A study of neuroendocrine dysfunction in patients of tuberculous meningitis

More, Aniruddha; Verma, Rajesh; Garg, Ravindra Kumar; Malhotra, Hardeep Singh; Sharma, Praveen; Uniyal, Ravi; Pandey, Shweta; Mittal, Madhukar

doi:10.1016/j.jns.2017.06.015

Cited by 15 publications

(16 citation statements)

References 24 publications

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“…Similar results were reported in a previous series of 75 patients, with a higher prevalence of TSH and ACTH deficiency (30.7% and 42.7% of the cases, respectively) (Dhanwal et al 2010). Remarkably, none had DI (Dhanwal et al 2010;More et al 2017), but nearly 10% of the patients had a syndrome of inappropriate antidiuretic hormone secretion (SIADH) (More et al 2017). Of note, hypopituitarism may be recognized as a long-term sequela, up to several years after TBC meningitis.…”

Section: Specific Bacterial Infectionssupporting

confidence: 87%

“…Visual impairment may occur as a result of a sellar/extrasellar tuberculoma or an optochiasmatic arachnoiditis. In the largest available prospective study from India, HP dysfunction was observed in 62 out of 115 patients affected by TBC meningitis (53.9%), with single and multiple axes dysfunction in 30.4% and 23.5% of the cases, respectively (More et al 2017). Hypogonadism was the most frequent (33.9%), possibly associated with hyperprolactinemia (22.6%), followed by TSH and ACTH deficiency (17.4% each).…”

Section: Specific Bacterial Infectionsmentioning

confidence: 97%

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Hypophysitis and Granulomatous Pituitary Lesions in Systemic Diseases

Jaffrain-Rea¹,

Filipponi²

2019

Endocrinology

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In clinical practice, expansive sellar lesions are largely represented by primary diseases of the pituitary gland, mostly pituitary tumors, which can be managed by endocrinologists and/or multidisciplinary pituitary teams. Hypophysitis has long been considered as a rare disease, and is classified on the basis of pathological findings, and as primary or secondary. Nowadays, an enlarging spectrum of pituitary and/or hypothalamic inflammatory, granulomatous, or even neoplastic disorders can be recognized, which may be part of systemic conditions and require appropriate multidisciplinary management involving a variety of specialists. For example, hypophysitis is being increasingly recognized in the setting of systemic IgG4-related disorders or as side effects of immune checkpoints inhibitors in oncological patients. Lymphocytic hypophysitis may sometimes be part of autoimmune polyendocrine syndromes. Significant knowledge has been added in the last decade in the pathogenesis and management of histiocytic disorders, which may infiltrate the pituitary and/or the hypothalamus Infective causes of pituitary inflammation should not be underestimated and are increasingly recognized in immunocompromised patients. Based on updated literature on these topics, this chapter aims to place pituitary inflammatory, granulomatous, and histiocytic disorders in their systemic context and stimulate multidisciplinary collaboration in order to optimize their diagnosis and clinical management.

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Section: Specific Bacterial Infectionssupporting

confidence: 87%

Section: Specific Bacterial Infectionsmentioning

confidence: 97%

Hypophysitis and Granulomatous Pituitary Lesions in Systemic Diseases

Jaffrain-Rea¹,

Filipponi²

2019

Endocrinology

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“…Two out of the 3 children who died within three days had SIADH 18 . Another study in 115 TBM patients reported endocrinal dysfunctions in 53% and SIADH in 9.6% 19 . In a prospective study on 76 TBM patients, 34 (44.7%) had hyponatremia, which was mild in 3, moderate in 23 and severe in 8 patients.…”

Section: Hyponatremia In Tuberculous Meningitis (Tbm)mentioning

confidence: 94%

Mechanism, spectrum, consequences and management of hyponatremia in tuberculous meningitis

