ABSTRACT
The authors report the case of a 74-years-old woman treated by immunotherapy for a metastatic renal cell carcinoma and having developed an important cholestasis with thrombocytosis, increased CRP, leucocytosis and hypoalbuminemia. Liver remained free of metastases at medical imaging. The diagnosis of a Stauffer syndrome was confirmed by the hepatic biopsy. A complete response of liver disorders was obtained after nephrectomy. From literature survey, Stauffer syndrome should be kept in mind in cancer patients, especially those suffering from a renal cell carcinoma, presenting with cholestasis with no underlying cause.
Subject(s)
Carcinoma, Renal Cell , Cholestasis , Kidney Neoplasms , Liver Diseases , Female , Humans , Aged , Carcinoma, Renal Cell/complications , Carcinoma, Renal Cell/diagnosis , Kidney Neoplasms/complications , Kidney Neoplasms/diagnosis , Kidney Neoplasms/pathology , Syndrome , Liver Diseases/diagnosis , Cholestasis/complicationsABSTRACT
Eighteen patients who survived an acute myocardial infarction were found to have a normal coronary arteriogram. Seven patients were younger than 35 years and six were female. The myocardial infarction was nontransmural in 11 cases. The mean follow-up was 21.6 months. Eleven patients developed residual chest pain at rest early after myocardial infarction. One, treated by beta-blockers, suffered a recurrent myocardial infarction. Eight became asymptomatic, and two improved under antispastic therapy. Another patient developed a severe form of variant angina three months after myocardial infarction; she died following plexectomy. Finally, two patients experienced rare episodes of angina at rest. The stress ECG was negative in all cases. Provocative test for spasm was positive in three out of nine patients. Diffuse narrowing associated with chest pain was demostrated in two patients at angiography. Thus, myocardial infarction and subsequent normal coronary angiogram are mainly found in young female patients, and infarction is often nontransmural. Clinical evidence of vasospastic phenomena and increased vasomotor tone are found in most patients. Whenever residual chest pain is controlled by antispastic therapy, the follow-up course seems benign.
Subject(s)
Coronary Angiography , Myocardial Infarction/diagnostic imaging , Adult , Angina Pectoris/drug therapy , Angina Pectoris/etiology , Coronary Vasospasm/diagnosis , Coronary Vasospasm/etiology , Exercise Test , Female , Follow-Up Studies , Humans , Male , Middle Aged , Myocardial Infarction/complications , Myocardial Infarction/etiology , PrognosisABSTRACT
In view of reports that prostaglandins influence insulin and glucagon secretion, we have studied PGE2, insulin and glucagon release from fragments (15-20 mg) of human insulinoma tissue incubated in vitro in the absence or presence of indomethacin (100 mumol/liter) an inhibitor of prostaglandin synthesis. Acid-ethanol extraction of this tissue showed the following hormonal contents : insulin : 7.17 U and glucagon 84.4 ng per g of tissue (wet weight). In the absence of indomethacin, the mean release of PGE2, insulin and glucagon into the incubation medium was 3.65 +/- 1.3 pmol, 10.5 +/- 1.2 mU and 708.4 +/- 141.8 pg in two hours (mean of 5 vials containing 2 fragments of 15-20 mg of tissue). PGE2 release was significantly inhibited in the presence of indomethacin (0.89 +/- 0.23 pmol). This effect was associated with a significantly higher insulin (16.8 +/- 1.9 mU/2 hours) and lower glucagon (176 +/- 19.7 pg/2 hours) release. These results support the view that insular tissue possesses a prostaglandin synthesis system which positively modulates glucagon secretion whereas it negatively influences insulin release.
