Bone metabolism in patients with primary hyperparathyroidism before and after surgery.

Primary hyperparathyroidism (PHPT) is accompanied with a reduced bone mineral density (BMD) and an increased risk of fracture. Surgery is the only option for cure. It is hypothesized that in patients with PHPT bone metabolism normalizes after parathyroidectomy (PTX) and that BMD gradually increases. Fifty-two patients with PHPT who underwent surgery were prospectively followed for 1 year. Biochemical analyses were performed at baseline and 1, 4, 7 days; 6 weeks; and 3, 6, and 12 months, and BMD before and one year after surgery. Parathyroid hormone (PTH), calcium, and the bone resorption marker dropped immediately, but transiently after PTX, bone formation decreased more slowly. Osteoprotegerin (OPG) as well as cathepsin K did not show significant changes. BMD of the lumbar spine, but not of the femoral neck, increased significantly within one year after surgery. Moderate correlations existed between the changes of total calcium, ionized calcium, as well as bone-specific alkaline phosphatase and changes of the lumbar BMD. Patients who needed postoperative supplementation with calcium and vitamin D had significantly higher PTH levels. Some gender-specific differences in patients with PHPT were observed. In patients with PHPT, males appear to be more severely affected than females. Within the first year after PTX, bone metabolism normalized, and BMD of the lumbar spine increased. Patients who needed a supplementation with calcium and vitamin D after PTX preoperatively had higher serum levels of PTH.

Persistent arterial stiffness and endothelial dysfunction following successful pancreas-kidney transplantation in Type 1 diabetes.

OBJECTIVE: Successful simultaneous pancreas-kidney transplantation (SPK) in Type 1 diabetic (T1DM) patients results in improved cardiovascular outcome and survival. However, it is doubtful whether the impairment of cardiovascular and endothelial function in T1DM can be completely reversed. METHODS: Pulse-wave velocity, stroke volume, heart rate, serological markers of endothelial dysfunction (soluble intercellular, vascular cell-adhesion molecules, E-selectin, and plasminogen-activator-inhibitor-1) were measured in 10 T1DM patients after SPK with non-diabetic glucose levels, 10 T1DM patients with poor [T1DM>8; glycated haemoglobin (HbA1c)>8%], and 10 with good glucose control (T1DM<7, HbA1c<7%), in 6 non-diabetic patients after kidney transplantation (KT) and 9 non-diabetic control subjects (CON), matching for major anthropometric characteristics. RESULTS: Pulse-wave velocity was increased in SPK (P < 0.02 vs. CON, KT, T1DM<7) and in T1DM>8 (P < 0.02 vs. T1DM<7). Systolic blood pressure was increased in SPK (P < 0.05 vs. CON). Stroke volume was reduced in SPK, T1DM>8 and T1DM<7 and KT (P < 0.01 vs. CON). Heart rate was elevated in SPK and in T1DM>8 (P < 0.0003 vs. CON and T1DM<7). In SPK, soluble intercellular and vascular cell-adhesion molecules were 100% and 44% higher (P < 0.03 vs. CON), respectively, while plasminogen-activator-inhibitor-1 was decreased in SPK (P < 0.02 vs. CON). CONCLUSION: T1DM patients after SPK experience arterial stiffness, a higher heart-rate and blood pressure, reduced stroke volume and serological signs of endothelial dysfunction. Thus, functional and structural cardiovascular alterations as a result of glucotoxicity, uraemia and hypertension in T1DM might not be completely resolved by SPK.

Effect of acute citrate load on markers of bone metabolism in healthy volunteers.

