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Manel Puig-Domingo, Gonzalo Díaz, Joanna Nicolau, Cristián Fernández, Sergio Rueda, and Irene Halperin

Objective

Hypoparathyroidism is usually controlled with calcium and vitamin-D supplements; in very few cases this treatment fails and teriparatide may be an alternative. We report the first case of hypoparathyroidism refractory to vitamin-D therapy requiring multipulse teriparatide treatment.

Case report

A 53 year-old woman presented severe hypocalcemia and hypomagnesemia after thyroidectomy. Preoperatively, mild hypercalciuria was detected with parathyroid hormone (PTH) 69 pg/ml (normal 10–45) and 25-OH-vitamin D 9 ng/ml (normal 20–40) and normal levels of magnesium. No response was seen with oral and i.v. calcium and magnesium, or even with 5 μg calcitriol/day, suggesting a vitamin-D resistance status. Calcium sensor and vitamin-D receptor gene mutation studies were negative.

Interventions and results

The following treatments were tried: i) s.c. recombinant human PTH (rhPTH) 1–34 plus oral calcitriol, calcium, and magnesium, was partially effective, but symptoms resumed 4 h after the injection of 20 μg rhPTH; stable calcemia was not achieved even with 4–6 injections/day of teriparatide; ii) two trials of heterologous parathyroid transplant were performed but rejection was detected 3 months after; iii) i.v. magnesium decreased rhPTH requirements but i.m. administration was not tolerated and iv) multipulse s.c. infusion of teriparatide achieved complete normalization of serum calcium, phosphate, magnesium, calciuria and magnesuria with relatively low rhPTH doses (25–35 μg/day) for more than a year.

Conclusions

Vitamin-D unresponsiveness leads to uncontrolled hypocalcemia when postsurgical hypoparathyroidism occurs; in situations of no response to usual or higher doses of vitamin-D and s.c. injections of rhPTH, treatment with teriparatide multipulse s.c. infusor is an effective and safe alternative.

Free access

Silvia Pellitero, María Luisa Granada, Eva Martínez, Jose María Balibrea, Elena Guanyabens, Assumpta Serra, Pau Moreno, Maruja Navarro, Ramon Romero, Antonio Alastrué, and Manel Puig-Domingo

Objectives

IGF1 is decreased in morbidly obese (MO) patients and its changes after bariatric surgery weight loss (WL) are not well known. The aim of this study was to analyse IGF1 modifications in MO patients after WL and its relationship to ghrelin and to different types of surgeries.

Design

Retrospective follow-up study at the University Medical Center.

Methods

One hundred and nine MO patients (age 44.1±9.3, BMI 51.74±8.75 kg/m2) were evaluated at baseline and 1 year after surgery: 28 sleeve gastrectomy (SG), 31 distal modified (m), and 50 ringed (r) Roux-en-Y gastric bypass (RYGBP) surgery. Changes in IGF1, IGFBP3, ratio IGF1:IGFBP3, and ghrelin were evaluated 1 year after surgery.

Results

Baseline prevalence of low IGF1 (defined by s.d. IGF1<−2) was 22%, and %WL 1 year after surgery was 34.9±8.9%. There was a significant decrease in IGFBP3 in all the procedures, an increase in IGF1:IGFBP3 ratio in rRYGBP and SG, but total IGF1 only increased significantly in SG. Albumin concentrations decreased in mRYGBP, did not change in rRYGBP, but increased in SG after surgery. Total ghrelin concentrations increased after both RYGBPs and decreased after SG (P<0.05 in all cases). The prevalence of low IGF1 decreased in SG (28.6 vs 10.1%, P=0.03) and did not change in RYGPBP techniques. The %albumin change was the only dependent variable associated with the % total IGF1 change.

Conclusions

Recovery of low IGF1 after bariatric surgery was specifically related to the albumin modifications induced by surgery and was not related to ghrelin modifications.

Restricted access

María Teresa Julián, Guillem Pera, Berta Soldevila, Llorenç Caballería, Josep Julve, Carlos Puig-Jové, Rosa Morillas, Pere Torán, Carmen Expósito, Manel Puig-Domingo, Esmeralda Castelblanco, Josep Franch-Nadal, Kenneth Cusi, Didac Mauricio, and Nuria Alonso

Objective: To investigate the prevalence and risks factors associated with the presence of significant liver fibrosis in subjects with nonalcoholic fatty liver disease (NAFLD) with and without type 2 diabetes mellitus (T2D).

Design and methods: This study was part of a population-based study conducted in the Barcelona metropolitan area among subjects aged 18-75 years old. Secondary causes of steatosis were excluded. Moderate-to-advanced liver fibrosis was defined as a liver stiffness measurement (LSM) ≥ 8.0 kPa assessed by transient elastography.

