PDF(Pubmed)
Abstract：
BACKGROUND: In the early literature, unintentional vitamin C deficiency in humans was associated with heart failure. Experimental vitamin C deficiency in guinea pigs caused enlargement of the heart. The purpose of this study was to collect and analyze case reports on vitamin C and pulmonary hypertension.
METHODS: We searched Pubmed and Scopus for case studies in which vitamin C deficiency was considered to be the cause of pulmonary hypertension. We selected reports in which pulmonary hypertension was diagnosed by echocardiography or catheterization, for any age, sex, or dosage of vitamin C. We extracted quantitative data for our analysis. We used the mean pulmonary artery pressure (mPAP) as the outcome of primary interest.
RESULTS: We identified 32 case reports, 21 of which were published in the last 5 years. Dyspnea was reported in 69%, edema in 53% and fatigue in 28% of the patients. Vitamin C plasma levels, measured in 27 cases, were undetectable in 24 and very low in 3 cases. Diet was poor in 30 cases and 17 cases had neuropsychiatric disorders. Right ventricular enlargement was reported in 24 cases. During periods of vitamin C deficiency, the median mPAP was 48 mmHg (range 29-77 mmHg; N = 28). After the start of vitamin C administration, the median mPAP was 20 mmHg (range 12-33 mmHg; N = 18). For the latter 18 cases, mPAP was 2.4-fold (median) higher during vitamin C deficiency. Pulmonary vascular resistance (PVR) during vitamin C deficiency was reported for 9 cases, ranging from 4.1 to 41 Wood units. PVR was 9-fold (median; N = 5) higher during vitamin C deficiency than during vitamin C administration. In 8 cases, there was direct evidence that the cases were pulmonary artery hypertension (PAH). Probably the majority of the remaining cases were also PAH.
CONCLUSIONS: The cases analyzed in our study indicate that pulmonary hypertension can be one explanation for the reported heart failure of scurvy patients in the early literature. It would seem sensible to measure plasma vitamin C levels of patients with PH and examine the effects of vitamin C administration.
METHODS: We searched Pubmed and Scopus for case studies in which vitamin C deficiency was considered to be the cause of pulmonary hypertension. We selected reports in which pulmonary hypertension was diagnosed by echocardiography or catheterization, for any age, sex, or dosage of vitamin C. We extracted quantitative data for our analysis. We used the mean pulmonary artery pressure (mPAP) as the outcome of primary interest.
RESULTS: We identified 32 case reports, 21 of which were published in the last 5 years. Dyspnea was reported in 69%, edema in 53% and fatigue in 28% of the patients. Vitamin C plasma levels, measured in 27 cases, were undetectable in 24 and very low in 3 cases. Diet was poor in 30 cases and 17 cases had neuropsychiatric disorders. Right ventricular enlargement was reported in 24 cases. During periods of vitamin C deficiency, the median mPAP was 48 mmHg (range 29-77 mmHg; N = 28). After the start of vitamin C administration, the median mPAP was 20 mmHg (range 12-33 mmHg; N = 18). For the latter 18 cases, mPAP was 2.4-fold (median) higher during vitamin C deficiency. Pulmonary vascular resistance (PVR) during vitamin C deficiency was reported for 9 cases, ranging from 4.1 to 41 Wood units. PVR was 9-fold (median; N = 5) higher during vitamin C deficiency than during vitamin C administration. In 8 cases, there was direct evidence that the cases were pulmonary artery hypertension (PAH). Probably the majority of the remaining cases were also PAH.
CONCLUSIONS: The cases analyzed in our study indicate that pulmonary hypertension can be one explanation for the reported heart failure of scurvy patients in the early literature. It would seem sensible to measure plasma vitamin C levels of patients with PH and examine the effects of vitamin C administration.
摘要：
背景：在早期文献中，人类无意中的维生素C缺乏与心力衰竭有关。豚鼠的实验性维生素C缺乏导致心脏增大。目的收集和分析维生素C和肺动脉高压的病例报告。
方法：我们搜索了Pubmed和Scopus的案例研究，其中维生素C缺乏被认为是肺动脉高压的原因。我们选择了通过超声心动图或导管检查诊断为肺动脉高压的报告，对于任何年龄,性别,或维生素C的剂量。我们提取了定量数据进行分析。我们使用平均肺动脉压（mPAP）作为主要目标的结果。
结果：我们确定了32例病例报告，其中21篇发表于过去5年。有69%的人报告呼吸困难,53％的患者水肿和28％的患者疲劳。维生素C血浆水平,在27个案例中测量，在24例中检测不到，在3例中检测不到。饮食不良30例，神经精神障碍17例。报告24例右心室扩大。在维生素C缺乏期间，mPAP中位数为48mmHg(范围29~77mmHg;N=28).开始服用维生素C后，mPAP中位数为20mmHg(范围12~33mmHg;N=18).对于后18例，维生素C缺乏时mPAP高2.4倍（中位数）。报告维生素C缺乏期间的肺血管阻力（PVR）9例，范围从4.1到41木材单位。维生素C缺乏期间的PVR比维生素C施用期间高9倍(中位数;N=5)。在8个案例中，有直接证据表明这些病例是肺动脉高压（PAH）。可能其余的大多数病例也是PAH。
结论：我们研究中分析的病例表明，肺动脉高压可能是早期文献中报道的镰刀病患者心力衰竭的一种解释。测量PH患者的血浆维生素C水平并检查维生素C给药的效果似乎是明智的。
方法：我们搜索了Pubmed和Scopus的案例研究，其中维生素C缺乏被认为是肺动脉高压的原因。我们选择了通过超声心动图或导管检查诊断为肺动脉高压的报告，对于任何年龄,性别,或维生素C的剂量。我们提取了定量数据进行分析。我们使用平均肺动脉压（mPAP）作为主要目标的结果。
结果：我们确定了32例病例报告，其中21篇发表于过去5年。有69%的人报告呼吸困难,53％的患者水肿和28％的患者疲劳。维生素C血浆水平,在27个案例中测量，在24例中检测不到，在3例中检测不到。饮食不良30例，神经精神障碍17例。报告24例右心室扩大。在维生素C缺乏期间，mPAP中位数为48mmHg(范围29~77mmHg;N=28).开始服用维生素C后，mPAP中位数为20mmHg(范围12~33mmHg;N=18).对于后18例，维生素C缺乏时mPAP高2.4倍（中位数）。报告维生素C缺乏期间的肺血管阻力（PVR）9例，范围从4.1到41木材单位。维生素C缺乏期间的PVR比维生素C施用期间高9倍(中位数;N=5)。在8个案例中，有直接证据表明这些病例是肺动脉高压（PAH）。可能其余的大多数病例也是PAH。
结论：我们研究中分析的病例表明，肺动脉高压可能是早期文献中报道的镰刀病患者心力衰竭的一种解释。测量PH患者的血浆维生素C水平并检查维生素C给药的效果似乎是明智的。
