CASE REPORT article

Front. Neurol., 11 February 2021

Sec. Stroke

Volume 11 - 2020 | https://doi.org/10.3389/fneur.2020.563037

Cyclosporine-A-Induced Intracranial Thrombotic Complications: Systematic Review and Cases Report

  • 1. Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, China

  • 2. Advanced Center of Stroke, Beijing Institute for Brain Disorders, Beijing, China

  • 3. Department of China-America Institute of Neuroscience, Xuanwu Hospital, Capital Medical University, Beijing, China

  • 4. Department of Neurosurgery, Wayne State University School of Medicine, Detroit, MI, United States

Abstract

This study reported two cases of intracranial thrombotic events of aplastic anemia (AA) under therapy with cyclosporine-A (CsA) and reviewed both drug-induced cerebral venous thrombosis (CVT) and CsA-related thrombotic events systematically. We searched PubMed Central (PMC) and EMBASE up to Sep 2019 for publications on drug-induced CVT and Cs-A-induced thrombotic events. Medical subject headings and Emtree headings were used with the following keywords: “cyclosporine-A” and “cerebral venous thrombosis OR cerebral vein thrombosis” and “stroke OR Brain Ischemia OR Brain Infarction OR cerebral infarction OR intracerebral hemorrhage OR intracranial hemorrhage.” We found that CsA might be a significant risk factor in inducing not only CVT but also cerebral arterial thrombosis in patients with AA.

Background

Cyclosporine-A (CsA) is widely used as an immunosuppressive agent in organ transplantation (13), ulcerative colitis (UC) (46), and aplastic anemia (AA) (7). Most commonly, the high incidences of thromboembolic complications in the renal vascular system were found in patients with CsA use after kidney transplantation (8, 9), which might be due to acute and chronic nephrotoxicity of CsA. However, thrombotic complications in other organs secondary to CsA use are not fully analyzed in the clinical settings (10). In particular, cases of CsA-induced intracranial thrombotic complications in patients with AA were rather rare (7). Herein, we presented two cases of AA with CsA-related intracranial thrombotic events, involved in cerebral venous sinuses and cerebral arteries, respectively. Besides, we conducted a systematic literature review of CsA-related thrombotic events to give more clinical references to physicians in this field.

Moreover, it is well-known that oral contraceptive (OCP) use is regarded as the iatrogenic risk factor inducing cerebral venous thrombosis (CVT). However, there is by far no review on if any other medications that could also cause CVT. Therefore, inspired by our case of CsA-induced CVT, we further comprehensively reviewed drug-induced CVT.

Case Presentation

Case 1

A 15-year-old female with a 4-year history of AA with treatment of CsA (50 mg, bid) complained of an intermittently severe headache on her left frontoparietal areas for 8 months. Her headache could initially attenuate after intravenous injection of mannitol (125 ml, q8h) for 7 days. However, her headache was recurrent and even became aggressively severe with nausea and projectile vomiting 20 days ago, which could no longer be relieved by the former treatment of mannitol. Physical examination revealed a body temperature of 36.4°C, blood pressure of 105/85 mmHg, heart rate of 78/min, and respiratory rate of 20/min. No abnormal finding was found in the neurological examination. Fundoscopy showed stage V papilledema measured by the Frisén scale (Supplementary Figure 1).

Her complete blood cell (CBC) test indicated moderate normocytic normochromic anemia and a decreased platelet level due to her primary disease. The serum iron test was normal, which further excluded the differential diagnosis of iron deficiency anemia. Baseline levels of inflammatory biomarkers, including C-reactive protein (CRP) (37.2 mg/L, normal 1.0–8.0 mg/L), high-sensitivity CRP (hs-CRP) (25.75 mg/L, normal 0.0–3.0 mg/L), and interleukin 6 (IL-6) (19.6 pg/ml, normal 0.0010–7.0 pg/ml) were all above the upper normal limits (Supplementary Table 1), which suggested acute inflammatory reaction secondary to the primary disease. An increased level of D-dimer (2.47 μg/ml, normal range 0.01–0.5 μg/ml) and fibrinogen (4.21 g/L, normal range 2.0–4.0 g/L) remained over the upper limit of the normal range for several days after admission, suggesting the formation of thrombosis at acute stage (Supplementary Table 1). Serum neuron-specific enolase (NSE) level at admission was 51.52 ng/ml (normal range 0.0–17.0 ng/ml). The elevated NSE was related to damage to both neurons and the blood–brain barrier (BBB). Investigation for vasculitis [antinuclear antibody (ANA), antineutrophil cytoplasmic antibody (ANCA), and antiphospholipid antibody (APLA)] was negative. The cerebrospinal fluid (CSF) profile revealed a slightly increased white blood cell (WBC) count (2 × 106/L), and lumbar puncture opening pressure (LPOP) was over 330 mm H2O. Contrast-enhanced magnetic resonance venography (CE-MRV) (Figure 1) and high-resolution MRI with black-blood thrombus image (MRBTI) of the brain (Figure 2) demonstrated subacute thrombosis in the superior sagittal sinus (SSS), straight sinus, right transverse sinus (TS), right sigmoid sinus (SS), and proximal part of right internal jugular vein (IJV). Moreover, no parenchymal lesion was found in MRBTI. The confirmed diagnosis of subacute CVT in multiple sites was made based on imaging findings, with involvement in cerebral venous sinuses and IJV. The CVT-induced cerebrospinal venous insufficiency could cause disturbance of CSF circulation, further leading to intracranial hypertension and related symptoms, such as severe headaches and projectile vomiting. However, the etiology of CVT development was hard to be explained in this case due to lacking common risk factors like other female CVT patients, such as obesity, pregnancy, or long-term OCP use. Moreover, no positive result was found in the workup of thrombophilia, including protein S (PS), protein C (PC), antithrombin-III (AT-III), Factor VII/VIII deficiency, or Factor V Leiden mutation. Then, we closely monitored her blood cell counts on an everyday basis. Her hypercoagulable state induced by moderate anemia secondary to AA and probable adverse effect of CsA on damaging venous vessel walls raised our attention. The procoagulant effect of the two factors might potentiate the formation of CVT.

