The AsSociation Between Type 2 Diabetes Mellitus, Hypothyroidism, and Thyroid Cancer.

This study aimed to investigate the association between type 2 diabetes mellitus (T2DM), antidiabetic therapy, hypothyroidism, and thyroid cancer. We analyzed data from 320 patients who underwent thyroid surgery for suspicion of cancer. The diagnosis of thyroid cancer was confirmed by histopathological analysis in 95 patients. No significant difference was found in the diagnosis of T2DM and hypothyroidism concerning the presence of thyroid cancer (p=0.13; p=0.85), nor in the gender of patients with T2DM and hypothyroidism with respect to the type of thyroid cancer (p=0.19; p=0.25). Patients with T2DM (Odds ratio [OR] 1.89; 95% CI, 0.856-4.163) and patients with hypothyroidism (OR, 1.05; 95% CI, 0.530-2.164) had higher prevalence of thyroid cancer, as did those who had both diagnoses combined (p=0.37; OR, 2.39; 95% CI, 0.333-17.278), compared with the patients who did not have those diagnoses. Men with T2DM (OR, 6.19; 95% CI, 1.180-32.513) had higher prevalence of thyroid cancer than women. Patients who were on oral antidiabetics (OR, 1.91; 95% CI, 0.804-4.512) had higher prevalence of thyroid cancer than those receiving insulin. According to the results of this study, we can conclude that there is an association between T2DM, hypothyroidism, oral antidiabetics, and thyroid cancer.

Kikuchi-Fujimoto disease: the first reported case in Croatia.

Kikuchi-Fujimoto disease (KFD) is an extremely rare disease known to have a worldwide distribution with higher prevalence among Japanese and other Asiatic individuals. KFD presents as benign and self-limited disorder, characterized by regional cervical lymphadenopathy with tenderness, usually accompanied with mild to high fever and night sweats. Less frequent symptoms include weight loss, nausea, vomiting and sore throat. Final diagnosis can only be determined on the basis of typical morphological changes in the lymph node, therefore lymph node biopsy is crucial for proving the diagnosis. Here we present a 16-year-old, native Croatian, Caucasian girl with KFD, as a first case of KFD reported in Croatia. We suggest that this disease should be considered as a possible cause of fever of the unknown origin followed by lymphadenopathy.

The significance of Helicobacter pylori in patients with nasal polyposis.

AIM: To determine the presence of Helicobacter pylori in nasal polyps and the transmission of H. pylori from stomach to nasal polyps. METHODS: In a prospective, controlled clinical research, 35 subjects with nasal polyps and 30 controls with concha bullosa (CB) were involved, and had been subjected to endoscopic sinus surgery (ESS). In the biopsies of removed polyps and CB, polymerase chain reaction (PCR) was used for detecting the H. pylori DNA. Blood samples of the test and control group were evaluated for H. pylori immunoglobulin (Ig) G and A antibodies by ELISA. The test and control group underwent esophagogastroduodenoscopy with taking biopsies from the stomach for PCR detection of H. pylori DNA. RESULTS: In blood samples, specific IgG and IgA antibodies to H. pylori were found in 30 (85.71%) of 35 polyp patients and in 16 (53.33%) of 30 controls. In 10 (28.57%) of 35 patients H. pylori DNA was identified in the nasal polyp tissue, but it was not detected in the CB specimens. H. pylori DNA was found in the stomach mucosa samples of all test and control group of subjects. Significant statistical difference was found in the H.pylori specific IgG and IgA between the test and control group (p less 0.006) and between the polyp and control biopsy specimens of H. pylori DNA by PCR (p less 0.001). CONCLUSION: This research points to the colonisation of nasal polyps with H. pylori, the transfer of H. pylori from stomach to nasal polyps and potential role of H. pylori in emergence of nasal polyps.

Non-functional parathyroid gland carcinoma, a rare malignant tumor of the head and neck.

