New-onset type II diabetes mellitus, hyperosmolar non-ketotic coma, rhabdomyolysis and acute renal failure in a patient treated with sulpiride
Ömer Toprak1,
Mustafa Cirit1,
R
fk
Ersoy1,
Atilla Üzüm1,
Ömer Özümer2,
Ay
egül Çobano
lu1,
Mehmet Tanr
sev1,
Demet Güleç3 and
evki Çetinkalp4
1 Department of Nephrology2
Department of 3rd Internal Medicine3
Department of Psychiatry
Ataturk Research and Training Hospital
Izmir4
Department of Endocrinology
Medical School of Ege University
Izmir
Turkey
Email: info{at}omertoprak.com
Sir,
Various drugs have been reported to cause myoglobinuric acute renal failure [14]. In this report, we present a case of oral sulpiride administration, complicated with new-onset type II diabetes mellitus, hyperosmolar non-ketotic coma, rhabdomyolysis and acute renal failure.
Case. A 44-year-old female patient consulted a psychiatrist for her complaints of anxiety and hallucination. At the time, her laboratory results were normal. Oral sulpiride had been administered at a dose of 200 mg per day and increased to 600 mg/day gradually. At admission to our hospital 3 days later, she was unconscious. On physical examination, her blood pressure was 90/60 mmHg and her temperature was 38.5°C; turgor-tonus was diminished and muscle rigidity was present. Abnormal laboratory analyses were as follows: white blood cell count 17 x 103/µl, serum glucose 389 mg/dl, blood urea nitrogen 76 mg/dl, serum creatinine 5.0 mg/dl, sodium 168 mmol/l, calcium 7.8 mg/dl, creatine phosphokinase 7070 U/l, aspartate transaminase 151 U/l, alanine transaminase 52 U/l, lactate dehydrogenase 654 U/l and blood osmolality 360 mosm/kg H2O. Her serum myoglobin level was 4360 ng/ml (normal range: 764) and her urinary myoglobin level was 7620 ng/ml (normal range: 0200). Serum islet cell antibody and glutamic acid decarboxylase antibodies were negative. Insulin and C-peptide were increased after the intravenous administration of 1 mg of glucagon. HbA1c was normal (5.0%). Urinary dipstick analysis was 2+ positive for glucose, 1+ positive for protein, negative for ketone and 3+ positive in the haem test. Urinary sediment showed a few red blood cells and 23 leukocytes per high-power field. No microbial agent was grown in cultures. Renal ultrasonography and electromyography (EMG) examination were normal. Sulpiride was withdrawn. She was treated with bicarbonate and intensive insulin. On the 12th day, her mental status, fever and laboratory analysis returned to normal (figure 1). On psychiatric evaluation, a brief psychotic disorder was diagnosed. One month after discharge, all laboratory analyses remained normal and the patient had no complaints.
Discussion. Sulpiride is a selective dopamine D2 antagonist with antipsychotic and antidepressant activity [5]. Sulpiride has been associated with many side effects [57]. Only one case of neuroleptic malignant syndrome with myoglobinuric acute renal failure after withdrawal of sulpiride and maprotiline therapy was described in the literature [2]. However, in this case, new-onset diabetes mellitus and hyperosmolar non-ketotic coma had not been reported. Our patient had no prior diagnosis of diabetes. New-onset diabetes mellitus due to administration of clozapine, olanzapine, risperidone and quetiapine has been reported previously [6]. However, there was no case of new-onset diabetes mellitus being caused by sulpiride intake. The precise mechanism of antipsychotic-associated diabetes is unclear. Rhabdomyolysis is frequently observed in diabetics [4,6]. We considered that dehydration, non-ketotic coma, hyperthermia, hyperosmolality due to severe hypernatraemia and neuroleptic malignant syndrome were the main causes of rhabdomyolysis in our case [1,3,4,7]. We thought that the trigger was sulpiride administration. We excluded the main causes of rhabdomyolysis according to history and laboratory tests. The kidney is the most common site of complication in rhabdomyolysis, and acute renal failure may occur [1]. In our case, acute renal failure also occurred and was improved with adequate therapy. On the 12th day of hospitalization, the insulin therapy was withdrawn and the serum glucose levels persisted in the normal range with diet regulation. The psychiatric symptoms disappeared, so antipsychotic therapy was no longer required. The complications of sulpiride therapy were observed to be temporary in our case.
In conclusion, physicians should be aware of the potential risks of new-onset diabetes mellitus, hyperosmolar non-ketotic coma, rhabdomyolysis and acute renal failure in patients receiving sulpiride treatment.
Conflict of interest statement. None declared.
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