Objectives
To describe the frequency and causes for the presence of a halo sign on the ultrasound of patients without a diagnosis of GCA.
Methods
In total, 305 patients with temporal artery colour Doppler ultrasound showing the presence of halo sign (intima-media thickness ≥0.34 mm for temporal arteries [TAs] and ≥1 mm for axillary arteries) were included, and their medical records were reviewed. The clinical diagnosis based on the evolution of the patient over at least one year was established as the definitive diagnosis.
Results
Fourteen of the 305 (4.6%) patients included showed presence of the halo sign without final diagnosis of GCA: 12 patients in the TAs (86%), and two patients with isolated AAs involvement (14%). Their diagnoses were PMR (n = 4, 29%); atherosclerosis (n = 3, 21%); and non-Hodgkin lymphoma type T, osteomyelitis of the skull base, primary amyloidosis associated with multiple myeloma, granulomatosis with polyangiitis, neurosyphilis, urinary sepsis and narrow-angle glaucoma (n = 1 each, 7%).
Conclusion
The percentage of halo signs on the ultrasound of patients without GCA is low, but it does exist. There are conditions that may also show the halo sign (true positive halo sign), and we must know these and always correlate the ultrasound findings with the patient’s clinic records.
In order to assess the association between empty sella (ES) and primary autoimmune hypothyroidism, and the possibility of a common pathogenesis. We retrospectively studied all patients with presumed ES diagnosed in the last 20 years, most of whom were treated by our Endocrinology Department. Subjects with a known etiology were excluded. Incomplete records or those with a doubtful diagnosis were also excluded. A total of 56 subjects were included in the study. ES was diagnosed by pituitary MRI. The measurement of free T4, TSH, and antithyroid antibodies (TPOAb and TgAb) was assayed using commercial kits. The cases of hypothyroidism obtained were compared with those in another group of similar patients, diagnosed with diabetes mellitus type 2, through chi2 test. A total of 15 (26.78%) patients of 56 with ES had autoimmune thyroid disease (subclinical or clinical hypothyroidism). Primary hypothyroidism with negative antithyroid autoantibodies was found in a further 13 patients (23.21%). The 46.42% of ES had primary hypothyroidism; this result had obtained a statistically significant difference when compared to the ratio obtained in the group of diabetes mellitus type 2 (P < 0.0029). There is an important association between ES and autoimmune thyroid disease, which reached 26.78% in our series. We suggest the possibility of a common pathogenesis for certain cases of ES and autoimmune thyroid disease, with the end point of ES in the pituitary, and atrophy in the thyroid gland.
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