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Query: UMLS:C0018681 (headache)
56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nasal cytograms, as an aid to diagnosis of pathological conditions of the nose and paranasal sinuses, have not been adopted by the majority of otolaryngologists. This situation exists because of technical problems with the preparation of a slide and the difficulty in finding someone competent and interested in its interpretation. The work of the Bryans has provided an analysis of the cytology of nasal secretions. Adopting their methods, we have been using the nasal cytogram in clinical practice and find it helpful in determining appropriate therapy for problems encountered in otolaryngological practice. In the authors' experience, profuse nasal mastocytosis is a consistent finding in cytograms from patients having varied symptoms that are associated with hypersensitivities that are not accompanied by positive objective findings. This is especially true in patients with constantly recurring headaches and those with a chronically obstructed nose. Once many mast cells are found by the cytogram, attempts are made to relieve these patients by selective dietary restrictions. These attempts are often successful. The nasal cytogram is also used to help explain periodic symptom flares in the long term allergy patient undergoing immunotherapy for inhalants, by identifying superimposed viral and bacterial infections.
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PMID:Cytology of nasal secretions: further diagnostic help. 5 60

A 25-year-old woman with documented mastocytosis developed hypoxemia with pruritus, diarrhea, headache, and hypotension on two separate occasions. The hypoxemia appeared to be related to a massive release of histamine. Resolution of the patient's symptoms was accompanied by the return of her arterial oxygen tension to normal levels.
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PMID:Respiratory distress and hypoxemia in systemic mastocytosis. 42 34

The case is described of a 42-year-old man with urticaria pigmentosa and documented systemic mastocytosis who had 2 episodes of loss of consciousness, headache, nasal stuffiness and faecal incontinence, following a swim in a river. Under controlled conditions the patient was subjected to immersion of the right hand to icewater for a period of 2 minutes, followed by 2 minutes of strenuous exercise. Similar symptoms involving change in conscious state were evoked with accompanying rises in plasma histamine levels. These findings suggest that histamine is at least one of the major mediators of the change in conscious state that is reported rarely in these patients and draws attention to the neurological facets of this rate disorder.
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PMID:Urticaria pigmentosa---change in conscious state associated with rise in plasma histamine levels. 55 Sep 41

A 48 year old male patient presented with maculopapular rash, pruritus, peptic ulcer disease and attacks of headache and vertigo. Rubbing of the cutaneous lesions led to urticarial whealing which is indicative of abnormal mast cell proliferation in the cutis. Histologic evidence of abnormal mast cell proliferation in biopsy specimens of skin and bone marrow led to the diagnosis of systemic mastocytosis. Treatment with H1 and H2 receptor antagonists was started.
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PMID:[Maculopapular rash, pruritus, upper abdominal pain, attacks of dizziness]. 174 78

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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PMID:Mastocytosis: one year's experience. 287 59

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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PMID:Systemic mastocytosis: management of an unusual case with histamine (H1 and H2) antagonists and cyclooxygenase inhibition. 288 Jun 86

Mastocytosis is a disease characterized by an increase in the number of tissue mast cells and a concomitant increase in mast cell-derived mediators. To demonstrate the spectrum of skin disease in mastocytosis in the pediatric population, five children with mastocytosis and complaints of urticaria (4/5), bullae/vesicles (3/5), abdominal pain (3/5), flushing (2/5), headache (1/5), and bone pain (1/5) are reviewed. Confirmation of the diagnosis of cutaneous mastocytosis was obtained by histologic examination of a biopsy of lesional skin; however, mast cell numbers in lesional skin did not correlate with plasma histamine levels or the extent of cutaneous involvement. Mastocytosis is a diagnosis that must be recognized in the differential diagnosis of pediatric urticarial diseases.
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PMID:Mastocytosis in infants and children: recognition of patterns of skin disease. 292 86

