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Proline at position 36: a new transthyretin mutation associated with familial amyloidotic polyneuropathy.

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Familial amyloidotic polyneuropathy (FAP) is associated with the deposition of an abnormal transthyretin (TTR) molecule. We have studied DNA from a family of Greek descent with FAP. The proband's TTR gene was asymmetrically amplified by using PCR and then was sequenced directly, to reveal a

Familial amyloid polyneuropathy in Taiwan: identification of transthyretin variant (Leu55-->Pro).

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We report a family with familial amyloid polyneuropathy (FAP), showing an early-onset and a fatal outcome before age 30. Transthyretin (TTR) gene analysis showed one point mutation (T-->C change) in the second base of codon 55, and the corresponding amino acid substitution of proline (Pro) for

Efficacy and safety of Privigen(®) in patients with chronic inflammatory demyelinating polyneuropathy: results of a prospective, single-arm, open-label Phase III study (the PRIMA study).

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This prospective, multicenter, single-arm, open-label Phase III study aimed to evaluate the efficacy and safety of Privigen(®) (10% liquid human intravenous immunoglobulin [IVIG], stabilized with L-proline) in patients with chronic inflammatory demyelinating polyneuropathy (CIDP). Patients received

Subcutaneous Immunoglobulin Therapy for Chronic Inflammatory Demyelinating Polyneuropathy: A Nursing Perspective.

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Chronic inflammatory demyelinating polyneuropathy (CIDP), an immune-mediated peripheral neuropathy, is frequently treated with long-term maintenance intravenous immunoglobulin (IVIG). However, disadvantages of IVIG are the systemic adverse reactions, lengthy infusions, and need for vascular access.

IgPro20, the Polyneuropathy and Treatment with Hizentra® study (PATH), and the treatment of chronic inflammatory demyelinating polyradiculoneuropathy with subcutaneous IgG.

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Subcutaneous IgG (SCIG) administration may be preferred over the intravenous route (IVIG) in chronic inflammatory demyelinating polyneuropathy (CIDP) because it minimizes 'end of cycle' treatment-related fluctuations, reduces systemic adverse effects, improves convenience/quality of life and

A new transthyretin variant (Ser 24) associated with familial amyloid polyneuropathy.

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An American kindred with systemic amyloidosis presenting with carpal tunnel syndrome, peripheral neuropathy, and cardiomyopathy is reported. The transthyretin gene of a patient was analysed by direct DNA sequencing and both cytosine and thymine were present at the first base of codon 24. This new

The crystal structure of amyloidogenic Leu55 --> Pro transthyretin variant reveals a possible pathway for transthyretin polymerization into amyloid fibrils.

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The x-ray crystal structure of the amyloidogenic Leu55 --> Pro transthyretin (TTR) variant, implicated as the causative agent in early-onset familial amyloidotic polyneuropathy (Jacobson, D. R., McFarlin, D. E., Kane, I., and Buxbaum, J. N. (1992) Hum. Genet. 89, 353-356), has been solved by

Rare myelin protein zero sequence variant in late onset CMT1B.

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Myelin protein zero (MPZ) mutations cause demyelinating neuropathies that range from severe neonatal to milder adult forms. We report a 65-year-old woman with slowly progressive leg weakness starting at 47. Examination revealed distal weakness and atrophy in all extremities, impaired light touch in

Amino acid synthesis deficiencies.

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In recent years the number of disorders known to affect amino acid synthesis has grown rapidly. Nor is it just the number of disorders that has increased: the associated clinical phenotypes have also expanded spectacularly, primarily due to the advances of next generation sequencing diagnostics. In

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