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PubMed1980

Autonomic neuropathy: cardiovascular, hormonal and metabolic studies.

In order to elucidate the physiological significance of autonomic neuropathy in juvenile diabetics, cardiovascular, hormonal and metabolic functions have been investigated in three groups of juvenile diabetics: One group had no signs of neuropathy, one group had presumably slight autonomic neuropathy (reduced beat-to-beat variation in heart rate during hyperventilation) and one group had clinically severe autonomic neuropathy, defined by presence of orthostatic hypotension. In all three experimental situations we found sympathetic dysfunction causing cardiovascular and/or hormonal maladjustments in patients with autonomic neuropathy. Regarding metabolic functions we found normal responses to graded exercise and insulin-induced hypoglycemia in patients with autonomic neuropathy in spite of blunted catecholamine responses, suggesting increased sensitivity of glycogen stores and adipose tissue towards the action of catecholamine in patients with autonomic neuropathy.

Blood Pressure↗
PubMed1980

The natural history of diabetic autonomic neuropathy.

Seventy-three diabetics (62 males and 11 females) who complained of symptoms suggestive of autonomic neuropathy were followed prospectively for up to five years. Thirty patients presented with impotence alone, while the other 43 presented with one or more of the following: postural hypotension, intermittent diarrhoea, hypoglycaemic unawareness, sweating abnormalities and gastric fullness. Most subjects with impotence alone had normal autonomic function tests (responses to the Valsalva manoeuvre and sustained handgrip) whereas the majority with other symptoms had abnormal tests. Twenty-six subjects (20 males and six females) died during the follow-up period. Of the 33 with initially normal autonomic function tests, five (15 per cent) died, whereas of the 40 with initially abnormal tests, 21 (53 per cent) died. Diabetics with symptoms of autonomic neuropathy and abnormal autonomic function tests, had a calculated mortality rate after two-and-a-half years of 44 per cent and after five years of 56 per cent. Half the deaths in those with abnormal tests were from renal failure, and the remainder were either sudden and unexpected, or from other causes which may have been associated with the autonomic neuropathy. Autonomic function testing repeated during the follow-up period showed that some normal tests later became abnormal, but once tests were abnormal, they usually remained abnormal. A number of subjects with impotence alone developed other features of autonomic neuropathy and abnormal tests during the follow up period. Symptoms of autonomic neuropathy, particularly postural hypotension, gastric symptoms and hypoglycaemic unawareness, together with abnormal autonomic function tests, carry a very poor prognosis. Diarrhoea and importence, on their own, cannot be relied on as symptoms of autonomic neuropathy. Autonomic function testing using simple cardiovascular reflexes give a good guide to the prognosis of diabetic autonomic neuropathy.

Adult↗
PubMed1993

[Coagulation and fibrinolytic parameters in patients with various angiopathies--analysis in cerebral thrombosis, diabetic and vasculitic neuropathies].

We measured the coagulation and fibrinolytic parameters in patients with various angiopathies to clarify the usefulness of the parameters for the evaluation of vascular involvement. The study included 65 patients with cerebral thrombosis at the chronic stage, 47 diabetics with neuropathy associated with diabetic microangiopathy, 15 diabetics without neuropathy, and 16 patients with vasculitic neuropathy associated with collagen diseases. Control subjects were 45 patients with other neurological disorders without symptomatic angiopathies. In cerebral thrombosis at the chronic stage, the coagulation factor VIII (FVIII), von Willebrand factor (vWF), and platelet factor IV were elevated significantly as compared with age-matched controls. Diabetics with neuropathy showed significantly elevated FVIII and vWF in comparison with diabetics without neuropathy and controls. No significant difference in parameters concerning glucose metabolism was observed between the two groups of diabetics. These findings suggest that elevated activities of the coagulation parameters reflect not merely the abnormalities in glucose metabolism but also the presence of microangiopathy which causes diabetic neuropathy. The patients with vasculitic neuropathy exhibited significantly elevated FVIII, vWF and fibrin/fibrinogen degradation products (FDP). The present study demonstrated that FVIII and vWF are useful parameters for the evaluation of the extent of vascular involvement in angiopathies of different etiologies. It is important for the treatment of patients with the angiopathies, to monitor the coagulation parameters which reflect vascular involvement in addition to parameters for the disease activity.

Aged↗
PubMed1996

[Pathophysiology of sensory ataxic neuropathy].

