The levels of circulating markers of atherosclerosis and inflammation in subjects with different degrees of body mass index: Soluble CD40 ligand and high-sensitivity C-reactive protein.

BACKGROUND: It is well demonstrated that obesity is an independent risk factor for cardiovascular diseases. Recent studies have shown that obesity, insulin resistance and atherosclerosis are closely related phenomena in which low-grade inflammatory state and prothrombotic condition has pivotal roles. It has been shown that CD40-soluble CD40 ligand (sCD40L) interactions might constitute an important mediator for vascular inflammation. The aim of the present study was to assess sCD40L in relation to hs-CRP and cardiovascular risk factors in relation to body mass index (BMI). MATERIALS AND METHODS: Serum sCD40L and hs-CRP concentrations were measured in 52 obese patients and 28 non-obese subjects by ELISA. Insulin resistance was calculated by homeostasis model assessment-insulin resistance (HOMA-IR). We divided the participants into three groups depending in their BMI levels (Group 1: BMI <25 kg/m(2), Group 2: BMI 30-34.9 kg/m(2), Group 3: BMI > or =35 kg/m(2)). RESULTS: We determined that the mean sCD40L of group 3 was significantly higher than group 1 and group 2 (p<0.05, p<0.05, respectively). However, there was no significant correlation between plasma sCD40L levels and BMI. Plasma levels of hs-CRP were higher in obese group than the non-obese group (p<0.001). The levels of sCD40L were not significantly different between the two groups. The mean hs-CRP levels increased gradually in accordance with groups of BMI, there was a strong correlation between hs-CRP levels and BMI (r=0.724, p<0.001). There was no significant correlation between sCD40L and hs-CRP levels in all participants. CONCLUSIONS: It is still a subject for debate whether sCD40L levels are increased or not in obesity. However, the results of this study showed that sCD40L is substantially increased in patients with severe obesity. In terms of causality, the relatively small sample size and cross-sectional design of this study are considered to be the limitation factors.

The relationship between insulin resistance assessed by HOMA-IR and serum osteoprotegerin levels in obesity.

AIM: We investigated the relationship between insulin resistance and serum osteoprotegerin (OPG) levels in healthy obese subjects and healthy lean controls. METHODS: Fifty obese subjects (age: 31+/-8 years) and 24 lean controls (age: 30+/-7 years) were included in the study. We used the homeostasis model assessment for insulin resistance (HOMA-IR) index as the index of insulin resistance. OPG levels were measured with the commercial ELISA kit. Obese subjects were studied in three groups: Group I (n = 25) HOMA-IR index < 2.24, Group II (n = 13) index 2.24-3.59, Group III (n = 12) index > 3.59. Group IV (n = 24) was the lean controls with HOMA-IR index < 2.24. RESULTS: Obese subjects with increased insulin resistance (Group III) had lower OPG values than other groups (11.88+/-7.43 pg/ml, 16.39+/-6.39 pg/ml, 17.37+/-9.61 pg/ml, and 18.1+/-6.65 pg/ml, respectively; Group I versus Group III p = 0.036; Group III versus Group IV p = 0.012). We also found significant inverse correlations between OPGc (corrected for BMI) and fasting glucose (r = -0.325, p = 0.005), fasting insulin (r = -0.404, p = 0.0001) as well as HOMA-IR (r = -0.428, p = 0.0001). Increased fibrinogen level was found in Group III than Group IV (9.32+/-1.97 micromol/l versus 7.47+/-1.65 micromol/l, respectively; p = 0.005). In conclusion, insulin resistance in obesity is associated with decreased serum OPG levels and increased fibrinogen levels. The relationship between serum OPG levels and HOMA-IR may provide an insight into vascular endothelial dysfunction in obesity.

Pulmonary alveolar proteinosis in a patient with acute lymphoid leukemia regression after G-CSF therapy.

Pulmonary alveolar proteinosis (PAP) is the intra-alveolar accumulation of periodic-acid schiff (PAS) positive material. PAP is one of the underrecognized causes of pulmonary infiltrates in patients with hematologic malignancies. Here, we present a patient with acute lymphoid leukemia (ALL) in first remission that developed fever and diffuse pulmonary infiltrates during the neutropenic stage of consolidation chemotherapy. The histopathologic examination of bronchoalveolar lavage (BAL) fluid and transbronchial biopsy specimen demonstrated the presence of PAS-positive eosinophilic material. Empirical antibiotherapy and granulocyte-colony stimulating factor (G-CSF) were given. After the correction of neutropenia with G-CSF, the patient's fever disappeared, acute phase reactants decreased, pulmonary infiltrates resolved. We present this case because it was the first patient in whom the correction of neutropenia with G-CSF was followed by resolution of PAP.

A primary Sjögren's syndrome patient with distal renal tubular acidosis, who presented with symptoms of hypokalemic periodic paralysis: Report of a case study and review of the literature.

Although renal tubular acidosis (RTA), secondary to autoimmune interstitial nephritis, develops in a large proportion of patients with Sjögren's syndrome (SS), most of the subjects are asymptomatic. Here, we shall present a 39-year-old female patient who came to us with hypokalemic periodic paralysis (HPP), and who was later diagnosed with distal RTA. The patient, who had xerostomia and xerophthalmia for a long period of time, was diagnosed with primary SS from serologic and histologic findings. The patient recovered by being prescribed potassium replacement therapy. Although renal biopsy was not performed, corticosteroids were administered because HPP indicated severe interstitial nephritis. HPP did not reoccur during a 2-year follow-up period. We also review cases with SS-related distal RTA and HPP.