This considerably reduced requirement for warfarin prompted a retrospective review of medical records at our hospital for the period 1981-6 to examine whether there might be an interaction between tamoxifen and warfarin. The records of women with breast cancer and a subsequent admission for a serious thromboembolism were examined. There were 18 such women: seven who had had deep venous thrombosis and 11 who had had a pulmonary embolus with probable deep venous thrombosis. Five of them were taking tamoxifen when they started taking warfarin. Two of them had complications after loading doses of warfarin: in one the prothrombin time after three daily doses of warfarin (10 mg, 10 mg, and 5 mg) rose to 50 seconds, and she developed a left subdural haematoma requiring warfarin to be withdrawn; in the other a similar loading dose regimen resulted in a prothrombin time of 49 seconds on day 7, the patient developed severe haematuria, and her anticoagulant treatment was changed to phenindione. The three other patients taking tamoxifen required daily doses of 2 mg, 2 mg, and 3 mg to maintain appropriate prothrombin times.The dose of warfarin that maintained appropriate prothrombin times in the 13 patients not taking tamoxifen varied from 4 to 10 mg (mean 6 25 mg) daily. None of these patients had complications in the first month of treatment with warfarin. CommentOur observations suggest that women with breast cancer requiring warfarin need a lower dose if they are taking tamoxifen. The mechanism of the interaction between the two drugs is unclear, but protein binding and competition for metabolic pathways may both play a part. Both warfarin and tamoxifen are metabolised by the microsomal enzyme systems in the liver. Warfarin is a racemic mixture and the (S) isomer is four to five times more physiologically active than the (R) isomer. This more active (S) isomer is converted to the 7-hydroxy metabolite, which is inactive, by the cytochrome P450 enzyme system.2 Three metabolites have been detected in the serum ofpatients taking tamoxifen. Normally tamoxifen accounts for 36% of the drug and metabolites present, desmethyltamoxifen for 58%, metabolite Y for 4%, and 4-hydroxytamoxifen for 1-5%.3 All of these metabolites have some affinity for the oestrogen receptor, but the affinity of the 4-hydroxy metabolite is 50-100 times greater than that of the parent drug.4 Accordingly, 4-hydroxytamoxifen is about 100 times more potent than tamoxifen in inhibiting the growth of MCF7 breast cancer cells in culture.5The hydroxylations are probably carried out by similar enzyme systems. In the case of warfarin competition for the enzymes may increase the concentration of the active parent drug and decrease the concentration of inactive metabolites. In the case of tamoxifen, however, the resultant changes in the amounts of metabolites present may have important implications for the activity of the drug. Altering the percentage of the 4-hydroxy metabolite present may have an effect on the response of the tumour.The hazards of an increased pha...

Shadow cells are characteristic of pilomatricoma, although they have been described in other cutaneous and visceral neoplasms, particularly endometrioid adenocarcinomas of the female genital tract. We describe a metastasis of an ovarian endometrioid adenocarcinoma with shadow cells to the skin that was initially misinterpreted as a pilomatricoma. We compare the histology of the ovarian neoplasm to 21 pilomatricomas. This is the first reported case of a cutaneous metastasis of a visceral neoplasm mimicking a primary pilomatrical neoplasm.

Introduction Lung cancer is the most common cause of cancer-related deaths globally. Metastatic disease is often found at the time of initial diagnosis in the majority of lung cancer patients. However, colonic metastases are rare. This report describes an uncommon case of colonic metastasis from lung adenocarcinoma. Case presentation A 64-year-old female presented to her gastroenterologist for progressively worsening abdominal pain and constipation. Exploratory colonoscopy revealed a large rectosigmoid mass resulting in near total rectal occlusion. Her specialist recommended she immediately go to her regional hospital for further workup. On admission, she complained of continued abdominal pain and constipation. Notably, she had a past medical history of non-small cell lung cancer (T1bN3M0 stage IIIB), diagnosed 1 year prior. She was thought to be in remission following radiation and immunotherapy with pembrolizumab. Upon hospital admission, she underwent an urgent colostomy, ileocecectomy and anastomosis, and rectosigmoid mass resection with tissue sampling. Pathology confirmed the diagnosis of colonic metastasis from primary lung adenocarcinoma. Treatment was with systemic chemotherapy followed by localized radiation to the pelvic region was started. She did not respond well to these therapies. Subsequent imaging showed refractory tumor growth in the pelvic region. Treatment could not be completed due to the patient experiencing a debilitating stroke, and she was transitioned to hospice care. Conclusions Clinicians should have a low threshold for intestinal investigation and considerations for colonic metastasis when patients with a history of primary lung cancer have abdominal symptoms.

A 55-year-old female presented to the emergency department with seizures, left hemiparesis, and memory loss. Her past medical history was notable for a right triple-negative breast adenocarcinoma that was diagnosed approximately two years prior. She underwent treatment with chemotherapy, right breast lumpectomy, and radiation near her rural hometown. Radiologic studies were performed in the emergency department. Brain imaging revealed a new 2-cm mass in the left breast and a 4-cm left frontal lobe brain lesion. She underwent an urgent craniotomy. Immunohistochemical staining of the brain tumor tissue suggested metastatic triple-negative breast adenocarcinoma. She was discharged with recommendations to follow up with her prior oncologist near her home for systemic chemotherapy. Three months after metastatic breast cancer to the brain was diagnosed, the patient experienced headaches, fever, and nuchal rigidity. MRI of the brain showed new leptomeningeal enhancement. A lumbar puncture with a cerebrospinal fluid analysis revealed the presence of malignant cells. Together with imaging and cerebrospinal fluid findings, leptomeningeal carcinomatosis was diagnosed. This case report presents an uncommon but well-known complication of breast cancer.

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