The main lesions of sensory ataxic neuropathy such as chronic idiopathic sensory ataxic neuropathy, (ISAN), carcinomatous neuropathy, Sjögren syndrome-associated neuropathy and acute autonomic and sensory neuropathy (AASN) are the large-diameter sensory neurons and dosal column of the spinal cord and the large myelinated fibers in the peripheral nerve trunks. In addition, afferent fibers to the Clarke's nuclei are also severely involved, suggesting Ia fibers being involved in these neuropathies. In NT-3 knockout mouse, an animal model of sensory ataxia, large-sized la neurons as well as muscle spindle and Golgi tendon organs are depleted, and are causative for sensory ataxia. Thus, the proprioceptive Ia neurons would play a role in pathogenesis of sensory ataxia in human sensory ataxic neuropathies, but the significance of dorsal column involvement in human sensory ataxia is still needed to evaluate.

Animals↗
PubMed1997

Diabetic neuropathy: prevalence, concordance between clinical and electrophysiological testing and impact of risk factors.

UNLABELLED: The aim of this study was to assess the prevalence of various forms of diabetic neuropathy (DN), by clinical and electrophysiological tests, on 374 diabetic patients (66 with type 1 and 308 with type 2 diabetes mellitus) and the concordance between clinical and electroneurological alterations and relative risk factors impact. The overall prevalence of DN, according to the Saint Antonio Conference criteria, was 44.9% (28.88% somatic, 14.44% mixed and 1.60% autonomic) without statistical difference between type 2 and type 1 diabetes (46.43% and 37.88% respectively). In 32.24% of patients nerve conduction velocity (NCV) abnormalities were present together with clinical signs or symptoms of neuropathy, while 12.68% presented only signs and/or symptoms. In addition 9.36% of patients showed alterations of NCV in the absence of clinical signs or symptoms of neuropathy. The most frequent form was asymptomatic (30.21%), followed by symptomatic neuropathy (12.83%); rare was the severe neuropathy. Relative risk increased for diabetes duration > 20 years (p < 0.0001). IN CONCLUSION: 1) the Saint Antonio Consensus Conference criteria can be considered the most complete test for neuropathy diagnosis; 2) NCV alterations may not be concordant with signs-symptoms of neuropathy; 3) the duration of diabetes seems to be the most important risk factor.

Adolescent↗
PubMed1997

[Genetic factors, Na K ATPase activity and neuropathy in diabetics].

A genetic predisposition to develop a polyneuropathy in case of diabetes seems to exist. Some ethnic groups such as North Africans are prone to develop a diabetic polyneuropathy. To identify this predisposition could help in targeting a preventive treatment. We have observed that red cell Na/K ATPase activity was lower among diabetic patients than controls and even lower when diabetic neuropathy was present. Now an impaired NA/K ATPase activity has been implicated in the pathogenesis of diabetic neuropathy and ethnic differences in this enzyme activity have been demonstrated. For these reasons, we have compared red cell Na/K ATPase activity of European and North African individuals with or without diabetes and in case of diabetes with or without neuropathy. Among European subjects, Na/K ATPase activity was higher in 46 control subjects than in 84 insulin-dependent diabetic patients (405 +/- 16 nmol.mg Prot-1h-1 versus 282 +/- 10 p. < 0.05) and in the diabetic group Na/K ATPase activity was lower in the patients presenting with neuropathy (242 +/- 19 versus 323 +/- 12 p. < 0.05). The mean red cell Na/K ATPase activity was lower in 16 North African control subjects than in their European counterparts (296 +/- 26 p. < 0.05). The same observation was made when comparing 24 North Africans insulin dependent diabetic patients to the European diabetics (246 +/- 20 p. < 0.05). A low Na/K ATPase activity appears to be a risk marker of diabetic neuropathy. It could explain the propensity of North African patients to develop this diabetic complication. A restriction polymorphism exist on the first intron of the ATP1 A1 gene coding for the ATPase alpha 1 isoform. This isoform is preponderent in the nervous tissue and exclusive in red cells. Among European diabetic individuals, the presence of the restricted allele is strongly associated to diabetic neuropathy, confering a relative risk of 6.5 (95%, confidence interval 3.3-13). The restricted allele is associated to a lower Na/K ATPase activity but only among diabetic patients and not in control subjects. This fact suggests an interaction between genetic factors (the restriction polymorphism of ATP1 A1 gene) and environmental factors (diabetes) to induce a decrease in Na/K ATPase activity which in turn could favor the development of diabetic neuropathy. Among North African individuals the impairement of Na/K ATPase activity is not explained by the presence of this polymorphism. Other genetic factors remain to be identified.

Adult↗
PubMed1998

The prevalence of peripheral neuropathy in newly diagnosed patients with non-insulin-dependent diabetes mellitus.

INTRODUCTION: Neuropathy is considered to be a longterm complication of diabetes. AIMS: To determine the prevalence of peripheral neuropathy in 112 Sri Lankan patients with recently diagnosed non-insulin-dependent diabetes and a control population of 100 people. METHODS: A diagnosis of peripheral neuropathy was made using a clinical symptom score, clinical examination, quantitative sensory testing and electrophysiological studies. RESULTS: 9.8% of diabetic patients at diagnosis had peripheral neuropathy, 2.6% had foot ulcers, 7.1% had signs of neuropathy, abnormal vibration perception threshold and nerve conduction abnormalities and 15.1% had abnormal nerve conduction velocity without signs or symptoms of neuropathy. The peroneal nerve conduction velocity was higher in diabetic patients when compared to controls. There was an inverse correlation between nerve conduction velocity and fasting blood glucose in diabetic patients (p < 0/05). This association was stronger for peroneal nerve conduction velocity (r = -0.73) than for median nerve motor conduction velocity (r = -0.42). CONCLUSIONS: Symptomatic peripheral neuropathy is common among Sri Lankans with newly diagnosed non-insulin-dependent diabetes. This may be due to a later presentation of diabetes or a genetic predisposition.

Adult↗
PubMedDate not supplied

Peripheral neuropathies of the median, radial, and ulnar nerves: MR imaging features.

The median, radial, and ulnar nerves of the upper limbs may be affected by various peripheral neuropathies, each of which may be categorized according to its cause, as either an entrapment or a nonentrapment neuropathy. Entrapment neuropathies, also referred to as nerve compression syndromes, include the supracondylar process syndrome, pronator syndrome, anterior interosseous nerve syndrome, carpal tunnel syndrome, posterior interosseous nerve syndrome, cubital tunnel syndrome, and Guyon canal syndrome. Nonentrapment neuropathies include traumatic nerve injuries, infectious and inflammatory conditions, polyneuropathies, and mass lesions at anatomic locations where entrapment syndromes typically do not occur. Although clinical examination and electrophysiologic testing are the cornerstone of the diagnostic work-up, in certain cases magnetic resonance (MR) imaging may provide key information about the exact anatomic location of a lesion or may help narrow the differential diagnosis. In patients with a diagnosis of peripheral neuropathy, MR imaging may help establish the cause of the condition and provide information crucial for conservative management or surgical planning. In addition, knowledge of the normal anatomy and of the possible causes, typical clinical findings, and MR imaging features of peripheral neuropathies that affect the median, radial, and ulnar nerves allows greater confidence in the diagnosis.

Humans↗
PubMed1990

Acute autonomic neuropathy. Two cases and a clinical review.

Acute autonomic neuropathy is an uncommon syndrome, usually affecting healthy young people. Presentation is often dramatic and initial misdiagnosis is common. We describe two young women with acute autonomic neuropathy who presented with gastrointestinal involvement heralding widespread dysautonomia and review 26 additional cases of acute autonomic neuropathy from the English language literature. Acute autonomic neuropathy can be primarily cholinergic without orthostatic hypotension (26%) or pandysautonomic (74%) involving sympathetic adrenergic functions. Onset has been temporally related to viral syndromes in 20% of cases, with autonomic deficits usually evolving over 1 to 3 weeks. Gastroparesis (69%) and syncope (12%) are frequent presenting complaints. Spinal fluid protein levels are often (75%) elevated in pandysautonomic subtypes. Prolonged and incomplete recovery is the rule (60%), with persistent gastroparesis and orthostatic hypotension. Other specific diseases that occasionally mimic acute autonomic neuropathy include botulism, porphyria, amyloidosis, and paracarcinomatous neuropathies. Acute autonomic neuropathy shares several clinical features with acute idiopathic polyneuropathy (Guillain-Barré syndrome), suggesting an immune-mediated pathogenesis.

Acute Disease↗
PubMed2005

Painful peripheral neuropathy associated with voriconazole use.