Figure 1

Figure 2

Intravenous injection of mannitol (125 mL, q8h) was continued after the admission. Subcutaneous injection enoxaparin sodium (0.6 ml, qd) was started when the diagnosis of CVT was confirmed and usage of CsA was suspended after consultation with the department of hematology. The usage of enoxaparin sodium was then bridged to rivaroxaban (20 mg, qd) when she was discharged. Outpatient follow-up after 6 months of standard anticoagulation was evaluated by the Patients' Global Impression of Change (PGIC) scale. The patient reported a definite improvement of her symptoms (PGIC score = 6) and was transferred to the department of hematology to further treat AA.

Case 2

A 34-year-old male with a 1-year treatment of CsA (50 mg, bid) for AA presented with right homonymous hemianopia for 20 days, accompanied by dizziness and right-hand numbness. There was no history of nausea and vomiting, motor or sensory symptoms in the limbs, facial bulbar symptoms, sphincter incontinence, and loss of consciousness or seizures. He denied a family history of blood clotting disorders. Physical examination showed his body temperature was 36.9°C, blood pressure was 130/84 mmHg, heart rate was 72 beats/min, and respiratory rate was 18 beats/min. Neurological examination revealed no positive findings.

Peripheral blood test demonstrated mild normocytic normochromic anemia (hemoglobin, 110 g/L, normal range 120–160 g/L; hematocrit 34.8%, normal range 38.0–50.8%). The evaluation of thrombophilia showed increased levels of fibrinogen (4.11 g/L, normal range 2.0–4.0 g/L), D-dimer (1.4 μg/ml, normal range 2.0–4.0 g/L), AT-III (134%, normal range 80.0–120.0%), and protein C (181%, normal range 65.0–140.0%). All the results of serological tests, including aPL, ANA, ANCA, and complements C3 and C4, were negative. Workups of proinflammatory biomarkers, such as CRP, hs-CRP, and IL-6, were all negative. LPOP was 200 mmH2O, and a slightly elevated level of protein (57 mg/dl, normal range 15.0–45.0 mg/dl) and WBC count in CSF was found (5 × 106/L). Serum NSE was more than two times higher than the normal upper limit (36.59 ng/ml, normal range 0.0–17.0 ng/ml). MRI indicated cerebral infarction in the left occipital lobe (Figure 3A) and both sides of the cerebellum (Figure 3B). Magnetic resonance angiography (MRA) showed focal stenosis in the distal branches of the left posterior cerebral artery (PCA) and a partial filling defect in both sides of the superior cerebellar arteries (Figure 4). CE-MRV excluded the possibility of CVT (Figure 5). As this patient has not been identified to have any vascular risk factors, such as diabetes mellitus (DM), hypertension, hyperlipidemia, obesity or smoking history, family history of small vessel disease, or state of hypercoagulability, and the evidence of systemic autoimmune diseases was also negative, we assumed that the cerebral atrial infarction was caused by emboli from cardiac source or thrombosis in situ secondary to certain unknown injuries. Then, to further evaluate the potential cause of stroke, transesophageal echocardiography (TEE) was conducted, with negative findings of atrial septal abnormalities [patent foramen ovale (PFO), atrial septal defect (ASD), or atrial septal aneurysm (ASA)]. Based on the patient's medical history of using CsA, the direct or indirect adverse effect of CsA may contribute to the damage in arterial vessel walls, which further initiated the formation of thrombosis in situ. The usage of CsA was withdrawn after consultation with the department of hematology due to his relatively well-controlled condition of AA. Aspirin (100 mg, qd) was prescribed at discharge.

Figure 3

Figure 4

Figure 5

MRI follow-up at 6 months post-stroke showed no new-onset parenchymal lesions, and his symptoms were partially relieved and evaluated by PGIC scale (PGIC score = 6).

Literature Review

We searched PubMed Central (PMC) and EMBASE up to Sep 2019 for publications on CsA-induced thrombotic events and drug-induced CVT. We used Medical subject headings and Emtree headings combining with the following keywords: “cyclosporine-A” and “cerebral venous thrombosis OR cerebral vein thrombosis” and “stroke OR Brain Ischemia OR Brain Infarction OR cerebral infarction OR intracerebral hemorrhage OR intracranial hemorrhage.” We also screened reference lists of included articles for additional relevant studies. Intracranial thrombotic events had to be diagnosed by MRI, conventional angiography, computed tomography (CT) angiography, or at surgery or autopsy. Articles written in languages other than English were only selected if they had an English abstract with sufficient data.