Carcinoma of the parathyroid gland is a very rare tumor of the head and neck. The largest number of carcinomas are discovered by chance. (intraoperatively, during surgery removal of the parathyroid gland are adenomas). Around 1% of the primary parathyreoidism is caused by the cancer of parathyroid glands. Only 10% of these rare tumors make up dysfunctional cancer of parathyroid glands. There have been 24 cases reported of this disease in the literature. The focus of our study is to present a case of this disease and to review the published literature to date.

Significance of the pepsin from the saliva in the diagnosis and treatment of laryngopharyngeal reflux disease.

Etiopathogenesis of the laryngopharyngeal reflux has not been sufficiently clarified. It is believed that damage to the lining of laryngopharynx in laryngopharyngeal disease occurs in the use of acid and pepsin. The diagnosis of reflux acidic 24-hour Dual probe pH-metry is considered the gold standard. However, since the laryngopharyngeal reflux is often non-acidic new diagnostic methods are been explored, safe diagnosis of the disease according to symptoms of this uncharacteristic disease. In our study on 45 patients with laryngopharyngeal disease, we have proved that tracking the value of pepsin in the saliva of a valuable diagnostic indicator of laryngopharyngeal reflux and a valuable indicator of the success of the treatment.

Angiosarcoma of the hypopharynx: case report.

Angiosarcomas are malignant neoplasias of rapid growth that emerge from endothelial cells. They are rarely found in the area of the head and neck and account less than 0.1% of all head and neck malignancies. In some cases it has been linked to trauma, radiation and angiectasia but the etiology mainly remains unknown. Here we report a case of angiosarcoma of pyriform sinus manifested by dysphagia and dysphonia. The patient underwent endoscopic hypopharyngeal excision followed by radiation therapy with a good result. Our patient remains tumor free after two years. The purpose of this article is to add another case of primary angiosarcoma of a rare site, the hypopharynx.

Sensorineural hearing loss in hemodialysis patients.

Chronic renal failure affects all organ systems. Senses are not exception and hearing impairment is common, particularly sensorineural hearing loss (SNHL). The term SNOS of unknown origin or uremic deafness is related to only a smaller part of the cases with unclear etiology of the impairment. The study searched for SNOS in 66 chronic hemodialysis (HD) patients, mean age 51.50 +/- 12.70 years. They were treated by HD for 69.70 +/- 53.80 months. The relation between the severity of the impairment and the patients' age, duration of HD treatment (months) and a set of laboratory parameters typical for chronic HD patients was examined. The aim of the study was to detect potential causes of the impairment. The increased hearing threshold (HT) of above 20 dB for all frequencies was found in 42 patients (mean HT 26 +/- 10.50 dB), for speaking area frequencies in 22 patients (mean HT 19.70 +/- 8.80 dB), and in 56 patients for high frequencies (mean HT 41.70 +/- 19.70 dB). The significant positive correlation of HT was found only with the patients' age (r = 0.49, p < 0.01). The patients older than 45 years had higher mean HT than those younger, and those older than 65 also had higher HT than the younger ones. Patients with pathological value of HT were significantly more common among the older subgroup of patients, when divided according to the age at both cutoff values of 45 and of 60 years. Mean HT did not differ significantly according to the duration of HD treatment (subgroups A- no longer than 60 months, B- from 61 to 120 months, and C- longer than 120 months). The patients with pathological HT did not differ significantly in frequency among those subgroups, and the subgroups were not different according to the mean age (A--50.30 +/- 13.20 years; B--51.40 +/- 12.75 years; C--55.80 +/- 10.55 years). In conclusion, our results along with other authors'published data report on SNHL as very frequent finding among chronic HD patients and suggest multifactorial etiology. Accurate proportion of those with SNHL of unknown origin is not possible to determine. Those cases are probably not caused by uremic polyneuropathy and/or preterm vascular aging only, although those factors are likely to play crucial roles.

Atmospheric pressure as a force that fills developing bones with marrow and air.

