Neurologic disorders in immunocompetent patients with autochthonous acute hepatitis E.
Patients and Methods
This retrospective multicenter study was conducted in France from January 2006 through June 2013. All members of the French Liver Association (Association Frangaise pour l'Etude du Foie, 500 members) were sent a newsletter inviting them to report cases of HEV infection in which neurologic symptoms were experienced. Data were recorded from patients with neurologic disorders, regardless of the symptoms exhibited during the course of acute HEV infection. This retrospective sampling was likely to capture most patients in France who had neurologic symptoms during acute HEV infection. A second newsletter was sent 6 months later to maximize the completeness of reporting. HEV infection was diagnosed by detecting anti-HEV IgM, HEV RNA, or both in serum or fecal samples from patients with elevated aminotransferase levels. All cases occurred in France, and all patients gave their informed consent.
The EIAgen (Adaltis, Eurobio, Bologna, Italy) and Wantai (Wantai Biologic Pharmacy Enterprise Co., Beijing, China) kits were used to detect antibodies (13). Both tests are highly specific and sensitive for detecting IgM against HEV. HEV RNA from serum, fecal samples, or cerebrospinal fluid (CSF) was detected by using a real-time PCR as described (3,14). All other causes of acute hepatitis were excluded, and patients had no co-infections. All patients were screened for other causes of disease with immunoassays (antinuclear antibodies, antipolynuclear neutrophil cytoplasmic antibodies) and underwent viral serologic testing (hepatitis B virus, hepatitis C virus, HIV, Epstein-Barr virus, cytomegalovirus). Campylobacter was also screened for. The cases of patients 5 and 12 have been reported (14).
Phylogenetic analyses were performed by sequencing a 347-nt fragment within the open reading frame 2 region as described (15). Nucleotide identity was analyzed with BioEdit software version 126.96.36.199 (http://www.mbio.ncsu. edu/BioEdit/bioedithtml).
Data are presented as their medians (ranges) or their means (SDs). Student t-test was used to compare the quantitative variables. A p value <0.05 was considered significant.
Patient Characteristics and Clinical Outcomes
Fifteen patients (7 women, 8 men) from 7 different hospitals were included in this study. The clinical characteristics of the patients are reported in Table 1. The median age was 55 years (range 25-77 years). The median follow-up period was 42 weeks (range 4-161 weeks). All patients were immunocompetent. All but 1 lived in southern France: 11 lived in the southwest, 3 in the southeast, and 1 in central France.
No patient had underlying chronic liver disease; 2 patients had jaundice, 10 had asthenia, 5 had arthromyalgia, and 3 had fever. Three patients had neurologic symptoms only. Their biological characteristics are reported in Table 2. All patients had elevated liver enzyme levels, and none experienced liver failure. Median enzyme levels at diagnosis were the following: alanine aminotransferase level at diagnosis was 495 IU/L (range 49-3,641 IU/L; reference range 10-41 IU/l), aspartate aminotransferase 124 IU/L (range 37-1,742 IU/L; reference range 15-41 IU/l), bilirubin 15 [micro]mol/L (range 4-101 [micro]mol/L; reference range 3-21 [micro]mol/l), alkaline phosphatase 254 IU/L (range 88-704 IU/L; reference range 36-126 IU/l), g-glutamyl transferase 185 IU/L (range 33-783 IU/L; reference range 7-64 IU/l). Median prothrombin time was 96% (range 76%-100%).
All patients had IgM against HEV; 13 had IgG against HEV and 2 did not. Serum specimens of 14 patients underwent HEV PCR, and specimens from 11 patients were positive for HEV (Table 2). The median plasma HEV RNA concentration was 4.40 log-copies/mL (range 2.12-5.83).
We were able to sequence 7 virus strains from the patients: all belonged to genotype 3f, the main genotype identified in France. Phylogenetic analyses were conducted with these strains and HEV strains obtained by the French National Reference Center from patients who did not exhibit a neurologic disorder (Figure). The strains were scattered across the phylogenetic tree and were only 87.0%-93.5% identical.