BACKGROUND AND OBJECTIVES: This study aims to investigate the possible effects of acute citrate administration on bone metabolism in healthy men. MATERIALS AND METHODS: A placebo-controlled, crossover trial was conducted on 10 male volunteers. The volunteers received either a standardized infusion of citrate at 1.5 mg/kg body weight/min or the equal volume of placebo, separated by a washout period of 14 days. Serial blood and urine samples were collected and analysed for bone biochemical markers and electrolytes. RESULTS: Infusion of citrate resulted in increased serum levels of the bone formation marker osteocalcin (OC) and bone resorption marker C-telopeptide of type 1 collagen (CTX). Increases in CTX and OC were positively correlated to the surge in the serum concentration of intact parathyroid hormone (iPTH) but only OC showed correlation to changes in ionized calcium. Citrate infusion showed no effect on serum concentrations of bone alkaline phosphatase, osteoprotegerin, and bone tartrate-resistant acid phosphatase 5b, or the expression of receptor activator of nuclear factor kappa B ligand. Variations in OC and CTX were short-term as both bone markers gradually declined within 90 min following citrate exposure. CONCLUSION: Acute citrate load resulted in profound alterations of the bone markers OC and CTX. The short-term increase of CTX suggests a temporary shift to a higher bone turnover rate, although the clinical consequence of the observed changes in bone markers remains open.

The bone marker plot: an innovative method to assess bone turnover in women.

BACKGROUND: Biochemical markers of bone turnover reflect the resorptive and reconstructive effects that act on the skeleton. Although elevated markers are commonly interpreted as a sign of an increased turnover rate, the balance between bone resorption and formation is mostly neglected. We introduce a graphic report combining both complementary processes. MATERIALS AND METHODS: Bone turnover markers were measured in 599 women (aged 25-74 years). To set up reference ranges, 269 from 599 women were selected because of having T-scores > -1 and inconspicuous basic laboratory data. Concentrations of resorption and formation markers were mathematically transformed to build up plots with four fields, symbolizing fast and slow resorption and fast and slow formation processes. The reference data of bone turnover were represented by a 95% confidence ellipse. For individual marker plots, we converted data of bone turnover markers from therapy follow-up profiles of patients in a similar manner. RESULTS: In pre-, peri- and postmenopausal women (n= 190, 39 +/- 6 years; n= 35, 51 +/- 6 years; n= 44, 55 +/- 5 years, respectively), the medians of the bone resorption marker CrossLaps and of the bone formation markers osteocalcin and aminoterminal propeptide of type I procollagen were 0.13/0.16/0.22 ng mL(-1), 21/21/25 ng mL(-1) and 36/35/45 ng mL(-1), respectively. In postmenopausal women, the marker plots revealed a shift towards accelerated bone resorption. A discrimination from osteopenic women (n= 138) failed. CONCLUSION: The proposed marker plot facilitates the intuitive perception of bone turnover in individual patients as well as in patient groups by a synopsis of the balance between bone formation and resorption with the rate of these processes.

Sporadic hypercalcitoninemia: clinical and therapeutic consequences.

'Calcitonin screening' is not accepted as the standard of care in daily practice. The clinical and surgical consequences of 'calcitonin screening' in a series of patients with mildly elevated basal calcitonin and pentagastrin stimulated calcitonin levels are presented. 260 patients with elevated basal (>10 pg/ml) and stimulated calcitonin levels (>100 pg/ml) were enrolled in this prospective study. None of the patients was member of a known medullary thyroid carcinoma family. Thyroidectomy and bilateral central and lateral neck dissections were performed. Testing for the presence of germ-line mutations was performed in all patients. Histological and immunohistochemical findings were compared with basal and stimulated calcitonin levels. All patients were subsequently followed biochemically. C-cell hyperplasia (CCH) was found in 126 (49%) and medullary thyroid cancer was found in 134 (51%) patients. RET proto-oncogen mutations were documented in 22 (8%) patients (medullary thyroid cancer:18, CCH:4). In 56 (46%) of 122 patients, sporadic CCH was classified neoplastic ('carcinoma in situ'). Of 97 (72%; 10 with hereditary medullary thyroid cancer) had pT1 (International Union against Cancer recommendations 2002) and 33 (25%) had pT2 or pT3 and 4 (3%) pT4 tumors. Of 39 (29.1%) had lymph node metastases. 106 (79.1%; 15 (38.5%) with lymph node metastases) patients were cured. Evaluation of basal and stimulated calcitonin levels enables the prediction of medullary thyroid cancer. All patients with basal calcitonin >64 pg/ml and stimulated calcitonin >560 pg/ml have medullary thyroid cancer. Medullary thyroid cancer was documented in 20% of patients with basal calcitonin >10 pg/ml but <64 pg/ml and stimulated calcitonin >100 pg/ml but <560 pg/ml.

