ObjectivesSeveral studies have demonstrated associations of birth weight with metabolic and reproductive abnormalities in adults. The aim of this study was to investigate the birth weight in women with PCOS and its correlation with clinical and biochemical characteristics of the syndrome.Materials and MethodsWe studied 288 women with PCOS according to the NIH criteria and 166 women with normal cycle and without clinical hyperandrogenism. Birth weight and anthropometric characteristics were recorded, and levels of serum androgens, SHBG, insulin and fasting glucose were measured.ResultsBirth weight data were available for 243/288 women with PCOS and age- and BMI-matched 101/166 controls. No differences were found (p> 0.05) in birth weight among women with PCOS and normal controls. Birth weight of PCOS women was negatively correlated with DHEAS levels (p = 0.031, r = -0.143) and positively correlated with waist circumference (p <0.001, r = 0.297) and body mass index (BMI) (p = 0.040, r = 0.132). Birth weight of controls was negatively correlated with SHBG levels (p = 0.021, r = -0.234). Women from both groups were further divided in 6 categories according to birth weight (A. <2.500 gr, B. 2.501-3.000 gr, C. 3.001-3.500 gr, D. 3.501-4.000 gr, E. 4.001-4.500 gr, F. > 4.500 gr). No statistically significant differences were observed in the distribution percentages between PCOS women and controls. (A. 7% vs 7.9%, B. 26.8% vs 20.8%, C. 39.1% vs 48.5%, D. 21.4% vs 20.8%, E. 4.9% vs 2%, F. 0.8% vs 0%), (in all comparisons, p> 0.05).ConclusionsWomen with PCOS do not differ from controls in birth weight distribution. However, birth weight may contribute to subtypes of the syndrome that are characterized by adrenal hyperandrogenism and central obesity.
Introduction: Leukocytosis and particularly neutrophilia are usually caused by acute infection, inflammation, and myeloproliferative neoplasms. However, leukocytosis can also occur in patients with malignancy either due to bone marrow metastases or in the context of a paraneoplastic syndrome. Case Presentation: An 86-year-old female was admitted to our hospital due to marked leukocytosis (white blood cells [WBC] > 40,000/μL), neutrophilia, and monocytosis. She was afebrile and reported hoarseness and mild difficulty swallowing. Upon physical examination, lung auscultation revealed inspiratory wheezing and a non-tender mass was observed in the anterior midline of the neck. Blasts and immature WBC were not found, and polymerase chain reaction for the detection of BCR/ABL gene was negative. A mass (5.4 cm in diameter) of abnormal parenchymal composition with calcifications occupying the right lobe, was seen on thyroid ultrasound. Cytology, after fine-needle aspiration, showed an anaplastic thyroid carcinoma (ATC). The cervical and chest computed tomography scan revealed a low-density lesion with calcifications that shifts and presses the trachea and multiple lung nodular lesions bilaterally. Since the case was inoperable and the airway was severely obstructed, a DUMON stent was placed. Biopsy of specimens from the trachea lesion revealed a tumor with significant atypical cells and focal squamoid features. The patient's WBC increased to 72,470/μL. Additionally, interleukin-6 (IL-6) was markedly elevated (20.2 pg/mL). The patient passed away due to respiratory arrest 55 days after her initial admission. Discussion: Excessive leukocytosis in a patient, having excluded infectious disease and myelodysplastic syndrome, could represent a manifestation of a paraneoplastic syndrome due to various cytokines secretion from the tumor. In our case, ATC synthesized and secreted IL-6, which seems to be the cause of severe leukocytosis.
Incomplete protection and response variability have been reported in chronic renal failure (CRF) and hemodialysis (HD) patients vaccinated against hepatitis B with the recombinant vaccine (rHBV). We vaccinated 12 consecutive patients (7 CRF and 5 HD), 7 males and 5 females, 61 years old (range 22-82); HD patients were on treatment from 1 to 12 months. CRF patients had a residual renal function (creatinine clearance) of 11 +/- 3 mL/min. Six patients had been already vaccinated unsuccessfully, as defined by the absence of detectable specific antibody S (Abs) 1 month after the completion of vaccination by the classical intramuscular method, with a median of 7 (range 3-18) doses of 20 micrograms. rHBV was given intradermally (i.d.) at the dose of 5 micrograms every fortnight up to 8 doses or until titers of Abs rose above 1000 mIU/mL. Levels above 10 mIU/mL were considered as protective. Abs titers were monitored during the whole vaccination period every 15 days and at the 1st, 3rd, and 6th month after its completion. Median number of i.d. doses given was 7 (range 4-8). Antibody titers rose gradually; surface antibodies (AbS) were detected as early as the end of the first month (2nd dose). Age and sex had no influence on the immune response, its duration, or antibody titers. i.d. administration of rHBV in repeated small injections was found to be absolutely effective, in both CRF and HD patients. AbS titers after multiple i.d. vaccination rose gradually in CRF and HD patients, and were protective for at least 6 months after the last injected dose. Protective levels were achieved even in patients not responding to multiple-double quantity intramuscular (i.m.) doses. Patients with stronger initial response to the vaccine (after the 4th dose) gave significantly higher AbS titers (at least in 50% of the follow-up measurements), although they received fewer injections and smaller total dose of vaccine.
A 59-year-old woman presented with flushing attacks accompanied by tachycardia and hypotension, which lasted approximately 30 to 60 minutes, underwent 18 years ago a gastrointestinal tumor resection. The histologic examination revealed a poorly differentiated mixed neuroendocrine/adenocarcinoma located in the caecum with regional metastases. Postoperatively, the patient received combined chemotherapy of 5-fluorouracil with interferon for six months and since has remained asymptomatic. Her examination revealed positivity for chromogranin A (CgA) and a-Fetoprotein (aFP) (580 ng/24 h, normal range 27–94, and 10 IU/mL, normal range 0–6, respectively). Urinary 5-hydroxy indole acetic acid excretion was remarkably high (41.8 mg/24 h, normal range 2–10 mg/24 h). An abdominal Magnetic Resonance Imaging scan revealed multiple focal loci in the liver whose histological examination revealed a carcinoid tumor confirmed by an Octreoscan. Additional uptake was noted on the right shoulder and the right sternum-clavicle joint confirmed by Tc-99m MDP scan. The patient received somatostatin analogue therapy followed by long-acting release octreotide analogue therapy (30 mg/month) showing a partial improvement of relevant biomarkers. Two years later, carcinoid syndrome symptoms reappeared and due to the tumors expression of somatostatin receptors the patient received peptide receptor radionuclide therapy with 177Lu-DOTATATE that resulted in both clinical and biochemical improvements.
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