Two patients had eaten game (wild boar and deer). All other patients had eaten pork. All patients had liver enzyme levels within the reference range at the last follow-up.
Fourteen patients had been hospitalized. Neurologic symptoms were classified into 4 categories: mononeuritis multiplex, PTS, meningoradiculitis, and acute inflammatory demyelinating polyradiculoneuropathy (Table 3).
Six patients (3 men and 3 women, patients 1-6) had mononeuritis multiplex; their median age was 54 years (range 25-77 years). Mononeuritis multiplex was defined by asymmetric, asynchronous involvement of the noncontiguous nerve trunks. All patients had experienced neuropathic pain and paresthesia in [greater than or equal to] 1 nerve segments with hyporeflexia or areflexia. For 3 patiens, an electromyogram showed asymmetric axonal neuropathy, and various patterns of nerve involvement were observed. Patients 1 and 6 had confluent but asymmetric (>50%) lower-limb neuropathy (musculocutaneous and external saphenous). Patients 3 and 4 had multiple radicular or proximal troncular neuropathies, and patient 5 had troncular median and internal brachial cutaneous-nerve involvement. Three patients had asthenia and 1 had jaundice; HEV RNA was detected by PCR in serum samples from 4 patients (patients 1, 2, 5, 6).
One patient (patient 6) received specific antiviral treatment. He was given ribavirin, initially at a dose of 400 mg for 7 days (5.5 mg/kg/d) and was then given 600 mg/day (8.5 mg/kg/d) for 3 months. A serum specimen was negative for HEV after 10 days of treatment. Patient 3 was given corticosteroids for 10 weeks. Five patients had no sequelae at the last follow-up (median 33 weeks [range 4-157 weeks]). One patient (patient 2), at the last follow-up at 4 weeks, had ongoing paresthesia in a nerve segment in the lower limbs.
Four patients (3 men and 1 woman, patients 7-10) exhibited PTS, also known as neuralgic amyotrophy. Their median age was 55.5 years (range 51-56 years). These patients sought treatment at the hospital for asthenia and acute neuropathic pain in the shoulder. PTS was bilateral but asymmetric in 3 patients. Asymmetric paresis and amyotrophia appeared within a few days, with the concomitant decrease in pain. Tendon reflexes were reduced or eliminated in 2 patients (patients 9 and 10). For 3 patients, an electromyogram confirmed bilateral patchy denervation, predominantly of the upper trunk of the brachial plexus. For 2 patients (patients 7 and 10), analysis of CSF showed high levels of proteins, levels of cells in reference ranges, and glucose level within reference range. HEV PCR of a CSF specimen was not done.
HEV was diagnosed after IgM against HEV was detected in 1 patient (patient 9) and after HEV RNA was detected in the serum of 3 patients (patients 7, 8, 10). Patients 7 and 10 were given ribavirin (for, respectively, 3 weeks and 2 months) at a dose of 800 mg/day. This treatment was well tolerated. They also received intravenous immunoglobulin (IVIg) at a dose of 25 g/day (patient 7) or 35 g/day (patient 10) for 5 days. All patients but 1 had persistent weakness at the last follow-up (median 71 weeks [range 16-126 weeks]); none had received a control electromyogram. Assessment of patients through disability scales was not possible because this study was retrospective and involved many centers. Notably, the only asymptomatic patient at follow-up was the patient that received both ribavirin and IVIg.
