- Email: [email protected]
Erythropoietin production and pH
1411
total visual loss. The patient was placed supine by her spouse, which resulted in a slow return of vision to baseline over the ensuing hours. Bromocriptine was immediately discontinued, and she was admitted for resection of a non-functioning pituitary tumour via the transphenoidal route 2 days later without complication. and release by patients have intolerable side-effects to even small doses, bromocriptine is well:tolerated by most, and has proven effective in almost 15 years of widespread use in the treatment of prolactinomas.The drug also decreases tumour size and improves visual function in patients with prolactin-secreting macroadenomas, in which surgical cure rates are low’ (only 49% of patients with tumours > 1 cm among our first 1000 patients achieved chemical cure [ < 20 ng/ml prolactin postoperatively]). Thus our practice is to place all patients with large or invasive pituitary tumours with endocrinologically documented prolactin secretion on a trial of bromocriptine, with All solid monitoring of clinical status and radiographic tumours should primary prolactin-secreting respond to the medication by reduction in tumour size and by reduction in prolactin. The aim is to produce normal prolactin concentrations, because prolonged hyperprolactinaemia may be associated with osteoporosis.5 The most common side-effects with bromocriptine are nausea and orthostatic hypotension, which often occur at onset of treatment. Thus medication is usually started in small doses.6,7 The most likely cause of our patient’s transient visual loss was postural hypotension with resultant decrease in perfusion pressure to a compromised visual system, which underlines the need for close observation during the initial phase of treatment in such patients.
Bromocriptine
suppresses
prolactin production
stimulation of dopamine receptors. Although
some
appearance.
Department of Neurological Surgery, University of Southern California School of Medicine, Los Angeles, California 90033, USA
WILLIAM T. COULDWELL MARTIN H. WEISS
1. Vance ML, Evans WS, Thomer MO. Bromocriptine Ann Intern Med 1984; 100: 78-91. 2. Landolt AM. Surgical treatment of pituitary prolactinomas: postoperative prolactin and fertility in seventy patients. Fertil Steril 1981, 35: 620-25. 3. Weiss MH, Wycoff RR, Yadley R, Gott P, Feldon S. Bromocriptine treatment of
prolactin-secreting tumours: surgical implications. Neurosurgery 1983; 12: 640-42. Surgical results for pituitary adenomas: results of an international survey. In: Black PMcL, Zervas NT, Ridgeway EC, eds. Secretory tumors of the pituitary gland New York: Raven, 1984. 377-85. Klibanski A, Biller BMK, Rosenthal DI, Schoenfeld DA, Saxe V. Effects of prolactin and estrogen deficiency in amenorrheic bone loss. J Glin Endocrinol Metab 1988; 67:
4. Zervas NT
5
124-30. 6. Parkes D. Bromocriptine. N Engl J Med 1979; 301: 873-78. 7. Vance ML, Thomer MO. Prolactinomas. Endocrinol Metab Clin North Am 1987; 16: 731-51.
Erythropoietin production and pH iK,—ivicLauoiic
acluusis
may
oe unuerenumaLeu m
cuinnouLmg
defective erythropoietin production, mainly in chronic renal failure. We have assayed serum immunoreactive erythropoietin in three consecutive patients with diabetes mellitus who were admitted for correction of severe ketoacidosis. Samples for arterial blood gas analyses and erythropoietin measurements were taken before and on the first day after treatment with sodium bicarbonate, electrolytes, and insulin. Patient 1 was a 34-year-old woman with type I diabetes mellitus and chronic renal failure (pH 7-09, base excess - 22 mmol/l, haemoglobin 8-4 g/dl, creatinine 650 umol/1). Patient 2 was an 80-year-old man with type IIdiabetes mellitus (pH 6’92, base excess - 29 mmol/1, haemoglobin 11-7 g/dl, creatinine 251 jmiol/1). Patient 3 was a 53-year-old man with type II diabetes mellitus (pH 712, base excess - 22 mmol/1, haemoglobin 12-3 g/dl, creatinine 217 lunol/1). Serum erythropoietin increased in all three patients within a day of treatment and the pH became normal (figure). This erythropoietin increase was not attributable to change in haemoglobin concentration or arterial p02. pH concentration affected erythropoietin production despite uraemia in patient 1. Plasma erythropoietin may increase in patients with chronic renal failure during hypoxaemial or after a switch from haemodialysis to chronic ambulatory peritoneal dialysis,2 which indicates that the capacity to produce erythropoietin is not necessarily abolished in uraemia. Laboratory studies in man and animals have shown that to
arterial
pH
Serum erythropoietin in patients 1-3 with diabetes mellitus before and on day after pH correction.