Pulmonary and systemic effects of inhaled PACAP38 in healthy male subjects.

BACKGROUND: Pituitary adenylate cyclase activating polypeptide 1-38 (PACAP38) displays biological activities (e.g. bronchodilatory, pulmonary vasodilatory and anti-inflammatory properties) that are relevant in several pulmonary diseases. The aim of this study was to assess the safety and tolerability and the pulmonary and systemic effects of inhaled PACAP38 in humans. MATERIALS AND METHODS: Twelve healthy male subjects (mean age 28) were studied in a randomized, double-blind, placebo-controlled dose escalation trial with inhalation of PACAP38 to a cumulative dose of 480 microg. Lung function was measured by body plethysmography. Systemic absorption was evaluated by plasma levels, skin blood flux (estimated by laser Doppler imager fluxmetry) and systemic haemodynamics. RESULTS: Inhalation of PACAP38 did not cause relevant adverse reactions or an increase of PACAP38 plasma levels. No statistically significant changes in lung function tests and no systemic effects (blood pressure, pulse rate or skin blood flux) occurred. CONCLUSION: Inhaled PACAP38 was well tolerated without systemic side-effects in healthy male subjects.

No effect of homocysteine-lowering therapy on vascular inflammation and haemostasis in peripheral arterial occlusive disease.

BACKGROUND: Although peripheral arterial occlusive disease (PAOD) is significantly associated with elevated homocysteine levels, the clinical relevance of hyperhomocysteinaemia for the prevention and progression of PAOD is still unknown. MATERIALS AND METHODS: A total of 65 patients suffering from symptomatic PAOD with elevated homocysteine levels were randomized onto placebo or B-vitamins (50 mg thiaminhydrochlorid, 50 mg pyridoxine, and 0.05 mg cyanocobalamin), plus 5 mg folic acid daily for 6 weeks. Serum levels of folic acid, vitamin B12, creatinine, ultra-sensitive C-reactive protein (usCRP), interleukin (IL)-6, IL-8, IL-18, monocyte-chemo-attractant-protein-1 (MCP-1) and plasma levels of homocysteine, tissue factor (TF) and tissue factor pathway inhibitor (TFPI) were determined on the 1st day and 42nd day. Primary outcome was reduction of homocysteine, secondary outcomes were reduction of usCRP, IL-6, IL-8, Il-18, MCP-1, TF and TFPI. RESULTS: The mean reduction of homocysteine concentration was 33% (95%CI 33.36-55.76, or 18.9+/-5.4 micromol L-1-12.6+/-2.8 micromol L-1, P=0) in the B-vitamin group compared with 1% in the placebo group. Folic acid (P=0) and vitamin B12 (P=0) increased significantly in the verum group, but both remained unchanged in the control group. No treatment effect of lowering of homocysteine on any markers of haemostasis (TF, TFPI) or inflammation (usCRP, IL-6, IL-8, IL-18 and MCP-1) was observed. CONCLUSION: Although homocysteine is associated with vascular disease risk in the general population and in particular with PAOD, marked lowering of homocysteine concentrations by folic acid and B-vitamin supplementation does not influence inflammatory responses involving usCRP, IL-6, IL-8, IL-18 and MCP-1, nor tissue factor. These results provide evidence against a major effect of hyperhomocysteinaemia on vascular chronic inflammation or coagulation in patients with symptomatic peripheral arterial occlusive disease.

Mode of delivery is associated with maternal and fetal endocrine stress response.

