polyneuropathies/albumin

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Increased permeability across the blood-nerve barrier of albumin glycated in vitro and in vivo from patients with diabetic polyneuropathy.

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The blood-nerve transfer of human plasma albumin glycated with D-glucose was investigated by measuring the permeability coefficient-surface area product (PS) of the blood-nerve barrier to radioiodinated albumin in normal adult rat sciatic nerve. Human albumin (ALB) from normal individuals, freshly

Loss of functional albumin triggers acceleration of transthyretin amyloid fibril formation in familial amyloidotic polyneuropathy.

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Transthyretin (TTR)-related familial amyloidotic polyneuropathy (FAP) is characterized by systemic accumulation of amyloid fibrils caused by a point mutation in the TTR gene. Despite the urgent need for alternative therapeutic strategies, the pathogenesis of FAP still remains elusive. In our study

Increased endoneurial albumin in diabetic polyneuropathy.

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Albumin was measured in the endoneurium of fascicular biopsies of sural nerves and in plasma from diabetic patients with polyneuropathy by solid phase radioimmunoassay, and normalized to total endoneurial and plasma protein, respectively, to obtain an index of the blood-nerve barrier (BNB-Index).

Effect of albumin on transthyretin and amyloidogenic transthyretin Val30Met disposition and tissue deposition in familial amyloidotic polyneuropathy.

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OBJECTIVE Transthyretin (TTR)-related familial amyloidotic polyneuropathy (FAP) is characterized by the systemic accumulation of amyloid fibrils caused by amyloidogenic. Our previous studies demonstrated that albumin played a role in the inhibition of TTR amyloid-formation. The aim of this study was

Successful management of critical illness polyneuropathy and myopathy in renal transplant recipients.

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Critical illness polyneuropathy and myopathy commonly occur in patients with multiorgan failure and sepsis. Distal muscle weakness and loss of deep tendon reflexes are usually found, with sparing of the cranial nerve musculature. Many risk factors have been identified, specifically hypoxia,

Eosinophilic Granulomatosis with Polyangiitis Presented as Acute Polyneuropathy and Cerebral Vasculitis.

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Eosinophilic granulomatosis with polyangiitis (EGPA) is an immune related systemic disease that is caused by vasculitis affecting multiple organ systems. It is characterized by asthma, fever, eosinophilia, cardiac problems, renal injury, and peripheral neuropathy. In this report, we describe a

[Indication of autologous stem cell transplantation in chronic inflammatory demyelinating polyneuropathy: Guidelines from the Francophone Society of Bone Marrow Transplantation and Cellular Therapy (SFGM-TC)].

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Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) is a chronic autoimmune disease involving the peripheral nervous system, characterized by focal and segmental demyelination accounting for neurological deficit. CIDP diagnosis is based on several criteria and requires the presence of specific

Abnormal Osmolality Gap Exists in Distal Symmetric Polyneuropathy.

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Distal symmetric polyneuropathy, represented by chronic inflammatory demyelinating polyneuropathy, is a popular neurological condition. Some cases are known to be associated with genetic mutations or serum auto-antibodies, but the exact mechanisms in most cases are unknown. Recently, osmotic factors

Sepsis and catecholamine support are the major risk factors for critical illness polyneuropathy after open heart surgery'.

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BACKGROUND Critical illness polyneuropathy (CIP) remains a problem after open heart surgery. Recently, we reported about a retrospectively performed study pointing out that sepsis, the application of higher amounts of catecholamines and intervention such as chronic venovenous hemodiafiltration may

Unwanted road to anaemia in transthyretin familial amyloid polyneuropathy may continue irrespective of tafamidis treatment.

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Background This retrospective longitudinal study was performed to determine whether tafamidis treatment leads to improvements in commonly used blood data for transthyretin familial amyloid polyneuropathy (TTR-FAP). Methods Commonly used blood data (complete blood count [including a haemogram], total

[Bivariate evaluation of laboratory findings: immunoglobulin G and albumin in cerebrospinal fluid (author's transl)].

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Using radial immunodiffusion, albumin and immunoglobulin G were determined in non-preconcentrated cerebrospinal fluid from 127 controls and from 239 patients. In controls the concentrations of albumin and immunoglobulin G followed normal distribution. The two variables were correlated linearly (r =

Neurophysiological study of critical illness polyneuropathy and myopathy in mechanically ventilated children; additional aspects in paediatric critical illness comorbidities.

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OBJECTIVE Critical illness polyneuropathy and myopathy (CIP/CIM) is being increasingly recognized as a significant clinical problem in critically ill children especially if they have spent long periods in the intensive care unit. So the aim was to determine the frequency of CIP/CIM amongst

Altered cerebrospinal fluid index of prealbumin, fibrinogen, and haptoglobin in patients with Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy.

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OBJECTIVE Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP) are autoimmune diseases of the peripheral nervous system. A clinical hallmark of GBS and CIDP is the albumino-cytologic dissociation in the cerebrospinal fluid (CSF). Changes in the CSF levels of

Post hoc analysis of nutritional status in patients with transthyretin familial amyloid polyneuropathy: impact of tafamidis.

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BACKGROUND Gastrointestinal symptoms are common among patients with transthyretin familial amyloid polyneuropathy (TTR-FAP). This post hoc analysis evaluated the nutritional status of TTR-FAP patients treated with tafamidis while enrolled in clinical trials. METHODS Nutritional status was measured

Argpyrimidine, a methylglyoxal-derived advanced glycation end-product in familial amyloidotic polyneuropathy.

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FAP (familial amyloidotic polyneuropathy) is a systemic amyloid disease characterized by the formation of extracellular deposits of transthyretin. More than 80 single point mutations are associated with amyloidogenic behaviour and the onset of this fatal disease. It is believed that mutant forms of

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