Hepatitis B and C in institutions for individuals with intellectual disability

People with intellectual disability are a well-known high-risk group for hepatitis B virus (HBV) infection. Hepatitis B virus is a major public health problem, but it is often neglected because of its largely asymptomatic course with long-term complications. Safe and effective vaccines have been available for over 15 years. However, universal vaccination strategies have not or have not completely been implemented to date, even though epidemiological data have indicated the effectiveness and efficacy of vaccination, and economic evaluations have shown that it is cost effective. Hepatitis C virus (HCV), which was discovered in 1989, has similar risk factors and is also a cause of chronic hepatitis. The prevalence of HCV amongst individuals with intellectual disability has not been clearly established. An overview of the literature on the prevalence of HBV and HCV in this population, as well as risk factors, transmission and prevention is presented in the present review. The literature cited in the present article was obtained by searches in MedLine using the following keywords and keyword combinations: hepatitis, hepatitis B virus, hepatitis C virus, mentally retarded, mentally handicapped, developmentally retarded, intellectual disability, institutionalization, Down's syndrome and hepatitis B vaccination. The search was done from 1980 to 1998. Beside this, the older articles found in the references were included if these were considered necessary for completeness.     

Severe exacerbation of hepatitis C-associated vasculitic neuropathy following treatment with interferon alpha: a case report and literature review

Vasculitic neuropathy may occur in association with chronic hepatitis C infection. Interferon alpha (IFN(alpha)), an effective treatment for chronic hepatitis C, can precipitate or worsen autoimmune diseases. We report a patient with chronic hepatitis C and mild indolent vasculitic sensorimotor peripheral polyneuropathy, who developed severe mononeuropathy multiplex soon after IFN(alpha) was initiated, and review the literature on worsening vasculitic neuropathy after IFN(alpha) treatment for chronic hepatitis C. Care should be taken after starting patient with chronic hepatitis C-associated vasculitic neuropathy on IFN(alpha), as there is evidence that IFN(alpha) may exacerbate the neuropathy.     

Hepatitis E–induced severe myositis

Introduction: Our objective was to compare the effect of different low‐frequency filters on jitter parameters when stimulating the orbicularis oculi. Methods: Ten healthy volunteers were studied. Jitter was expressed as the mean consecutive difference (MCD). The low filter settings compared were 1, 2, and 3 kHz . Results: No significant difference in mean MCD or outliers was found with the different filter settings. No significant difference in mean MCD was seen when the number of potentials analyzed was reduced. Conclusion: Different low‐frequency settings do not influence the mean MCD when using a peak detection system. Muscle Nerve 54 : 317–319, 2016     

精神科住院患者病毒性肝炎感染状况调查

目的调查精神科住院患者病毒性肝炎感染的阳性率。方法对2004年1月～2005年12月的住院精神科患者4990例采用ELISA方法进行HBsAg、抗-HBs、HBeAg、抗-HBe、抗-HBc、抗-HCV、抗HEV-IgG检测。结果4990例住院精神科患者中HBsAg阳性174例,阳性率为3.5%;抗-HCV阳性28例,阳性率为0.56%;抗HEV-IgG阳性9例,阳性率为0.18%。结论根据精神科患者的特点,应加强病房患者管理,防止病毒性肝炎的院内感染。     

Mononeuropathy Multiplex in a Patient with Chronic Active Hepatitis B

Background

Mononeuropathy multiplex is a rare complication during the course of chronic hepatitis B, despite various neuropathies following acute hepatitis B having been reported previously.

Case Report

A 30-year-old man presented with sensorimotor symptoms in multiple peripheral nerves. The serological tests for hepatitis were consistent with chronic active hepatitis B. After treatment with oral prednisone combined with an antiviral agent, the sensory and motor symptoms improved and hepatitis B virus replication was reduced.

Conclusions

We suggest that chronic immune-mediated neuropathy associated with hepatitis B virus infection should be considered in the differential diagnosis of patients with hepatitis B.     

