330
Journal of the Royal Society of Medicine Volume 83 May 1990
Case reports
Retroperitoneal fibrosis, hypercholestrolaemia and acute myocardial infarction
P A Routledge MD FRCP Department ofPharmacology and Therapeutics, University of Wales College of Medicine, Heath Park, Cardiff CF4 4XN Keywords: retroperitoneal fibrosis; acute myocardial infarction; hypercholesterolaemia
Idiopathic retroperitoneal fibrosis is a rare disease possibly caused by an allergic reaction to insoluble lipid leaking through thinned arterial walls from atheromatous plaques'. I report two cases of this condition occurring shortly after acute myocardial infarction in two patients with hypercholesterolaemia. Case reports Case 1: A 60-year-old man was admitted with chest pain due to inferior myocardial infarction. He was being treated with allopurinol for prophylaxis against gout and there was a strong family history of ischaemic heart disease. Examination was unremarkable. His serum creatinine was 80 Amol/l and his erythrocyte sedimentation rate (ESR) was (Westergren) 26 mm/h. He was discharged on timolol 10 mg twice a day, allopurinol and ibuprofen. Twelve weeks later he complained oflower abdominal pain. Whilst awaiting investigation he developed acute left ventricular failure. Serum creatinine was 750 ,mol/l and his ESR was 96 mm/h. Intravenous pyelogram showed bilateral hydronephrosis and hydroureter with a normal sized bladder. At operation, the R ureter was mobilized and histology of the fibrous tissue showed appearances consistent with retroperitoneal fibrosis. He made a good recovery but was noted to have a bilateral arcus and measurement of his fasting serum cholesterol showed a persistently raised cholesterol of 8.1 mmol/l (triglyceride 1.8 mmol/1). Case 2: A 48-year-old man was admitted with chest pain due to antero-lateral myocardial infarction. He had known familial hypercholesterolaemia for which he was receiving diet only. Examination revealed bilateral arcus senilis and tendon xanthomata and his fasting cholesterol was 10.9 mmol/l and his triglycerides 1.9 mmol/l. His serum creatinine was 86 itmol/l. ESR was raised, at 90 mm/h. Subsequent cardiac failure was treated with frusemide, spironolactone and isosorbide dinitrate and he was discharged after 10 days. Twelve weeks later he complained of dull ache in his back and his creatinine had risen to 413 jAmol/l and his ESR was 108 mm/h. Intravenous pyelography conflrmed bilateral
hydronephrosis and hydroureter with normal sized bladder and decompression was performed, followed by elective ureterelysis for retroperitoneal fibrosis. Discussion Recent studies have shown that idiopathic retroperitoneal fibrosis occurs only in areas where the walls of an artery, normally the aorta, have severe atheromatous plaques with evidence of breaching'. It is thought that this may allow insoluble lipid (ceroid) to leak into tissue around the aorta and induce an immune response with inflammation and chronic periaortitis2'3. Although idiopathic retroperitoneal fibrosis is thus associated with atheromatous disease, to my knowledge no link between hypercholesterolaemia and the condition has been previously reported. The relationship of retroperitoneal fibrosis to recent acute myocardial infarction in these two patients may merely have been fortuitous (since the latter disease is common), or the myocardial infarct might have helped to trigger the immune response leading to the development of retroperitoneal fibrosis. It should be noted that one subject (case 1) was receiving timolol as secondary prevention after myocardial infarction. His case was reported previously to indicate the possibility that timolol may be associated with retroperitoneal fibrosis4. It has been since suggested, however, that the association may occur because beta blockers are often used to treat hypertension caused by the unrecognized retroperitoneal fibrosis5. In the second patient, the raised ESR during admission for acute myocardial infarction might indicate that the retroperitoneal fibrotic process might have been already present. However, he was asymptomatic and the raised ESR could have been related to another cause. In conclusion it is possible that hypercholesterolaemia and myocardial infarction may be risk factors for retroperitoneal fibrosis and further studies are indicated. Acknowledgments: I thank Dr D Fisher for valuable criticism. References 1 Dixon AK, Mitchinson MJ, Sherwood T. Computed tomographic observations in periaortitis: a hypothesis. Clin Radiol 1984; 35:39-42 2 Parums D, Mitchinson MJ. Demonstration of immunoglobulin in the neighbourhood of advanced atherosclerotic plaques. Atherosclerosis 1981;38:211-16 3 Parums DV, Chadwick DR, Mitchinson MJ. The localisation of immunoglobulin in chronic periaortitis. Atherosclerosis 1986; 61:117-23 4 Rimmer E, Richens A, Forster ME, Rees RWM. Retroperitoneal fibrosis associated with timolol. Lancet 1983;ii:300 5 Pryor JP, Castle WM, Dukes DC, Smith JC, Watson ME, Williams JL. Do beta-adrenoceptor blocking drugs cause retroperitoneal fibrosis? Br Med J 1983;287:639-41
(Accepted 29 March 1989)
0141-0768/90/ 050330-01/$02.00/0 © 1990 The Royal Society of Medicine