Three patients (2 women and 1 man, patients 11-13) had meningoradiculitis. They were, respectively, 74, 54, and 33 years of age. These patients sought treatment for meningitis symptoms (headache, photophobia) and radiculitis with pain and paresthesia restricted to 1 or a few radicular topographies. CSF was clear and showed lymphocytic meningitis with >90% lymphocytes, a high level of protein (0.79-1.37 g/L, reference range 0.28-0.53 g/L), and glucose levels within reference ranges. Patient 11 had jaundice. PCR of all serum samples from all patients with meningoradiculitis showed HEV RNA. For 2 patients, PCR of CSF was positive for HEV (patients 11 and 12). One woman was breast feeding (patient 13); HEV was detected in her serum but not in breast milk. PCR detected HEV in fecal samples from 2 patients (patients 11 and 13). Patient 11 was treated with IVIg at 0.5 g/kg/day for 4 days. No patient was symptomatic at the last follow-up visit. The median time to follow-up was 119 weeks (range 77-161 weeks).
Acute Inflammatory Demyelinating Polyradiculoneuropathy
Two patients exhibited acute inflammatory demyelinating polyradiculoneuropathy: 1 had GBS, and 1 had Miller-Fisher syndrome. Patient 14, a 60-year-old woman, was hospitalized for GBS. Initially, she had asthenia and acute low back pain. She had a positive viral load for HEV IgG and IgM. A neurologic examination revealed generalized areflexia and weakness in the lower limbs. GBS was confirmed in nerve-conduction studies. She had no hepatic symptoms. CSF analysis showed a high level of protein (2 g/L, reference range 0.28-0.53 g/L) and no HEV RNA. She was treated with IVIg for 5 days at a dose of 400 mg/day, and the symptoms partially regressed. By 5 weeks later, weakness of the lower limbs had improved, but she still experienced persistent areflexia.
Patient 15, a 54-year-old man, was hospitalized for weight loss. A neurologic examination revealed quadridistal hypoesthesia with ataxia, areflexia, and diplopia due to paresia of the right VI nerve. CSF protein concentration was elevated (1.46 g/L, reference range 0.28-0.53 g/L), and albumino-cytologic dissociation was found. Nerve-conduction studies confirmed demyelinating neuropathy. These findings were conclusive for Miller-Fisher syndrome. He had no hepatic symptoms. Serum was positive for IgM against HEV. Serum and fecal samples were negative for HEV by PCR. He received IVIg for 5 days at a dosage of 2 g/kg and was hospitalized for 1 week. His neurologic symptoms improved but did not totally disappear until >13 weeks of follow-up (persistent ataxia).
This study shows the wide spectrum of neurologic injuries associated with patients with an acute HEV autochthonous infection. Because the study was retrospective, it was not possible to identify the prevalence of HEV infection in patients with neurologic symptoms or the prevalence of neurologic symptoms in patients with HEV infection.
Neurologic symptoms could be divided into 4 entities. Notably, the first dominant finding was mononeuritis multiplex, observed in 6 of the 15 patients, with asymmetric, asynchronous, and painful segmental nerve involvement. This condition was also the main entity in the original report, which also included immunocompromised patients with chronic HEV-3 infection (5). In previous reports in immunocompetent patients, painful peripheral neuropathy has rarely been reported (8). However, mononeuritis multiplex is a common complication in immune and viral diseases. A vasculitis process can be hypothesized, but none of the patients in this study underwent a nerve biopsy. Additional investigations, including anatomopathologic exploration, would be needed to further explore the physiopathologic (antiviral and/or immunosuppressive) pathways.
The next most frequent manifestation was PTS, also called brachial neuritis or neuralgic amyotrophy, which was found in 4 patients. PTS is a rare pathologic condition, defined by sudden, acute, and unbearable pain across the top of the shoulder, followed by severe amyotrophy. As was exhibited by the patients described here, PTS can be unilateral or bilateral but is asymmetric. A recent study reported cases of acute HEV infection in a cohort of 47 patients from Cornwall (UK) and the Netherlands (12); 5 cases (10.6%) of acute HEV infection were identified, indicating that HEV may be a major cause of PTS in industrialized countries with a high prevalence of HEV. That study also suggested that HEV-associated brachial neuritis more commonly produces bilateral symptoms and signs than brachial neuritis produced by other causes. In our study, 3 of 4 patients had bilateral symptoms. Three of the 4 patients with PTS had neurologic sequelae at the last follow-up (71 weeks), which suggests that concomitant HEV infection may represent a poor prognostic factor. Van Eijk et al. (12) found that all 5 of their HEV-positive patients exhibited persistent weakness at 6 months.