We identified 322 publications related to drug-induced cerebral venous sinus thrombosis (CVST), of which 109 were selected for full-length review (Figure 6). Among these, 79 articles with a total of 706 patients were included based on our inclusion criteria. However, nine articles within the inclusion criteria were not collected due to no access to full texts despite that we searched for several times and tried to contact corresponding authors by e-mail. Herein, we listed these nine references in Supplementary Materials. Most of the eligible studies were case reports or case series (n = 68) and retrospective studies (n = 9), and only one meta-analysis and one prospective study were found (Table 1) (1189). Western countries reported 95% of the cases, followed by eastern countries (4%), while only one case was from African countries. The mean age of patients was 33.8 ± 17.9 years, and 68.5% of patients were female. There were 94 pediatric cases (94/706, 13.3%). The most common symptoms were seizures (48.6%), headaches (38.1%), nausea/vomiting (19.5%), altered mental status (drowsiness, confusion, syncope, or coma) (17.6%), motor/sensory disorder (12.9%), visual disturbance (9.0%), and aphasia/dysphasia (7.6%). The least common symptoms were personality/behavior change (aggressiveness, n = 1; irritability, n = 4; poor personal care, n = 1) (2.9%) and ataxia (2.4%). Only few cases reported symptoms like general malaise/fatigability (n = 2), fever (n = 2), diarrhea (n = 2), and urinary incontinence (n = 1). CVT was confirmed by CE-MRV (n = 55) and MRI (n = 18). Although digital subtraction angiography (DSA) was considered the gold standard, only 13 cases conducted DSA to make the defined diagnosis. Besides, CT (n = 5), CT venography (CTV) (n = 5) and autopsy (n = 5) were also mentioned as method to detect CVT. Among all sinuses, SSS (n = 123) was most likely involved in drug-induced CVT, followed by the TS (n = 119), SS (n = 97), and straight sinus (n = 80). Thrombosis was usually formed bilaterally in the TS (n = 26), while it was less common in the left TS (LTS) (n = 23) and the right TS (RTS) (n = 14). However, the left SS (LSS) more potentially formed thrombosis (n = 18) than the right SS (RSS) (n = 9); 60.3% of cases had multiple sinus thromboses (105/174). CVST combined with cortical vein thrombosis (CoVT) and isolated CoVT were reported in 102 cases and 6 cases, respectively. Drug-induced deep cerebral vein thrombosis was only found in a vein of Galen, combined with CVST (n = 2). Furthermore, CVST was also found to coexist with jugular system thrombosis (n = 70), while isolated jugular system thrombosis was very rare (n = 2). Nineteen articles indicated contraceptive drug-induced CVT, and 14 studies reported heparin-induced thrombocytopenia (HIT) that resulted in CVT. l-Asparaginase was widely used in patients with acute lymphoblastic leukemia (ALL), while 10 publications demonstrated the close relationship between CVT and l-asparaginase. Furthermore, CsA use was also a risk factor for CVT (n = 7).