Hepatitis A post-viral encephalitis

We report a seven-year-old girl who developed a hepatitis A viral infection and encephalitis. The patient developed fever, abdominal pains and jaundice. Five days later she became delirious, combative, and did not respond to verbal commands. Laboratory studies showed elevated liver enzymes and elevated serum immunoglobulin M (IgM) and immunoglobulin G (IgG) antibodies to hepatitis A virus. Cerebrospinal fluid contained IgG antibodies to hepatitis A virus but not IgM antibodies. Polymerase chain reaction, which amplifies a portion of the hepatitis A virus genome, did not demonstrate viral nucleic acid in cerebrospinal fluid. These studies suggest that the patient may have suffered from a post-viral hepatitis A encephalitis from which she fully recovered.     

Assessment for evidence of non a-non b hepatitis in patients given n-heptane-suspended heat-treated clotting factor concentrates

Nineteen patients, (2 adults, 17 children) with inherited bleeding disorders were infused with n-heptane-suspended-heated clotting factor concentrates. Twelve of the nineteen were previously untreated. Six patients were infused with Profilnine Heat-Treated® and 13 with Profilate Heat-Treated. Five separate centers participated and were given various lots of concentrates for use. Blood from the seventeen children was sampled prior to entry, at infusion, 2 weeks, 6 weeks, 12 weeks and 6 months after the first infusion. The two adults were sampled every 2 weeks. Twelve of the 19 patients were followed beyond six months. Three patients demonstrated a rise in ALT during the first six months of observation with levels above 2.5 times the upper limit of normal. One of these patients showed a parallel increment in a-CMV IgM titer and a second patient, an adult, had previously received many units of single donor blood components. During the second 6 month observation interval, two patients showed a rise in ALT. One of these patients had been exposed to only one lot of concentrate with no other viral cause being determined. Two additional patients had a moderate increase in ALT up to 98 U/L (normal <50). No patients were clinically ill or showed jaundice during these episodes. The hepatitis episode at 11 months in the patient using one lot of concentrate, might suggest a non-viral mechanism in this instance. This study indicates that these concentrates may be associated with episodes of ALT above 2.5 times the upper limit of normal in approximately 20% of the patients treated, but the etiology of the raised ALT may not always be Non A-Non B hepatitis.     

Olfactory neural pathway in mouse hepatitis virus nasoencephalitis

Summary The mechanism of brain infection with mouse hepatitis virus-JHM was studied in BALB/cByJ mice following intranasal inoculation, and found to be a consequence of direct viral spread along olfactory nerves into olfactory bulbs of the brain. Infection was followed sequentially from nose to brain, using microscopy, immunohistochemistry and virus quantification. Lesions, antigen and virus were observed in the olfactory bulb and anterior brain as early as 2 days and posterior brain by 4 days after inoculation. Viral antigen extended through nasal mucosa into submucosa, then coursed along the olfactory nerve perineurium and fibers, through the cribriform plate into the olfactory bulbs. On days 4 and 7, viral antigen was found in the antero-ventral brain, along ventral meninges, olfactory tracts and anterior ramifications of the lateral ventricles. Virus was cleared from nose by 10 days and anterior brain by 20 days, but persisted in posterior brain for 20 days after inoculation. Mice also developed disseminated infection, with viremia and hepatitis. Infection of brain did not correlate with presence of viremia. In contrast to intranasally inoculated mice, orally-inoculated mice did not develop encephalitis, despite evidence of disseminated infection.Supported by USPHS grant RR-02039 from the Division of Research Resources, National Institutes of Health, Bethesda, Md, USA     

Hepatitis C and depression

Although the incidence of hepatitis C virus (HCV) is declining, a large reservoir of patients with chronic hepatitis C exists. Unless effective HCV antiviral regimens are developed, many patients with asymptomatic HCV will develop clinical symptoms in the next 15 to 20 years. Mood disorders are common in patients with HCV referred for psychiatric consultation. Interferon is the primary treatment for chronic hepatitis C but can induce depression and other mental and neuropsychiatric syndromes. Mood disorders associated with hepatitis C may respond to psychiatric intervention. Psychiatrists need to be aware of the clinical issues in the diagnosis and treatment of depression complicating chronic hepatitis C. Depression and Anxiety 7:188–193, 1998. © 1998 Wiley-Liss, Inc.     