Many theories try to explain the existence and function of paranasal sinuses. This paper is an attempt to correlate process of paranasal sinus development in human with bone pneumatization processes in animals. It is here proposed that this mechanism starts in utero and continues after birth. During endochondral development, a solid hyaline cartilage model transforms into long bones. Central chondrocytes hypertrophy and their lacunae become confluent. Dissolving of the cartilage intercellular matrix forms a primitive marrow cavity. It is soon invaded by the periostal bud. Once circulation is established in the developing bone, the dissolved hyaline matrix can be slowly washed away from the bone cavity. Circulation in the bone cavity can develop slight subatmospheric pressures, similar to negative interstitial pressures in subcutaneous tissues. The amniotic fluid conducts atmospheric pressure to the fetal body. The pressure is trying to fill enlarging bone cavities through the existing vascular openings, or to create new openings. Bone walls of developing paranasal bones are to weak to resist the pressure gradient on their walls. New openings form on the weakest spots allowing airway mucosa to form initial paranasal sinuses. The enlarging cavities of long bones that are remote from the body surface and airway also develop a slightly subatmospheric pressure that fills them with cellular elements. These elements enter bone through the feeding vessels and form bone marrow. During after birth skeletal growth, bone remodeling shapes paranasal sinuses in a process of slow evolution that do not require measurable pressure gradients. When two sinuses come in vicinity, their growth rate declines, since the remaining thin and fragile bone lamella between them does not retract anymore.

A calcium homeostasis model: orchestration of fast acting PTH and calcitonin with slow calcitriol.

Calcitriol is in plasma bound to transcalciferin and this results in a long calcitriol half-life in plasma (5-12h). Abundance of bound calcitriol molecules prevents the exact and quick control of its effects and makes it an inert regulator with a time lag between the changes of calcitriol synthesis and its effect on peripheral tissues. The added regulatory inertia is here defined as: calcitriol(bound)/calcitriol(free) and it approaches value of 99. Estrogens increase transcalciferin levels. It is possible that the estrogen-induced increase in the total calcitriol plasma pool makes calcitriol effects even more inert, augmenting and prolonging the calcitriol effects and thus improving calcium balance in women. Since calcitriol synthesis in kidneys depends on the PTH level, it can be assumed that the size of the total calcitriol pool in plasma reflects more the average PTH secretion during previous hours, than the high or low peaks of PTH secretion in the same period. In other words, one or more PTH tides of short duration are followed with a late calcitriol tide that lasts for hours, and even longer lasting rise in calcitriol effects. Bone integrity depends also on the cortisol level. A possible speculation is that the main result of all profound bone effect of hypecortisolemia, might be reduction of the bone amino acids uptake, thus allowing redistribution of available proteins. Both PTH and calcitriol prevent dangerous hypocalcemia. PTH is quick in mobilizing bone calcium, while calcitriol tends to increase absorption of dietary calcium. In case of low or no dietary calcium, calcitriol mobilizes bone calcium and thus increase PTH initiated demineralization. In the case of calcium abundance, increased plasma calcium reduces PTH levels. Calcitriol plasma level (reflecting previous PTH surges) can induce both calcium absorption and bone demineralization. This two-blade action is tuned by calcitonin that reduces osteoclastic bone resorption, allowing bone deposition of abundant calcium. An overnight fast with a reduced absorption of dietary calcium, might decrease plasma calcium below the regulatory set point, inducing an increase in PTH secretion. Increased average nighttime PTH secretion induces more calcitriol to be synthesized in kidneys. The resultant late calcitriol morning and daytime tide would stimulate calcium absorption from gut, or from bone, depending on the availability of dietary calcium. Due to the described time lag in calcitriol effects, increased calcium absorption might continue during daytime, regardless of the plasma calcium level. If plasma calcium is above the set point, calcitonin will allow excess calcium to deposit in bones. A speculation based on this model is that it might be more efficient to avoid calcium rich food for dinner or supper, and to administer calcium supplementation in the morning, during the calcitriol tide.