Intravenous immunoglobulin treatment in patients with chronic inflammatory demyelinating neuropathy not responsive to other treatments.

Nemni, Raffaello; Amadio, Stefano; Fazio, Raffaella; Galardi, Giuseppe; Previtali, Stefano C.; Comı, Gıancarlo

doi:10.1136/jnnp.57.suppl.43

Cited by 17 publications

(12 citation statements)

References 13 publications

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“…Our results are comparable to those of previous trials and of the ICE trial at 6‐ and 24‐week time‐points . However, in our study these results were achieved by administering IVIg following individualized regimens, whereas doses and frequencies were fixed in the ICE trial.…”

Section: Discussionsupporting

confidence: 89%

Long‐term outcome in chronic inflammatory demyelinating polyneuropathy patients treated with intravenous immunoglobulin: A retrospective study

et al. 2013

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Section: Discussionsupporting

confidence: 89%

Long‐term outcome in chronic inflammatory demyelinating polyneuropathy patients treated with intravenous immunoglobulin: A retrospective study

et al. 2013

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“…49 We therefore emphasize that fewer than one-half of patients with CIDP-I respond to the first treatment, but the majority will improve i f alternative therapies are used. Simmons et a1.l and van der Meche and van found that almost one-third of their initial nonresponders improved with a second or third treatment modality.…”

Section: Methodsmentioning

confidence: 98%

Chronic inflammatory demyelinating polyneuropathy

Gorson¹,

Allam²,

Ropper³

1997

Neurology

314

202

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We report the clinical and EMG details of 67 consecutive patients with strictly defined chronic inflammatory demyelinating polyneuropathy (CIDP) during a 4-year period and compare responses to treatment in patients with idiopathic CIDP (CIDP-I) and CIDP with monoclonal gammopathy of uncertain significance (CIDP-MGUS). Patients were examined an average of 28 months after first symptoms. There were several variant presentations that still conformed to the clinical and electrophysiologic definitions of CIDP, including a pure motor syndrome (10%), sensory ataxic variant (12%), mononeuritis multiplex pattern (9%), paraparetic pattern (4%), and relapsing acute Guillain-Barré syndrome (16%). Pain was more frequent than in previous studies (42%). Conduction block was the commonest EMG abnormality (detected in at least one nerve in 73% of patients), but only 31% had a pure demyelinating neuropathy and the majority had some degree of axonal change. Patients with CIDP-MGUS had less severe weakness, greater imbalance, leg ataxia, vibration loss in the hands, and absent median and ulnar sensory potentials, but were as likely as CIDP-I patients to respond to plasma exchange. Seventeen of 44 patients (39%) with idiopathic CIDP improved for at least 2 months with an initial therapy. Although the response rates among plasma exchange, IVIG, and steroids were similar, functional improvement (Rankin score) was greatest with plasma exchange. Of 26 patients who failed to respond to an initial therapy, 9 (35%) benefited from an alternative treatment, and of the 11 who required a third modality 3 (27%) improved. Overall, 66% responded to one of the three main therapies for CIDP.

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“…There is strong evidence suggesting that IVIg is beneficial in CIDP 10. As the biological effects in vivo have yet to be fully elicited, the mechanisms underlying recovery remain equivocal.…”

Section: Discussionmentioning

confidence: 99%

Human immunoglobulin for diabetic amyotrophy—a promising prospect?

Courtney

McDonnell

Patterson

2001

Postgraduate Medical Journal

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Diabetic neuropathies are universally recognised and cause significant morbidity. At present improving glycaemic control is the only recognised treatment. A man with type 2 diabetes presented with disabling asymmetric lower limb proximal neuropathy. Rapid clinical, functional, and electrical improvement followed treatment with intravenous immunoglobulin. The aetiology of diabetic amyotrophy remains controversial but there is evidence for an immune mediated process and this case suggests a role for immunoglobulin in the management of this debilitating condition. (Postgrad Med J 2001;77:326-328) Keywords: diabetes mellitus; neuropathy; immunoglobulin Case report A 63 year old former labourer presented with a five month history of progressive proximal leg weakness and weight loss. Previously well, his walking distance had been unrestricted and he had been riding a bicycle. A steady decline led to mobilisation with a Zimmer frame and great diYculty climbing stairs. He complained of a painful burning sensation in his left shin and numbness of the left leg. There had been a 12 kg weight loss in four months. Diabetes mellitus had been diagnosed six months previously and dietary treatment initiated.On examination he was pale and thin (body mass index 20) with quadriceps wasting and fasciculation. Tone was normal, power (Medical Research Council scoring) was reduced: left hip flexion, 4+; right hip flexion, 3; left knee flexion and extension, 4. Both knee jerks were absent but both ankle jerks were present. Plantar responses were bilaterally flexor. Below the left knee light touch sensation was diminished and vibration sensation was absent.Investigations revealed a raised glycated haemoglobin of 9.7% (standardised to Diabetes Control and Complications Trial, normal <7%), and creatine kinase was less than 20 U/l. Full blood picture, liver function tests, and urea and electrolytes were normal. Nerve conduction velocities were generally slowed: median and ulnar nerves 40 m/s (normal >50 m/s) and lateral popliteal 24 m/s (normal >40 m/s). Responses were of low amplitude but there was no evidence of conduction block. Electromyography was mildly abnormal with neurogenic type changes, particularly in the lower limbs. Muscle histology revealed variation in fibre diameter with occasional fibre degeneration, and scattered angulation. Although there was no evidence of vasculitis, a macrophage reaction was noted in the interstitium and in relation to the degenerating fibres. The overall findings were consistent with denervation.The patient was treated with intravenous human immunoglobulin (IVIg), 2 g/kg of body weight in divided doses over five days. A basal bolus insulin regimen was started to improve glycaemic control. After three days of IVIg there was significant subjective and objective improvement in lower limb function. By the time of discharge after one week, there was full power in all muscle groups and knee reflexes had returned. The only remaining sensory abnormality was of absent vibration sense at the left gr...

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Intravenous immunoglobulin treatment in patients with chronic inflammatory demyelinating neuropathy not responsive to other treatments.

Cited by 17 publications

References 13 publications

Long‐term outcome in chronic inflammatory demyelinating polyneuropathy patients treated with intravenous immunoglobulin: A retrospective study

Long‐term outcome in chronic inflammatory demyelinating polyneuropathy patients treated with intravenous immunoglobulin: A retrospective study

Chronic inflammatory demyelinating polyneuropathy

Human immunoglobulin for diabetic amyotrophy—a promising prospect?

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