Cotrimoxazole-Induced Hypoglycaemia in a Patient with Churg-Strauss Syndrome

Senanayake, Russell; Mukhtar, Mamoun

doi:10.1155/2013/415810

Cited by 9 publications

(7 citation statements)

References 15 publications

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“…Interestingly, we present co-trimoxazole-induced hypoglycaemia despite a normal random cortisol and concomitant prescription of a corticosteroid (prednisolone), which in theory should be protective against this adverse effect owing to its promotion of insulin resistance 20. This phenomenon was also described by Senanayake et al ,20 who also report a reduction in serum glucose parallel to a reduction in steroid dosage, further suggesting the sulfonylurea-like effect of co-trimoxazole 2…”

Section: Discussionsupporting

confidence: 70%

Severe co-trimoxazole-induced hypoglycaemia in a patient with microscopic polyangiitis

2017

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A 69-year-old man presented to the emergency department with lower respiratory tract infection and febrile neutropaenia. He was recently discharged following a 50-day hospital stay with newly diagnosed microscopic polyangiitis, complicated by pulmonary haemorrhage and severe renal dysfunction requiring renal replacement therapy, plasma exchange and immunosuppression (cyclophosphamide and methylprednisolone). High risk of pneumocystis pneumonia (PCP) led to an escalation in treatment from prophylactic to therapeutic oral co-trimoxazole, alongside broad-spectrum antibiotics. The patient suffered from severe and protracted hypoglycaemia, complicated by a tonic-clonic seizure 7 days after escalation to therapeutic co-trimoxazole. Endogenous hyperinsulinaemia was confirmed and was attributed to co-trimoxazole use. Hypoglycaemia resolved 48 hours after discontinuation of co-trimoxazole. PCP testing on bronchoalveolar lavage was negative. Owing to the prescription of heavy immunosuppression in patients with vasculitis and the subsequent risk of PCP warranting co-trimoxazole prophylaxis, we believe that the risk of hypoglycaemia should be highlighted.

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Section: Discussionsupporting

confidence: 70%

Severe co-trimoxazole-induced hypoglycaemia in a patient with microscopic polyangiitis

2017

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“…In this case, long-term steroid use was also a risk for prolonged hypoglycemia due to tertiary adrenal insufficiency, because steroids suppress the secretion of corticotropin-releasing hormone from the hypothalamus [30]. Senanayake et al reported a case of hypoglycemia caused by a prophylactic dose of TMP/SMX in a patient with eosinophilic granulomatosis with polyangiitis using prednisolone for immunosuppressive therapy, although the patient was without renal impairment [24]. Symptoms of hypoglycemia were ameliorated by increasing the prednisolone dosage.…”

Section: Discussionmentioning

confidence: 91%

“…The structural similarity of SMX with sulfonylurea may result in pancreatic insulin secretion, particularly at higher doses and in patients with renal impairment [6]. We reviewed previously reported 22 cases of TMP/ SMX-associated hypoglycemia [4,[6][7][8][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25] (Table 2). In most of the cases (77%), patients had renal impairment (serum creatinine > 1.1 mg/dL and/or on renal replacement therapy).…”

Section: Discussionmentioning

confidence: 99%

Severe hypoglycemia during pneumocystis pneumonia treatment associated with trimethoprim–sulfamethoxazole use in a patient on peritoneal dialysis

et al. 2017

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Background: Trimethoprim-sulfamethoxazole (TMP/SMX) is an essential antimicrobial agent for treating pneumocystis pneumonia (PCP). Furthermore, the risk of hypoglycemia is increased with the co-administration of sulfonylurea due to the presence of the same sulfanilamide structural group in SMX and sulfonylurea. However, hypoglycemia caused by a single administration of TMP/SMX is a rare adverse reaction, and not many cases have been reported. Renal failure is a risk factor for hypoglycemia with single TMP/SMX administration. Case presentation: A 54-year-old Japanese woman on peritoneal dialysis (PD) for 10 years was admitted to our hospital for the suspicion of PCP. She underwent immunosuppressive treatment with oral prednisolone (3 mg/day) and a subcutaneous injection of adalimumab (40 mg) every 2 weeks for rheumatoid arthritis. We initiated the administration of a low-to-moderate dose of TMP/SMX (TMP equivalent to TMP/SMX, approximately 8 mg/kg/day) in the patient, considering that she was on PD. At 10 days after administration, the patient became unconscious, and blood test results showed that her blood glucose level was low (15 mg/dL). Unlike hypoglycemia, her serum insulin levels were abnormally high (69.4 μU/mL) at that time. Glucose injection was used for correcting the hypoglycemia, but it was refractory. Highly concentrated glucose infusion was needed to maintain her blood glucose level normal. Her serum insulin level was confirmed to have returned to normal (4.0 μU/mL) at 9 days after completing the TMP/SMX treatment. Conclusions: We suspected that the refractory hypoglycemia in this case was caused by high levels of insulin secretion due to the accumulation of TMP/SMX. One of the risk factors in this patient was the low excretion rate of TMP/SMX into the PD fluid. Although hypoglycemia is a rare complication of TMP/SMX, we should consider this risk during TMP/SMX use in patients, especially those on PD.

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“…6 This is because it is structurally similar to sulphonylureas, and it is thus thought to stimulate pancreatic beta-cell insulin secretion. 7 In fact, sulphonylureas were first created from the discovery of sulphonamide-induced hypoglycaemia in 1942. 6 Despite this link, hypoglycaemia is a surprisingly rare side effect of co-trimoxazole.…”

Section: Discussionmentioning

confidence: 99%

Co-trimoxazole-induced hypoglycaemia in an immunosuppressed intensive care patient

Richards

Raby

2016

Journal of the Intensive Care Society

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An 18-year-old female inpatient on a neurosciences intensive care unitwith new onset super-refractory epilepsy became hypoglycaemic 48 h after commencing co-trimoxazole. She had been placed on this for prophylaxis against Pneumocystis jiroveci infection in the context of significant immunosuppression with high-dose corticosteroid therapy. In order to maintain glucose control, she required a continuous infusion of 10% dextrose at rates of 15-25 ml/h. Recurrent attempts to wean this were limited by further hypoglycaemia, until she spontaneously regained normoglycaemia after 73 days. This case report will discuss this unusual case of refractory hypoglycaemia, and the proposed pathophysiology of hypoglycaemia related to co-trimoxazole therapy.

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Cotrimoxazole-Induced Hypoglycaemia in a Patient with Churg-Strauss Syndrome

Cited by 9 publications

References 15 publications

Severe co-trimoxazole-induced hypoglycaemia in a patient with microscopic polyangiitis

Severe co-trimoxazole-induced hypoglycaemia in a patient with microscopic polyangiitis

Severe hypoglycemia during pneumocystis pneumonia treatment associated with trimethoprim–sulfamethoxazole use in a patient on peritoneal dialysis

Co-trimoxazole-induced hypoglycaemia in an immunosuppressed intensive care patient

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