There is no specific treatment identified for PTS, but it is known to be immune mediated. However, we cannot exclude direct infection of the brachial plexus. Three of the 4 patients in our study had serum samples positive for HEV by PCR, indicating active replication. Two patients were treated with ribavirin as an antiviral therapy. This antiviral therapy is recommended to treat chronic hepatitis E in organ-transplant recipients (16,17). Case reports on the treatment of acute HEV infection in immunocompetent patients have been published, with promising results (18-21). We found that the only patient who had no persisting symptoms at the last follow-up had been treated with a combination of ribavirin and IVIg.
The third neurologic entity we found was meningoradiculitis in 3 patients. HEV was detected in the CSF of 1 case-patient, indicating neurotropism and the direct effect of HEV. This condition is probably the only one in which HEV may be directly responsible for the neurologic manifestations. No neurologic sequelae were seen in this group. A previous study found quasispecies compartmentalization in an immunocompromised patient with neurologic manifestations, and its temporal association suggests that neurologic symptoms could be linked to the emergence of neurotropic variants (22). The factors associated with HEV neurotropism need to be investigated further.
The last entity was acute inflammatory demyelinating polyradiculoneuropathy, which was seen in 2 patients. This condition can be classically triggered by many viruses, including hepatotropic viruses (23). An immune response that cross-reacts with axonemal or Schwann cell antigens is elicited and results in damage to the peripheral nerves. Both patients had persisting neurologic symptoms, commonly seen in this disease (11). Although several studies have demonstrated that HEV infection can induce GBS, this condition was found in only 2 of our patients. In a cohort of GBS case-patients from Bangladesh, seroprevalence of IgM against HEV was 11%, compared with 2% in a control group of patients with other neurologic disease (7). The frequency of HEV infection was recently determined in a cohort of 201 patients with GBS in the Netherlands and was found to have occurred in 5% (11).
The number of patients in this study is too small to draw definitive conclusions on the sex ratio for these conditions, but the ratio was highest in the PTS group. We also found that neurologic disorders occurred only in those with a HEV 3f genotype, although this is the most common genotype in France (24), so other HEV subtypes and genotypes may induce neurologic symptoms (5). Moreover, because only patients with elevated liver enzyme levels were included, neurologic complications were probably underestimated in this study, in particular, for GBS and PTS, for which conditions the neurologic symptoms are often delayed after the initial event is triggered.
Patients with PTS had significantly higher values in liver enzyme tests (aspartate aminotransferase, g-glutamyl transpeptidase) than patients with mononeuritis multiplex. We have no definitive explanation, but this finding could be due to the earlier appearance of PTS symptoms during the course of HEV infection.
Three patients were treated with ribavirin with the aim of shortening the disease's duration: the 2 PTS patients and 1 patient with mononeuritis multiplex. One needed blood transfusions and erythropoietin. Whether ribavirin shortened the evolution of neurologic symptoms, particularly for patients with PTS, needs to be studied further.
One limitation of our study is the retrospective sampling by emailing through the French Liver Association. Although this method provides the advantage of reaching most practitioners who diagnose HEV infection throughout France, it may have induced an ascertainment bias, that is, the true frequency of the neurologic symptoms during HEV infection is difficult to assess. In addition, patients with neurologic symptoms who were not referred to a hepatologist obviously were not accounted for.
In summary, HEV-3 infection can induce a wide range of neurologic symptoms, including mononeuritis multiplex, PTS, meningoradiculitis, and inflammatory demyelinating polyradiculoneuropathy. Sequelae were seen with mononeuropathy multiplex, PTS, and inflammatory demyelinating polyradiculoneuropathy. Only 2 patients had overt hepatitis with jaundice. Therefore, we recommend screening patients with elevated liver enzyme levels and neurologic symptoms for HEV infection, regardless of other symptoms. Treatment with ribavirin needs to be assessed further.
