普罗布考抗动脉粥样硬化作用机制及研究进展

普罗布考(probucol)又名丙丁酚,化学名为4,4'-[(1-甲基亚乙基)双(硫基)]双[2,6-双(1,1-二甲基乙基苯酚],分子式为C13H48O2S2.早期大量的药理及临床实验发现普罗布考具有调脂、抗氧化和抗动脉粥样硬化(AS)作用,但由于其可降低高密度脂蛋白胆固醇(HDL-C),使其在临床上的应用受到影响.     

17 α-雌二醇抑制低密度脂蛋白的氧化

〔英〕／Dittrich R…∥Exp Clin Endocrinol Diabetes．-1999，107．-53～57 研究了17α-雌二醇对铜诱导的低密度脂蛋白(LDL)氧化的影响，并与17β-雌二醇、雌三醇和普罗布考(probucol，一种有抗氧化剂性质的降脂药)的作用进行了比较。 方法与结果采集健康男性隔夜空腹≥12 h的血样，用超速离心、凝胶过滤等方法分离LDL，在LDL溶液中分别加入0.2、0.4和1 μmol／L的试验物质(17α-雌二醇、17β-雌二醇、雌三醇和普罗布考)，再加入新鲜配制的CuSO4水溶液起动氧化反应，234 nm处吸收光谱的改变反映共轭二烯的形成，即反映LDL氧化，用分光光度计测定。共轭二烯形成的第一时相迟滞期是试验物质抗氧化的标志。结果显示加入3种浓度的试验物分别将LDL氧化的迟滞期延长为，17α-雌二醇：1.3(±0．09 SD)，1．7(±0．14 SD)和2.7(±0.25 SD)倍；17β-雌二醇：1.4(±0.14 SD)，1.8(±0.1 SD)和2.6(±0.16 SD)倍；雌三醇：1.1(±0.07 SD)，1.4(±0.11 SD)和1.6(±0.11 SD)倍；普罗布考：1.4(±0.14 SD)，1.6(±0.1 SD)和3.0(±0.21 SD)倍。即4种试验物均可延长LDL氧化修饰的迟滞期，且抑制LDL氧化的作用呈浓度依赖性。17α-雌二醇的抗氧化作用与17 β-雌二醇和普罗布考的作用相当，而强于雌三醇。 结论体外试验显示17α-雌二醇具有与17β-雌二醇相同的延迟LDL氧化的活性,而体内生理浓度的17α-雌二醇具有抗动脉粥样化作用，又因为17-α雌二醇无雌激素受体介导的作用，所以在非17 β-雌二醇适应症(如男性)的情况下，也许可使用17α-雌二醇来预防动脉硬化。 (张进安摘高慧校)     

普罗布考对冠心病合并糖尿病患者PCI术后对比剂肾病的影响

【】目的：观察普罗布考对冠心病合并糖尿病患者PCI术后对比剂肾病(CIN)的预防作用,探索其可能机制。方法：将90例择期行PCI合并糖尿病的冠心病患者随机分为治疗组及对照组。治疗组在常规治疗基础上,于术前3-5天开始服用普罗布考,0.5/次,2次/日。测患者入院时及术后24h、48h、72h血肌酐(SCr)和胱抑素C(CysC)水平,检测患者术前及术后3天超敏C反应蛋白(hsCRP)、脂质过氧化物(MDA)、一氧化氮(NO)、内皮素-1(ET-1)浓度变化。结果：普罗布考组CIN发生率(6. 5%)显著低于对照组(15. 9%,P < 0.05);普罗布考组术后3天hsCRP、MDA及ET-1水平低于对照组(P < 0.05),而术后3天血浆NO水平高于对照组(P < 0.05)。结论：普罗布考能抑制PCI术后炎症反应,减轻脂质过氧化损伤,改善内皮功能,预防CIN发生。     

