***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: 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 Question naire 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 Acetyl-L-carnitine ( ALC ) improves  non-oncological neuropathies .  We tested oral ALC ( 1 g tid ) for 8 weeks in 25 patients with neuropathy grade 3 ( common toxicity criteria --CTC ) during paclitaxel or cisplatin therapy , or grade 2 persisting for at least three months after discontinuing the drugs . An independent neurologist assessed patients before and after ALC . All patients except one reported symptomatic relief , and only two described grade 1 nausea . The sensory neuropathy grade improved in 15 of 25 ( 60 % ) , and motor neuropathy in 11 of 14 patients ( 79 % ) . Total neuropathy score ( TNS ) that included neurophysiological measures improved in 23 ( 92 % ) . Amelioration of sensory amplitude and conduction velocity ( sural and peroneal nerves ) was measured in 22 and 21 patients , respectively . Symptomatic improvement persisted in 12 of 13 evaluable patients at median 13 months after ALC . In view of its effect in improving established paclitaxel- and cisplatin-neuropathy , we recommend ALC testing in preventing progression or revert symptoms during neurotoxic chemotherapy Purpose Retreatment with bortezomib ( B ) is often considered for patients with relapsed multiple myeloma ( MM ) , but this strategy is hindered by uncertainty of response and emergence of B-induced peripheral neuropathy ( PN ) . We incorporated acetyl-l-carnitine ( ALCAR ) to prevent PN and allow for adequate dosing . We also investigated the correlation between B-inducible NF-κB activation and response to therapy . Methods Nineteen patients with relapsed/refractory MM received up to 8 cycles of intravenous bortezomib , doxorubicin and oral low-dose dexamethasone ( BDD ) to evaluate response and toxicity . Thirteen additional patients received prophylactic ALCAR ( BDD-A ) . Patients receiving BDD-A were evaluated by FACT-GOG-TX , FACIT-Fatigue , Neuropathic Pain index ( NPI ) and Grooved Pegboard ( GP ) testing . Primary MM cells from 11 patients were tested for B-inducible NF-κB activation . Results Seventy-six percent of subjects were refractory to previous treatment , 39 % refractory to bortezomib . Median cycles received were 5 . CR + PR for the entire group were 53 % and did not differ between groups . Incidence of ≥3 PN was 32 % in the BDD group versus 15 % in the BDD-A group ( p = ns ) . Patient-reported fatigue and PN measured by FACT-GOG-TX increased throughout the treatment period in the BDD-A group , although time to complete GP testing declined . In a sub- study examining constitutive bortezomib-inducible NF-κB activity in primary subject-specific MM cells , the presence of NF-κB activation correlated with lower likelihood of response . Conclusions Addition of ALCAR to BDD did not alter the incidence or severity of PN in relapsed MM patients receiving a B-based regimen . Bortezomib-inducible NF-κB activation in patient-derived primary MM cells may be associated with poorer response The aim of this study was to investigate the antioxidant effect of acetyl-L-carnitine ( ALC ) against gamma-irradiation-induced oxidative damage in liver and lung tissue after total body irradiation with a single dose of 6Gy . To achieve the ultimate goal of this study , 40 adult rats were r and omly divided into 4 groups of 10 animals each . Group I was injected intraperitoneally with saline solution for 5 consecutive days and served as control group . Group II was irradiated with a single dose of 6Gy . Group III was daily injected with ALC ( 250 mg kg(-1 ) , i.p . ) for 5 consecutive days . Group IV received a daily i.p . injection of ALC ( 250 mg kg(-1 ) , i.p . ) for 5 consecutive days and 1h after the last dose , rats were irradiated with a single dose ( 6Gy ) . The animals were sacrified after 24h . Administration of ALC for 5 consecutive days result ed in a significant increase in the activities of both superoxide dismutase ( SOD ) and glutathione peroxidase ( GSHPx ) and the level of reduced glutathione ( GSH ) , in lung and liver tissues which were reduced by radiation treatment . Also , ALC result ed in a significant decrease in total nitrate/nitrite ( NO(x ) ) and malondialdehyde ( MDA ) levels in both lung and liver tissues and a significant decrease in triglycerides , low-density lipoprotein-cholesterol ( LDL ) , high-density lipoprotein-cholesterol ( HDL ) , total cholesterol , Serum alanine aminotransferase ( ALT ) , aspartate aminotransferase ( AST ) levels and Gamma glutamyl transpeptidase ( GGTP ) compared to irradiated group . In conclusion , data obtained from this study indicate that ALC could increase the endogenous antioxidant defense mechanism in rat and there by protect the animals from radiation-induced organs toxicity Abstract Aims / Introduction To assess the efficacy and safety of acetyl‐L‐carnitine ( ALC ) on diabetic peripheral neuropathy compared with methylcobalamin ( MC ) . Material s and methods This was a multicenter , r and omized , parallel‐group , double‐blind , double‐dummy , positive‐controlled , non‐inferior phase II clinical trial . Diabetic patients with abnormal nerve conduction test results were r and omized in a 1:1 ratio to receive oral ALC 500 mg t.i.d . or MC 0.5 mg t.i.d . for 