Markers of hepatitis B virus (HBV) and delta agent were prospectively tested in sera of 107 intravenous drug abusers with acute hepatitis positive for hepatitis B surface antigen (HBsAg) associated with delta infection and compared with the findings in addicts with acute classical hepatitis B. On the basis of the presence and titer of IgM antibody to hepatitis B core antigen, 86 of the addicts with delta infection had simultaneously acquired HBV and delta agent, and 21 were chronic carriers of HBsAg experiencing acute delta superinfection. The frequencies of biphasic and severe hepatitis were significantly higher (P less than .05) in delta agent-infected patients than in controls, but the acute clinical and biochemical features of the two varieties of delta disease were not distinguishable. However, in analogy to the clinical outcome of classical hepatitis B, all patients with nonfatal acute HBV/delta coinfection had self-limited illness, whereas 20 of 21 HBsAg carriers superinfected by delta agent developed chronic active hepatitis.
Antiretroviral toxic neuropathy causes morbidity in human immunodeficiency virus (HIV) patients under dideoxynucleoside therapy, benefits only partially from medical therapy, and often leads to drug discontinuation. Proposed pathogeneses include a disorder of mitochondrial oxidative metabolism, eventually related to a reduction of mitochondrial DNA content, and interference with nerve growth factor activity. Carnitine is a substrate of energy production reactions in mitochondria and is involved in many anabolic reactions. Acetyl carnitine treatment promotes peripheral nerve regeneration and has neuroprotective properties and a direct analgesic role related to glutamatergic and cholinergic modulation. The aim of this study was to evaluate acetyl-l-carnitine in the treatment of painful antiretroviral toxic neuropathy in HIV patients. Twenty subjects affected by painful antiretroviral toxic neuropathy were treated with oral acetyl-l-carnitine at a dose of 2,000 mg/day for a 4-week period. Efficacy was evaluated by means of the modified Short Form McGill Pain Questionnaire with each item rated on an 11-point intensity scale at weekly intervals and by electromyography at baseline and final visit. Mean pain intensity score was significantly reduced during the study, changing from 7.35 +/- 1.98 (mean +/- SD) at baseline to 5.80 +/- 2.63 at week 4 (p = 0.0001). Electrophysiological parameters did not significantly change between baseline and week 4. In this study, acetyl-l-carnitine was effective and well tolerated in symptomatic treatment of painful neuropathy associated with antiretroviral toxicity. On the contrary, no effect was noted on neurophysiological parameters.
The aim of this work was first to determine whether the cutaneous silent period (CSP), a marker of small-nerve-fibre function, was altered in human immunodeficiency virus (HIV)-positive subjects with predominantly sensory symmetrical polyneuropathy and, second, to assess whether such alterations were predictive of an impairment in the largest calibre sensory and motor nerve fibres of the upper limb (UL) peripheral nerves. CSP was assessed in three groups of subjects: healthy control subjects, HIV-positive subjects with peripheral neuropathy (PN) of the lower limbs, and HIV-positive patients with clinical and neurophysiological involvement of the four limbs. CSP study showed a significant increase of the latency compared to the controls both in HIV-positive cases with no impairment in the UL (p=0.006) and in patients with four-limb neuropathy (p=0.002). CSP study in HIV-positive patients with mild lower limb distal sensory polyneuropathy can detect an early involvement of the UL peripheral nerves. CSP latency increase could therefore be addressed as the first sign of PN spreading to the UL.
Sera from 162 patients with acute or chronic hepatitis and from patients with autoimmune diseases have been investigated for autoantibodies by indirect immunofluorescence on human and animal tissues. A small proportion (14.2%) of young patients with chronic δ hepatitis has been found positive for cytoplasmic staining which was maximal in hepatocytes and renal proximal tubules. This autoantibody has been found to react with microsomal antigenic determinant different from the classic liver-kidney microsomal LKM antigen as demonstrated by fluorescence absorption experiments with purified subcellular organelles and by fluorescence-blocking tests. The microsomal autoantibody displayed also organ and species-specificity different from those shown by the LKM-positive sera. The positive patients showed persistence of the microsomal autoantibody during the follow-up without other serological markers of autoimmunity. There was no evidence of a particular course of chronic δ hepatitis in patients positive for the microsomal autoantibody.
Introduction: Acetyl‐L‐Carnitine (ALC) is a safe and well‐tolerated drug in the treatment of peripheral neuropathy in HIV infected patients. Its efficacy is focused on its role in modulating TNF‐alpha expression and on the restoration of endogenous acetylcarnitine. Peripheral nervous system is frequently involved during HIV infection and distal sensitive polyneuropathy is one of the most common neurological complications (up to 30% of AIDS patients). Etiology is still unknown. One of the pathogenetic hypotheses is the role of proinflammatory cytokines (TNF‐alpha) in causing neuropathic pain. Method: Twenty HIV‐ positive patients affected by neuropathic pain with EMG‐evidence of axonal alterations were enrolled; we excluded patients with mini‐mental test score < 24, acute CMV infection, chronic demyelinating neuropathies. All patients were treated with ALC at the dose of 1 gram t.i.d. for 4 weeks. A visual analogue scale (VAS) was used to evaluate characteristics of patient's pain before, during, and after treatment. EMG and neurographic assessment was performed before and after treatment. To evaluate changes in VAS score we used non‐parametric Friedman's test (F). Wilcoxon's test (W) was performed to timing the appearance of pain improvement, and to evaluate neurophysiological data. Results: The changes in VAS score were statistically significant during ALC treatment (mean score: before 6.7 ± 2.1 – after treatment 5.0 ± 2.1)(F = P < 0.001). The appearance of therapeutic effect was reached during the first week (W = P < 0.03) and during the fourth week (W = P < 0.05) of treatment. Analysis of neurophysiological data showed a statistically significant improvement of peroneal nerve motor parameters: reduced motor distal latency (W = P < 0.02), increased amplitude of the compound motor action potential at distal (W = P < 0.02) and proximal (W = P < 0.05) site of stimulation. Conclusions: Our data show the efficacy of ALC in the treatment of neuropathic pain, confirming previous results. Moreover, the analgesic effects appear during the first week of treatment according with pre‐clinical data in different experimental models of pain. Among mechanisms for ALC efficacy in patients with HIV‐related polyneuropathy, there is a neurotrophic effect as evidenced from patch‐skin biopsy evaluation.
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