OBJECTIVE: To determine whether mode of delivery is associated with the endocrine stress response in mother and child. DESIGN: Prospective observational study. SETTING: Tertiary care centre, University hospital. POPULATION: A total of 103 nulliparous women with uncomplicated singleton pregnancies at term undergoing either spontaneous labour for vaginal delivery or delivering by caesarean section without labour. Thirty women delivered vaginally without any pain relief, 21 women delivered vaginally with epidural anaesthesia, 23 women had ventouse extraction and 29 women underwent caesarean section with epidural analgesia. METHODS: After delivery, maternal and umbilical cord blood was collected for determination of different stress-associated hormones. MAIN OUTCOME MEASURES: Concentrations of epinephrine (EP), norepinephrine (NOR), adrenocorticotropic hormone (ACTH), cortisol (CORT), prolactin (PRL), corticotropin-releasing factor and beta-endorphin (BE). RESULTS: Caesarean section was associated with significantly lower maternal concentrations of EP, NOR, ACTH, CORT, PRL and BE and lower newborn levels of EP, NOR and CORT compared with all other modes of delivery. Concentrations of EP, ACTH and BE differed significantly in newborns delivered by normal vaginal delivery, vaginal delivery with epidural anaesthesia and ventouse extraction. CONCLUSIONS: The mode of delivery and analgesia used during birth are associated with maternal and fetal endocrine stress responses.

Early diagnosis and curative therapy of medullary thyroid carcinoma by routine measurement of serum calcitonin in patients with thyroid disorders.

To identify patients with medullary thyroid carcinoma (MTC) at a potentially curable stage of the disease, serum concentrations of calcitonin (hCT) were determined in 14,000 patients (including 10,158 patients with thyroid nodules) referred to a thyroid outpatient clinic. Excluding patients in whom elevated basal hCT concentrations had already been known at the time of their referral, 507 patients with thyroid nodules presented basal concentrations of hCT of more than 10 pg/ml. Following stimulation by IV pentagastrin (0.5 microg/kg BW), hCT concentrations of more than 100 pg/ml were seen in 103 patients. This group included 32 new cases of MTC (29 patients with sporadic MTC and 3 new index cases of the familial form) and 43 patients with C cell hyperplasia (CCH). Among the 3,843 patients without thyroid nodules, 2 were found to harbor sporadic MTC while 4 had CCH. As compared to 1.1 cases of MTC per 1,000 patients with nodular thyroid diseases diagnosed in our institution before hCT screening was begun, 3.2 cases of MTC per 1,000 patients were identified when hCT was determined in all patients with thyroid nodules. The determination of hCT in all patients with thyroid nodular disease facilitates the timely diagnosis of MTC, thus providing the chance of curative surgery.

Primary hyperparathyroidism as the leading symptom in a patient with a Y791F RET mutation.

Primary hyperparathyroidism (PHP; serum calcium 2.75 mmol/L, PTH 226 pg/ml) had been the first clinical manifestation of MEN-2A in a female patient (aged 55 years) with a mutation (Y791F, TAT-->TTT) in exon 13 of the RET proto-oncogene. The patient has a pentagastrin-induced rise in serum calcitonin (up to 57 pg/ml) considered normal for noncarriers but abnormal in family members of MEN-2 patients. This is the first case of MEN-2 due to this specific mutation with primary hyperparathyroidism as the first manifestation of the disease. In addition, the patient harbored, within the Menin gene, a polymorphism (D418D) reportedly associated with sporadic primary hyperparathyroidism. This case report indicates that molecular biological tests in MEN- 2 may only suggest a certain phenotype but cannot predict it with certainty. It may also suggest that genetic screening for MEN-2 may be advisable in patients with primary hyperparathyroidism and a borderline-high pentagastrin stimulation test, even in the absence of a positive family history.

Hormonal profile and fertility in patients with Anderson-Fabry disease.

