theophylline

1
Reactions 1167 - 1 Sep 2007 S Theophylline Hypercalcaemia: case report A woman developed hypercalcaemia during treatment with theophylline for asthma. At the age of 46 years in 1998, the woman started receiving theophylline 200 mg/day internally; she had been receiving prednisolone for 10 years and had started receiving calcium lactate and alfacalcidol after being diagnosed with compressive lumbar vertebral fracture, marked anterior curvature and corticosteroid-induced osteoporosis in 1997. In 2001, she was found to have increased calcium levels (11–15 mg/dL), but did not receive any treatment. At the end of March 2003, she presented with renal dysfunction and, at this time, she had an increased serum calcium level (15.1 mg/dL) along with blood urea nitrogen and creatinine levels of 11 mg/dL and 2.58 mg/dL, respectively. Calcium lactate and alfacalcidol were discontinued as the woman’s high serum calcium levels were attributed to the treatment with these drugs. Infusion was performed and she also received elcatonin. However, 2 months later, her serum calcium levels had not decreased (11–13 mg/dL). She then received two doses of pamidronic acid and, 1 week later, her serum calcium had normalised. About 2 weeks later, her serum calcium level again increased and, on 19 June 2003, she was hospitalised. At hospitalisation, infusion was increased and elcatonin was restarted at a higher dosage. Laboratory examinations showed a theophylline concentration of 7.9 µg/mL, a calcium level of 13.4 mg/dL, an intact parathyroid hormone (PTH) level of 8 pg/mL, PTH-related protein below the measurement sensitivity level (< 1.0 pmol/L) and a decreased level of active vitamin D (4.8 pg/ml). Her increased levels of serum cAMP (27 pmol/L) and free thyroxine (2.14 ng/dL), and suppressed thyroid-stimulating hormone receptor activity (1.5%), indicated hyperthyroidism. She tested positive for thyroid antibodies and had increased levels of cross-linked N-terminal telopeptide of Type-1 collagen and deoxypyridinoline. Urinalysis confirmed renal dysfunction with a daily calcium excretion of 163.35mg. Drug-induced hypercalcaemia was suspected. On 4 August 2003, theophylline was discontinued. Infusion and elcatonin were then discontinued, but her serum calcium levels did not increase. She was subsequently discharged and, at this time, her serum calcium level had decreased to 1.41 mg/dL and her renopathy had improved. At the last follow-up, her serum calcium levels were normal and her serum creatinine level had improved (1.12 mg/dL). Author comment: It was considered possible that a normally non-overt condition had triggered hypercalcaemia as a result of the administration of theophylline together with hyperthyroidism reinforcing the action of PTH. Itoh Y, et al. A case of theophylline-induced hypercalcemia. Nippon Jinzo Gakkai Shi 49: 446-451, No. 4, 2007 [Japanese; summarised from a translation] - Japan 801081824 1 Reactions 1 Sep 2007 No. 1167 0114-9954/10/1167-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved

Upload: phungtuong

Post on 17-Mar-2017

219 views

Category:

Documents


2 download

TRANSCRIPT

Reactions 1167 - 1 Sep 2007

STheophylline

Hypercalcaemia: case reportA woman developed hypercalcaemia during treatment with

theophylline for asthma.At the age of 46 years in 1998, the woman started receiving

theophylline 200 mg/day internally; she had been receivingprednisolone for 10 years and had started receiving calciumlactate and alfacalcidol after being diagnosed withcompressive lumbar vertebral fracture, marked anteriorcurvature and corticosteroid-induced osteoporosis in 1997. In2001, she was found to have increased calcium levels(11–15 mg/dL), but did not receive any treatment. At the end ofMarch 2003, she presented with renal dysfunction and, at thistime, she had an increased serum calcium level (15.1 mg/dL)along with blood urea nitrogen and creatinine levels of11 mg/dL and 2.58 mg/dL, respectively.

Calcium lactate and alfacalcidol were discontinued as thewoman’s high serum calcium levels were attributed to thetreatment with these drugs. Infusion was performed and shealso received elcatonin. However, 2 months later, her serumcalcium levels had not decreased (11–13 mg/dL). She thenreceived two doses of pamidronic acid and, 1 week later, herserum calcium had normalised. About 2 weeks later, herserum calcium level again increased and, on 19 June 2003, shewas hospitalised. At hospitalisation, infusion was increasedand elcatonin was restarted at a higher dosage. Laboratoryexaminations showed a theophylline concentration of7.9 µg/mL, a calcium level of 13.4 mg/dL, an intact parathyroidhormone (PTH) level of 8 pg/mL, PTH-related protein belowthe measurement sensitivity level (< 1.0 pmol/L) and adecreased level of active vitamin D (4.8 pg/ml). Her increasedlevels of serum cAMP (27 pmol/L) and free thyroxine(2.14 ng/dL), and suppressed thyroid-stimulating hormonereceptor activity (1.5%), indicated hyperthyroidism. She testedpositive for thyroid antibodies and had increased levels ofcross-linked N-terminal telopeptide of Type-1 collagen anddeoxypyridinoline. Urinalysis confirmed renal dysfunctionwith a daily calcium excretion of 163.35mg. Drug-inducedhypercalcaemia was suspected. On 4 August 2003,theophylline was discontinued. Infusion and elcatonin werethen discontinued, but her serum calcium levels did notincrease. She was subsequently discharged and, at this time,her serum calcium level had decreased to 1.41 mg/dL and herrenopathy had improved. At the last follow-up, her serumcalcium levels were normal and her serum creatinine level hadimproved (1.12 mg/dL).

Author comment: It was considered possible that anormally non-overt condition had triggered hypercalcaemia asa result of the administration of theophylline together withhyperthyroidism reinforcing the action of PTH.Itoh Y, et al. A case of theophylline-induced hypercalcemia. Nippon Jinzo GakkaiShi 49: 446-451, No. 4, 2007 [Japanese; summarised from a translation] -Japan 801081824

1

Reactions 1 Sep 2007 No. 11670114-9954/10/1167-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved