SummaryAlthough bone disease and stone disease are the universally accepted classical manifestations of primary hyperparathyroidism, clinical parathyroid bone disease is rarely seen today in the United States (<5% of patients) and Western Europe. Nevertheless, in a given patient, classical skeletal involvement can be the first sign of primary hyperparathyroidism, but not recognized because it is not usually included, anymore, in the differential diagnosis of this manifestation of skeletal disease. We describe four cases of primary hyperparathyroidism in which the first clinical manifestation of the disease was a pathological fracture that masqueraded as a malignancy. The presence of large osteolytic lesions gave rise to the initial diagnosis of a primary or metastatic cancer. In none of the reported cases was primary hyperparathyroidism with osteitis fibrosa considered as the diagnosis. It would seem to us that this course is best explained by the fact that in many countries such manifestations of primary hyperparathyroidism have become a rarity. In fact, the incidence of osteitis fibrosa among patients with primary hyperparathyroidism in the US is estimated as so rare, that in majority of medical centers routine x-ray examinations of the bones in these patients is not recommended. The X-ray or computed tomography scan findings of osteitis fibrosa cystica include lytic or multilobular cystic changes. Multiple bony lesions representing brown tumors may be misdiagnosed on computed tomography scan as metastatic carcinoma, bone cysts, osteosarcoma, and especially giant-cell tumor. Distinguishing between primary hyperparathyroidism and malignancy is made readily by the concomitant measurement of parathyroid hormone which in primary hyperparathyroidism, again, will be markedly elevated. In the hypercalcemias of malignancy, such elevations of parathyroid hormone are virtually never seen.ConclusionWhen radiographic evidence of a lytic lesion and hypercalcemia are present, primary hyperparathyroidism should always be considered in the differential diagnosis.

Primary hyperparathyroidism (PHPT) during pregnancy is a rare, but may cause many maternal and fetal complications. Most cases are mild and very often remain undiagnosed throughout the whole pregnancy period, especially since its symptoms overlap those occurring in normal pregnancy. Additionally, physiological changes in calcium metabolism and PTH secretion may make the diagnosis difficult. Some current data indicate, that in pregnant women with mild PHPT the risk of obstetrical complications do not increase. However, according to others some complications, including miscarriage, intrauterine growth retardation or preeclampsia continue to occur even in subjects with mild hypercalcemia or those previously successfully treated for PHPT. Additionally, the course of PHPT during pregnancy may exacerbate, and rapid severe worsening of hypercalcemia may occur in the postpartum period. Parathyroidectomy, optimally performed during the second trimester, remains the main and the only definite treatment of PHPT, especially, when the serum calcium level exceeds 2,75 mmol/l. In patients with mild, asymptomatic PHPT some experts recommend conservative treatment with postponing surgery to the postpartum period. There are no medical guidelines regarding the treatment of PHPT during pregnancy. Therefore, to achieve optimal care of pregnant women with PHPT, they should be diagnosed, monitored and treated in reference centers by multidisciplinary teams of closely cooperating specialists. Conservative treatment is possible only on condition of close monitoring of the mother and child during pregnancy and after delivery.