Journal of the Royal Society of Medicine Volume 83 May 1990
Case reports
Retroperitoneal fibrosis, hypercholestrolaemia and acute myocardial infarction
P A Routledge MD FRCP Department ofPharmacology and Therapeutics, University of Wales College of Medicine, Heath Park, Cardiff CF4 4XN Keywords: retroperitoneal fibrosis; acute myocardial infarction; hypercholesterolaemia
Idiopathic retroperitoneal fibrosis is a rare disease possibly caused by an allergic reaction to insoluble lipid leaking through thinned arterial walls from atheromatous plaques'. I report two cases of this condition occurring shortly after acute myocardial infarction in two patients with hypercholesterolaemia. Case reports Case 1: A 60-year-old man was admitted with chest pain due to inferior myocardial infarction. He was being treated with allopurinol for prophylaxis against gout and there was a strong family history of ischaemic heart disease. Examination was unremarkable. His serum creatinine was 80 Amol/l and his erythrocyte sedimentation rate (ESR) was (Westergren) 26 mm/h. He was discharged on timolol 10 mg twice a day, allopurinol and ibuprofen. Twelve weeks later he complained oflower abdominal pain. Whilst awaiting investigation he developed acute left ventricular failure. Serum creatinine was 750 ,mol/l and his ESR was 96 mm/h. Intravenous pyelogram showed bilateral hydronephrosis and hydroureter with a normal sized bladder. At operation, the R ureter was mobilized and histology of the fibrous tissue showed appearances consistent with retroperitoneal fibrosis. He made a good recovery but was noted to have a bilateral arcus and measurement of his fasting serum cholesterol showed a persistently raised cholesterol of 8.1 mmol/l (triglyceride 1.8 mmol/1). Case 2: A 48-year-old man was admitted with chest pain due to antero-lateral myocardial infarction. He had known familial hypercholesterolaemia for which he was receiving diet only. Examination revealed bilateral arcus senilis and tendon xanthomata and his fasting cholesterol was 10.9 mmol/l and his triglycerides 1.9 mmol/l. His serum creatinine was 86 itmol/l. ESR was raised, at 90 mm/h. Subsequent cardiac failure was treated with frusemide, spironolactone and isosorbide dinitrate and he was discharged after 10 days. Twelve weeks later he complained of dull ache in his back and his creatinine had risen to 413 jAmol/l and his ESR was 108 mm/h. Intravenous pyelography conflrmed bilateral
hydronephrosis and hydroureter with normal sized bladder and decompression was performed, followed by elective ureterelysis for retroperitoneal fibrosis. Discussion Recent studies have shown that idiopathic retroperitoneal fibrosis occurs only in areas where the walls of an artery, normally the aorta, have severe atheromatous plaques with evidence of breaching'. It is thought that this may allow insoluble lipid (ceroid) to leak into tissue around the aorta and induce an immune response with inflammation and chronic periaortitis2'3. Although idiopathic retroperitoneal fibrosis is thus associated with atheromatous disease, to my knowledge no link between hypercholesterolaemia and the condition has been previously reported. The relationship of retroperitoneal fibrosis to recent acute myocardial infarction in these two patients may merely have been fortuitous (since the latter disease is common), or the myocardial infarct might have helped to trigger the immune response leading to the development of retroperitoneal fibrosis. It should be noted that one subject (case 1) was receiving timolol as secondary prevention after myocardial infarction. His case was reported previously to indicate the possibility that timolol may be associated with retroperitoneal fibrosis4. It has been since suggested, however, that the association may occur because beta blockers are often used to treat hypertension caused by the unrecognized retroperitoneal fibrosis5. In the second patient, the raised ESR during admission for acute myocardial infarction might indicate that the retroperitoneal fibrotic process might have been already present. However, he was asymptomatic and the raised ESR could have been related to another cause. In conclusion it is possible that hypercholesterolaemia and myocardial infarction may be risk factors for retroperitoneal fibrosis and further studies are indicated. Acknowledgments: I thank Dr D Fisher for valuable criticism. References 1 Dixon AK, Mitchinson MJ, Sherwood T. Computed tomographic observations in periaortitis: a hypothesis. Clin Radiol 1984; 35:39-42 2 Parums D, Mitchinson MJ. Demonstration of immunoglobulin in the neighbourhood of advanced atherosclerotic plaques. Atherosclerosis 1981;38:211-16 3 Parums DV, Chadwick DR, Mitchinson MJ. The localisation of immunoglobulin in chronic periaortitis. Atherosclerosis 1986; 61:117-23 4 Rimmer E, Richens A, Forster ME, Rees RWM. Retroperitoneal fibrosis associated with timolol. Lancet 1983;ii:300 5 Pryor JP, Castle WM, Dukes DC, Smith JC, Watson ME, Williams JL. Do beta-adrenoceptor blocking drugs cause retroperitoneal fibrosis? Br Med J 1983;287:639-41
(Accepted 29 March 1989)
0141-0768/90/ 050330-01/$02.00/0 © 1990 The Royal Society of Medicine