Epo
=
erythropoietin
erythropoietin response to anaemia, hypoxaemia, or cobalt is suppressed in acidosis and enhanced in alkalosis when induced artificially.3 Based on our measurements in patients with diabetes mellitus, we propose that pH changes exert a significant influence on plasma erythropoietin in human disease. the
treatment
Department of Internal Medicine, Medical University of Lubeck, Lubeck, Germany
P. M. ROB
Department of Physiology, University of Bonn, 5300 Bonn 1, Germany
J. FANDREY W. JELKMANN
1. Chandra M, McVicar M, Clemons G, Mossey RT, Wilkes BM. Role of erythropoietin m the reversal of anemia of renal failure with continuous ambulatory peritoneal dialysis. Nephron 1987; 46: 312-15. 2. Chandra M, Clemons GK, McVicar MI. Relation of serum erythropoietin levels to renal excretory function: evidence for lowered set point for erythropoietin production in chronic renal failure. J Pediatr 1988; 113: 1015-21. 3. Jelkmann W. Erythropoietin: structure, control of production, and function. Physiol Rev 1992; 72: 449-89.
Living-related liver transplantation in fulminant hepatic failure SIR,-Fulminant hepatic failure (FHF) is an indication for liver transplantation. However, no guarantee can be given that a donor will be available when required, and death while waiting for a transplant is not uncommon. As outlined by Dr Takas (Nov 7, p 1164) there are obstacles to defining brain death and organ transplantation in Japan. Therefore FHF is treated by plasmapheresis. When a cadaveric donor is not available, livingrelated donor liver transplantation is an alternative. We report a case of FHF thus treated. A 15-year-old boy of 48 kg developed influenza-like symptoms on July 20,1992, and took medicines which had been prescribed for his mother by a family doctor. On Aug 2, he became jaundiced. Serological examination excluded infection with hepatitis A, B, or C viruses, cytomegalovirus, Epstein-Barr virus, adenovirus, and Coxsackie virus. A drug lymphocyte-stimulation test was positive for diclofenac (index 346%). Interferon-Qt, glucagon/insulin infusion, prostaglandin E1, and acetylcysteinel were started but were not effective. On Aug 14, hepatic encephalopathy developed, and plasmapheresis was started (3200 ml, 14 times). However, there was no improvement; the patient’s encephalopathy worsened and considerable liver contraction was observed. On August 21, the patient was referred to Shinshu University for the possibility of a transplant. As there were no contraindicating factors, a transplant from his father was planned. 500 ml of the patient’s fresh-frozen plasma was stored and computed tomography (CT), magnetic resonance imaging, and coeliac arteriography were done. The total volume of the father’s liver according to CT was 1192 cm3, the left lobe
total visual loss. The patient was placed supine by her spouse, which resulted in a slow return of vision to baseline over the ensuing hours. Bromocriptine was immediately discontinued, and she was admitted for resection of a non-functioning pituitary tumour via the transphenoidal route 2 days later without complication. and release by patients have intolerable side-effects to even small doses, bromocriptine is well:tolerated by most, and has proven effective in almost 15 years of widespread use in the treatment of prolactinomas.The drug also decreases tumour size and improves visual function in patients with prolactin-secreting macroadenomas, in which surgical cure rates are low’ (only 49% of patients with tumours > 1 cm among our first 1000 patients achieved chemical cure [ < 20 ng/ml prolactin postoperatively]). Thus our practice is to place all patients with large or invasive pituitary tumours with endocrinologically documented prolactin secretion on a trial of bromocriptine, with All solid monitoring of clinical status and radiographic tumours should primary prolactin-secreting respond to the medication by reduction in tumour size and by reduction in prolactin. The aim is to produce normal prolactin concentrations, because prolonged hyperprolactinaemia may be associated with osteoporosis.5 The most common side-effects with bromocriptine are nausea and orthostatic hypotension, which often occur at onset of treatment. Thus medication is usually started in small doses.6,7 The most likely cause of our patient’s transient visual loss was postural hypotension with resultant decrease in perfusion pressure to a compromised visual system, which underlines the need for close observation during the initial phase of treatment in such patients.
Bromocriptine
suppresses
prolactin production
stimulation of dopamine receptors. Although
some
appearance.
Department of Neurological Surgery, University of Southern California School of Medicine, Los Angeles, California 90033, USA
WILLIAM T. COULDWELL MARTIN H. WEISS
1. Vance ML, Evans WS, Thomer MO. Bromocriptine Ann Intern Med 1984; 100: 78-91. 2. Landolt AM. Surgical treatment of pituitary prolactinomas: postoperative prolactin and fertility in seventy patients. Fertil Steril 1981, 35: 620-25. 3. Weiss MH, Wycoff RR, Yadley R, Gott P, Feldon S. Bromocriptine treatment of
prolactin-secreting tumours: surgical implications. Neurosurgery 1983; 12: 640-42. Surgical results for pituitary adenomas: results of an international survey. In: Black PMcL, Zervas NT, Ridgeway EC, eds. Secretory tumors of the pituitary gland New York: Raven, 1984. 377-85. Klibanski A, Biller BMK, Rosenthal DI, Schoenfeld DA, Saxe V. Effects of prolactin and estrogen deficiency in amenorrheic bone loss. J Glin Endocrinol Metab 1988; 67:
4. Zervas NT
5
124-30. 6. Parkes D. Bromocriptine. N Engl J Med 1979; 301: 873-78. 7. Vance ML, Thomer MO. Prolactinomas. Endocrinol Metab Clin North Am 1987; 16: 731-51.