Anderson-Fabry disease is a glycosphingolipid storage disorder with an X-linked recessive inheritance. The alpha-galactosidase A deficiency leads to a progressive accumulation of globotriaosylceramide in the endothelium and tissue cells of various organs. The kidney, heart and brain are predominantly affected. Reports on endocrine function and fertility rates in patients with Anderson-Fabry disease are sparse. In the present study, we assessed ovarian, testicular and adrenal function in a cohort of patients with Anderson-Fabry disease. Plasma follicle-stimulating hormone, luteinizing hormone, prolactin, estradiol, testosterone, sex hormone-binding globulin, somatotropin, insulin-like growth factor-I and serum cortisol were measured in 13 patients (six female and seven male), currently observed in an outpatient clinic. The profile revealed an undisturbed hormonal function and a normal fertility rate in both male and female Anderson-Fabry patients when compared with the corresponding Austrian population.

Effects of parathyroidectomy on lead mobilization from bone in patients with primary hyperparathyroidism.

Since lead (Pb) accrued from environmental exposure accumulates in bone with a half life time between 6 and 10 years, a release of bone Pb into the circulation and/or urine (PbU) should be expected in diseases with increased bone metabolism such as hyperparathyroidism. We studied 60 patients with primary hyperparathyroidism (pHPT, 50 women, 10 men, aged 61.4 +/- 10.6 and 64.1 +/- 9.9 years, respectively) (a) before, (b) 1-6 months, and (c) 6-12 months after parathyroidectomy. Besides lead in blood (PbB) and lead in 24-h urine samples (PbU), parathyroid hormone (PTH), serum Ca2+, osteocalcin (OC), phosphate (PO4), and serum pyridinoline cross-linked telopeptide (cTP) were determined. Control data were determined in 20 healthy age-matched subjects. As expected, Ca2+ decreased after parathyroidectomy. Mean PbB in patients with pHPT was in the same range as in controls. A decrease of PbB after parathyroidectomy was found in the interval beyond 6 months. In contrast, mean PbU initially increased after surgery (3.05 +/- 1.94 vs. 4.25 +/- 2.65 microg/l, P = 0.004) and was not different beyond 6 months in comparison with preoperative values at (c). Investigating only patients with PTH < 150 ng/l, no significant PbB or PbU alterations were detected before and after parathyroidectomy. In patients with PTH > 150 ng/l, the decrease of PbB at (c) was more pronounced as was the increase of PbU at (b). In these patients, PbB and OC as well as PbB and cTP were correlated preoperatively. In conclusion, our data show that in environmentally lead-exposed (by food or by pollution) hyperparathyroid individuals, there is no hazardous PbB release from bone. The preoperative correlation between PbB and OC in pHPT patients with PTH > 150 ng/l provides evidence that in fact there is a Pb release from bone into the blood-pool by bone remodeling. The increase of PbU after parathyroidectomy is suspected to be caused by PTH-dependent Pb accumulation in the kidney, which seems to be restored with decreasing PTH. Moreover, our data confirm prior findings that bone remodeling seems to be normalized 6 months after parathyroidectomy.

Bone metabolism in patients more than five years after bone marrow transplantation.

We investigated the bone metabolism of 22 patients (median age 38 years) over 6 years after allogeneic bone marrow transplantation (BMT). Biplanar roentgenograms of the thoracic and lumbar spine were used to diagnose vertebral deformities caused by fractures. The actual bone mineral density (BMD) of the lumbar spine and the femoral neck were measured. Laboratory tests included calcium, phosphate, parathyroid hormone, a marker of bone resorption (beta-crosslaps, CTX), markers of bone formation (osteocalcin, bone-specific alkaline phosphatase), osteoprotegerin (OPG)--antagonist of the osteoclast differentiation factor RANKL, and sex hormone status. One patient had a vertebral fracture. Seven patients (28%) had osteopenia in the lumbar spine while 12 patients (48%) had osteopenia in the femoral neck. Bone resorption was increased in nine patients (43%) and bone formation was increased in four patients (20%). BMT recipients had significantly increased serum levels of OPG (P=0.029). Three women (75%) and four men (25%) were hypogonadal. The data showed that BMD is reduced and bone metabolism is still disturbed more than 6 years after BMT. The RANKL/osteoprotegerin system appears to play an important role in the pathophysiology of late post transplantation osteoporosis.

Frequency of RET proto-oncogene mutations in patients with normal and with moderately elevated pentagastrin-stimulated serum concentrations of calcitonin.

The possibility of germline mutations of the RET proto-oncogene (exons 10, 11, 13, 14, and 16) was investigated in 75 patients (57 men, 18 women) with a negative family history for medullary thyroid carcinoma (MTC), elevated (> 10 pg/mL) basal serum concentrations of human calcitonin (hCT) and a pentagastrin (PG)-stimulated serum hCT ranging from 50-100 pg/mL. Seventy patients (50 men, 20 women) with basal serum calcitonin concentrations in the normal range served as controls. Among the 75 patients with elevated basal serum hCT concentrations we identified 1 man with the mutation S649L and 2 patients (1 man and 1 woman) with the mutation Y791F. Among the 70 individuals with normal basal calcitonin 1 man and 1 woman presented with the mutation Y791F. No other mutations (such as those in codons 618 or 634, considered to be of greater clinical relevance) were identified in either group. On the other hand, the RET proto-oncogene mutation Y791F, characterized by a low penetrance, occurs comparatively frequently among patients with normal serum calcitonin concentrations. To preselect patients for RET screening by moderately (50-100 pg/mL) pentagastrin stimulation hCT concentrations does not increase the number of identified cases of familial MTC.

Effect of systemic vitamin C on free fatty acid-induced lipid peroxidation.

OBJECTIVES: Plasma malondialdehyde (MDA), a reactive product of lipid peroxidation, may be influenced by anti-oxidant therapy. The aim of the present study was to investigate if elevated MDA as induced by increased free fatty acids (FFA) correlates with endothelial function and is affected by high doses of vitamin C. METHODS: The study design was randomised, placebo-controlled, double blind, 2-way cross over. Plasma MDA concentrations and forearm blood flow (FBF) responses to intra-arterial acetylcholine (ACh) and glyceryl trinitrate were assessed during co-administration of vitamin C or placebo in the presence of increased plasma FFA by Intralipid/heparin infusion in 10 healthy male subjects. RESULTS: The seven-fold rise in plasma FFA was associated with an increase in plasma MDA concentrations (r=0.7, p<0.001) and decreased FBF responses to ACh (r=-0.4, p<0.01). Co-administration of vitamin C restored the impaired reactivity of FBF to ACh but had no effect on elevated MDA concentrations. CONCLUSIONS: Anti-oxidant vitamin C improves lipid-induced impairment of endothelium-dependent vasodilation, but does not alter MDA formation or breakdown.

Serum concentrations of dehydroepiandrosterone sulfate and leptin in obese patients with normal serum cholesterol.

Normal (< 200 mg/dL) serum concentrations of cholesterol and a favorable ratio of cholesterol/high-density lipoprotein (HDL)-cholesterol are frequently seen in morbidly obese (body mass index [BMI] > 35 kg/m2) patients. Because it is unknown whether this subgroup is characterized by differences in other potential markers of cardiovascular disease, serum concentrations of dehydroepiandrosterone sulfate (DHEAS) and leptin were determined in 155 obese patients (BMI > 35 kg/m2, aged 20 to 50 years) with normal (n = 72) or with elevated (n = 83) total serum cholesterol. We found that seemingly negative marginal correlations between serum concentrations of DHEAS and cholesterol, as well as between DHEAS and the ratio cholesterol/HDL-cholesterol, were not any more apparent after correction for age, sex, and BMI. A negative correlation between serum leptin concentrations and the ratio cholesterol/HDL-cholesterol persisted after correction for age, sex, and BMI. In morbid obesity, there appears to be an association between serum concentrations of leptin and a more favorable lipid profile, whereas there is no direct interrelation between serum concentrations of cholesterol and DHEAS.

Transcapillary insulin transfer in human skeletal muscle.