Figure 6

Table 1

DrugAge/genderPrimary diseaseSymptomsCVSTReferencesCountryArticle typeStudy size
ModalityLocation
Contrast
Iopamidol36/FMyelographyNRDSASSS(11)FranceCase report1
24/MRecurrent left sciatica (Myelography)Headache (severe), nausea and vomitingDSASSS, RLS(12)FranceCase report1
Recreational drug
MDMA type synthetic drugs
   Ecstasy22/FNoneHeadache, nausea, visual disturbance (photophobia, visual fortification spectra), expressive dysphasia, and right hemisensory loss.DSATS(13)UKCase report1
   Speed19/FNoneUncontrollable aggressivenessMRVLTS(14)SpainCase report1
   Cocaine30/MNoneHeadache (Occipital) and vomitingMRVSSS, TS(15)UKCase report1
Phosphodiesterase-5 (PDE5) inhibitors
Tadalafil45/MNoneHeadache (severe, posterior, sudden-onset, 3-day), and seizure (generalized tonic-clonic)MRIRCoVT(16)JapanCase report1
Sildenafil57/MTwo episodes of venous thrombosis (DVT; hemorrhoid plexus thrombosis)Headache (occipital, 2-week) and visual disturbance (blurry vision)MRVSSS, RSS, RTS(17)ItalyCase report1
IVIG16/FITPHeadache (severe), neck rigidity, and vomitingMRISSS(18)USACase report1
11/MITPHeadache (severe, transient frontotemporal)CTVSSS(19)CanadaCase report1
11/MHumoral immunodeficiency (Bruton's disease)Expressive aphasia, right upper extremity heavinessCTVSSS(20)LebanonCase report1
13/FITPHeadacheMRILIJV(21)USACase report1
Others
Dulaglutide52/FDM-2Headache (3-day) and visual disturbance (blurry vision)MRVRTS(22)IndiaCase report1
Romiplostim45/FITPHeadache (severe, occipital)MRVSSS, TS(23)TaiwanCase report1
Epoetin alfa37/FEnd stage renal diseaseHeadache (progressive, several-day)MRVSSS, SS(24)USACase report1
Dietary supplements63/Mwell-controlled hypertensionSeizure (generalized tonic-clonic)DSASS, vein of Galen(25)USACase report1
Lithum30/FBipolar disorderHeadache (progressive), confusion, visual disturbance (blurry vision), and left hemiparesis.DSASSS, LSS, LTS, straight sinus(26)USACase report1
Finasteride35/M (case 1)
41/M (case 2)
Male-pattern hair lossHeadache and seizures (case 1);
Headache (case 2)
CTVSSS(27)JapanCase report2
Combination tacrolimus/sirolimus67/MRenal transplantationSeizure (generalized) and right hemiparesisMRITS(28)AustraliaCase report1
Clozapine30/FChronic paranoid schizophreniaVomiting, irritability, fatigability, poor personal care (5-day)MRVSSS, ISS, RTS, RIJV(29)USACase report1
Levetiracetam6.5/MNoneHeadache and vomiting (2-day), then seizures (generalized)MRILTS, LSS(30)UKCase report1
Synthetic sex steroids
Oral contraception
Phytoestrogens52/FNoneHeadache (diffuse and continuous, 2-month)MRVLLS, LSS(31)PortugalCase report1
Third-generation CHCs (containing desogestrel or gestoden)16–49/FCVThSeizure (n = 52)CTV/MRVCVT: dural sinuses, DCVT, CoVT, IJV(32)USARetro57
Ethinylestradiol/
levonorgestrel
21/FNoneHeadache (severe, 4-day)CTVSSS, CoVT, RTS, RSS(33)USACase report1
NR18/F (case 1)
23/F (case 2)
Protein C resistance (case 1);
Anti-thrombin III deficiency (case 2)
Headache, nausea, vomiting and visual disturbance (photophobia) (case 1);
Headache, vomiting, altered sensorium (case 2)
MRISSS, TS, LSS (case 1)
SSS (case 2)
(34)IndiaCase report2
NR18/F (case 1)
18/F (case 2)
None (case 1);
ADHD and bipolar disorder (case 2)
Headache (intermittent right-sided) and visual disturbance (blurry vision) (3-day) (case 1);
Headache (intermittent right-sided) and visual disturbance (double vision) (6-week) (case 2)
MRVLTS, LSS (case 1);
RTS, IJV (case 2)
(35)USACase report2
NR27/F (case 1)
23/F (case 2)
NoneHeadache (retroauricular), vomiting, drowsiness, fever (several days) (case 1);
Headache, vomiting, increasing drowsiness and extra-pyramidal movements (1 day) (case 2).
DSA (case 1)
MRI (case 2)
LTS, SS (case 1);
SSS, SS (case 2)
(36)ItalyCase report2
Ethinylestradiol/
desogestrel
24/FNoneHeadache (severe, 1 week), vomiting.DSASSS, RLS, RSS, vein of Galen(37)Czech RepublicCase report1
Noracyclina (case 1)
Ovulenb (case 2)
50/F (case 1)
41/F (case 2)
None (case 1);
Thrombosis of left common carotid (case 2)
Fluctuated conscious status, aphasia, right arm weakness, and several epileptic seizures (case 1);
Right hand numbness and rapid-onset unconsciousness (case 2)
NecropsySSS, CoVT (case 1, 2);(38)SwitzerlandCase report2
Lyndiol 2, 5 (case 1)
Metrulen-M (case 2)
Anovlar (case 3)
Gynovlar (case 4)
Nuvacon (case 5)
24/F (case 1)
49/F (case 2)
30/F (case 3)
23/F (case 4)
29/F (case 5)
RIJVS (case 1)
Diabetes (case 2)
Right pulmonary embolus (case 3)
Thrombosis of choroid plexus (case 4)
Marfan's syndrome; thrombosis of iliac vein (case 5)
Headache, vomiting and drowsiness (5-day) (case 1);
Headache, vomiting, seizure (generalized, left-sided) (case 2);
Deeply comatose (case 3);
Diarrhea, headache (severe) and further unconsciousness (case 4);
Abdominal pain, headache (severe, 1-day), and vomiting (5-day) (case 5).
NecropsySSS, RTS, SS, CoVT, IJV (case 1);
SSS, RTS, LTS, CoVT (case 2, 3, 5);
All sinuses thrombosis, CoVT (case 4)
(39)NRCase report5
Norethynodrel and mestranol35/FEclampsia during pregnancy; obesityHeadache (severe, persistent, temporal) (4-day), vomiting, diarrhea, seizure, urinary incontinence, upper limb weakness (left-sided), and visual disturbance (photophobia)NecropsySSS, LTS, CoVT(40)NRCase report1
Enovid (case 1)
Ortho novum (case 2)
29/F (case 1, 2)Multiple arterial thrombi; thrombosis of left opththalmic vein;
Marfan's syndrome (case 2)
NRNecropsyAll sinuses thrombosis, CoVT (case 1);
SSS (case 2)
(41)NRCase report2
Combined oral contraceptives (COCs), progestin-only contraceptives or cyproterone acetate.15–49/FFormer thromboembolic event (including PE, CVT, ischemic stroke, or MI)NRNRCVT(42)FranceRetro452
Yasmin 28c18/FNoneHeadache (Throbbing, frontal and occipital, 1-month)MRVRTS, RSS, IJV, CoVT(43)USACase report1
NR22/FNoneSevere headache (1 week)CT/MRV/DSALTS, LSS(44)ChinaCase report1
Cyproterone/gestodene50/FHeterozygous factor II polymorphismNRNRCVST(45)ItalyRetro1/28
NR23–45/FProthrombin mutation G20210A (n = 2)Headache (n = 11), vomiting (n = 2), aphasia (n = 1)MRA (n = 10)
DSA (n = 7)
