unusual disorder of unknown etiology characterized by an abnormal proliferation of tissue mast cells. We present a case of a young woman with systemic mastocytosis with malabsorption secondary to small bowel invasion by mast cells, myelofibrosis, and massive exudative ascites secondary to mass cell invasion of the intraabdominal lymph nodes. The patient responded favorably to a combined therapy with histamine H1 and H2 receptor antagonists and corticosteroids. We include a review of the literature.
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