Upon completion of this activity, participants will be able to:
* Distinguish overall aspects of neurologic disorders occurring in immunocompetent patients infected with hepatitis E virus, based on a retrospective case series
* Discuss mononeuritis multiplex occurring in immunocompetent patients infected with hepatitis E virus
* Discuss Parsonage-Turner syndrome occurring in immunocompetent patients infected with hepatitis E virus.
Carol E. Snarey, MA, Copyeditor, Emerging Infectious Diseases. Disclosure: Carol E. Snarey, MA, has disclosed no relevant financial relationships.
Laurie Barclay, MD, freelance writer and reviewer, Medscape, LLC. Disclosure: Laurie Barclay, MD, has disclosed no relevant financial relationships.
Disclosures: Helene Blasco-Perrin, MD; Pascal Cintas, MD; Florence Abravanel, PharmD, PhD; Rene Gerolami, MD, PhD; Louis d'Alteroche, MD; Jean-Noel Raynal, MD; Emmanuel Dupuis, MD; Laurent Prudhomme, MD, PhD; Emmanuel Vaucher, MD; Patrice Couzigou, MD; Jean-Michel Liversain, MD; Louis Buscail, MD, PhD; Jean-Pierre Vinel, MD; Nassim Kamar, MD, PhD; Jacques Izopet, PharmD, PhD; and Jean-Marie Peron, MD, PhD, have disclosed no relevant financial relationships. Laurent Alric, MD, PhD, has disclosed the following relevant financial relationships: served as an advisor or consultant for MSD, BMS, Gilead; served as a speaker or a member of a speakers bureau for MSD; received grants for clinical research from Roche, Janssen, MSD, Gilead. Christophe Bureau, MD, PhD, has disclosed the following relevant financial relationships: served as an advisor or consultant for Norgine Inc.; served as a speaker or a member of a speakers bureau for W.L. Gore & Associates, Inc.; received grants for clinical research from W.L. Gore & Associates, Inc.
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1. Your patient is a 52-year-old man with an acute onset of severe shoulder pain and weakness and moderate elevation in transaminase levels. According to the retrospective case series by Blasco-Perrin and colleagues, which of the following statements about the overall aspects of neurologic disorders occurring in immunocompetent patients infected with hepatitis E virus (HEV) is correct?
A. The 4 syndromes reported were mononeuritis multiplex, Parsonage-Turner syndrome (PTS), ischemic stroke, and hemorrhagic stroke
B. Ten of the 15 patients had overt hepatitis with jaundice
C. All of the patients had complete, spontaneous resolution of their neurologic symptoms without HEV treatment
D. Patients with acute neurologic manifestations and abnormalities in transaminase levels should be screened for HEV
2. According to the retrospective case series by Blasco-Perrin and colleagues, which of the following statements about mononeuritis multiplex occurring in immunocompetent patients infected with HEV is correct?
A. Two of the 15 patients had mononeuritis multiplex
B. This condition is characterized by asymmetric, asynchronous, and painful segmental-nerve involvement
C. Nerve biopsy result proved that this was a vasculitic process
D. All of the patients had neurologic sequelae at last follow-up
3. According to the retrospective case series by Blasco-Perrin and colleagues, which of the following statements about PTS occurring in immunocompetent patients infected with HEV is correct?