BACKGROUND: Transcapillary insulin transfer is considered a rate-limiting step in insulin action at supraphysiological insulin concentrations. However, it remains unclear whether this concept also applies for physiological conditions. MATERIALS AND METHODS: In the present study we set out to characterize transcapillary insulin transfer by measuring insulin concentrations in plasma and interstitial space fluid of skeletal muscle during an oral glucose tolerance test and euglycaemic hyperinsulinaemic clamp conditions, respectively. For this purpose we employed in vivo microdialysis of skeletal muscle in conjunction with an ultrasensitive insulin assay in eight healthy lean male volunteers (aged 25 +/- 1 years). RESULTS: Insulin concentrations at baseline were 48 +/- 8 pmol x L(-1) in plasma and 19 +/- 4 pmol x L(-1) in the interstitium (P = 0.002). The mean interstitium to plasma ratio at baseline was 0.48 +/- 0.09 pmol x L(-1). During the oral glucose tolerance test the interstitium to plasma ratio remained unchanged (0.43 +/- 0.12, P = NS vs. baseline), but was significantly reduced during euglycaemic hyperinsulinaemic clamp conditions at steady-state hyperinsulinaemia (0.12 +/- 0.01, P = 0.01 vs. baseline). CONCLUSION: In summary there is a substantial transcapillary insulin gradient in healthy human skeletal muscle under baseline and glucose-stimulated conditions. Our findings support the hypothesis of a saturable transcapillary insulin transport representing a partly rate-limiting step for insulin action.

The role of intraoperative quick PTH measurements in primary hyperparathyroidism.

BACKGROUND: In patients with primary hyperparathyroidism (PHPT), circulating concentrations of intact parathyroid hormone (PTH), decline dramatically within minutes following surgical excision of hyperfunctioning parathyroid tissue. The magnitude of this decay correlates with the completeness of resection of hyperfunctioning parathyroid tissue and can be monitored during the operation. METHOD: Intraoperative Quick PTH (QPTH) monitoring and pitfalls of more than 350 patients, who were operated because of primary hyperparathyroidism are analyzed. Special attention is given to correct baseline values and interpretation of QPTH values. RESULTS: QPTH monitoring is able to distinguish reliably between single and multiple gland disease and is an indispensable prerequisite for any form of limited parathyroid exploration. Experience with QPTH monitoring is necessary to achieve the excellent results known from bilateral neck exploration. CONCLUSION: Applying correct baseline values and cautious interpretation of QPTH values results in excellent results. Nevertheless more data must be collected to allow reliable interpretation of QPTH monitoring in all patients with PHPT.

Homocysteine levels in patients with Raynaud's phenomenon.

BACKGROUND: Patients with Raynaud's phenomenon (RP) have vasomotor dysregulation, mainly cause by dysfunction of the endothelium. Since homocysteine has been found to be damaging to endothelial cells, we investigated the concentrations of plasma homocysteine, folate and vitamin B12 in patients with primary or secondary RP compared to healthy individuals. PATIENTS AND METHODS: We measured the concentrations of plasma fasting homocysteine, folate and vitamin B12 in a group of healthy individuals (n = 45) and in patients with primary (n = 26) or secondary RP (n = 42). RESULTS: Median homocysteine levels in healthy controls and in patients with primary RP, secondary RP were 7.9 (IQR 4.1 to 11.8) 9.8 (IQR 5.1 to 14.4), and 10.6 (6.0 to 15.3) mumol/L, respectively. Patients with primary and secondary RP had significantly higher homocysteine concentration compared to healthy controls (Kruskal Wallis p = 0.01). After matching for age and sex, patients with either primary or secondary RP showed significantly higher homocysteine levels (Wilcoxon p < 0.0001). No significant differences between the three groups were found concerning serum levels of vitamin B12 (p = 0.9) and serum folate levels (p = 0.2). CONCLUSION: These data demonstrate that patients with RP have higher plasma levels of homocysteine. No significant differences in folate and vitamin B12 levels were found between patients with primary RP, secondary RP, and healthy individuals. These data suggest that homocysteine may play a role in RP and may provide new clues in understanding of the vasomotor dysregulation.