普罗布考对经皮冠状动脉介入治疗术后造影剂肾病的预防作用

目的:探讨普罗布考对经皮冠状动脉介入治疗(PCI)术后造影剂肾病(CIN)的预防作用及其可能机制。方法:入选行PCI术患者共250例,随机将其分为普罗布考组125例和对照组125例。2组均给予足量水化,普罗布考组每日给予普罗布考500mg每天2次口服,对照组仅给予常规治疗。观察2组患者PCI术前及术后48~72h血尿素氮(BUN)、肌酐(Scr)、肾小球滤过率(eGFR)、C-反应蛋白(CRP)、白细胞介素-6(IL-6)、丙二醛(MDA)的变化,记录2组患者CIN发生情况。CIN定义为Scr水平较原有基础升高25%或者绝对值升高44.2μmol/L以上。结果:2组PCI术前血BUN、Scr、eGFR、CRP、IL-6、MDA差异无统计学意义(P0.05)。2组术后72h血Scr、CRP、IL-6、MDA均较术前增高;术后72h,普罗布考组CRP、IL-6、MDA水平低于常规组,eGFR高于对照组(P0.05或P0.01)。普罗布考组有3例发生CIN,CIN发生率为2.4%;对照组有12例发生CIN,发生率为9.6%,差异有统计学意义(χ2=5.75,P0.05)。多元Logistic回归分析结果显示普罗布考是CIN独立保护因素(OR=0.079,95%CI:0.009~0.725,P=0.025)。结论:普罗布考对降低PCI术后CIN的发生具有保护作用,可能与普罗布考抗氧化应激及抗炎症反应有关。     

普罗布考对老年下肢动脉硬化症患者内皮舒张功能的影响

目的　评价普罗布考对老年下肢动脉硬化症患者内皮舒张功能的影响。方法　采用随机、单盲、自身对照和组间对照方法 ,将 5 4例老年下肢动脉硬化症患者分为两组 ,其中普罗布考治疗组 33例 ,服用普罗布考 0 .5g,2次 /d ,同时服用阿司匹林 10 0mg ,1次 d ;常规治疗组 2 1例 ,仅服用阿司匹林 10 0mg,1次 d ,疗程均为 12周。采用高分辨率超声技术 ,对治疗前后血管内皮舒张功能进行检测。结果　 (1)治疗前老年下肢动脉硬化症患者肱动脉血流介导的舒张功能 (FMD)和硝酸甘油介导的舒张功能 (NMD)均明显低于健康人群 ;(2 )治疗后 ,普罗布考治疗组总胆固醇 (TC)、低密度脂蛋白胆固醇 (LDL C)及高密度脂蛋白胆固醇 (HDL C)明显降低 ;(3)治疗后 ,普罗布考治疗组FMD明显增加 ,而NMD无显著性改变。结论　 (1)老年下肢动脉硬化症患者内皮依赖的舒张功能降低 ;(2 )普罗布考能够改善老年下肢动脉硬化症患者内皮功能 ,并具有良好的调脂作用 ;(3)普罗布考引起的HDL降低并不影响其改善内皮功能的作用。     

抗氧化剂普罗布考对冠心病介入后患者主要不良心血管事件的Meta分析

目的评价抗氧化剂普罗布考对改善冠心病介入后患者主要不良心血管事件(MACE)的作用。方法检索PubMed、EMBASE、Science Direct和Cochrane临床对照试验中心注册库(the cochrane central register of clinical trial)、中文学术期刊全文数据库(CNKI)和万方数据库(WFDP)等电子数据库进行检索。中英文检索词包括"抗氧化剂"或"普罗布考"或"维他命C"或"维他命E"或"N-乙酰半胱氨酸"和"血管成形术"或"支架"和"随机"。采用Cochrane协作网提供的RevMan5.3软件进行Meta分析。结果在纳入的349篇文献中,有7篇文献对冠心病介入后患者发生MACE事件进行了报告,普罗布考组(n=352)发生MACE事件72例,发生率为20.5%;对照组(n=354)发生MACE事件111例,发生率为31.4%。与对照组比较,普罗布考组明显降低MAEC发生率(RR:0.65,95%CI 0.51～0.84,P=0.0008)。经进一步分析,与对照组比较,普罗布考组有52例患者发生再次血运重建事件,发生率为14.8%,显著低于对照组(86例,发生率为24.3%,95%CI 0.44～0.83,P=0.002)。两组再次心肌梗死和全因死亡率差异无显著性(P=0.34,P=0.49)。此外,与对照组比较,普罗布考组显著降低介入后患者总胆固醇和低密度脂蛋白水平(SMD-0.68, 95%CI-0.87～-0.49,P0.00001; SMD-0.28, 95%CI-0.46～-0.11,P=0.001)。结论与冠心病介入后常规治疗比较,抗氧化剂普罗布考联合常规治疗可明显降低MACE发生率,该作用与普罗布考降低再次血运重建,改善总胆固醇和低密度脂蛋白水平相关。     