BACKGROUND: Voriconazole is a new antifungal agent that has been recently introduced into clinical practice. We found no published reports of painful peripheral neuropathy associated with its use. OBJECTIVE: To describe a unique case of painful peripheral neuropathy associated with voriconazole use. SETTING: University hospital. PATIENT: A 43-year-old patient who had undergone liver transplantation received voriconazole for invasive deep sinus aspergillosis and developed intolerable pain in all extremities. RESULTS: A laboratory workup and electromyographic and nerve conduction studies were performed to exclude other causes of neuropathy in this complicated patient. Results of electromyographic and nerve conduction studies were suggestive of a demyelinating neuropathy. Symptoms and signs of neuropathy disappeared shortly after voriconazole discontinuation, suggesting a possible role in the development of neuropathy. The patient continues to do well 10 months after this event. CONCLUSIONS: To our knowledge, this is the first reported case of voriconazole-associated peripheral neuropathy. Awareness of this association and careful monitoring for neurological signs are necessary for patients receiving voriconazole.

Adult↗
PubMed1985

Quantitative computed tomography of Graves' ophthalmopathy. Extraocular muscle and orbital fat in development of optic neuropathy.

Quantitative assessment of computed tomographic (CT) scans was performed on 98 orbits of 49 patients with Graves' ophthalmopathy. Extraocular muscle volume and orbital fat volume were determined, according to whether optic neuropathy was absent, had developed during follow-up, or was present at the time of scanning. No differences in muscle volume were found between the group already having optic neuropathy and the group in which optic neuropathy developed during follow-up. Both optic neuropathy groups, however, had significant increases in extraocular muscle volume compared with the group without optic neuropathy. The absolute amount of orbital fat was the same for all groups, but the relative amount of orbital fat tended to decrease as total orbital volume increased with development or presence of optic neuropathy. This study establishes a quantitative relationship between optic neuropathy and extraocular muscle enlargement in Graves' ophthalmopathy. Orbital fat, however, does not play an important role in the disease.

Adipose Tissue↗
PubMed2003

Immunotherapy for IgM anti-Myelin-Associated Glycoprotein paraprotein-associated peripheral neuropathies.

BACKGROUND: Serum monoclonal anti-Myelin Associated Glycoprotein antibodies may be pathogenic in some patients with IgM paraprotein and demyelinating neuropathy. Immunotherapies aimed at reducing the level of these antibodies might be expected to be of benefit in the treatment of the neuropathy. Many potential therapies have been described in small trials, uncontrolled studies and case reports. OBJECTIVES: To examine the efficacy of any form of immunotherapy in reducing disability and impairment resulting from IgM anti-Myelin Associated Glycoprotein paraprotein-associated demyelinating peripheral neuropathy. SEARCH STRATEGY: We searched the Cochrane Neuromuscular Disease Group register (August 2002) and MEDLINE (January 1966 - August 2002) and EMBASE (January 1980 - August 2002) for controlled trials, checked the bibliographies to identify other controlled trials and contacted authors and other experts in the field. SELECTION CRITERIA: Types of studies: randomised or quasi-randomised controlled trials. TYPES OF PARTICIPANTS: patients of any age with anti-Myelin Associated Glycoprotein antibody associated demyelinating peripheral neuropathy with monoclonal gammopathy of undetermined significance of any severity. Types of interventions: any type of immunotherapy. Types of outcome measures: Primary: improvement in the Neuropathy Disability Score or Modified Rankin Scale six months after randomisation Secondary: Neuropathy Disability Score and/or the Modified Rankin Score 12 months after randomisation. Ten metre walk time, subjective clinical scores and electrophysiological parameters at six and 12 months after randomisation. IgM paraprotein levels and anti-Myelin Associated Glycoprotein antibody titres six months after randomisation. Adverse effects of treatments. DATA COLLECTION AND ANALYSIS: We identified six randomised controlled trials of which five were included after discussion between the authors. One author extracted the data and the other checked them. No missing data could be obtained from authors. MAIN RESULTS: The five eligible trials used four of the many available immunotherapy treatments. Only two had comparable interventions and outcomes but these were only short-term studies. There were no significant benefits of the treatments used in the predefined outcomes. However intravenous immunoglobulin showed benefits in terms of improved Modified Rankin Scale at two weeks and 10 metre walk time at four weeks. Serious adverse effects of intravenous immunoglobulin are known to occur from observational studies but none were encountered in these trials. REVIEWER'S CONCLUSIONS: There is inadequate reliable evidence from trials of immunotherapies in anti-Myelin Associated Glycoprotein paraproteinaemic neuropathy to recommend any particular immunotherapy treatment. Intravenous immunoglobulin is relatively safe and may produce some short-term benefit. Large well designed randomised trials are required to assess the efficacy of promising new therapies.

