Hulusi Atmaca

The effect of Helicobacter pylori on insulin resistance.

Helicobacter pylori causes a lifelong infection in the stomach after exposure. H. pylorihas been shown to be associated with peptic ulcer and gastric cancer development. Moreover, it is held responsible for some other nongastric diseases. Among them, coronary heart disease attracts much debate. Many studies have demonstrated a close relationship between insulin resistance and atherosclerosis. Chronic inflammation and alterations in counter-regulatory hormones are deemed responsible for the etiology of insulin resistance. We aimed to examine the effect of H. pylori on insulin resistance. Sixty-three patients were enrolled in the study. Patients were divided into two groups according to H. pylori presence. HOMA-IR (homeostasis model assessment of insulin resistance) level was used to assess insülin resistance. Thirty-six patients were H. pylori positive and 27 were H. pylori negative. There was no difference between the two groups with regard to age, gender, or body mass index. HOMA-IR level was 1.73± 1.1 in the H. pylori-negative group, whereas it was 2.56 ± 1.54 in the H. pylori-positive group (P < 0.05). This study provides the first direct evidence for an association between chronic H. pylori infection and insulin resistance.

Serum levels of tumor necrosis factor-α, interleukin-6 and interleukin-8 are not increased in dyspeptic patients with Helicobacter pylori-associated gastritis

INTRODUCTION: Helicobacter pylori (H. pylori) is a non-invasive microorganism causing intense gastric mucosal inflammatory and immune reaction. H. pylori-induced gastric mucosal cytokine overproduction has been clearly documented previously. The stomach has a large surface area and continuous spill-over of locally produced cytokines into the blood stream is a possibility. There are few and conflicting data on circulatory proinflammatory cytokine levels in patients with H. pylori infection. MATERIALS AND METHODS: Forty-two dyspeptic patients were enrolled into the study. The presence of H. pylori infection was diagnosed with antral histopathologic examination. After overnight fasting; serum samples were obtained from each patient to determine circulating interleukin (IL)-6, IL-8 and tumor necrosis factor-alpha (TNF-alpha) levels. RESULTS: H. pylori was shown in 30 cases using Giemsa stain in antral histopathologic evaluation. Twelve cases were negative for H. pylori staining. Both the age and sex distribution had an insignificant difference in both H pylori-positive and H. pylori-negative groups. The mean circulatory levels of IL-6, IL-8 and TNF-a in both groups were not different. The situation was same in respect to the serum levels of these cytokines and the degree of inflammation, H. pylori density and activation scores according to Sydney classification. CONCLUSION: We could not show elevated circulatory levels of IL-6, IL-8 and TNF-alpha in H. pylori-infected cases. We believe that H. pylori-related cytokine activation become concentrated on gastric mucosa and this pathogen-induced local inflammatory cascade does not cause changes in circulatory levels of these cytokines. Moreover, there is no correlation between the levels of serum cytokines and Sydney parameters.

Nephropathy and retinopathy in type 2 diabetic patients living at moderately high altitude and sea level.

Background: High-altitude-induced hypoxia results in various diseases, such as chronic mountain sickness and high altitude retinal edema, and may affect severity and incidence of some cardiovascular diseases. In order to evaluate the effects of moderately high altitude on diabetic nephropathy and retinopathy, a cross-sectional study was planned. Material Method: Long-term type II diabetic residents of sea level (n = 75, 38 male, 37 female, mean age 51.9 ± 10.5 in Trabzon and Zonguldak cities) and moderately high altitude (h = 1,727 m, n = 73, 28 male, 45 female, mean age 48.3 ± 12.1, Van city) were compared. Results: No difference was observed in terms of age, gender, diabetes duration, body mass index, smoking, systolic, diastolic, and mean arterial blood pressure values, serum glucose levels, cholesterol, high-density lipoprotein (HDL)-cholesterol, low-density lipoprotein (LDL)-cholesterol, hemoglobin, HbA1C, hypertension control, or blood pressure medications and retinopathy incidence. Mean 24 h protein excretion (210.0 ± 139.9, 127.8 ± 112.1 mg; P = 0.00), proteinuria prevalence (57.5% versus 33.3%, p = 0.003), and serum creatinine levels (1.04 ± 0.22 versus 0.84 ± 0.21, p = 0.00) were significantly higher in the highlanders, glomerular filtration rate (GFR) was significantly lower in sea level (SL) patients (90.9 ± 26.5 versus 83 ± 21.1, p = 0.05). Conclusion: Tendency to diabetic nephropathy as indicated by higher proteinuria and creatinine levels is increased among type 2 diabetic patients living at moderately high altitude. Prospective studies are needed to confirm these findings.