氧化应激对心房颤动犬心房肌细胞凋亡及凋亡相关蛋白影响的研究

目的 观察普罗布考(probucol)对长期心房快速起搏诱发心房颤动(房颤)犬心房肌细胞凋亡及凋亡相关蛋白表达的影响,探讨氧化应激在房颤心房结构重构中的作用.方法 杂种犬20只,随机分为假手术组(n=6)、对照组(n=7)和普罗布考组(n=7).无菌条件下开胸后在犬右心房缝植4对心外膜记录电极,电极尾端经皮下由犬背部穿出;在右心耳缝植螺旋型起搏电极,连接实验用AOO高频起搏器(400次/min),心房快速起搏6周,建立房颤犬模型;假手术组犬仅缝植心外膜记录电极和起搏电极但不起搏;对照组及普罗布考组犬心房快速起搏6周;普罗布考组于起搏前一周开始服用普罗布考(100 mg·kg-1·d-1),直至起搏结束.TUNEL法检测心房肌细胞凋亡情况;免疫组化方法及免疫印记法检测凋亡相关蛋白caspase-3、bcl-2和bax表达情况;免疫组化方法检测calpain Ⅰ表达;比色法检测心房肌总抗氧化能力(T-AOC)、丙二醛(MDA)和抗超氧阴离子(抗O2-)水平;于起搏前、起博6周后,经心外膜电极记录各组犬房颤诱发情况.结果 与假手术组犬相比,对照组犬左、右心房肌凋亡细胞数量显著增加[(44.3±9.7)% vs (1.36±0.70)%,(42.1±11.9)% vs (1.07±0.50)%,P＜0.01],心房肌caspase-3、bax和calpain Ⅰ表达明显上调(P＜0.01),bcl-2表达显著下调(P＜0.01).与对照组犬相比,普罗布考组犬左、右心房肌凋亡细胞数量明显减少[(21.4±5.8)% vs (44.3±9.7)%,(20.1±6.1)% vs (42.1±11.9)%,P＜0.01],calpain Ⅰ、caspase-3和bax表达显著下调(P＜0.01),bcl-2表达增加(P＜0.05).与假手术组犬相比对照组犬心房肌MDA水平明显增加(P＜0.01),T-AOC、抗O2-水平明显降低(P＜0.01);与对照组犬相比,普罗布考组犬心房肌MDA水平显著降低(P＜0.05),T-AOC、抗O2-水平显著增加(P＜0.01).对照组和普罗布考组起搏后房颤诱发率和平均持续时间均较起搏前显著增加(P＜0.05);起搏后普罗布考组房颤诱发率较对照组降低(P＜0.05),房颤平均持续时间显著减少(P＜0.01).结论 普罗布考可能通过抑制氧化应激,增加bcl-2表达,降低calpain Ⅰ、caspase-3和bax表达,阻止长期心房快速起搏诱发房颤犬心房肌细胞凋亡,对房颤心房结构重构防治有益,能够减少房颤发生.     

普罗布考对不稳定型心绞痛患者血清明胶酶的影响

目的:探讨普罗布考对不稳定型心绞痛(UAP)患者血清明胶酶的影响。方法:连续入选UAP患者80例,随机分为普罗布考治疗组(40例)和常规治疗组(40例)。常规治疗组采用硝酸酯类、阿司匹林、β受体阻滞剂等常规药物治疗;普罗布考组在常规治疗基础上加用普罗布考口服,观察治疗前及治疗一个月后血清明胶酶水平。结果:与治疗前比较,普罗布考治疗组治疗后基质金属蛋白酶(MMP)-2[(54.04±6.54)ng/ml比(32.43±1.81)ng/ml]、MMP-9[(56.33±7.25)ng/ml比(34±1.45)ng/ml]水平均明显下降(P均<0.01),且明显低于常规治疗组治疗后[MMP-2:(37.21±2.86)ng/ml、MMP-9:(39.96±1.75)ng/ml],P<0.05。结论:普罗布考能促进不稳定型心绞痛患者血清明胶酶水平的下降,起到稳定粥样斑块的作用。     