Demyelinating Diseases↗
PubMed1999

Anti-myelin-associated glycoprotein antibodies predict the development of neuropathy in asymptomatic patients with IgM monoclonal gammopathy.

We examined 52 asymptomatic patients with IgM monoclonal gammopathy and correlated anti-myelin-associated glycoprotein (anti-MAG) IgM with the presence of subclinical neuropathy and, in 24 of these patients, with the development of symptomatic neuropathy during a follow-up interval of 40 to 144 months (mean, 75.3 months). Three of 6 patients (50%) with high (>1/6,400) anti-MAG IgM had subclinical neuropathy at entry compared with 2 of 46 patients (4.3%) with low or no reactivity. At follow-up, a symptomatic neuropathy occurred in 3 of 4 patients with high reactivity and in 3 of 21 patients with low or no reactivity. The correlation of high anti-MAG IgM with the presence of subclinical neuropathy or the development of symptomatic neuropathy supports its pathogenetic role in the neuropathy.

Adult↗
PubMed2003

Schwann cell expression of PLP1 but not DM20 is necessary to prevent neuropathy.

Proteolipid protein (PLP1) and its alternatively spliced isoform, DM20, are the major myelin proteins in the CNS, but are also expressed in the PNS. The proteins have an identical sequence except for 35 amino acids in PLP1 (the PLP1-specific domain) not present in DM20. Mutations of PLP1/DM20 cause Pelizaeus-Merzbacher Disease (PMD), a leukodystrophy, and in some instances, a peripheral neuropathy. To identify which mutations cause neuropathy, we have evaluated a cohort of patients with PMD and PLP1 mutations for the presence of neuropathy. As shown previously, all patients with PLP1 null mutations had peripheral neuropathy. We also identified 4 new PLP1 point mutations that cause both PMD and peripheral neuropathy, three of which truncate PLP1 expression within the PLP1-specific domain, but do not alter DM20. The fourth, a splicing mutation, alters both PLP1 and DM20, and is probably a null mutation. Six PLP1 point mutations predicted to produce proteins with an intact PLP1-specific domain do not cause peripheral neuropathy. Sixty-one individuals with PLP1 duplications also had normal peripheral nerve function. These data demonstrate that expression of PLP1 but not DMSO is necessary to prevent neuropathy, and suggest that the 35 amino acid PLP1-specific domain plays an important role in normal peripheral nerve function.

Adolescent↗
PubMed1989

Anti-myelin-associated glycoprotein IgM antibody titers in neuropathy associated with macroglobulinemia.

Twenty-seven patients with neuropathy and IgM monoclonal gammopathy were tested for antigen specificity of the M-protein and for anti-myelin-associated glycoprotein (MAG) IgM levels by immunoblot. In 16 patients (59.2%) the M-protein reacted with MAG and with cross-reactive glycoconjugates. Anti-MAG IgM titers in these patients ranged between 1:12,800 and 1:100,000. A fainter IgM reactivity with MAG and related glycoconjugates was detected in 3 additional patients with neuropathy, but also in 8 of 24 patients with IgM M-protein without neuropathy (33.3%). This reactivity was not due to the M-protein and corresponded to antibody titers of 1:400 or less in all but 1 patient with a titer of 1:3,200. Low titers of anti-MAG IgM (1:200 or less) were also detected in 17 of 101 control patients without IgM M-proteins (16.8%), while 1 patient with neuropathy of unknown cause had anti-MAG IgMK titers of 1:25,600. In 1 patient with neuropathy and IgM M-protein that was not anti-MAG, the M-protein bound to other antigens in nerve, while in 6, other possible causes or mechanisms for the neuropathy were found. In this study, high titers of anti-MAG IgM antibodies were always associated with neuropathy. The presence of low levels of anti-MAG IgM in a significant proportion of controls suggests that monoclonal expansion of naturally occurring B-cell clones secreting anti-MAG IgM may be responsible for the high incidence of this antigen specificity of the M-protein.

Adult↗
PubMed1994

Frequency and clinical correlates of anti-neural IgM antibodies in neuropathy associated with IgM monoclonal gammopathy.