An unusual case of pancytopenia associated with Sheehan’s syndrome

Dear Editor, Sheehan’s syndrome is characterized by varying degrees of anterior pituitary dysfunction due to postpartum ischemic necrosis of the pituitary gland after massive bleeding [1]. The most frequent hematologic finding is normochromic anemia. Pancytopenia is rarely observed in patients with Sheehan’s syndrome. We described a patient with pancytopenia due to hypocellular bone marrow in whom the diagnosis of Sheehan’s syndrome was established later during the evaluation of pancytopenia. A 57-year-old woman with complaints of malaise, fatigue, and dyspnea was referred to our hematology clinic for pancytopenia. Physical examination revealed no lymphadenopathy and hepatosplenomegaly. Complete blood count showed a white blood cell count of 2.3×10/l with a neutrophil count of 1.0×10/l, the hemoglobin level of 9.0 g/dl, and the platelet count of 90×10/l. Reticulocyte count was 0.3%. Serum iron, total iron binding capacity, ferritin, folic acid, and vitamin B12 levels were normal. Bone marrow examination revealed decreased hematopoiesis with hypocellularity (Fig. 1). After a careful interview, we found out that she had excessive bleeding after the last delivery at age 36; subsequently, lactation failed and menstruation did not resume. Sheehan’s syndrome was suspected from the history and the physical examination, and hormone study was made. Hormone profile was consistent with panhypopituitarism: adrenocorticotropic hormone, <10 pg/ml (10–46); growth hormone, <0.05 ng/ml (<10); follicle-stimulating hormone, 0.58 mIU/ml (21–153); luteinizing hormone, 0.18 mIU/ml (11–40); thyroid-stimulating hormone, 1.42 μIU/ml (0.4–4); free T3, 1.31 pg/ml (1.8– 4.2); free T4, 0.43 ng/dl (0.8–1.9); cortisol, <1 μg/dl (5–25). Magnetic resonance images of hypophisis demonstrated empty sella. The diagnosis of Sheehan’s syndrome was established. She received 0.1 mg L-thyroxine and 7.5 mg prednisolone. After 3 months of hormone replacement treatment, full hematologic recovery was observed. A normochromic anemia occurs frequently in the course of Sheehan’s syndrome. The anemia associated with hypopituitarism is related to hypocortisolism, hypothyroidism, hypogonadism, and growth hormone deficiency. In patients with anemia associated with panhypopituitarism, bone marrow examination shows either normal marrow or deficiency of erythroblasts [2]. Pancytopenia is rarely observed in patients with Sheehan’s syndrome. There have been few reports of pancytopenia with hypocellular bone marrow associated with Sheehan’s syndrome in the literature [2–4]. Pathogenesis of pancytopenia is uncertain but loss of direct effect of pituitary hormones on metabolic reactions concerned in hematopoiesis was suggested to play a role in pancytopenia associated with hypopituitarism [2, 3]. Our patient was treated Ann Hematol (2007) 86:307–308 DOI 10.1007/s00277-006-0233-y

Clinical characterization of patients with macroprolactinemia and monomeric hyperprolactinemia.

Macroprolactinemia is often a cause of misdiagnosis, unnecessary expensive investigation, and unsuitable treatment. The aim of the present study was to investigate the clinical findings and the concentrations of macroprolactin in patients with hyperprolactinemia in our region. Eighty‐four female hyperprolactinemic patients were screened for macroprolactinemia. Prolactin was measured by chemiluminesans method on an Immulite 2000 analyzer (Siemens Health Diagnostics, Deerfield, IL, USA). Recoveries less than or equal to 40% after polyethylene glycol precipitation were indicative of macroprolactinemia. Clinical features and biochemical values were compared in true hyperprolactinemic and macroprolactinemic patients. Macroprolactinemia was detected in 31 patients (36.9%), with 84 hyperprolactinemic female patients. There was no difference in frequency of galactorrhea and oligomenorrhea/amenorrhea between the two groups. When we evaluated the clinical features of patients according to prolactin levels, no significant difference was found between the groups. In conclusion, our initial data show that no clinical features could reliably differentiate macroprolactinemic from true hyperprolactinemic patients, but at least one of these symptoms was present in most macroprolactinemic patients.

Gonadal function in male mountain bikers.

Yamaner, F, Atmaca, H, Bayraktaroglu, T, Aydin, M, and Aydemir, S. Gonadal function in male mountain bikers. J Strength Cond Res 25(8): 2311-2315, 2011—Some studies reported testicular disorders associated with biking in mountain cyclists, which include injuries, erectile dysfunction, and higher scrotal temperatures. But none of these studies evaluated gonadal function. Therefore, the aim of this study was to evaluate gonadal function in male mountain bikers. Twenty-two male professional mountain bikers and 30 healthy noncyclist controls were included in the study. The mean age and body mass index were similar in both groups. Fasting blood samples for the measurement of the levels of total testosterone (TT), sex-hormone binding globulin (SHBG), luteinizing hormone (LH), and follicle-stimulating hormone (FSH) were obtained from all study participants before any physical activity. In addition, because insulin sensitivity and leptin modulate gonadal function, the concentrations of insulin, glucose, and leptin were also measured in the same samples. Calculated free testosterone (cFT) and bioavailable testosterone (bioT) were calculated from SHBG and TT. Basal hormonal levels including insulin, leptin, LH, FSH, SHBG, TT, glucose, and homeostasis model assessment scores were similar between the groups. However, bioT and cFT levels were significantly lower (p ≤ 0.05) in the mountain bikers than those in the controls. Despite the lower mean testosterone levels in the study group, the levels of LH and FSH were similar to controls. Insulin and leptin do not contribute to lower testosterone levels. In conclusion, male mountain bikers have lower testosterone concentrations compared to controls. This alteration cannot solely be explained by testicular dysfunction. The etiology of lower testosterone levels in cyclists appears to be complex and requires further research. The influence of such a decline on the athletes performance, quality of life, and muscle strength is not known as yet.