四种药物对兔动脉粥样硬化消退治疗的作用

目的 :探讨辛伐他汀、普罗布考、卡托普利和中药对动脉粥样硬化消退作用。　　方法 :55只兔饲养高胆固醇饲料 ,12周末将 40只兔随机分为自然消退组、辛伐他汀组、普罗布考组、卡托普利组和中药组 ,每组 8只 ;于实验开始、 12周末、 2 4周末测量腹主动脉内中膜厚度和内中膜校正的声学密度值 (% )。对比超声测量的内中膜厚度与病理测值。　　结果 :病理测量的腹主动脉内中膜厚度与超声测值差异无统计学意义 (P >0 0 5) ;4个药物治疗组内中膜厚度均显著低于自然消退组 (P均 <0 0 5) ,服药后内中膜厚度依次为辛伐他汀组 <普罗布考组 <中药组 <卡托普利组 <自然消退组。消退治疗后内中膜校正回声强度 (% )均显著增高 (P <0 0 5) ,依次为普罗布考组 >辛伐他汀组 >中药组或卡托普利组。　　结论 :辛伐他汀、普罗布考、卡托普利和中药均有不同程度消退实验兔动脉粥样硬化的作用 ,其中以辛伐他汀效果最佳。高频超声技术可作为定性和定量随访动脉粥样硬化动态变化的可靠方法     

普罗布考对高脂血症患者血脂及血管内皮舒张功能的影响

目的　评价普罗布考降血脂的同时对高脂血症患者血管内皮舒张功能的影响。方法　采用自身对照和组间对照 ,将 5 2例原发性高脂血症患者分为两组 ,其中普罗布考组 (36例 ) ,服用普罗布考 0 .5 ,Bid;普伐他汀组 (16例 ) ,服用普伐他汀 10 mg,QN,疗程均为 4周。选择血脂正常的 2 0例健康者为空白对照组。采用高分辨率超声技术 ,对治疗前后血管内皮舒张功能进行检测。结果　 1高脂血症患者治疗前肱动脉血流介导的舒张功能 (FMD)明显低于正常对照组 [(4.6± 3.2 ) %比 (12 .8± 3.5 ) % ,P<0 .0 1],而对硝酸甘油的反应 (NMD)正常。 2普罗布考明显降低总胆固醇 (TC)、低密度脂蛋白胆固醇 (L DL - c)和高密度脂蛋白胆固醇 (HDL - c) ,三酰甘油变化不明显。 3普罗布考使 FMD明显增强 ,NMD无显著性改变。 4普罗布考降 TC及对 FMD的改善作用均不比普伐他汀差 (分别P<0 .0 1和 P<0 .0 5 )。 5 FMD的改善与 TC及 L DL - c无相关性。结论　普罗布考短期治疗即可显著降低血脂 ,并明显改善 FMD,可作为良好的保护内皮功能的药物 ,其改善 FMD的作用与降脂无关     

Three layer functional model and energy exchange concept of aging process

Relying on a certain degree of abstraction, we can propose that no particular distinction exists between animate or living matter and inanimate matter. While focusing attention on some specifics, the dividing line between the two can be drawn. The most apparent distinction is in the level of structural and functional organization with the dissimilar streams of ‘energy flow’ between the observed entity and the surrounding environment. In essence, living matter is created from inanimate matter which is organized to contain internal intense energy processes and maintain lower intensity energy exchange processes with the environment. Taking internal and external energy processes into account, we contend in this paper that living matter can be referred to as matter of dissipative structure, with this structure assumed to be a common quality of all living creatures and living matter in general. Interruption of internal energy conversion processes and terminating the controlled energy exchange with the environment leads to degeneration of dissipative structure and reduction of the same to inanimate matter, (gas, liquid and/or solid inanimate substances), and ultimately what can be called ‘death.’ This concept of what we call dissipative nature can be extended from living organisms to social groups of animals, to mankind. An analogy based on the organization of matter provides a basis for a functional model of living entities. The models relies on the parallels among the three central structures of any cell (nucleus, cytoplasm and outer membrane) and the human body (central organs, body fluids along with the connective tissues, and external skin integument). This three-part structural organization may be observed almost universally in nature. It can be observed from the atomic structure to the planetary and intergalactic organizations. This similarity is corroborated by the membrane theory applied to living organisms. According to the energy nature of living matter and the proposed functional model, the decreased integrity of a human body's external envelope membrane is a first cause of the structural degradation and aging of the entire organism. The aging process than progresses externally to internally, as in single cell organisms, suggesting that much of the efforts towards the restoration and maintenance of the mechanisms responsible for structural development should be focused accordingly, on the membrane, i.e., the skin. Numerous reports indicate that all parts of the human body, like: bones, blood with blood vessels, muscles, skin, and so on, have some ability for restoration. Therefore, actual revival of not only aging tissue of the human body's membrane, but the entire human body enclosed within, with all internal organs, might be expected. We assess several aging theories within the context of our model and provide suggestions on how to activate the body's own anti-aging mechanisms and increase longevity. This paper presents some analogies and some distinctions that exist between the living dissipative structure matter and inanimate matter, discusses the aging process and proposes certain aging reversal solutions.     

