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Thiamine deficiency (TD) is recognized in various kinds of disease with associated loss of appetite including cancer. However, it has not been recognized to date in bereaved partners after spousal loss from cancer.
From a series of bereaved partners who lost a spouse to cancer, we report on those who developed TD after bereavement.
Case 1 was a 57-year-old woman who sought consultation at our “bereavement clinic.” Her husband had been diagnosed with pancreatic cancer one year earlier and had died one month previously. At the first visit, she was observed to suffer depression, anxiety, and decreased appetite. Neurological, blood, and biochemical examinations did not reveal any noteworthy findings. She was diagnosed with uncomplicated bereavement. Detailed examination revealed that her appetite had been markedly decreased for approximately five weeks. The diagnosis of TD was supported by her abnormally low serum thiamine level. Case 2 was a bereaved 73-year-old male who had lost his wife to hypopharyngeal cancer one month previously after a five-year illness. He had shown a lack of energy for the month preceding his wife's death, but because there was no improvement after her death, his family recommended he seek consultation at our “bereavement clinic.” He was suffering from major depressive disorder. Detailed examination revealed that his appetite had been decreased for more than two weeks. Again, the diagnosis of TD was supported by his abnormally low serum thiamine level.
Significance of results
These reports demonstrate that there is a possibility that bereaved could develop TD after the loss of a loved one. TD should be considered whenever there is a loss of appetite lasting for more than 2 weeks, and medical staff should pay careful attention to the physical condition of the bereaved to prevent complications because of TD.
Thiamine deficiency (TD) is recognized in various kinds of disease with associated loss of appetite including cancer; however, TD has not been recognized in the family caregivers of cancer patients to date.
From a series of cancer patient caregivers, we reported an aged family caregiver who developed TD while caring for the cancer patient.
The caregiver was a 90-year-old male. He had been accompanying his wife, who was diagnosed with colon cancer 4 years previously, on hospital visits as the primary caregiver, but because of psychological issues, he was recommended to visit the psycho-oncology department's “caregiver's clinic” for a consultation. Detailed examination revealed that his appetite had been only about 50% of usual from about one year before, and he had lost 12 kg in weight in one year. The diagnosis of TD was supported by his abnormally low serum thiamine level.
Significance of the results
This report demonstrates that there is a possibility that care providers could develop TD from the burdens associated with caregiving. TD should be considered whenever there is a loss of appetite lasting for more than 2 weeks, and medical staff should pay careful attention to the physical condition of care providers to prevent complications resulting from TD.
Wernicke encephalopathy (WE) is a neuropsychiatric disorder caused by thiamine deficiency, and is sometimes overlooked because of the diversity of clinical symptoms.
From a series of WE patients with cancer, we report a lung cancer patient who developed WE, the main symptom of which was agitation.
A 50-year-old woman with lung cancer was referred to our psycho-oncology clinic because of agitation lasting for three days. No laboratory findings or drugs explaining her agitation were identified. Although the patient did not develop delirium, ophthalmoplegia, or ataxia, WE was suspected because she experienced a loss of appetite loss lasting 5 weeks. This diagnosis was supported by abnormal serum thiamine and disappearance of agitation one hour after intravenous thiamine administration.
Significance of results
This report emphasizes the clinical diversity of WE and indicates the limits of the ability to diagnose WE from typical clinical symptoms. The presence of a loss of appetite for more than two weeks may be the key to the accurate diagnosis of WE.
Thiamine is an essential coenzyme for oxidative metabolisms; however, it is not synthesized in the human body, and the average thiamine storage capacity is approximately 18 days. Therefore, thiamine deficiency (TD) can occur in any condition of unbalanced nutrition. If TD is left untreated, it causes the neuropsychiatric disorder Wernicke encephalopathy (WE). Although WE is a medical emergency, it is sometimes overlooked because most patients with WE do not exhibit all of the typical symptoms, including delirium, ataxia, and ophthalmoplegia. If all of the typical clinical symptoms of WE are absent, diagnosis of TD or WE becomes more difficult.
