Inappropriate antidiuretic hormone secretion in Wernicke’s encephalopathy

Cooles, Philip E.; Borthwick, L J

doi:10.1136/pgmj.58.677.173

Cited by 5 publications

(4 citation statements)

References 12 publications

(12 reference statements)

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“…In this later phase, targeted structures, notably the mammillary bodies, become atrophic (13,14). To date, only one report has demonstrated a relationship between SIADH and WE (15). Thus, Korsakoff syndrome may be related to the cause of SIADH and the mechanism of occurrence of Takotsubo cardiomyopathy with severe hyponatremia in the present case.…”

Section: Discussionmentioning

confidence: 47%

Takotsubo Cardiomyopathy in a Patient with Severe Hyponatremia Associated with Syndrome of Inappropriate Antidiuretic Hormone

Kawano¹,

Matsumoto²,

Arakawa³

et al. 2011

Intern. Med.

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Section: Discussionmentioning

confidence: 47%

Takotsubo Cardiomyopathy in a Patient with Severe Hyponatremia Associated with Syndrome of Inappropriate Antidiuretic Hormone

Kawano¹,

Matsumoto²,

Arakawa³

et al. 2011

Intern. Med.

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“…As far as the authors know, hyponatremia and hypotension were only reported in some WE cases, respectively. [7–9] Therefore, as a very rare example, this case showed all above symptoms. Therefore, this case was reported here to highlight the possibility of WE when patients with nutrition supplemental deficiency developed hypothalamic syndrome.…”

Section: Discussionmentioning

confidence: 75%

“…To our knowledge, 1 report of WE in the literature indicated syndrome of inappropriate antidiuretic hormone secretion (SIADH), [9] whereas another WE report revealed cerebral salt-wasting syndrome (CSWS), [8] although both cases showed hyponatremia. However, SIADH shows dilutional hyponatremia, a decreased urine volume, and euvolemia or hypervolemia because of the excessive release of antidiuretic hormone, whereas CSWS shows hyponatremia, serum hypoosmality, concentrated urine, and natriuresis with dehydration.…”

Section: Discussionmentioning

confidence: 99%

Hypothalamic sydrome as an initial presentation of Wernicke encephalopathy

et al. 2019

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Rationale: Wernicke encephalopathy (WE) is a syndrome characterized by an acute or subacute onset of ataxia, ophthalmoplegia, and mental status changes. To our knowledge, hypothalamic syndrome is rare in WE. Patient concerns: A 73-year-old female patient with acute cerebral infarct, who showed initial symptoms of vomiting, nausea, ataxia, and subsequent anorexia, was treated with parenteral nutritional supplement for 20 days. Nevertheless, the patient still developed refractory hyponatremia despite the appropriate sodium supplement given for a week following parenteral nutritional supplement. In fact, after 14 days of parenteral nutritional supplement, the patient gradually showed hypotension and apathy. Hyponatremia, hypotension, anorexia and apathy were signs of hypothalamic syndrome. Diagnoses: Finally, the patient was diagnosed as WE by head magnetic resonance imaging, which showed symmetrical lesions in T2-weighted imaging images and FLAIR high signal intensity in the periaqueduct, hypothalamus, thalamus, mammiliary bodies, medulla oblongata, and vermis cerebelli. Interventions: The patient was given thiamine supplementation. Outcomes: The patient regained consciousness within 3 days. The sings of hyponatremia, hypotension, and apathy were relieved subsequently. Lessons: When patients develop unexplained hypothalamic syndrome, we should think of the possibility of WE. The concomitant presence of hyponatremia, hypotension, anorexia, and apathy in WE is rare. Therefore, this case is reported here for discussion.

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“…Methotrexate toxicity may induce both SIADH and WE, or there might be a causal relationship between these two diseases. Only one study was found on this issue, however: a case report showing that WE may cause SIADH . Thus, in order to determine whether WE causes SIADH or vice versa, more research is needed.…”

Section: Discussionmentioning

confidence: 99%

Wernicke's encephalopathy in a child with Down syndrome, undergoing treatment for acute lymphoblastic leukemia

Yıldırım

Bilgili

Akman

et al. 2016

Pediatrics International

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Wernicke's encephalopathy (WE), the early diagnosis of which is crucial to prevent permanent sequelae, is an acute neurologic disorder that develops due to thiamine deficiency, and which is associated with considerable morbidity and mortality. A 10-year-old boy diagnosed with Down syndrome and acute lymphoblastic leukemia had severe vomiting and impaired consciousness following methotrexate treatment at a dose of 1 g/m 2 . Biochemistry was consistent with the syndrome of inappropriate anti-diuretic hormone secretion. Level of consciousness did not improve following meticulous correction of hyponatremia, therefore cranial magnetic resonance imaging was done, which indicated specific findings consistent with WE. It should be kept in mind that Down syndrome patients are more likely to incur toxic side-effects of chemotherapeutic agents, and thus neurological complications such as WE may occur.

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Inappropriate antidiuretic hormone secretion in Wernicke’s encephalopathy

Cited by 5 publications

References 12 publications

Takotsubo Cardiomyopathy in a Patient with Severe Hyponatremia Associated with Syndrome of Inappropriate Antidiuretic Hormone

Takotsubo Cardiomyopathy in a Patient with Severe Hyponatremia Associated with Syndrome of Inappropriate Antidiuretic Hormone

Hypothalamic sydrome as an initial presentation of Wernicke encephalopathy

Wernicke's encephalopathy in a child with Down syndrome, undergoing treatment for acute lymphoblastic leukemia

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