The immunoneuroendocrine role of melatonin

Abstract: A tight, physiological link between the pineal gland and the immune system is emerging from a series of experimental studies. This link might reflect the evolutionary connection between self-recognition and reproduction. Pinealectomy or other experimental methods which inhibit melatonin synthesis and secretion induce a state of immunodepression which is counteracted by melatonin. In general, melatonin seems to have an immunoenhancing effect that is particularly apparent in immunodepressive states. The negative effect of acute stress or immunosuppressive pharmacological treatments on various immune parameters are counteracted by melatonin. It seems important to note that one of the main targets of melatonin is the thymus, i.e., the central organ of the immune system. The clinical use of melatonin as an immunotherapeutic agent seems promising in primary and secondary immunodeficiencies as well as in cancer immunotherapy. The immunoenhancing action of melatonin seems to be mediated by T-helper cell-derived opioid peptides as well as by lymphokines and, perhaps, by pituitary hormones. Melatonin-induced-immuno-opioids (MHO) and lymphokines imply the presence of specific binding sites or melatonin receptors on cells of the immune system. On the other hand, lymphokines such as -γ-interferon and interleukin-2 as well as thymic hormones can modulate the synthesis of melatonin in the pineal gland. The pineal gland might thus be viewed as the crux of a sophisticated immunoneuroendocrine network which functions as an unconscious, diffuse sensory organ.     

Unusual responses of nocturnal pineal melatonin synthesis and secretion to swimming: Attempts to define mechanisms

Abstract: The effect of swimming at night on rat pineal melatonin synthesis was compared with that of light exposure at night. Rats were forced to swim at 0030 hr (lights out at 2000 hr) and sacrificed by decapitation 15 and 30 min later, immediately after swimming. Other groups of animals were exposed to white light (650μW/cm²) for 15 and 30 min at same time. Swimming caused a rapid and highly significant drop in the melatonin content in the pineal gland; however, the activity of N-acetyltransferase (NAT), the supposed rate limiting enzyme in the melatonin production, was not changed. Despite the drop in pineal melatonin levels, serum concentrations of the indole remained elevated in the rats that swam. In contrast, melatonin levels in the pineal and serum of light exposed rats fell precipitously, accompanied by a significant suppression of NAT activity. Since we anticipated that the strenuous exercise associated with swimming may induce release of artrial natriuretic peptide (ANP) from the heart, which in turn could cause the release of pineal melatonin, in a second study we injected physiological saline intravenously to stretch the cardiac muscle and release ANP. Three milliliters of normal saline was injected during the day into the jugular vein of anesthetized rats that were pretreated with isoproterenol to stimulate pineal melatonin production. Animals were killed 15 min after the saline injection, and pineal NAT activity and pineal melatonin levels were measured. The saline injections caused no alteration in the elevated levels of either NAT or melatonin. These data suggest that the disparity in pineal NAT activity (which was high) and pineal melatonin (which was low), in animals swum at night, may not be caused by ANP which is released during strenuous exercise such as swimming.     

Melatonin and photoperiodic time measurement: Seasonal breeding in the sheep

Abstract: Well-established circadian physiology supports the view that photoperiodic time measurement utilizes the coincidence between the presence of light and a photosensitive phase of a 'biological clock' to alter reproductive status—the so-called external coincidence model of seasonal breeding. In this review, we examine the mechanism whereby photoperiod interacts with presumed suprachiasmatic nuclei activity to allow endogenous melatonin to normally synchronize reproductive activity to the optimal time of year. The Romney Marsh sheep is particularly explored as an experimental model. It is suggested that the on/off activity of seasonal reproduction may be a robust mechanism able to be predictably manipulated by the judicious use of the light/dark cycle and exogenous melatonin, but firmly based on circadian principles.     

