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Nodular regenerative hyperplasia and thrombocytopenia: case report A 61-year-old woman developed nodular regenerative hyperplasia and thrombocytopenia during treatment with trastuzumabemtansine [duration of treatment to reaction onset not stated; not all outcomes stated]. In 2003, the woman was diagnosed invasive ductal carcinoma with hormonal receptors and HER2 positive and received initial neoadjuvant chemotherapy epirubicin, paclitaxel and gemcitabine and underwent modified mastectomy of left breast followed by radiotherapy and tamoxifen. In October 2006, bone metastasis was noted and she received radiotherapy followed by trastuzumab and tamoxifen for 22 months (until November 2009). Between January 2010 and October 2012, she received lapatinib and capecitabine due to the worsening of right occipital condyle metastasis. Thereafter, small metastasis in her left rib was observed and her treatment with switched to trastuzumab-emtansine 3.6 mg/kg every three weeks [route not stated]. During treatment with trastuzumab-emtansine, she developed progressive stellate angiomas. Numerous abdominal CT-scans were carried out and it showed a stable hypodensity lesion in segment IV-A with a small element of steatosis without portal thrombosis or hepatic metastasis. A CT-scan performed in April 2014, showed sign of portal hypertension in the lower mesenteric veins (i.e after 24th cycle of trastuzumab-emtansine). Her portal hypertension was not clinically significant and no ascites was observed. Also, morphology of the liver was normal. However, over several months during treatment with trastuzumab-emtansine, transaminase enzymes increased and platelet count decreased (thrombocytopenia). Laboratory investigation prior to the 9th cycle, showed AST and ALT approximately twice the upper normal value. In December 2014, liver biopsy was performed because of increased stellate angiomas. Her initial cirrhosis evaluation was negative for anti-smooth muscle antibodies, viral hepatitis B and C, antimitochondrial antibodies, ferritin, antiparietal cell antibodies and alpha-1 antitrypsin. In January 2015, histological examination confirmed nodular regenerative hyperplasia. The Naranjo scale showed a probable association between trastuzumab-emtansine and nodular regenerative hyperplasia. Hence, the woman’s treatment with trastuzumab-emtansine was discontinued after 39 cycles (27 months). At that time, no cancer progression was observed under trastuzumab-emtansine therapy. Due to prior good response to trastuzumab, she was restarted on it along with exemestane in March 2015. Following three months of trastuzumab-emtansine discontinuation, a significant improvement in stellate angiomas was observed. Also, abdominal CT-scan, showed no progression of the hypodensity lesion. Her liver enzymes also normalised after six months of discontinuation. She further received 22 cycles of trastuzumab March 2015 and May 2016. However, she died of cancer progression a month later. The most likely hypothesis for nodular regenerative hyperplasia was that i