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Biomedical subjects

Cristina Boccalandro

Publications and source records attributed to Cristina Boccalandro.

6 recordsLinked to original sources
PubMed2006

Endocrine failure after traumatic brain injury in adults.

OBJECTIVE: To review histopathological and clinical data linking endocrine failure to traumatic brain injury (TBI) during acute neurosurgical treatment and rehabilitation. METHODS: A focused search of the Medline (PubMed) medical literature database and the authors' files were used to identify selected publications. RESULTS: Endocrine failure may produce clinically important consequences during acute and convalescent care after TBI, and may be caused by direct injury to the hypothalamic- pituitary axis (HPA), neuroendocrinological effects from catecholamines and cytokines, or from systemic infection/inflammation that produces primary gland failure. Autopsy evidence of hemorrhage or ischemia in the HPA is common soon after TBI. The estimated incidence of acute hormone reduction is adrenal 15%, thyroid 5 - 15%, growth hormone 18%, vasopressin 3 - 37%, and gonadal (25 - 80%). Hyperprolactinemia occurs in more than 50% of patients. Inappropriate secretion of antidiuretic hormone (SIADH) and the euthyroid sick syndrome are common. Acute adrenal failure, central hypothyroidism, SIADH, and diabetes insipidus (DI) may cause poor neurological outcomes including death, hypo/hypernatremia, hypotension, and increased vasoactive drug requirements. Treatment of those conditions is warranted. Delayed diagnosis of hypopituitarism is often mistaken for symptoms of residual head injury. Some chronic hormone deficiency occurs in 30 - 40% of selected patients after TBI, more than one deficiency in 10 - 15%, growth hormone in 15 - 20%, gonadal hormones in 15%, and hypothyroidism in 10 - 30%. Chronic adrenal failure and DI are reported over a wide incidence. Prolactin is elevated in 30%. All clinical symptoms respond favorably to replacement therapy. CONCLUSIONS: Severe TBI associated with basilar skull fracture, hypothalamic edema, prolonged unresponsiveness, hyponatremia, and/or hypotension is associated with a higher occurrence of endocrinopathy. Greater awareness of this possible complication of TBI and appropriate testing are encouraged.

Adrenal Insufficiency↗
PubMed2004

Characterization of an aquaporin-2 water channel gene mutation causing partial nephrogenic diabetes insipidus in a Mexican family: evidence of increased frequency of the mutation in the town of origin.

A Mexican family with partial congenital nephrogenic diabetes insipidus (NDI) that resulted from a mutation in the aquaporin-2 water channel (AQP2) was characterized, and the source of this rare mutation was traced to the family's town of origin in Mexico. Affected individuals with profound polyuria and polydipsia were homozygous for an autosomal recessive missense V168M mutation in the AQP2 gene. Expression in oocytes revealed that, although retained in the endoplasmic reticulum (ER) to a great extent, a considerable amount of the partially functional AQP2-V168M was expressed at the plasma membrane, and that its ER retention was less than AQP2-T126M, a functional mutant in severe recessive NDI. None of the affected AQP2-V168M individuals had neurologic deficits, which also suggested a milder form of the disease. The homozygous individuals reported subjective improvement in polyuria and polydipsia with the use of dDAVP (1-desamino-8-D-arginine-vasopressin). When clinically tested, infusion of dDAVP at variable doses produced a partial increase in the urinary osmolality in homozygous individuals and decreased their water intake. Heterozygotes were unaffected when compared with controls. Samples were obtained from the population of the Mexican town of origin of the family; 30% of the population was heterozygous for the V168M AQP2 mutation and 1% was homozygous for the mutation. The high frequency of this rare mutation in the town provides evidence for an important health care problem in the village with consequences for future generations.

Aquaporin 2↗
PubMedDate not supplied

Severe reversible dilated cardiomyopathy and hyperthyroidism: case report and review of the literature.

OBJECTIVE: To describe a case of a 46-year-old woman with Graves' disease and reversible low-output congestive heart failure and present a comparative analysis of 23 similar cases reported in the literature. METHODS: A detailed case report is presented. In addition, a review of the pertinent literature published between 1960 and 2002 was performed to identify similar cases of dilated cardiomyopathy and thyrotoxicosis and to assess the findings in these patients. RESULTS: A 46-year-old woman without primary heart disease was admitted to the hospital with Graves' thyrotoxicosis and severe low-output congestive heart failure. Her left ventricular ejection fraction (LVEF) at the time of initial assessment was less than 20%, and her condition was categorized as New York Heart Association (NYHA) functional class III. Nineteen months after she was treated for hyperthyroidism, her LVEF was 49% and her status was NYHA class I. A severe hypotensive episode occurred when b-adrenergic blockade therapy was initiated. The group of 23 similar cases from the literature plus our currently described patient had a mean age of 45 years, a male-to-female ratio of 1:1.2, Graves' disease as the principal cause, and LVEF improvement from 29% to 58%. CONCLUSION: Dilated cardiomyopathy is an unusual manifestation of hyperthyroidism with unclear cause. Clinicians should be aware of this entity because it is treatable and hypotension can occur if b-adrenergic blockade treatment is initiated.

Adrenergic beta-Antagonists↗