Cancer Chemotherapy-Related Thrombotic Thrombocytopenic Purpura: Biological Evidence of Increased Nitric Oxide Production

Porta, Camillo; Danova, Marco; Riccardi, Alberto; Bobbio-Pallavicini, E; Ascari, E

doi:10.4065/74.6.570

Cited by 18 publications

(11 citation statements)

References 30 publications

(3 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These vascular lesions are similar to those seen in aHUS induced by other chemotherapeutic agents such as vinblastine, bleomycin, and cisplatin [23]. Porta and colleagues showed that patients with chemotherapy-associated aHUS have increased circulating levels of nitrate compared with those with acquired idiopathic TTP or healthy controls, consistent with massive disruption of endothelial integrity [24]. Other investigators found that in vitro exposure of umbilical cord endothelial cells to nonlethal doses of mitomycin induced decreased prostacyclin concentration, further supporting the notion of endothelial dysfunction [23].…”

Section: Discussionmentioning

confidence: 66%

Is therapeutic plasma exchange indicated for patients with gemcitabine‐induced hemolytic uremic syndrome?

Gore

Jones

Marques

2009

J of Clinical Apheresis

View full text Add to dashboard Cite

Atypical hemolytic uremic syndrome (aHUS) has been described as an uncommon complication of gemcitabine. In this review, we discuss the diagnosis of gemcitabine-induced aHUS (GiHUS) and the published experience with therapeutic plasma exchange (TPE). To illustrate GiHUS, we present a patient who developed hypertension and peripheral edema while receiving gemcitabine and subsequently was found to have thrombocytopenia, hemolytic anemia, renal failure, and normal ADAMTS-13 activity. Although laboratory parameters improved on suspending gemcitabine, they worsened after reinstitution of the drug. Thrombocytopenia and hemolysis ceased once the drug was permanently discontinued without therapeutic plasma exchange (TPE). The pathological characteristics of GiHUS suggest damage of the glomeruli endothelial lining, leading to occlusion by fibrin-rich thrombi. Among 26 patients described in the literature not treated with TPE, 56% recovered from GiHUS, whereas only 30% of 18 patients treated with TPE did. The difference in recovery rate may have been confounded by the severity of GiHUS as suggested by the rate of dialysis in each group: 10/26 (38%) patients who did not receive TPE were dialyzed compared with 11/18 (61%) of those who had plasma exchange. Thus, although the currently available evidence is not decisive for use or non use of TPE, we suggest that the most important therapeutic intervention in GiHUS is discontinuation of the drug. Apheresis medicine specialists should be aware of this specific type of aHUS and provide treatment advice based on the currently available evidence.

show abstract

Section: Discussionmentioning

confidence: 66%

Is therapeutic plasma exchange indicated for patients with gemcitabine‐induced hemolytic uremic syndrome?

Gore

Jones

Marques

2009

J of Clinical Apheresis

View full text Add to dashboard Cite

show abstract

“…Previous literature has not reported that cyclophosphamide alone with moderate dosage can induce TMA [26,27]. This patient only received cyclophosphamide with a total dosage of 1 g and had maintained stable renal function, normal hemoglobin and platelet count over the next three years.…”

Section: Discussionmentioning

confidence: 82%

A case of lipoprotein glomerulopathy with thrombotic microangiopathy due to malignant hypertension

