Breast cancer is the most common cancer in women. The common sites of metastasis include the lungs, liver, and, infrequently, the gastrointestinal (GI) tract. A 72-year-old Caucasian female presented to the hospital with nausea and vomiting, diarrhea, intermittent abdominal pain, and unintentional weight loss. She had had a past medical history of bilateral lobular breast carcinoma and severe iron-deficiency anemia treated with iron transfusions. On arrival, the examination was significant for hypotension and pallor. Laboratory investigations revealed abnormal liver enzymes and raised tumor markers Ca-125 and carcinoembryonic antigen. Imaging studies established a diagnosis of distal small bowel obstruction. The surgical intervention showed the presence of a small bowel tumor, the biopsy findings of which were consistent with metastatic breast cancer, with ER and PR positive but HER-2 negative. She was managed with a selective estrogen receptor degrader and CDK4/6 inhibitor and has been in remission since. Metastasis to the small bowel from the breast is a very rare occurrence. Clinicians should thus maintain a modest amount of suspicion when encountering an uncommon GI presentation of primary breast malignancy. We describe the case of metastatic breast cancer with an atypical GI presentation.

Acquired thrombotic thrombocytopenic purpura is a combination of thrombocytopenia with microangiopathic hemolytic anemia. A 62-year-old female was transferred from an outside hospital for rapidly worsening mental status and severe thrombocytopenia. Laboratory studies were significant for reduced hemoglobin and platelet count along with raised blood urea nitrogen, creatinine, and serum lactate dehydrogenase levels. Peripheral smear showed numerous schistocytes and further testing showed low ADAMTS13 activity, high ADAMTS13 inhibitor, and positive hepatitis C virus antibody with a high hepatitis C virus ribonucleic acid (RNA) load. The patient was diagnosed with acquired thrombotic thrombocytopenic purpura and started on plasma exchange and steroids. Since no response was achieved until day four of treatment, weekly rituximab was initiated. After the initial two doses of rituximab, she showed significant improvement clinically. ADAMTS13 levels returned back to normal. Cyclosporine was added, following which platelet counts were normalized. Cyclosporine was discontinued, plasma exchange and steroids were slowly tapered off. Follow-up visits showed that the patient is off treatment and continues to be in remission and on regular treatment for hepatitis C. Acquired thrombotic thrombocytopenic purpura is a hematological emergency. Our patient remained refractory to standard therapies and required rituximab and immunosuppressive agents like cyclosporine. We describe the association of active hepatitis C with acquired thrombotic thrombocytopenic purpura that was refractory to plasma exchange, high dose steroids and rituximab. As per our knowledge, this is the first case in the literature to describe a possible association between active hepatitis C and acquired thrombotic thrombocytopenic purpura.