Chronic anisakiasis is a rare entity, and its diagnosis is difficult. We report a case of chronic anisakiasis with multiple gastrointestinal manifestations presenting as a palpable mesenteric mass, diagnosed by specific serology and histologic findings. We describe the computed tomographic appearance of this mass and the pathologic correlations. To our knowledge, this is the first time this mesenteric location has been detected by imaging before surgery.
The subclinical Cushing′s syndrome (SCS) is found in 20% of incidental adrenal tumors (AI). The overnight 1 mg oral dexamethasone suppression test (DST) with the measurement of circulating cortisol (F) is a sensitive method to rule out SCS. The assessment of salivary cortisol (SAF) as a surrogate of F became a non-invasive methodological advance. There are few data on the functional evaluation of AI through SAF in DST (SAFdex). The aim of this retrospective study was to investigate the utility of SAFdex for the detection of SCS in patients with AI. Subjects and Methods: 20 subjects with AI (7 male and 13 women; 65.0 ± 11.0 y/o; BMI: 26.5 ± 1.4) were studied. Sixteen had unilateral and 4 bilateral tumors (size: 10.0 - 90.0 mm; density (UH) was <10.0 in 17 cases and ≥ 10.0 in 3). They were not on drugs that may affect the HPA axis. Eight patients (1 male and 7 women; 20.0–60.0 y/o; BMI: 27.0 ± 3.0) with overt non ACTH dependent Cushing Syndrome (CS) were included as the reference group of active hypercortisolism. CS had unilateral adrenal tumors in 6 cases and bilateral in 2 (size: 11.0 -200.0 mm; density (UH) <10.0: n= 7 and >10.0: n=1).All subjects collected 24-hour urine for urinary free cortisol (UFC). After the urine collection, they obtained whole saliva samples at 23 h for cortisol (SAF23). Subsequently, they received 1 mg oral dexamethasone. The following day at 8 h, simultaneous blood (Fdex) and saliva (SAFdex) samples were obtained. F, SAF and UFC were determined by RIA and ACTH by IRMA. Reference values from our laboratory (n= 100): UFC ≤90.0 µg / 24hs; ACTH: 10.0–50.0 pg / ml, SAF23: 0.5–3.8 nM / l; SAFdex: 0.5–2.0 nM; Fdex: 13.8–50.0 nM. Statistics were performed by Mann-Whitney and Spearman tests, p <0.05 was considered significant. In AI: ACTH 22.0 ± 11.0 pg /ml; UF:C 47.0 ± 20.0 µg / 24hs; SAF23: 1.5 ± 0.9 nM); SAFdex: 1.0 ± 0.5 nM and Fdex: 35.6 ± 10.0 nM were normal and significantly different from CS: 5.6±1.8 pg /ml; 391.0 ± 406.0 µg / 24hs; 20.0 ± 32.0 nM; 27.0 ± 24.0 nM and 674.0 ± 339.0 nM, respectively; p <0.05 in all cases. A positive and significant correlation was demonstrated between SAFdex and Fdex in AI (r = 0.830) and CS (r = 0.905); p <0.05 in both. Interestingly, a woman with overt CS and moderate signs of hypercortisolism, had normal SAF23 (1.5 nM) and UFC (76.0 µg / 24hs), while SAFdex (3.0 nM) and Fdex (69.0 nM) showed absence of suppression. Surgical resection of the adrenal tumor (an adrenocortical adenoma) and postoperative hypocorticism confirmed the diagnosis of CS.
Conclusion: SCS was excluded in all AI. The dexamethasone suppression test using saliva as a diagnostic fluid was a sensitive and practical method to rule out hypercortisolism in these patients.
Introduction:
Acromegaly results from the chronic and persistent elevation of growth hormone (GH) circulating levels. Several isoforms of the receptor of GH have been identified; one contains exon 3 giving rise to the full form of the GHR or full-length (fl), and another one lacking this exon (d3). This isoform heterogeneity results in the following genotypes: homozygous fl, heterozygous d3/fl and homozygous d3.
Objective:
To determine if the GHR genotype influences the clinical and/or biochemical expression of acromegaly.
Methods
: Forty-nine (30 women/19 men) acromegalic patients and forty-one control subjects (22 women/19 men), aged 30 to 76 years, who attended the Endocrinology Department of a Hospital in Buenos Aires, Argentina, were evaluated. Genotyping of the GHR was performed by a multiplex polymerase chain reaction (GAP-PCR). Clinical data were recorded, and general biochemical and hormonal determinations were carried out (IGF-1, GH and PRL). To measure tumor dimension, Magnetic Resonance Imaging (MRI) of the sellar area was performed in all patients.
Results:
The frequency of the genotypes was 61.2% homozygous fl, 34.7 % heterozygous d3/fl and 4.1 % homozygous d3 in acromegalic patients and 48.8% homozygous fl, 41.5% heterozygous d3/fl and 9.7% homozygous d3 in control subjects. The frequency of the genotypes in the studied population was in Hardy-Weinberg equilibrium (p = 0.8878). In this group of acromegalic patients, we did not observe any associations of the genotypes with the body mass index (BMI), the presence of micro or macroadenomas, the response to treatment, the presence of hypertension, diabetes or dyslipidaemia, neither with GH, IGF-1 or PRL levels.
Conclusion:
The present study confirms that the distribution of the allele coding for the isoform without the exon 3 of GHR in this group of acromegalic patients is similar to that observed in healthy subjects and to that reported in the literature. On the other hand, the presence of the polymorphism of the GHR is not related to BMI, tumor size, response to treatment, metabolic alterations or to hormonal levels in this group of acromegalic patients evaluated.
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