A. PTS, also called brachial neuritis or neuralgic amyotrophy, occurred in 4 of the 15 patients
B. PTS is a common condition associated with sudden, acute, severe elbow pain followed by severe amyotrophy
C. All of the patients with PTS had neurologic resolution by the last follow-up
D. This condition is known to be caused only by direct HEV infection of the affected nerve(s)
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Author affiliations: Hopital Purpan-CHU Toulouse, Toulouse, France (H. Blasco Perrin, P. Cintas, F. Abravanel, L. Alric, C. Bureau, J.-P. Vinel, J. Izopet, J.M. Peron); Hopital de La Conception-CHU Marseille, Marseille, France (R. Gerolami); Hopital Trousseau-CHU Tours, Tours, France (L. d'Alteroche); Clinique de l'Union, l'Union, France (J.- N. Raynal); Clinique Pasteur, Toulouse (E. Dupuis); CHIC Castres-Mazamet, Castres-Mazamet, France (L. Prudhomme); CH Narbonne, Narbonne, France (E. Vaucher); Hopital du Haut-Leveque-CHU Bordeaux, Bordeaux, France (P. Couzigou); CH Mont de Marsan, Mont de Marsan, France (J.-M. Liversain); Hopital Ranguei-CHU Toulouse, Toulouse (L. Buscail, N. Kamar)
Dr. Blasco-Perrin was an intern from 2010 to 2015 at the Toulouse University hospital in the gastrointestinal and hepatology units. She will be a fellow in the hepatology unit, Purpan Hospital, CHU Toulouse, France, in 2016. . Her research interests focus on viral hepatitis, in particular, hepatitis E.
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Address for correspondence: J.-M. Peron, CHU Toulouse, Purpan-Service Hepato Gastro Enterologie, Place du Dr Baylac, Pavilion Dieulafoy, Toulouse 31039, France; email: firstname.lastname@example.org
Table 1. Clinical characteristics of 15 patients with hepatitis E virus-linked neurologic disorders, France, January 2006-June 2013 * Patient Neurologic Age, Treatment Other symptoms no. pathology y/sex 1 MM 59/M None Asthenia 2 MM 44/F None Fever, asthenia, arthromyalgia 3 MM 65/M Corticosteroids Asthenia 4 MM 25/F None None 5 MM 49/M None None 6 MM 77/F RBV None 7 PTS 51/M RBV + IVIg Arthromyalgia, asthenia 8 PTS 55/F None Asthenia, arthromyalgia 9 PTS 56/M None Asthenia 10 PTS 56/M RBV + IVIg Asthenia 11 MR 74/M IV Ig Arthromyalgia, asthenia 12 MR 54/F None Fever, nausea 13 MR 33/F None Fever, arthromyalgia 14 GBS 60/F IV Ig Asthenia, acute low back pain 15 MFS 54/M IV Ig Asthenia, anorexia Patient Neurologic Follow up no. symptoms times, wk at last follow-up 1 No 10 2 Yes 4 3 No 157 4 No 33 5 No NA 6 No 44 7 No 100 8 Yes 126 9 Yes 42 10 Yes 16 11 No 77 12 No NA 13 No 161 14 Yes 5 15 Yes 13 * MM, mononeuritis multiplex; PTS, Parsonnage-Turner syndrome; MR, meningoradiculitis; GBS, Guillain-Barre syndrome; MFS, Miller-Fisher syndrome; RBV, ribavirin; IVIg, intravenous immunoglobulin; NA, not available. Table 2. Liver test results and virologic characteristics of 15 patients with hepatitis E virus-linked neurologic disorders, France, January 2006-June 2013 * Patient Diagnosis