Iodine supplementation during pregnancy of hypothyroid women treated with L-thyroxine neither influences neonatal TSH nor prevents decrease in maternal free thyroid hormone concentrations in second and third trimesters Suplementacja jodowa u ciężarnych z niedoczynnością tarczycy leczonych L-tyroksyną nie wpływa na stężenia TSH noworodków ani nie zapobiega obniżeniu stężeń wolnych hormonów tarczycy u matek w drugim i trzecim trymestrze AbstractIntroduction: Pregnant women require about 250 μg of iodine daily. Hypothyroid women treated with L-thyroxine do not utilise iodine, and metabolism of L-thyroxine tablets is an additional source of iodine for their foetuses. The aim of the study was to evaluate the influence of iodine supplementation in hypothyroid pregnant women treated with L-thyroxine on neonate TSH concentration and maternal thyroid parameters. Material and methods: Ninety-two pregnant women with primary hypothyroidism on adequate thyroid hormone replacement were voluntarily divided into two groups: "thyroxine" (n = 38) treated with L-thyroxine only, and "thyroxine + iodine" (n = 54) treated additionally with 150 μg/day of iodine since 10 th gestational week. Primary outcomes were the maternal thyroid function tests (TSH, fT4, fT3) and neonatal TSH concentrations at the 3-4 th day of life. Urinary iodine concentration was measured at first and third trimester to compare iodine status in both groups. Results: Iodine supplementation significantly increased median urinary ioduria in the third trimester (from 95.15 μg/L to 151.50 μg/L), but did not prevent the decrease of maternal fT4 and fT3 concentrations in the second and third trimester. Median neonate TSH concentration in both groups was within normal range, but was 33% higher in the "thyroxine + iodine" than in the "thyroxine" group (1.91 mU/L vs. 1.34 mU/L). Moreover, 8.77% of newborns in the "thyroxine + iodine" group had TSH > 5 mIU/L. Conclusions: We did not find evidence for a positive influence of iodine supplementation on thyroid function of either hypothyroid pregnant women sufficiently treated with L-thyroxine or their neonates. (Endokrynol Pol 2016; 67 (4): 367-374)

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Declarations Ethics approval and consent to participate Not applicable Consent for publication Not applicable Availability of data and materials Not applicable Competing interests The author declares no conflict of interests. Funding Not applicable Peer review This short paper underwent the journal's standard peer review process for supplements.

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S u m m a r yVitamin D is one of the most important factors regulating calciuam and phosphorus homeostasis and bone metabolism. In the last years increasing evidences suggest an important role of vitamin D deficiency in many extra-skeletal disorders, such as metabolic syndromes, cardiovascular diseases, cancers, infections and autoimmune disorders, including rheumatoid arthritis, Crohn disease, multiple sclerosis and type 1 diabetes mellitus. Many studies has shown also an association of vitamin D deficiency with occurrence and development of autoimmune thyroid diseases including Hashimoto's thyroiditis, postpartum thyroiditis and Graves' disease. In recent years there are increasing data indicating that vitamin D supplementation may prevent these pathologies or alleviate their course. Some studies suggest also that vitamin D may influence thyroid function. This review presents current data on the relationship of vitamin D and thyroid autoimmunization and function. The effects of vitamin D supplementation on the development and progression of autoimmune thyroid disease have also been discussed. S t r e s z c z e n i e Witamina D jest jednym z głównych czynników regulujących homeostazę wapnia i fosforu oraz metabolizm kostny. W ostatnich latach coraz więcej dowodów wskazuje na ważną rolę niedoboru witaminy D w wielu schorzeniach spoza układu kostnego, takich jak zespoły metaboliczne, choroby układu sercowo-naczyniowego, nowotwory, infekcje oraz zaburzenia autoimmunizacyjne, w tym reumatoidalne zapalenie stawów, choroba Leśniowskiego-Crohna, stwardnienie rozsiane czy cukrzyca typu 1. Wiele badań wykazało także związek między niedoborem witaminy D a chorobami autoimmunizacyjnymi tarczycy, w tym zapaleniem tarczycy Hashimoto, poporodowym zapaleniem tarczycy i chorobą Gravesa-Basedowa. W ostatnich latach coraz więcej danych wskazuje na to, że uzupełnianie niedoboru witaminy D może zapobiegać tym patologiom lub łagodzić ich przebieg. Niektóre badania sugerują także, że witamina D może mieć wpływ na czynność hormonalną gruczołu tarczowego. W artykule przedstawiono najnowsze doniesienia dotyczące związku witaminy D z procesami autoimmunizacyjnymi w tarczycy i jej czynnością hormonalną. Omówiono także wpływ suplementacji witaminą D na rozwój i przebieg autoimmunizacyjnych chorób tarczycy.