Results: Among 930 subjects with NAFLD, the prevalence of moderate-to-advanced liver fibrosis was higher in subjects with T2D compared those without (30.8% vs. 8.7%). By multivariable analysis, one of the main factors independently associated with increased LSM in subjects with NAFLD was atherogenic dyslipidemia, but only in those with T2D. The percentage of subjects with LSM ≥ 8.0 kPa was higher in subjects with T2D and atherogenic dyslipidemia than in those with T2D without atherogenic dyslipidemia, both for the cut-off point of LSM ≥8.0 kPa (45% vs 24%, p=0.002) and 13 kPa (13% vs 4%, p=0.020). No differences were observed in the prevalence of LSM ≥8.0 kPa regarding glycemic control among NAFLD-diabetic subjects.

Conclusions: Factors associated with moderate-to-advanced liver fibrosis in NAFLD are different in subjects with and without T2D. Atherogenic dyslipidemia was associated with the presence of moderate-to-advanced liver fibrosis in T2D with NAFLD but not in non-diabetic subjects. These findings highlight the need for an active search for liver fibrosis in subjects with T2D, NAFLD and atherogenic dyslipidemia.

Restricted access

Marjorie Reyes, Lorena González, Kevin Ibeas, Rubén Cereijo, Siri D. Taxerås, Silvia Pellitero, Eva Martínez, Jordi Tarascó, Pau Moreno, Paloma Malagón, Carmen Higueras, Andrea Soria, Manel Puig Domingo, Francesc Villarroya, Dolors Serra, Laura Herrero, and David Sánchez-Infantes

Context

The endocrine and immunological properties of subcutaneous vs. visceral adipose tissue (sWAT and vWAT, respectively) have turned a milestone in the study of metabolic diseases. The cytokine S100A4 is increased in obesity and has a role in adipose tissue dysfunction. However, the cellular source and its potential role in hepatic damage in obesity has not been elucidated.

Objective

We aim to study the regulation of S100A4 in immune cells present in sWAT and vWAT, as well as its potential role as a circulating marker of hepatic inflammation and steatosis.

Design

A cohort of 60 patients with obesity and distinct metabolic status was analyzed. CD11b+ myeloid cells and T cells were isolated from sWAT and vWAT by magnetic-activating cell sorting, and RNA was obtained. S100A4 gene expression was measured, and correlation analysis with clinical data was performed. Liver biopsies were obtained from 20 patients, and S100A4 circulating levels were measured to check the link with hepatic inflammation and steatosis.

Results

S100A4 gene expression was strongly upregulated in sWAT- vs. vWAT-infiltrated CD11b+ cells, but this modulation was not observed in T cells. S100A4 mRNA levels from sWAT (and not from vWAT) CD11b+ cells positively correlated with glycemia, triglycerides, TNF-α gene expression and proliferation markers. Finally, circulating S100A4 directly correlated with liver steatosis and hepatic inflammatory markers.

Conclusion

Our data suggest that sWAT-infiltrated CD11b+ cells could be a major source of S100A4 in obesity. Moreover, our correlations identify circulating S100A4 as a potential novel biomarker of hepatic damage and steatosis.

Free access

Mónica Marazuela, Tomás Lucas, Cristina Alvarez-Escolá, Manel Puig-Domingo, Nuria Garcia de la Torre, Paz de Miguel-Novoa, Alejandra Duran-Hervada, Rafael Manzanares, Manuel Luque-Ramírez, Irene Halperin, Felipe F Casanueva, and Ignacio Bernabeu

Context

Pegvisomant is an effective treatment for somatostatin analogue-resistant acromegaly, but the determinants defining the response to this treatment are largely unknown.

Objective

To investigate the efficacy of pegvisomant treatment in resistant acromegalic patients (e.g. serum IGF1 at least 1.25×upper normal limit) in a clinical setting and the factors conditioning this response.

Design and setting

A retrospective cross-sectional study performed in six Spanish University hospitals from 2004 to 2007.

Patients

Forty-four acromegalic patients (61.4% female, mean age: 49±14), 95% of whom had undergone pituitary surgery and 61% having received pituitary radiotherapy. The mean follow-up was 22.7±11.2 months.

Main outcome measures

IGF1 levels reflected treatment efficacy, and the influence of gender, age, weight, previous radiotherapy and duration of treatment was assessed.

Results

IGF1 normalisation was achieved in 84% of the patients. Male gender (P<0.05), previous irradiation (P<0.05) and the treatment duration (r=0.364, P<0.02) were associated with a better response to pegvisomant therapy. There was a significant decrease in HbA1c (P<0.001) and in the mean insulin dose (P<0.01) in acromegalic diabetic patients. Although 25% of patients experienced mild adverse events, pegvisomant was only withdrawn in four patients due to side effects (two cases of tumour growth, one liver dysfunction and one headache).

Conclusions

Long-term pegvisomant is a very effective therapy in resistant acromegaly. Male gender and prior radiotherapy influence the therapeutic response rate.