We studied the frequency and clinical correlates of different IgM specificities in 75 patients with neuropathy associated with IgM monoclonal gammopathy. Patients were tested for IgM reactivity with the myelin-associated glycoprotein, P0, neurofilaments, and tubulin by immunoblot; with GM1, asialo-GM1, GM2, GD1a, GD1b, sulfatide, and chondroitin sulfate C by enzyme-linked immunosorbent assay; and with brain and nerve glycolipids by overlay high-performance thin-layer chromatography. Forty-two patients (56%) had high titers of IgM antibodies to MAG; 4 (5%), to sulfatide (1 also to myelin-associated glycoprotein); 4 (5%), to the 200-kd neurofilament (2 also to myelin-associated protein); and 1 each, to GD1b and chondroitin sulfate C. No reactivity was found in 26 patients (35%). More patients with anti-myelin-associated glycoprotein IgM (62%) than with unknown IgM reactivity (31%) had a predominantly sensory neuropathy (p < 0.025). Nerve conduction findings were consistent with a demyelinating neuropathy in 77% of patients reactive to myelin-associated glycoprotein and 24% with unknown reactivity (p < 0.0001) and the mean conduction velocity of peroneal nerve was lower in the former group (22.9 m/sec) than in the latter group (39.6 m/sec) (p < 0.000001). Patients with anti-sulfatide IgM had a sensorimotor neuropathy with morphological evidence of demyelination while anti-neurofilament IgM was not associated with homogeneous findings. Patients with anti-GD1b or anti-chondroitin sulfate C IgM had a predominantly motor impairment. The frequent occurrence of anti-neural IgM antibodies in neuropathy associated with IgM gammopathy, and their frequent, though not constant association with similar neuropathy features, support their possible pathogenetic role in the neuropathy.

Adult↗
PubMed1995

Peripheral neuropathy with necrotizing vasculitis in rheumatoid arthritis. A clinicopathologic and prognostic study of thirty-two patients.

OBJECTIVE: To examine the clinicopathologic features of the noncompressive neuropathies in rheumatoid arthritis (RA). METHODS: We studied 32 patients with RA and peripheral neuropathy whose nerve and/or muscle biopsy specimens exhibited necrotizing vasculitis. Morphologic analysis of nerve specimens included light and electron microscopy studies and teased fiber preparation. Survival was evaluated, and the prognostic values of clinical, biologic, and pathologic features were assessed by Cox proportional hazards model. A prognostic assessment based on the significant variables was devised to estimate the probability of survival of any individual patient. RESULTS: Epi- and/or perineurial vasculitis was observed with the same frequency in the 17 patients with sensory and motor deficit and the 15 patients with sensory neuropathies and was associated with axonal degeneration of an average of 77.7% of the nerve fibers. The mean followup was 7.2 years, and the overall survival rate at 5 years was 57%. A full prolonged remission of the vasculitis was observed in 53% of the patients; relapse occurred in 25%. The factors correlated with mortality, in decreasing order of significance, were clinical cutaneous vasculitis (P = 0.0003), neuropathy affecting 3 or 4 limbs (P = 0.03), and depressed level of C4 (P < 0.05). The prognostic assessment indicated a wide range of 5-year probabilities of survival, from < 1% to 93%. CONCLUSION: Necrotizing vasculitis is responsible for the different patterns of noncompressive neuropathies in RA, including mononeuritis multiplex and distal symmetric sensory or sensorimotor neuropathy. Cutaneous vasculitis, multifocal neuropathy, and depressed C4 level were the 3 independent variables which best predicted mortality. We propose a prognostic assessment according to these variables, to stratify patients to receive more aggressive or less aggressive therapy.

Adult↗
PubMed1996

Presence of autonomic neuropathy is a poor prognostic indicator in patients with advanced liver disease.

Autonomic neuropathy (AN) is seen in both alcohol-induced and non-alcohol-induced liver disease, and when present is an independent predictor of mortality. We postulated that patients who were awaiting liver transplantation are likely to have a high prevalence of autonomic neuropathy with an associated increase in mortality. To test our hypothesis, we evaluated the presence of autonomic neuropathy using a battery of tests in 33 patients awaiting liver transplantation and prospectively followed them to determine their prognosis. Twenty-two of 33 (67%) patients with liver disease had evidence of autonomic neuropathy; of these, 12 (36%) had evidence of definite and 10 (31%) had early autonomic neuropathy. The prevalence of AN was similar in alcohol-induced and non-alcohol-induced liver disease. Using Child-Pugh classification, 14.3% Child A, 31.3% Child B, and 60% Child C had definite autonomic neuropathy. Six patients died during a median observation period of 10 months, and all had AN. Kaplan-Meier survival analysis showed a significantly higher mortality (P=.05) in patients with AN. On the basis of this observation, we suggest that consideration should be given for early liver transplantation in patients with advanced liver disease and autonomic neuropathy.

Adult↗