{'fraction_non_alphanumeric': 0.0452841973766396, 'fraction_numerical': 0.03653966271080575, 'mean_word_length': 4.7504488330341115, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 3, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Reversible diabetes insipidus in a patient with multiple myeloma.

We present a case of reversible diabetes insipidus in a 64-year-old man with multiple myeloma. Central diabetes insipidus developed in association with a myelomatous lesion of the clivus, but without evidence of macroscopic pituitary compression. Resolution of this patient’s diabetes insipidus was observed following treatment of his myeloma. A 64-year-old man presented with bone pain and weight loss. Blood tests revealed serum IgA 12.8 g/L (normal range 0.8–4.0), serum free lambda light chains 857 mg/L (6–26), beta-2 microglobulin 7.5 mg/L (0.0–3.2), corrected calcium 3.41 mmol/L (2.10–2.55), albumin 41 g/L (38–52) and creatinine 134 umol/L (60–105). X-rays demonstrated multiple long bone lytic lesions. A diagnosis of advanced IgA lambda multiple myeloma (MM) was made and the patient commenced chemotherapy with cyclophosphamide, dexamethasone and bortezomib. On the day of his third weekly dose of the first cycle of chemotherapy, he required hospital admission with profound dehydration and hypotension. He reported that he had been passing six litres of urine per day and drinking copious fluids. In retrospect, he had noticed increased thirst and urine output for six months, but had not mentioned it previously. His regular medications at this time were aciclovir, trimethoprim/sulfamethoxazole, ezetimibe, allopurinol, aspirin, cilazapril and dexamethasone. Admitting blood tests showed a creatinine of 152 umol/L (60–105), corrected calcium of 2.22 mmol/L (2.10–2.55) and a sodium of 137 mmol/L (135– 145). His anti-hypertensive agent (cilazapril) was discontinued and he was rehydrated with IV fluids. An overnight water deprivation test was suggestive of diabetes insipidus (DI), with a urine osmolality of 288 mOsm/kg (normal >750) and a matched serum osmolality of 293 mOsm/kg (normal urine/serum osmolality >2.4). He then underwent a formal 7-hour water deprivation test, as per the local protocol.1 Despite being nil by mouth he continued to produce 75–200mL urine per hour. At the end of the test his urine osmolality was inappropriately low at 270 mOsm/kg with a serum anti-diuretic hormone (ADH) of only 0.8 pmol/L (normal >1.0). Following administration of 2mcg of IV desmopressin his urine osmolality increased to 359 mOsm/kg and urine volume reduced to 30mL/hour (Table 1). A diagnosis of central DI was made1 and nasal desmopressin prescribed. The patient reported resolution of his nocturia and return to a normal fluid intake. There was no evidence of anterior pituitary dysfunction and he had a morning serum cortisol of 430 nmol/litre (200–700). He had a normal plasma glucose and none of his medications were known to cause central DI. An MRI pituitary was arranged (Figure 1). The pituitary gland was normal, apart from absence of the posterior pituitary bright spot. There were mottled changes of the skull base, in particular the clivus, confirmed as lytic lesions on a subsequent CT head scan (Figure 2). The bone lesions were consistent with myeloma. On the MRI scan there was also anomalous cerebral vasculature with a primitive trigeminal artery that caused distortion of the pituitary gland.