A patient reported that she developed various shock-like symptoms upon intake of alcohol, acetylsalicylic acid, or after injection of contrast medium. After provocation with alcohol applied orally and following endoscopy flush, tachycardia, and a severe headache followed immediately by painful diarrhea were observed. According to our diagnosis the patient had urticaria pigmentosa involving the bone marrow and an enlarged liver and spleen, respectively. The suspected intestinal mastocytosis was confirmed histologically by a biopsy from the jejunum. It was concluded that the symptoms were the result of a direct activation of the accumulated intestinal mast cells. The differential diagnosis of mastocytosis as opposed to allergic gastroenteritis, sprue, and carcinoid is discussed.
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PMID:[Mastocytosis simulating a food allergy]. 686 85

Mastocytosis is a rare disease of mast-cell proliferation with involvement of the reticuloendothelial systems including skin, bone, gastrointestinal tract, liver, lungs, spleen, and lymph nodes. Systemic mastocytosis is characterized by a combination of symptoms that relate to the mast cells' release of vasoactive substances, such as histamine. These symptoms include urticaria pigmentosa, flushing, syncope with hypotension, headaches, nausea, vomiting, diarrhea, and occasional bronchospasm. The diagnosis of mastocytosis is typically based on the presence of the characteristic extraosseus manifestations. A well recognized roentgenographic feature seen in 70-75% of patients with mastocytosis is diffuse osteolysis and osteosclerosis, affecting primarily the axial skeleton and the ends of the long bones. Rarely, the bony involvement consists of generalized osteoporosis, which may lead to pathologic fracture, or solitary lesions (mastocytomas) which may cause symptoms of localized pain. Four patients with previously diagnosed systemic mastocytosis had unusual skeletal lesions. Clinical and laboratory evaluation of these patients eventually led to the correct diagnosis of systemic mastocytosis. We report these four cases to emphasize the need for thorough evaluation of unusual musculoskeletal findings in association with extraosseus symptoms that are characteristic of mastocytosis. Knowledge of a wide differential diagnosis of unusual skeletal lesions should include systemic mastosytosis.
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PMID:Mastocytosis presenting as a skeletal disorder. 912 84

Mast cells (MC) are multipotent hemopoietic effector cells producing diverse mediators like histamine, heparin, or tissue type plasminogen activator. We report a 75-year-old male patient with myelodysplastic syndrome (MDS) of recent onset (3 months' history) associated with a massive leukemic spread of immature tryptase+ MC (tentative term: myelomastocytic leukemia). The patient presented with pancytopenia, bleeding, hypofibrinogenemia, and an increased cellular tryptase level. Moreover, an excessive elevation of plasmin-antiplasmin complexes (9,200 ng/ml; normal range: 10-150), an elevated D-dimer, and an increase in thrombin-antithrombin III complexes were found. The identity of the circulating MC was confirmed by immunophenotyping (CD117/c-kit+, CD123/IL-3R alpha-, CD11b/C3biR-), biochemical analysis (cellular ratio [ng:ng] of tryptase to histamine >1), and electron microscopy. Bone marrow (bm) examination showed trilineage dysplasia (17% blasts), 30% diffusely scattered MC, and a complex karyotype. No dense, compact MC infiltrates (mastocytosis) were detectable in bm sections. Despite hyperfibrinolysis and mediator syndrome (flushing, headache), the patient received remission induction polychemotherapy (DAV) followed by two cycles of consolidation with intermediate dose ARA-C (2 x 1 g/m2/day on days 1, 3, and 5). He entered complete remission after the first chemotherapy cycle without evidence of recurring MDS. Moreover, in response to chemotherapy, the hyperfibrinolysis and mediator syndrome resolved, and the circulating c-kit+ MC disappeared. We suggest consideration of polychemotherapy as a therapeutic option in patients with high-risk MDS of recent onset, even in the case of MC lineage involvement.
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PMID:Hyperfibrinolysis in a case of myelodysplastic syndrome with leukemic spread of mast cells. 1033 14


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