Misra

2019

Wellcome Open Res

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Hyponatremia is the commonest electrolyte abnormality in hospitalized patients and is associated with poor outcome. Hyponatremia is categorized on the basis of serum sodium into severe (< 120 mEq/L), moderate (120-129 mEq/L) and mild (130-134mEq/L) groups. Serum sodium has an important role in maintaining serum osmolality, which is maintained by the action of antidiuretic hormone (ADH) secreted from the posterior pituitary, and natriuretic peptides such as atrial natriuretic peptide and brain natriuretic peptide. These peptides act on kidney tubules via the renin angiotensin aldosterone system. Hyponatremia <120mEq/L or a rapid decline in serum sodium can result in neurological manifestations, ranging from confusion to coma and seizure. Cerebral salt wasting (CSW) and syndrome of inappropriate secretion of ADH (SIADH) are important causes of hyponatremia in tuberculosis meningitis (TBM). CSW is more common than SIADH. The differentiation between CSW and SIADH is important because treatment of one may be detrimental for the other; evidence of hypovolemia in CSW and euvolemia or hypervolemia in SIADH is used for differentiation. In addition, evidence of dehydration, polyuria, negative fluid balance as assessed by intake output chart, weight loss, laboratory evidence and sometimes central venous pressure are helpful in the diagnosis of these disorders. Volume contraction in CSW may be more protracted than hyponatremia and may contribute to border zone infarctions in TBM. Hyponatremia should be promptly and carefully treated by saline and oral salt, while 3% saline should be used in severe hyponatremia with coma and seizure. In refractory patients with hyponatremia, fludrocortisone helps in early normalization of serum sodium without affecting polyuria or functional outcome. In SIADH, V2 receptor antagonist conivaptan or tolvaptan may be used if the patient is not responding to fluid restriction. Fluid restriction in SIADH has not been found to be beneficial in TBM and should be avoided.

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“…Neuroendocrine‐associated metabolic abnormalities are common in TBM. In an observational study of patients newly diagnosed with TBM, neuroendocrine dysfunction occurred in half . This is likely due to the tendency for TBM to affect the basal structures such as the interpeduncular fossa, cisterna ambiens and cisterna pontis, which surround the pituitary gland, pituitary stalk, and hypothalamus (Fig.…”

Section: Pathogenic and Pathophysiologic Mechanisms Within The Brain mentioning

confidence: 99%

“…). Exudates here lead to edema, perivascular infiltration, and subsequent microglial reactions known collectively as “borderzone encephalitis.” Subsequent metabolic abnormalities include gonadotropin deficiency, hyperprolactinemia, thyrotropin deficiency, corticotropin deficiency, and somatotropic hormone deficiency . Hyponatremia is also common, although the mechanism by which is occurs is debated.…”

Section: Pathogenic and Pathophysiologic Mechanisms Within The Brain mentioning

confidence: 99%

The pathogenesis of tuberculous meningitis

Davis

Rohlwink

Proust

et al. 2019

Journal of Leukocyte Biology

132

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Tuberculosis (TB) remains a leading cause of death globally. Dissemination of TB to the brain results in the most severe form of extrapulmonary TB, tuberculous meningitis (TBM), which represents a medical emergency associated with high rates of mortality and disability. Via various mechanisms the Mycobacterium tuberculosis (M.tb) bacillus disseminates from the primary site of infection and overcomes protective barriers to enter the CNS. There it induces an inflammatory response involving both the peripheral and resident immune cells, which initiates a cascade of pathologic mechanisms that may either contain the disease or result in significant brain injury. Here we review the steps from primary infection to cerebral disease, factors that contribute to the virulence of the organism and the vulnerability of the host and discuss the immune response and the clinical manifestations arising. Priorities for future research directions are suggested. K E Y W O R D S mycobacterial, endothelial cells, granulocytes, microglia cells, monocytes/macrophages, myeloid cells, neutrophils, T Lymphocytes, Th17 cells at the site of infection activates macrophages and DCs to produce cytokines and antimicrobial factors that contribute to containment of the TB bacillus. 2 This inflammatory process results in the formation of a granuloma, which encapsulates the infected cells and retards the replication of TB bacilli and can lead to latent infection. However, in

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A study of neuroendocrine dysfunction in patients of tuberculous meningitis

Cited by 15 publications

References 24 publications

Hypophysitis and Granulomatous Pituitary Lesions in Systemic Diseases

Hypophysitis and Granulomatous Pituitary Lesions in Systemic Diseases

Mechanism, spectrum, consequences and management of hyponatremia in tuberculous meningitis

The pathogenesis of tuberculous meningitis

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