Hepatitis B vaccine related‐myelitis?*

We present four incidental cases that developed partial myelitis following the administration of hepatitis B vaccine in 1998. The first two cases, a 33-year-old man and a 42-year-old woman developed progressive sensory symptoms without motor involvement within 4 weeks following the vaccination. Their magnetic resonance imaging (MRI) disclosed similar lesions consistent with myelitis at their cervical spinal cord. A comparable inflammatory lesion was seen at the T9-T10 levels of the spinal cord in the third case, who was a 40-year-old woman presenting with numbness in her legs and urinary retention following the vaccination. The fourth case who was a 42-year-old woman, presented with sensory symptoms in her left extremities, which developed 3 months after the vaccination. Her MRI showed a hyperintense lesion at C6. She also had two tiny lesions in her cranial MRI. In all cases, there was no history of preceding infections and no clinical evidence suggestive of any other disorders that may cause myelopathy. All patients recovered completely within 3 months with the exception of the third patient who developed new neurological symptoms after 12 months. Similar clinical and imaging presentation of myelitis following hepatitis B vaccination within a 1 year period with no other demonstrable clinical and laboratory evidence for any other disorder raise the probability of a causal link between these two events.     

丙型肝炎病毒阳性受者肾移植后的安全性分析

背景：对于丙肝病毒阳性患者接受肾移植后安全性的问题是目前大家关注的热点。 目的：丙型肝炎病毒感染者接受肾移植后临床观察及处理对策。 方法：纳入22例患者,肾移植前肝炎病毒RNA均为阳性,其中14例患者肝功能轻度升高。移植后定期检测患者的肝、肾功能,积极防治可能的排斥反应。主要观察患者一般情况、肝、肾功能、肝炎病毒基因学情况及死亡率。 结果与结论：移植后随访6~36个月,20例患者移植后4周~6个月内出现不同程度的肝功能异常,予护肝治疗后肝功能均恢复正常,1例移植后HCV-RNA 阳性患者,因自行改变抗排斥方案于移植后1.5年出现严重的肝功能衰竭而死亡;4例患者移植后应用干扰素和利巴韦林治疗,HCV-RNA转阴,其余18例患者HCV-RNA均呈阳性,需长期护肝治疗。表明,对丙肝病毒阳性受者,移植后应进行严格的随访,出现肝功能异常时,及时采取相应处理和护肝治疗。     

精神分裂症患者乙型肝炎病毒感染调查

目的:调查精神分裂症患者的乙型肝炎病毒(HBV)感染与肝功能异常情况。方法:对312例精神分裂症住院患者的HBV感染及丙氨酸氨基转移酶(ALT)异常进行流行病学调查,以健康体检者279名为对照。结果:精神分裂症患者的HBV感染率为71.8%,ALT异常率为29.5%,明显高于对照组,精神分裂症患者中两性间HBsAg阳性率以男性显著较高。再次住院患者的HBV感染显著比首次住院患者高。结论:对精神分裂症患者应加强隔离措施,特别是HBsAg阳性的患者,防止交叉感染;加强健康教育,加强饮食营养支持和乙肝疫苗的接种等措施。     

Endothelial protein C receptor plasma levels increase in chronic liver disease, while thrombomodulin plasma levels increase only in hepatocellular carcinoma

INTRODUCTION: Thrombomodulin (TM) and endothelial protein C receptor (EPCR) are two transmembrane endothelial receptors involved in the protein C pathway, that regulates coagulation and inflammation processes. We postulated that soluble thrombomodulin and EPCR are plasmatic markers of progression to hepatocellular carcinoma (HCC) and prognostic indicators in cirrhotic patients. MATERIALS AND METHODS: Plasma levels of TM and EPCR were measured in 104 patients affected by different stages of liver diseases (66 patients with HCC, and 38 without HCC), and in 52 healthy controls. RESULTS: EPCR levels were higher in patients than in controls (239+/-1.8 ng/mL vs. 127+/-1.5 ng/mL, p<0.0001). TM levels were higher in patients with HCC than in those without (42.1+/-2.0 ng/mL vs. 28.3+/-2.1 ng/mL; p=0.039), while EPCR levels were similar in the two groups. No association between TM and clinical outcome was found, while high levels of EPCR were associated with death and thrombosis of the portal vein. CONCLUSIONS: We surmise a possible role for high levels of TM as a marker of HCC development in patients with cirrhosis, whereas high levels of EPCR are a possible marker of worse HCC prognosis, being a sign of endothelial damage of large vessels.     