Conservative management of perforated duodenal diverticulum： A case report and review of the literature

Duodenal diverticula are a relatively common condition. They are asymptomatic, unless they become complicated, with perforation being the rarest but most severe complication. Surgical treatment is the most frequently performed approach. We report the case of a patient with a perforated duodenal diverticulum, which was diagnosed early and treated conservatively with antibiotics and percutaneous drainage of secondary retroperitoneal abscesses. We suggest this method could be an acceptable option for the management of similar cases, provided that the patient is in good general condition and without septic signs.     

Changes in connexin43, the gap junction protein of astrocytes, during development of the rat pineal gland

Abstract: The abundance of gap junctions between rat pineal astrocytes formed by connexin43 (Cx43) was studied during development. Levels and distribution of Cx43 were measured by immunoblotting and indirect immunofluorescence, respectively. The amount of Cx43 in cells located within the gland was low until about the 7th postnatal day and increased to adult values between the 14th and 21st days postpartum. Although astrocytes, recognized by their vimentin immunoreactivity, were scarce before birth, they were abundant by the 7th postnatal day suggesting that the low levels of Cx43 found at this age corresponded to a low expression of this protein. Localization of the immunoreactivity to Cx43 and vimentin showed a close correlation, indicating that mature or immature pineal astrocytes form gap junctions made of Cx43. Since Cx43 levels attained their adult values at about the time the innervation and the functional state of the gland reached maturity (2–3 weeks after birth), it is proposed that astrocyte gap junctions are involved in the function of the adult rat pineal gland.     

Language of CTO interventions – Focus on hardware

The knowledge of variety of chronic total occlusion (CTO) hardware and the ability to use them represents the key to success of any CTO interventions. However, the multiplicity of CTO hardware and their physical character and the terminology used by experts create confusion in the mind of an average interventional cardiologist, particularly a beginner in this field. This knowledge is available but is scattered. We aim to classify and compare the currently used devices based on their properties focusing on how physical character of each device can be utilized in a specific situation, thus clarifying and simplifying the technical discourse.     

High prevalence of distal sensory polyneuropathy in antiretroviral-treated and untreated people with HIV in Tanzania

Objectives To describe the prevalence of distal sensory polyneuropathy (DSP), a complication of both advanced HIV disease and of antiretroviral therapy (ART), amongst Tanzanians with HIV, on and off ART (including stavudine) with CD4 counts above and below 200 cells/μl. Methods We recruited participants attending ART clinic into four groups: >6 months ART exposure and (i) CD4 < 200 cells/μl or (ii) CD4 > 200 cells/μl (ART/CD4 < 200 and ART/CD4 > 200, respectively); ART‐naïve and (iii) CD4 < 200 cells/μl or iv)CD4 > 200 cells/μl (noART/CD4 < 200 and noART/CD4 > 200, respectively). Primary outcome was DSP, as defined by presence of at least one symptom and one sign. Results Of 326 evaluable participants, 81 (32 men, median age 38 years, median CD4 142 cells/μl) were enrolled in the ART/CD4 < 200 group, 78 (17 men, median age 37 years, median CD4 345 cells/μl) in ART/CD4 > 200, 81 (30 men, median age 37 years, median CD4 128 cells/μl) in noART/CD4 < 200 and 86 (22 men, median age 33 years, median CD4 446 cells/μl) in noART/CD4 > 200. Numbness was the most commonly reported symptom. DSP prevalence ranged from 43.2% in ART/CD4 < 200 to 20.9% in noART/CD4 > 200. DSP was more common among men (adjusted odds ratio [aOR] 1.9, 95% confidence interval [CI] 1.2–3.3) and older participants (aOR 2.7, 95% CI 1.1–6.2 for age 40 + vs. <30 years). Conclusion Distal sensory polyneuropathy is common amongst those attending this clinic, even those with no ART exposure and a CD4 count above 200 cells/μl. Stavudine and didanosine expose HIV‐infected patients to an additional avoidable risk of DSP. Access to non‐neurotoxic ART regimes as well as earlier HIV diagnosis and initiation of ART is needed.