AST, ALT, Bilirubin, no. IU/L IU/L [micro]mol/L i MM 69 256 8.6 2 MM 507 756 17 3 MM NA 3,641 90 4 MM 54 120 10 5 MM 50 118 14 6 MM 71 119 14 7 PTS 897 1,834 42 8 PTS 1.330 1,900 15 9 PTS 601 1,376 15 10 PTS 135 495 17 11 MR 1.742 822 101 12 MR 221 566 11 13 MR 100 246 4.7 14 AIDP 113 384 34.2 15 AIDP 37 49 7 Patient ALKP, GGT, PT, % GT no. Iu/L IU/L i 254 323 92 3f 2 540 187 90 3f 3 NA NA 80 NA 4 NA 95 100 NA 5 90 95 95 NA 6 430 131 100 3f 7 336 383 88 NA 8 194 182 95 NA 9 231 601 95 NA 10 659 740 100 3f 11 704 528 76 3f 12 124 184 100 NA 13 248 33 98 3f 14 474 783 100 3f 15 88 48 94 NA Patient Serology Serum viral PCR PCR no. load, log stools CSF copies/mL i IgG+/IgM+ 4.92 NA NA 2 IgG+/IgM+ 5 Pos NA 3 IgG+/IgM+ Neg Neg NA 4 IgG+/IgM+ Neg Neg NA 5 IgG+/IgM+ Pos NA Neg 6 IgG-/IgM+ 5.57 Pos NA 7 IgG+/IgM+ 2.12 NA NA 8 IgG+/IgM+ 2.81 NA NA 9 IgG+/IgM+ NA NA NA 10 IgG+/IgM+ 3.89 Pos NA 11 IgG+/IgM+ 5.83 Pos Pos 12 IgG+/IgM+ Pos NA Pos 13 IgG-/IgM+ 2.9 Pos Neg 14 IgG+/IgM+ Pos Pos Neg 15 IgG+/IgM+ Neg Neg Neg * AST, aspartate aminotransferase; ALT, alanine aminotransferase; ALKP, alkaline phosphatase; GGT, [gamma]-glutamyl transpeptidase; PT, prothrombin time; GT, genotype; CSF, cerebrospinal fluid; MM: mononeuritis multiplex, NA, not available; Pos, positive; Neg, negative; PTS: Parsonage-Turner syndrome; MR: meningoradiculitis; AIDP, acute inflammatory demyelinating polyradiculoneuropathy. Table 3. Average biological values of the 4 groups of patients with hepatitis E virus-linked neurological disorders * Disorder Age, y Sex AST, IU/L ([+ or -] SD) (range) ratio MM 54 (25-77) 1 150 ([+ or -] 200) ([dagger]) PTS 55 (51-56) 6 740.7 ([+ or -] 503) MR 54 (33-74) 2 687.7 ([+ or -] 915) AIDP 57 (54-60) 1 75 ([+ or -] 54) Disorder ALT, IU/L ([+ or -] SD) PT, % ([+ or -] SD) MM 835 ([+ or -] 1,396) 92.8 ([+ or -] 7.5) PTS 1,401.25 ([+ or -] 647) 94.5 ([+ or -] 4.9) MR 544.67 ([+ or -] 288) 91.3 ([+ or -] 13.3) AIDP 216 ([+ or -] 236) 97 ([+ or -] 4) Disorder Bilirubin, ALKP, IU/L [micro]mol/L ([+ or -] SD) ([+ or -] SD) MM 25.6 ([+ or -] 32) 328.5 ([+ or -] 198) PTS 22.2 ([+ or -] 13) 355 ([+ or -] 211) MR 38.9 ([+ or -] 54) 358.67 ([+ or -] 305) AIDP 20.6 ([+ or -] 19) 281 ([+ or -] 272) Disorder GGT, IU/L ([+ or -] SD) MM 166.2 ([+ or -] 95) ([dagger]) PTS 476.5 ([+ or -] 245) MR 248.3 ([+ or -] 253) AIDP 415 ([+ or -] 519) * AST, aspartate aminotransferase; ALT, alanine aminotransferase; PT, prothrombin time; ALKP, alkaline phosphatase; GGT, [gamma]-glutamyl transpeptidase; MM, mononeuritis multiplex; PTS, Parsonage-Turner syndrome; MR, meningoradiculitis; AIDP, acute inflammatory demyelinating polyradiculoneuropathy. ([dagger]) p < 0.05 when compared with PTS.
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|Author:||Perrin, H. Blasco; Cintas, P.; Abravanel, F.; Gerolami, R.; d'Alteroche, L.; Raynal, J.-N.; Alric, L|
|Publication:||Emerging Infectious Diseases|
|Date:||Nov 1, 2015|
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