Motor-axonal polyneuropathy associated with hepatitis C virus

The association between hepatitis C virus (HCV) infection, the presence of mixed cryoglobulinemia and peripheral neuropathy is well-documented (Apartis et al., 1996). HCV is the chief cause of essential mixed cryoglobulinemia (type II cryoglobulinemia) with cryoglobulins present in up to half of patients with HCV infection (Akriviadis et al., 1997). More recently it has been stated that peripheral polyneuropathy may be associated with HCV chronic infection without mixed cryoglobulinemia (Lidove et al., 2001). Patients usually present with a clinical and electrophysiology--predominantly sensory axonopathies (Apartis et al., 1996; Heckmann et al., 1999) or less frequently with fulminating vasculitis and mononeuropathy multiplex syndrome (David et al., 1996)--especially when associated with cryoglobulinemia. We report, for the first time, the association between pure motor-axonal polyneuropathy and HCV infection without cryoglobulinemia.     

Hemiballism with insular infarction as first manifestation of Takayasu's arteritis in association with chronic hepatitis B

Background: Takayasu's arteritis is a chronic inflammatory idiopathic disease involving large arteries like the aorta and its primary branches. Cell-mediated autoimmunity leading to vascular injury has been suspected in its pathogenesis although the antigen inducing the process remains unknown. Case report: A 50-year-old male patient suffered from acute hemiballism. Neuroimaging showed an infarction of right temporal insular cortex. Neurosonology and MR-Angiography revealed bilateral long-distant subtotal stenosis of the common carotid artery and left-sided occlusion of the subclavian artery. Positive hepatitis B serology with active viral replication was found. In the absence of other vasculitis or inflammation markers, Takayasu's arteritis was diagnosed and steroid therapy was started. Conclusions: Unilateral insular lesions may lead to transient hemiballistic movements which could be the result of decreased inhibitory output of the insula to basal ganglia. The hepatitis B virus possibly contains a surface antigen inducing a specific cellular immune response leading to Takayasu's arteritis. Received: 25 May 2002, Received in revised form: 25 September 2002, Accepted: 9 October 2002 Correspondence to Dr. Thorleif Etgen     

In vivo detection of hepatitis C virus (HCV) RNA in the brain in a case of encephalitis: evidence for HCV neuroinvasion

We report here a 27-year-old woman who presented with encephalitis of unknown origin. Magnetic resonance imaging (MRI) of the brain revealed leukoencephalopathy, cerebrospinal fluid showed signs of inflammation. Serum and brain biopsy tissue was tested positive for hepatitis C virus (HCV). Neuropathological investigation supported the hypothesis of viral encephalitis. C3, C4 and cryoglobulins as well as cerebral MR-angiography were normal. Neurological complications of HCV infection other than hepatic encephalopathy are generally attributed to parainfectious phenomena. This is the first case of HCV-RNA detection in vivo in human brain in literature and it raises the possibility that HCV is able to induce encephalitis caused by neurotrophism. This is supported by the fact that there is a growing body of literature on HCV-induced cerebral dysfunction and laboratory findings indicating HCV neuroinvasion.     

Severe course of neuromyelitis optica in a female patient with chronic C hepatitis

Neuromyelitis optica (NMO) is a rare, disabling, recurring inflammatory demyelinating disease affecting the spinal cord and optic nerves with predominance in women.We present the case of a female patient with chronic C hepatitis, who, despite treatment, developed severe symptoms of NMO during pregnancy and postpartum.