Straight sinus (n = 15)
TS (n = 7)
(46)SpainRetro15
Other contraceptive drugs
Norethisterone enanthate injection23/FNoneHeadaches (progressive), vomiting (repeated) and syncope (2–3 min)MRVSSS, RTS, RSS(47)USACase report1
Vaginal contraceptive ringd28/FNoneHeadacheCTLSS, TS(48)USACase report1
33/FNoneSeizures (multiple tonic-clonic), headachesCTLTS, LSS, LIJV(49)CanadaCase report1
Androgen analog
Oxymetholone40/FAANRMRISSS, LTS(50)South KoreaCase report1
Nandrolone decaonoate22/MNoneHeadaches and vomiting (repeated) (3-day)MRVSSS, TS(51)IranCase report1
Fluoxymesterone52/F (case 1)
39/F (case 2)
Hypoplastic anemiaHeadaches (severe), seizures, aphasia and hemiplegia, coma (case 1)
Headaches (severe) and seizure (focal) (case 2)
DSASSS (case 1)
SSS, CoVT (case 2)
(52)USACase report3
Methenolone-enanthate26/F (case 3)Headaches, visual disturbance (blurred vision), and hemiparesis (right-sided) (case 3)SSS, CoVT (case 3)
Danazole40/MAAHeadache (acute onset) and altered sensoriumCTCoVT(53)IndiaCase report1
19/MIHAHeadache and visual disturbance (transient obscurations of vision)DSASSS, CoVT, straight sinus(54)USACase report1
Steroid32/FRelapsing-remitting multiple sclerosisNumbness and weakness (both legs)MRVLTS, LSS(55)TurkeyCase report1
31/MIHAHeadaches, anorexia, general malaiseDSASSS, CoVT, straight sinus(52)JapanCase report1
HIT-related CVST
LMWH60/FBilateral extensive varicose veins in legsRight focal seizures with secondary generalization followed by headache, slurred speech, and altered sensoriumMRI/CTVLTS, LSS(56)IndiaCase report1
52/FKyphoplasty and posterior spinal fusionAcute onset altered mental status with significant agitation and non-sensical speech.MRVLTS, LSS, LIJV(57)USACase report1
55/FPartial gastrectomyNRMRVSSS, SS, LIJV(58)GermanyCase report1
57/FAntiphospholipid syndrome and possible systemic lupus erythematosusFever, altered mental status, and aphasia (expressive and sensory)MRVSSS, LSS, LIJV(59)GreeceCase report1
69/FKnee replacement for osteoarthritisSeizures (right arm focal type)MRVSSS, CoVT(60)USACase report1
72/MLeft knee joint surgeryComatoseNecropsySSS, SS, CoVT(61)GermanyCase report1
38 ± 28NRNRMRVCVT(62)GermanyRetro3/120
Unfractionated heparin61/FRetinal transient ischemic attack; DVT of the legHeadache (progressive) and aphasiaMRILLS(63)FranceCase report1
18/MExtensive UCHeadache (severe), nausea and vomitingMRIRTS, confluence area(64)SwedenCase report1
45/FCystic pituitary adenoma.Aphasia and visual disturbancesMRILTS, LSS(65)USACase report1
67/FNRNRCTVSSS(66)GermanyCase report1
63/FPolycythemia veraSeizures (right-sided focal type)Contrast-enhanced CTSSS(67)USACase report1
36/FPNHHeadache, nausea, then developed dysphasia and right hemiparesisMRVLTS, LSS(68)JapanCase report1
67/FAntiphospholipid syndromeHeadache (transient), vertigo, tinnitus and right hemifacial par-aesthesia with propagation down to the ipsilateral arm.MRVRTS, RSS, IJV(69)SwitzerlandCase report1
Anti-cancer drugs
Tamoxifen40/FBreast cancerHeadache and hemiparesis (left-sided) (10-day)MRISSS, RLS, RIJV(70)TurkeyCase report1
30/FBreast cancerHeadache (acute-onset) and hemiparesis (left-sided)DSA/MRISSS(71)South KoreaCase report1
46/FBreast cancerHeadache (severe) and nausea (subacute onset, 2-week)MRI/CTSSS, straight sinus(72)South KoreaCase report1
47/FBreast cancerHeadache (Severe), seizure (generalized tonic-clonic)MRVSSS, CoVT(73)USACase report1
L-asparaginase15/MALLAcute severe headache and recurrent vomitingMRVSSS, TS, straight sinus(74)GermanyCase report1
10/M (case 1)
13/F (case 2)
ALL (case 1)
Acute mixed phenotypic leukemia (case 2)
Headache, vomiting, seizures and loss of consciousness (case 1)
Headache and focal seizure (case 2)
MRVSSS (case 1 & 2)(75)IndiaCase report2
5–16ALL (n = 8)
Non-Hodgkin lymphoma (n = 1)
Headaches (chronic, daily), and seizures (partial-complex)gMRVLTS, LSS, LIJV (case 1)
CVST (case 2)
SSS (case 3)
TS (case 4)
(76)USARetro9/200
2.3/M (case 1)
3.5/F (case 2)
ALL (case 1 & 2)Seizure (left focal seizure evolving into generalized tonic-colonic seizure and subsequently status epilepticus) (case 1);
Seizure (left focal seizure evolving into status epilepticus) (case 2)
MRV (case 1 & 2)SSS (case 1 & 2)(77)IndiaCase report2
(1–17)/(38/10, M/F)ALLHeadache (n = 14), a decreased level or loss of consciousness (n = 15), visual impairment (n = 3), focal or generalized seizures (n = 18), photophobia (n = 1), vomiting (n = 8), irritability (n = 3), hemiparesis (n = 5), ataxia (n = 2), speech impairment (n = 6), and cranial nerve palsy (n = 1).CT (n = 38), MRV (n = 27)CoVT (n = 3),
CVST (n = 26),
CVST combined with CoVT (n = 4)
(78)ItalyRetro33/48
5.6 (1.0–17.0)/(38/33, M/F)ALLNRMRICVT(79)AustriaPro3/71
9/MALLHeadache (Acute-onset, severe) and then seizures (left-sided focal type) and right arm sensory disturbance.MRISSS(80)Saudi ArabiaCase report1
32 (15–59)/(144/96, M/F)ALL or lymphoblastic lymphomaNRNRCVT(81)FranceRetro5/214
NAALLNRNRCVT(82)ItalyMeta-analysis26/1,752
16/MALLHeadache, vomiting, and multiple episodes of seizuresContrast enhanced CTCoVT(83)IndiaCase report1
L-asparaginase or Tamoxifenf44.5 (10-71)/(16/4, M/F)Hematologic malignancies (n = 9); Solid tumor (n = 11)Headache (n = 8), seizure (n = 6), nausea/vomiting (n = 5), hemiparesis/aphasia (n = 4), altered metal status/coma (n = 3), dizziness (n = 3), visual disturbance (n = 2), gait disturbance (n = 1), incidental finding (n = 1), not available (n = 1)MRVSSS (n = 13), TS (n = 8), SS (n = 5), IJV (n = 4), straight sinus (n = 1)(84)USARetro20
Cisplatin and BEP16/FImmature teratomaHemiparesis (left-sided)MRISSS(85)TunisiaCase report1
Thalidomide74/FMultiple myelomaHeadache (right-sided, frontal), confusion and speech difficulty (acute-onset)MRILTS, straight sinus, CoVT, LIJV(86)USACase report1
Methotrexate12/MALLHemiparesis (right-sided), aphasia, altered mental status, persistent seizure activity, and progressive neurological deteriorationMRILTS, LSS(87)USACase report1
ATRA22/FAPMLVisual disturbance (blurred vision on the right eye)MRVSSS, RSS, TS, IJV(88)MalaysiaCase report1

