Prognostic indicators in guillain barre syndrome with special reference to serum albumin
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Date
2019-12
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SCTIMST
Abstract
Guillain Barre syndrome (GBS) is a common cause of neuromuscular paralysis, the
annual incidence of which is reported to be 0.81–1.89 per 100,000 person–years.1
It is
characterised by the combination of rapidly progressive symmetrical weakness in the
limbs with or without sensory disturbances, hypoflexia or areflexia, with or without
involvement of respiratory muscles or cranial nerve-innervated muscles, with or
without autonomic dysfunction, in the absence of a CSF cellular reaction. 2 According
to the clinical criteria, maximum weakness is reached within 4 weeks, but most
patients usually reach their maximum weakness within 2 weeks.34
Patients then have a
plateau phase of varying duration, ranging from 2 days to 6 months (median duration
7 days), followed by a usually much slower recovery phase. 4,5. In patients with GBS
who have inability to walk (severely affected patients), about 25% eventually need
artificial ventilation because of weakness of the respiratory muscles. Despite
treatment with IVIg or Plasma exchange, about 20% of severely affected patients
remain unable to walk after 6 months. 6 Hence, the prognosis of GBS is tough to
predict because of the considerable variation in outcome. In the past few decades, the
GBS Disability Scale by Hughes et al has been used as an outcome scale in the
majority of clinical trials in GBS. 7 Nevertheless, it is essential to foresee the outcome
of GBS, as those likely to have a severe disease may require more aggressive therapy.
Certain indicators postulated to be of prognostic significance are - higher age (>40 or >50 years), preceding diarrhoea, severe weakness with consequent low MRC score on
admission and high early GBS disability grade. Electrophysiologically, the most
consistently described finding predictive of poor outcome has been low mean or
summated CMAPs. 7,8 The Erasmus GBS outcome score has been used to predict
inability to walk independently after 6 months, and consists of—the GBS disability
score at 2 weeks after admission, age and presence of preceding diarrhea. 9
Hence, the current prognostic models are based predominantly on clinical features,
but there is a lack of a serologic biomarker to enhance these models. At present no
biomarkers are available to assess the extent of peripheral nerve damage or to predict
outcomes in immune-mediated neuropathies. Serum albumin has already been
established as a prognostic marker in various pathological conditions like
amyotrophic lateral sclerosis, cancer,in geriatric long-term care facility
residents,individuals undergoing surgical interventions,patients with kidney disorders,
and predicts failure of IVIG therapy in Kawasaki disease. It is unclear whether in
these conditions albumin levels are a marker of patients’ nutritional status or chronic
inflammatory state, which decreases the hepatic synthesis of albumin through the
production of proinflammatory cytokines 10
.
In this study, we aim to ascertain if serum albumin levels can serve as a prognostic
biomarker in patients with GBS. This would help in anticipating treatment outcomes,
and in deciding which patients need early and more aggressive therapy in clinical
practice