hypergammaglobulinemia/homa

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Hyperimmunoglobulinemia D and periodic fever syndrome (HIDS) in a child with normal serum IgD, but increased serum IgA concentration.

Watumiaji waliosajiliwa tu ndio wanaweza kutafsiri nakala

Ingia / Ingia

This report describes a boy with hyperimmunoglobulinemia D and periodic fever syndrome (HIDS). The serum IgD level was normal, but the serum IgA concentration was markedly elevated. In addition, he had a history of orchitis on two occasions, a previously unreported manifestation of HIDS. This report

Pseudodominant inheritance of the hyperimmunoglobulinemia D with periodic fever syndrome in a mother and her two monozygotic twins.

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Ingia / Ingia

Hyperimmunoglobulinemia D with periodic fever syndrome (HIDS) is a recessively inherited recurrent fever syndrome. We describe a family of 2 monozygotic twins and their mother with characteristic symptoms of HIDS, but normal levels of IgD and IgA, and with a dominant inheritance pattern. Mevalonate

Location of the gene causing hyperimmunoglobulinemia D and periodic fever syndrome differs from that for familial Mediterranean fever. International Hyper-IgD Study Group.

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Ingia / Ingia

The hyperimmunoglobulinemia D and periodic fever (hyper-IgD) syndrome is typified by recurrent febrile attacks with abdominal distress, joint involvement (arthralgias/arthritis), headache, skin lesions, and an elevated serum IgD level (> 100 U/ml). This familial disorder has been diagnosed in 56

Henoch-Schönlein purpura in a child with hyperimmunoglobulinemia D and periodic fever syndrome.

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Ingia / Ingia

This report describes a 3-year-old girl with a long history of periodic fever who presented with Henoch-Schönlein purpura. She was diagnosed with hyperimmunoglobulinemia D and periodic fever syndrome by means of mutation analysis of the mevalonate kinase gene. The serum IgA concentration was

Elevated serum level and altered glycosylation of alpha 1-acid glycoprotein in hyperimmunoglobulinemia D and periodic fever syndrome: evidence for persistent inflammation.

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Ingia / Ingia

Crossed affinoimmunoelectrophoresis using concanavalin A and Aleuria aurantia lectin as diantennary glycan- and fucose-specific affinocomponents, respectively, was applied to study changes in the concentration and glycosylation of the acute phase protein alpha 1-acid glycoprotein (AGP) in sera

Novel mutations of MVK gene in Japanese family members affected with hyperimmunoglobulinemia D and periodic fever syndrome.

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Ingia / Ingia

Hyperimmunoglobulinemia D with periodic fever syndrome (HIDS) is a recessively inherited recurrent fever syndrome. We describe a family of eldest son and monozygotic twin younger sisters with characteristic syndrome of HIDS, but normal level of IgD. Mevalonate kinase (MK) activity was deficient in

[Hyperimmunoglobulinemia D and periodic fever syndrome. A phenotypical analysis of a Spanish family].

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Ingia / Ingia

BACKGROUND Hyperimmunoglobulinemia D and periodic fever syndrome (HIDS) is a disorder diagnosed with low frequency, that produces a very prolonged and recurrent fever with other symptoms and analytical markers of inflammation. Its origin seems to be hereditary with a recessive autosomic pattern, but

Periodic fever in children with hyperimmunoglobulinemia D and mevalonate kinase mutations.

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Ingia / Ingia

Hyperimmunoglobulinemia D syndrome (HIDS) is one cause of periodic fevers in children. HIDS is associated with mutations in the mevalonate kinases gene on chromosome 12. Most cases of HIDS have been reported from the Netherlands and surrounding European countries. It is likely that HIDS is

Interleukin 6-producing gastric carcinoma with fever, hypergammaglobulinemia, and plasmacytosis in bone marrow.

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Ingia / Ingia

A 42-year-old man with a remittent fever was found to have both para-aortic and hepatic tumors with generalized lymphadenopathy. The pathological findings from biopsy specimens from the para-aortic lymph node and hepatic tumor by laparotomy and from left supraclavicular lymphadenectomy showed

Favorable preliminary experience with etanercept in two patients with the hyperimmunoglobulinemia D and periodic fever syndrome.

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Ingia / Ingia

OBJECTIVE The hyperimmunoglobulinemia D and periodic fever syndrome (HIDS; MIM 260920) is caused by recessive mutations in the mevalonate kinase gene (MVK), which encodes an enzyme involved in cholesterol and nonsterol isoprenoid biosynthesis. HIDS is characterized by persistently elevated

Molecular analysis of the MVK and TNFRSF1A genes in patients with a clinical presentation typical of the hyperimmunoglobulinemia D with periodic fever syndrome: a low-penetrance TNFRSF1A variant in a heterozygous MVK carrier possibly influences the phenotype of hyperimmunoglobulinemia D with periodic fever syndrome or vice versa.

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Ingia / Ingia

OBJECTIVE To describe biochemical findings and the spectrum of mevalonate kinase (MVK) gene mutations as well as an associated TNFRSF1A low-penetrance variant in a series of patients with clinical features of the hyperimmunoglobulinemia D with periodic fever syndrome (HIDS). METHODS The MVK gene was

AA amyloidosis complicating hyperimmunoglobulinemia D with periodic fever syndrome: a report of two cases.

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Ingia / Ingia

AA amyloidosis is the most serious potential complication of the inherited autoinflammatory syndromes and frequently results in end-stage renal failure. Although this complication is well recognized in familial Mediterranean fever, tumor necrosis factor receptor-associated periodic syndrome, and

Treatment with anakinra in the hyperimmunoglobulinemia D/periodic fever syndrome.

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Ingia / Ingia

Hyperimmunoglobulinemia D/periodic fever syndrome is caused by recessively inherited mutations in the mevalonate kinase gene and is characterized by persistently high polyclonal serum IgD titre and recurrent febrile attacks. No conventional therapy exists for preventing the typical recurrent

Hyperimmunoglobulinemia D and periodic fever syndrome; treatment with etanercept and follow-up.

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Ingia / Ingia

The hyperimmunoglobulinemia D and periodic fever syndrome (HIDS) is an autoinflammatory syndrome. It is caused by the mutations of the mevalonate kinase gene. There is no consensus for specific therapy of HIDS, but there are some case reports and studies in regards to its treatment with drugs like

First report of systemic reactive (AA) amyloidosis in a patient with the hyperimmunoglobulinemia D with periodic fever syndrome.

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Ingia / Ingia

Systemic reactive (AA) amyloidosis, leading to renal failure, is a severe complication of most hereditary periodic fever syndromes. The risk of developing this life-threatening condition varies widely among these disorders, being higher for patients affected by familial Mediterranean fever and tumor

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