Drug induced cerebral venous thrombosis.

R, right; L, left; SS, sigmoid sinus; SSS, superior sagittal sinus; TS, transverse sinus; LS, lateral sinus; CVT, cerebral venous thrombosis; CVST, cerebral venous sinus thrombosis; CoVT, cortical vein thrombosis; IJVS, internal jugular vein stenosis; DVT, deep vein thrombosis; ALL, acute lymphoblastic leukemia; APML, acute promyelocytic leaukaemia; HIT, Heparin-induced thrombocytopenia; AA, Aplastic anemia; DM, diabetes mellites; PNH, Paroxysmal nocturnal hemoglobinuria; UC, ulcerative colitis; MI, myocardial infarction; ADHD, attention deficit hyperactivity disorder; IHA, immune hemolytic anemia; ITP, immune thrombocytopenia; PE, pulmonary emboli; MRI, magnetic resonance imaging; CTV, CT venography; MRV, magnetic resonance venography; DSA, digital subtraction angiography; CHCs, combined hormonal contraceptives; ATRA, All-trans retinoic acid; BEP, bleomycin and etoposide; IVIG, Intravenous immunoglobulins; Retro, retrospective; Pro, prospective; NR, not reported.

a

Noracyclin = Lynestrenol/mestranol.

b

Ovulen = Ethinodiol diacetate/mestranol.

c

Yasmin 28 = drospirenone.

d

Vaginal contraceptive ring (NuvaRing): etonogestrel and ethinyl-estradiol per day.

e

Danazol is an attenuated androgen derived from ethisterone (17 α-ethinyltestosterone).

f

This study enrolled patients with hematologic malignancies or solid tumors.

g

All patients survived, with 4 experiencing complications possibly related to CVST. In this article, report these four patients in detail.

h

Female patients with diagnosed cerebral venous thrombosis (CVT) of the dural sinuses, involvement of the deep venous system (DCVT), cortical venous thrombosis, or with thrombosis of the jugular system.

We further searched articles related to CsA-induced thrombotic events to explore if CsA would bring extensive damage to different kinds of blood vessels. One hundred forty articles were identified, and full texts of 67 articles were screened (Figure 7). Only studies with sufficient information and a clear description of the relationship between CsA and thrombosis were finally included (n = 29). CsA was more likely associated with venous thrombotic events (n = 16), followed by capillary thrombotic events (n = 9) and arterial thrombotic events (n = 8). CVT was the most common thrombosis in CsA-induced thrombotic events (Table 2) (19, 90109). Thrombosis in the renal vessel system was more likely formed due to CsA use in renal transplantation (n = 13).