From a series of cancer patients, we reported three patients who developed TD without the typical clinical symptoms of WE.
A 69-year-old woman with pancreatic body cancer receiving chemotherapy with paclitaxel and gemcitabine for six months. Her performance status (PS) was 1. A detailed interview revealed that she had appetite loss for six months. Another 69-year-old woman with ovarian cancer received nedaplatin; her PS was 0. A detailed interview revealed that she had appetite loss for three months. A 67-year-old woman with colon cancer receiving ramucirumab in combination with second-line fluorouracil with folinic acid and irinotecan. Her PS was 1. A detailed interview revealed that she had appetite loss for three weeks. None exhibited typical clinical signs of WE, but they developed appetite loss for six months, three months, and three weeks, respectively. The diagnosis of TD was supported by abnormally low serum thiamine levels.
Significance of the results
This report emphasizes the possibility of TD in cancer patients even when patients do not develop typical clinical signs of WE. The presence of appetite loss for more than two weeks may aid in diagnosing TD. Patients receiving chemotherapy may be at greater risk for developing TD.
Wernicke encephalopathy (WE) is a neuropsychiatric disorder caused by thiamine deficiency. Several reports of WE in cancer patients are known. WE is sometimes overlooked because most patients do not exhibit its typical symptoms (e.g., delirium, ataxia, ocular palsy). If delirium is not present, a diagnosis of WE is difficult because delirium is the hallmark symptom of WE.
Taken from a series on WE in cancer, we report two patients who developed WE without delirium during periodic psycho-oncology outpatient visits.
Case 1. A 61-year-old woman with non-Hodgkin lymphoma who was periodically attending a psycho-oncology outpatient clinic developed an unsteady gait. WE was suspected because she also developed appetite loss for two weeks, and we could find no other laboratory findings to explain her unsteady gait. Our diagnosis was supported by abnormal serum thiamine and disappearance of the gait disturbance after intravenous thiamine administration. Case 2. A 50-year-old woman with breast carcinoma with bone metastasis developed an unsteady gait. WE was suspected because she also developed loss of appetite for two weeks, and no other laboratory findings could explain her unsteady gait. The diagnosis was supported by abnormal serum thiamine and disappearance of the gait disturbance after administration of intravenous thiamine.
Significance of Results:
Our report emphasizes the importance of being aware of WE, even when patients do not present with delirium. The presence of loss of appetite for more than two weeks may be the key to a diagnosis of WE.
The aim of this study was to investigate the effects of the administration of oral arachidonic acid (AA) in rats with or without dextran sulphate sodium (DSS)-induced inflammatory bowel disease. Male Wistar rats were administered AA at 0, 5, 35 or 240 mg/kg daily by gavage for 8 weeks. Inflammatory bowel disease was induced by replacing drinking water with 3 % DSS solution during the last 7 d of the AA dosing period. These animals passed loose stools, diarrhoea and red-stained faeces. Cyclo-oxygenase-2 concentration and myeloperoxidase activity in the colonic tissue were significantly increased in the animals given AA at 240 mg/kg compared with the animals given AA at 0 mg/kg. Thromboxane B2 concentration in the medium of cultured colonic mucosae isolated from these groups was found to be dose-dependently increased by AA, and the increase was significant at 35 and 240 mg/kg. Leukotriene B4 concentration was also significantly increased and saturated at 5 mg/kg. In addition, AA at 240 mg/kg promoted DSS-induced colonic mucosal oedema with macrophage infiltration. In contrast, administration of AA for 8 weeks, even at 240 mg/kg, showed no effects on the normal rats. These results suggest that in rats with bowel disease AA metabolism is affected by oral AA, even at 5 mg/kg per d, and that excessive AA may aggravate inflammation, whereas AA shows no effects in rats without inflammatory bowel disease.