Chen

Yang

et al. 2013

BMC Nephrol

View full text Add to dashboard Cite

BackgroundLipoprotein glomerulopathy (LPG) is a rare inherited renal disease characterized by intraglomerular lipoprotein within the lumina of severely dilated glomerular capillaries. The common clinical presentation of LPG includes proteinuria or nephrotic syndrome. Hypertension and anemia were thought to be mild in LPG. Thrombotic microangiopathy (TMA) in LPG has not been previously reported. In this report, we present a patient with LPG that developed TMA. To the best of our knowledge, this is the first report of TMA in LPG.Case presentationFour years ago (2005), a 19-year-old Chinese woman was diagnosed with nephrotic syndrome and provided prednisone treatment. A combination of prednisone and cyclophosphamide did not have any effect and was discontinued after six months. Although she was steroid-resistant, over the next subsequent three years, she maintained normal renal function without anemia and thrombocytopenia. In February 2009, she had a severe headache and blurry vision and presented at a local hospital with severe hypertension. Blood pressure was 220/160 mmHg. Laboratory data showed hemoglobin 3.8 g/dL; platelet counts 29×109/L; urinary protein 7.90 g/d; total bilirubin 29.9 umol/L; indirect bilirubin 28.2 umol/L; LDH 1172 U/L; ALB 2.66 g/dL; urea nitrogen 52 mg/dL; serum creatinine 3.2 mg/dL; triglyceride 253 mg/dL; total cholesterol 273 mg/dL. ANA, ds-DNA, ANCA, anti-GBM antibody and anticardiolipin were all negative. A renal biopsy revealed LPG with TMA. Genetic evaluation showed the patient carried the APOE Kyoto mutation. Adequate control of blood pressure improved microangiopathic anemia and thrombocytopenia, however, renal function did not improve and she eventually developed uremia and became hemodialysis dependent.ConclusionWe report on a rare case of TMA probably due to malignant hypertension in LPG. Early lipid-lowering and antihypertensive treatment may improve outcome. The pathophysiologic relationship between LPG and TMA should be investigated further.

show abstract

“…In patients with cancer, various cancer chemotherapeutic agents have been implicated; mitomycin C [6,[25][26] has been most commonly associated with both TTP and hemolytic uremic syndrome, and other agents, including cisplatin [27], deoxycoformycin [28], the regimen of cisplatin, bleomycin, and a vinca alkaloid [29], the combination of daunorubicin and cytosine arabinoside [30], and combination regimens containing cisplatin [31], have also been implicated. In addition, cancer itself has been suspected to cause TTP [22][23][24], but neither a clear link between cancer and the development of TTP nor a risk factor for TTP in cancer patients has been identified.…”

Section: Discussionmentioning

confidence: 99%

“…In cancer patients, at least two causes for TM have been identified. One is the complication from chemotherapy [6,[25][26][27][28][29][30][31], and the other is the manifestation of the cancer itself without any relationship to chemotherapy. No specific pathologic feature, This material is protected by U.S.…”

Section: Introductionmentioning

confidence: 99%

Thrombotic Thrombocytopenic Purpura Associated with Bone Marrow Metastasis and Secondary Myelofibrosis in Cancer

Chang

Naqvi

2003

The Oncologist

View full text Add to dashboard Cite

To examine the relationship between cancer and development of thrombotic microangiopathy (TM), the medical records of patients with known TM were examined in one institution from January 1981 to December 2002. Nine out of 93 patients with the established diagnosis of TM had active cancer. All nine of those patients had thrombotic thrombocytopenic purpura (TTP). Among those patients, two patients received chemotherapy prior to the development of TTP. Six of the seven patients who received no chemotherapy had extensive bone marrow metastasis and secondary myelofibrosis. There were two patients each with breast cancer, lung cancer, and stomach cancer. Severe anemia and thrombocytopenia with leukoerythroblastosis were prominent clinical features in all six patients. Four patients had neurological (mental) changes and three developed fever, but none had significant renal dysfunction. Upon establishing the diagnosis of TTP, four patients were treated with exchange plasmapheresis (EP) and two patients were treated with chemotherapy because there were no neurological changes. Three patients achieved complete remission of TTP, one with EP alone and two with chemotherapy. The one patient who achieved remission with EP alone was later treated with chemotherapy and survived for 2 1/2 years. The other three patients treated with EP alone died within 2 months after the diagnosis of TTP. Since TTP occurred in association with bone marrow metastasis and myelofibrosis in six patients among seven chemotherapy-untreated cancer patients, this marrow change was considered to be the possible cause of the development of TTP. It is recommended that all cancer patients with unexplained anemia and thrombocytopenia be evaluated for the coexistence of bone marrow metastasis and TTP.

show abstract

Cancer Chemotherapy-Related Thrombotic Thrombocytopenic Purpura: Biological Evidence of Increased Nitric Oxide Production

Cited by 18 publications

References 30 publications

Is therapeutic plasma exchange indicated for patients with gemcitabine‐induced hemolytic uremic syndrome?

Is therapeutic plasma exchange indicated for patients with gemcitabine‐induced hemolytic uremic syndrome?

A case of lipoprotein glomerulopathy with thrombotic microangiopathy due to malignant hypertension

Thrombotic Thrombocytopenic Purpura Associated with Bone Marrow Metastasis and Secondary Myelofibrosis in Cancer

Contact Info

Product

Resources

About