Figure 7

Table 2

Age/genderThrombosis locationPrimary diseaseReferencesCountryStudy sizeArticle type
NRDVT (n = 25),
PE (n = 4),
DVT with PE (n = 11)
Renal transplantation(90)UK40/480Retro
41 ± 12DVTRenal transplantation(91)Switzerland9/97Pro
52/M (case 1)
26/M (case 2)
32/M (case 3)
61/M (case 4)
11/M (case 5)
54/M (case 6)
45/F (case 7)
Glomerular capillary;
Renal afferent artery
Renal transplantation (cadaver-donor)(92)UK7Case report
NACyclosporine-associated arteriopathy (acute tubular necrosis; acute vasculitis; glomerular ischemia; interstitial intimate; Intima proliferation; venous thrombosis)Renal transplantation (cadaver-donor)(93)USA16/200Retro
36.7 ± 1.3/(49/41, M/F)PE (n = 10),
Renal vein (n = 1),
DVT (n = 3),
Hemorrhoidal artery (n = 3)
Renal transplantation (cadaver-donor)(8)Belgium13/90Retro
35.9 ± 13.8DVTRenal transplantation (cadaver-donor, living-donor)(94)Sweden9/97Pro
53/F (case 1) 33/M (case 2)
48/F (case 3)
HUS,
Glomerular capillaries,
Renal artery
Renal transplantation(95)Canada3Case report
33/FGlomerular capillariesRenal transplantation (cadaver-donor)(96)UK1Case report
NAGlomerular capillaries (Platelet microthrombi)Renal transplantation(97)UK12/32Retro
NARenal arteryRenal transplantation (cadaver-donor, living-donor)(98)China1/14Retro
6 (case 1)
6 (case 2)
17 (case 3)
48 (case 4)
53 (case 5)
51 (case 6)
Renal veinRenal transplantation (cadaver-donor, living-donor)(99)UK6/791Retro
NAHUS, Glomerular capillariesBehcet's disease(100)France2Case report
NACVSTSSINS(101)UK1/53Retro
45.1 ± 12.3Renal veinRenal transplantation (cadaver-donor)(102)UK16Pro
NAEyeground arteryRecurrent nephrotic syndrome(103)Japan1Case report
NACVTRenal transplantation(104)Spain1Case report
25.0 ± 26.4HUSRenal transplantation(105)USA10/672Retro
NAHepatic veinInflammatory bowel disease and latent thrombocythemia(106)France1Case report
19/MCVSTSevere active UC(5)Japan1Case report
48/FCVST (LTS, LSS), LIJVSChronic UC(4)USA1Case report
NAThrombotic microangiopathySPK transplantation(107)Belgium1/102Retro
(18–55)Pancreas graft thrombosis (n = 10),
Kidney graft thrombosis (n = 1)
SPK transplantation(9)Belgium11/102Pro
31 ± 11Graft thrombosis (combined arterial and venous thrombotic occlusion, n = 5; arterial occlusion, n = 3, venous occlusion, n = 1)SPK transplantation(3)Austria9/67Retro
30/FCentral retinal veinRenal transplantation (cadaver-donor)(108)Croatia1Case report
56.7 ± 10.1Coronary arteryHeart transplantation(2)Canada18/129Retro
25/MCVST (SSS, TS)Renal transplantation (living-donor)(1)Sri Lanka1Case report
23/FCVTNeuro-Behcet's disease(109)Brazil3/40Retro
18–64/(28/33, F/M)Venous thrombosisAcute steroid-refractory or dependent UC(6)Finland1/61Pro
44/FCVSTAA(7)China1Case report

Cyclosporine-A induced thrombosis.

R, right; L, left; CVT, cerebral vein thrombosis; CVST, cerebral vein sinus thrombosis; CoVT, cortical vein thrombosis; SSS, superior sagittal sinus; TS, transverse sinus; DVT, deep vein thrombosis; PE, Pulmonary emboli; SPK transplantation, Simultaneous pancreas-kidney transplantation; HUS, Hemolytic Uremic Syndrome; AA, Aplastic anemia; SSINS, steroid sensitive idiopathic nephrotic syndrome; UC, ulcerative colitis; IBD, inflammatory bowel disease; Retro, retrospective; Pro, prospective; NR, not reported.

Statistical Analysis

Quantitative variables with a normal distribution were specified as mean ± standard deviation. Analyses were performed with Stata software (version 15.0 SE, Stata Corp, LP, Texas, USA).

Discussion

This was the first systematic review on drug-induced CVT and CsA-related thrombosis based on the clinical cases. CVT is a rare subtype of stroke, accounting for <1% of all strokes (110). Severe CVT can be fatal. Common etiologies of CVT are postpartum period, infection, and coagulopathies (111). However, drug-induced CVT should not be neglected, as this kind of CVT could be reversible and preventable if we avoid certain drugs when treating primary diseases, for instance, the two cases presented in this study. In line with CVT of other etiologies, the most common symptoms in drug-induced CVT were seizures (48.6%) and headaches (38.1%). Furthermore, women or young people were mainly involved. Both CE-MRV and black-blood thrombus image (BBTI) are useful imaging tools to make a definitive diagnosis.

It would be worth noticing that CsA can induce not only CVT but also cerebral arterial thrombosis, as in Case 2 of this report. Interestingly, drug-induced CVT is more likely involved in multiple sinuses, cortical veins, or IJV, such as Case 1 in this paper. It is well-known that OCP can promote CVT in women, whereas CsA-related CVT should also raise our concern.