24 weeks . The neuropathy symptom score , neuropathy disability score and neurophysiological parameters were measured during follow up . Results A total of 232 patients were r and omized ( ALC n = 117 , MC n = 115 ) , 88 % of which completed the trial . At week 24 , patients from both groups had significant reductions in both neuropathy symptom score and neuropathy disability score with no significant difference between two groups ( neuropathy symptom score reduction : ALC vs MC 2.35 ± 2.23 , P < 0.0001 vs 2.11 ± 2.48 , P < 0.0001 , intergroup P = 0.38 ; neuropathy disability score reduction ALC vs MC 1.66 ± 1.90 , P < 0.0001 vs 1.35 ± 1.65 , P < 0.0001 , intergroup P = 0.23 ) . Neurophysiological parameters were also improved in both groups . No significant difference was found between groups in the development of adverse events . Conclusions ALC is as effective as MC in improving clinical symptoms and neurophysiological parameters for patients with diabetic peripheral neuropathy over a 24‐week period with good tolerance OBJECTIVE We evaluated frozen data bases from two 52-week r and omized placebo-controlled clinical diabetic neuropathy trials testing two doses of acetyl-L-carnitine ( ALC ) : 500 and 1,000 mg/day t.i.d . RESEARCH DESIGN AND METHODS Intention-to-treat patients amounted to 1,257 or 93 % of enrolled patients . Efficacy end points were sural nerve morphometry , nerve conduction velocities , vibration perception thresholds , clinical symptom scores , and a visual analogue scale for most bothersome symptom , most notably pain . The two studies were evaluated separately and combined . RESULTS Data showed significant improvements in sural nerve fiber numbers and regenerating nerve fiber clusters . Nerve conduction velocities and amplitudes did not improve , whereas vibration perception improved in both studies . Pain as the most bothersome symptom showed significant improvement in one study and in the combined cohort taking 1,000 mg ALC . CONCLUSIONS These studies demonstrate that ALC treatment is efficacious in alleviating symptoms , particularly pain , and improves nerve fiber regeneration and vibration perception in patients with established diabetic neuropathy Aims and background In addition to bone marrow suppression and renal toxicity , neurotoxicity is a commonly occurring side effect of widely used chemotherapeutic agents like taxanes , cisplatin and vinca alkaloids . Neurotoxicity can cause antitumor therapy discontinuation or dose regimen modification . The aim of the present exploratory study was to investigate the activity of acetyl-L-carnitine in reversing peripheral neuropathy in patients with chemotherapy-induced peripheral neuropathy . Methods and study design Twenty-seven patients ( 16 males and 11 females ) with paclitaxel and /or cisplatin-induced neuropathy ( according to WHO recommendations for the grading of acute and subacute toxic effects ) were enrolled . Patients received at least one cisplatin- ( n = 5 ) or one paclitaxel- ( n = 11 ) based regimen , or a combination of both ( n = 11 ) . Patients with chemotherapy-induced peripheral neuropathy were treated with acetyl-L-carnitine 1 g/die iv infusion over 1 - 2 h for at least 10 days . Results Twenty-six patients were evaluated for response having completed at least 10 days of acetyl-L-carnitine therapy ( median , 14 days ; range , 10 - 20 ) . At least one WHO grade improvement in the peripheral neuropathy severity was shown in 73 % of the patients . A case of insomnia related to ALC treatment was reported in one patient . Acetyl-L-carnitine seems to be an effective and well-tolerated agent for the treatment of chemotherapy-induced peripheral neuropathy . Conclusions Our preliminary results should be confirmed in double-blind , placebo controlled studies Background : Nucleoside analogue reverse transcriptase inhibitors ( NRTI ) disrupt neuronal mitochondrial DNA synthesis , impairing energy metabolism and result ing in a distal symmetrical polyneuropathy ( DSP ) , an antiretroviral toxic neuropathy ( ATN ) that causes significant morbidity in HIV disease . Serum acetyl-l-carnitine ( ALCAR ) levels are decreased in neuropathy associated with NRTI therapy . ALCAR enhances neurotrophic support of sensory neurons and promotes energy metabolism , potentially causing nerve regeneration and symptom relief . Objective : To assess the efficacy of oral ALCAR ( 1500 mg twice daily ) for up to 33 months in an open cohort of 21 HIV-positive patients with established ATN . Methods : Skin biopsies were excised from the leg before ALCAR treatment , at 6–12 month intervals thereafter and from HIV-negative non-neuropathic controls . Fibre types in epidermal , dermal and sweat gl and innervation were quantified immunohistochemically . Results : After 6 month 's treatment , mean immunostaining area for small sensory fibres increased ( epidermis 100 % , P = 0.006 ; dermis 133 % , P < 0.05 ) by more than that for all fibre types ( epidermis 16 % , P = 0.04 ; dermis 49 % , P < 0.05 ; sweat gl and s 60 % , P < 0.001 ) or for sympathetic fibres ( sweat 
    Output:
    
Clinical trials also showed beneficial effects on nerve conduction parameters and nerve fiber regeneration , with a good safety profile .
These data indicate that ALC provides an effective and safe treatment in patients with painful peripheral neuropathy .