Erythropoietin production and pH iK,—ivicLauoiic
acluusis
may
oe unuerenumaLeu m
cuinnouLmg
defective erythropoietin production, mainly in chronic renal failure. We have assayed serum immunoreactive erythropoietin in three consecutive patients with diabetes mellitus who were admitted for correction of severe ketoacidosis. Samples for arterial blood gas analyses and erythropoietin measurements were taken before and on the first day after treatment with sodium bicarbonate, electrolytes, and insulin. Patient 1 was a 34-year-old woman with type I diabetes mellitus and chronic renal failure (pH 7-09, base excess - 22 mmol/l, haemoglobin 8-4 g/dl, creatinine 650 umol/1). Patient 2 was an 80-year-old man with type IIdiabetes mellitus (pH 6’92, base excess - 29 mmol/1, haemoglobin 11-7 g/dl, creatinine 251 jmiol/1). Patient 3 was a 53-year-old man with type II diabetes mellitus (pH 712, base excess - 22 mmol/1, haemoglobin 12-3 g/dl, creatinine 217 lunol/1). Serum erythropoietin increased in all three patients within a day of treatment and the pH became normal (figure). This erythropoietin increase was not attributable to change in haemoglobin concentration or arterial p02. pH concentration affected erythropoietin production despite uraemia in patient 1. Plasma erythropoietin may increase in patients with chronic renal failure during hypoxaemial or after a switch from haemodialysis to chronic ambulatory peritoneal dialysis,2 which indicates that the capacity to produce erythropoietin is not necessarily abolished in uraemia. Laboratory studies in man and animals have shown that to
arterial
pH
Serum erythropoietin in patients 1-3 with diabetes mellitus before and on day after pH correction.
Epo
=
erythropoietin
erythropoietin response to anaemia, hypoxaemia, or cobalt is suppressed in acidosis and enhanced in alkalosis when induced artificially.3 Based on our measurements in patients with diabetes mellitus, we propose that pH changes exert a significant influence on plasma erythropoietin in human disease. the
treatment
Department of Internal Medicine, Medical University of Lubeck, Lubeck, Germany
P. M. ROB
Department of Physiology, University of Bonn, 5300 Bonn 1, Germany
J. FANDREY W. JELKMANN
1. Chandra M, McVicar M, Clemons G, Mossey RT, Wilkes BM. Role of erythropoietin m the reversal of anemia of renal failure with continuous ambulatory peritoneal dialysis. Nephron 1987; 46: 312-15. 2. Chandra M, Clemons GK, McVicar MI. Relation of serum erythropoietin levels to renal excretory function: evidence for lowered set point for erythropoietin production in chronic renal failure. J Pediatr 1988; 113: 1015-21. 3. Jelkmann W. Erythropoietin: structure, control of production, and function. Physiol Rev 1992; 72: 449-89.
Living-related liver transplantation in fulminant hepatic failure SIR,-Fulminant hepatic failure (FHF) is an indication for liver transplantation. However, no guarantee can be given that a donor will be available when required, and death while waiting for a transplant is not uncommon. As outlined by Dr Takas (Nov 7, p 1164) there are obstacles to defining brain death and organ transplantation in Japan. Therefore FHF is treated by plasmapheresis. When a cadaveric donor is not available, livingrelated donor liver transplantation is an alternative. We report a case of FHF thus treated. A 15-year-old boy of 48 kg developed influenza-like symptoms on July 20,1992, and took medicines which had been prescribed for his mother by a family doctor. On Aug 2, he became jaundiced. Serological examination excluded infection with hepatitis A, B, or C viruses, cytomegalovirus, Epstein-Barr virus, adenovirus, and Coxsackie virus. A drug lymphocyte-stimulation test was positive for diclofenac (index 346%). Interferon-Qt, glucagon/insulin infusion, prostaglandin E1, and acetylcysteinel were started but were not effective. On Aug 14, hepatic encephalopathy developed, and plasmapheresis was started (3200 ml, 14 times). However, there was no improvement; the patient’s encephalopathy worsened and considerable liver contraction was observed. On August 21, the patient was referred to Shinshu University for the possibility of a transplant. As there were no contraindicating factors, a transplant from his father was planned. 500 ml of the patient’s fresh-frozen plasma was stored and computed tomography (CT), magnetic resonance imaging, and coeliac arteriography were done. The total volume of the father’s liver according to CT was 1192 cm3, the left lobe