Cyclosporine thrombogenicity manifested mostly with CVT. However, the underlying mechanism is still controversial. Several adverse effects of CsA had been reported in patients: Firstly, CsA enhanced secretion of von Willebrand factor (VWF), a classic platelet agonist, from endothelial cells (112). Then, platelet aggregation was increased due to a higher level of VWF in circulation (113). Thirdly, CsA-induced endothelial cell dysfunction by suppressing nitric oxide production and initiating intrinsic coagulation pathway (10, 114). Further, CsA was associated with increased D-dimer and fibrinogen levels, which were observed in our patients after the onset of the thrombotic event, which was consistent with other studies (4, 8, 115). However, some animal and clinical studies showed that CsA therapy was not related to thrombosis in renal transplant and even provided strong protection from both reperfusion injury (97) and congestive heart failure (116) or improved recovery after treatment of coronary thrombosis with angioplasty (117).

Moreover, apart from the thrombogenic effect of CsA, patients with AA frequently presented with decreased levels of WBC, RBC, or platelet. Anemia secondary to AA could also be associated with both CVT (118) and arterial ischemic stroke (AIS) (119). More importantly, anemia was correlated with stroke severity and poor clinical outcomes in AIS patients (120, 121). Thus, a well-controlled condition of AA is vital to prevent cerebral thrombotic events. Besides, a stronger association between anemia and CVT in men than in women (118), which reminded us that the potential confounders, such as age and gender, should also be taken into consideration when treating AA patients with thrombotic complications.

Although we cannot prove the clear relationship between the potential adverse effect of CsA, anemia secondary to AA, and intracranial thrombotic events in these two cases due to the rarity of similar cases, CsA-induced intracranial thrombosis in AA patients was firstly reported. This observation may at least warrant caution of monitoring thrombotic events during CsA treatment in patients with AA. Therefore, we suggested that future studies could shed more light on the mechanism of the prothrombotic effects of Cs-A in the treatment of AA patients. Additionally, the systematic literature review on CsA-related thrombotic events and drug-induced CVT would give more clinical references to physicians in this field, especially when treating patients with unknown reasons for stroke.

Summary Table

What Is Known About This Topic?

  • A possible association may exist between cyclosporine-A use and thrombotic events in patients with aplastic anemia.

  • Currently, there is a lack of information on comprehensive review on drug-induced cerebral venous thrombosis and cyclosporine-A-related thrombotic events.

What Does This Paper Add?

  • This real-world study provides two cases with aplastic anemia that developed intracerebral thrombotic events due to cyclosporine-A use.

  • Articles on cyclosporine-A-related thrombotic events were reviewed. CsA-induced thrombosis may involve the arteries, veins, and capillaries. Damage to the renal vascular system was most commonly reported due to the acute and chronic nephrotoxicity of CsA.

  • Studies on drug-induced cerebral venous thrombosis were selected, of which we summarized features of clinical characteristics and neuroimaging findings.

Statements

Data availability statement

The original contributions presented in the study are included in the article/Supplementary Material, further inquiries can be directed to the corresponding author.

Ethics statement

The studies involving human participants were reviewed and approved by Xuanwu Hospital, Beijing, China. The patients/participants provided their written informed consent to participate in this study. Written informed consent was obtained from the individual(s) for the publication of any potentially identifiable images or data included in this article.

Author contributions

RM drafted and revised the manuscript and provided the study concept and design. S-YS drafted and revised the manuscript, provided the study concept and design, and carried out collection, assembly, and interpretation of the data. RM, S-YS, Y-CD, Z-AW, and X-MJ wrote the manuscript and gave final approval of the manuscript. Y-CD intensively edited the revised version and contributed to the critical revision. All authors contributed to the article and approved the submitted version.

Funding

This study was sponsored by the National Key R&D Program of China (2017YFC1308400), the National Natural Science Foundation (81371289), and the Project of Beijing Municipal Top Talent for Healthy Work of China (2014-2-015).

Acknowledgments

We would like to thank the two patients for allowing us to publish their medical experience for scientific use.

Conflict of interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Supplementary material

The Supplementary Material for this article can be found online at: https://www.frontiersin.org/articles/10.3389/fneur.2020.563037/full#supplementary-material

Supplementary Figure 1

Funduscopic imaging of Case 1.

Supplementary Table 1

Follow up of abnormal examination in Case 1.

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Summary

Keywords

cyclosporine-A, cerebral venous sinus thrombosis, cerebral arterial infarction, case report, systematic review

Citation

Song S, Wang Z, Ding Y, Ji X and Meng R (2021) Cyclosporine-A-Induced Intracranial Thrombotic Complications: Systematic Review and Cases Report. Front. Neurol. 11:563037. doi: 10.3389/fneur.2020.563037

Received

17 May 2020

Accepted

23 December 2020

Published

11 February 2021

Volume

11 - 2020

Edited by

Sara Martinez De Lizarrondo, INSERM U1237 Physiopathologie et imagerie des troubles Neurologiques (PhIND), France

Reviewed by

David Gomez-almaguer, Autonomous University of Nuevo León, Mexico; Marialuisa Zedde, Local Health Authority of Reggio Emilia, Italy

Updates

Copyright

*Correspondence: Ran Meng

This article was submitted to Stroke, a section of the journal Frontiers in Neurology

Disclaimer

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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