Pyloric giant Brunner's gland hamartoma as a cause of both duodenojejunal intussusception and obscure gastrointestinal bleeding.

Obscure gastrointestinal bleeding is an important dilemma. Brunner's gland hamartoma is an extremely rare tumor generally localized in the duodenal bulb. We present a 34-year-old woman who had suffered from several episodes of melena for the past three years. Endoscopic examinations were normal. Computed tomography showed a large target lesion over the right abdomen and an image representing intestinal malrotation, which was supported by enteroclysis. At exploratory laparotomy, ligamentum of Treitz was located in the mid-to-right side of the columna vertebralis, and the duodenal bulb was found to be invaginated into the proximal jejunum. After longitudinal duodenotomy, a pedunculated ring-shaped large polyp originating from the pyloric ring was seen and excised. Histology was consistent with Brunner's gland hamartoma. This case with obscure bleeding was original with respect to its rarity and being a huge, ring-shaped tumor with pyloric localization. Moreover, the patient had a rare clinical presentation of duodenojejunal intussusception with accompanying intestinal malrotation.

Analysis of inherited thrombophilic mutations and natural anticoagulant deficiency in patients with idiopathic portal hypertension.

Idiopathic portal hypertension (IPH) is characterized by non-cirrhotic presinusoidal intrahepatic portal hypertension. The etiopathogenesis of the disease is poorly understood. Obliteration with microthrombosis of the small portal vein branches may lead to lesions underlying portal hypertension. We aimed to put forward a comprehensive thrombophilic mutation profile in IPH and its probable contribution to pathogenesis. Eleven patients and 12 controls were included. We used the CVD-StripAssay which is based on the reverse-hybridization principle to identify a total of 12 thrombophilic gene mutations: Factor V R506Q, Factor V H1299R, prothrombin G20210A, Factor XIII V34L, beta-Fibrinogen -455 G-A, PAI-1 4G/5G, platelet GPIIIa L33P, MTHFR C677T, MTHFR A1298C, ACE I/D, Apo B R3500Q and Apo E2/E3/E4, respectively. We also evaluated some blood parameters and protein C, protein S, AT-III levels using commercially available assays. IPH patients and controls were similar in respect to gender distribution (P = 1.000). Mean age was 31.2 in patients and 29.1 in controls (P = 0.622). Pica history was present in 54.5% of the patients. Mean protein C and AT-III levels were lower in patients than that of controls (P = 0.002 and 0.001, respectively). Factor XIII V34L, PAI-1, GPIIIa L33P, MTHFR C677T and MTHFR A1298C frequencies of genetic polymorphisms were found to be significantly higher among patients than that of controls. Apolipoprotein E2/E3/E4 analysis showed an inverse relationship with IPH when E2 plus E4 compared with E3. A higher frequency of Beta-Fibrinogen -455G-A mutation was observed in patients, but this difference did not reach a statistical significance. Our data represent the most comprehensive study to date with respect to thrombophilic gene polymorphisms in IPH. The data support a possible pathogenetic role in IPH, at least by some of the prothrombotic mutations. In order to confirm or refuse this proposal, a larger cohort of patients is needed.

The effects of nonsteroidal anti-inflammatory drugs on platelet function and severity of upper gastrointestinal haemorrhage.

Nonsteroidal anti-inflammatory drugs (NSAIDs) cause gastrointestinal (GI) damage primarily due to the inhibition of prostaglandin synthesis in gastric mucosa, which is an important factor in mucosa protection. Platelets are a cardinal feature of vascular repair. A variety of angiogenic stimulators are stored in platelets and are released during clotting at the wound. When there is a defect in any of these functions and/or platelet number, haemostasis is usually impaired and there may be an associated increased risk and severity of bleeding. While the mechanism of mucosal injury and bleeding are well documented with the use of NSAIDs, very little is known about the platelet function abnormalities and their effects on severity of upper GI bleedings. We performed a prospective analysis of 49 patients who had a history of NSAIDs use to investigate the association between the platelet function impairment associated with NSAIDs and severity of upper GI haemorrhages. Thirty-six of 49 patients (73.5%) had deteriorated platelet function. Mean severity score of patients with deteriorated platelet functions was 3.39, and that of patients with normal platelet functions was 2.46. Mean severity score was statistically significantly higher in patients with deteriorated platelet functions. In conclusion, impaired platelet functions associated with NSAIDs may cause more severe upper GI bleeding. Clinicians should be alert for GI complications especially in older patients and in those with a history of ulcer bleeding.

Two cases of bacterial meningitis accompanied by thalidomide therapy in patients with multiple myeloma: is thalidomide associated with bacterial meningitis?

Morbidity and mortality in multiple myeloma is often attributed to life-threatening infections. A defect in humoral immunity has been proposed for the predisposition to bacterial infections. Most of the infections are of bacterial origin, and the most serious are septicemia, meningitis, and pneumonia. Thalidomide is a drug with pleiotropic effects. The immunomodulatory effects of thalidomide are at least partially mediated through its ability to down-regulate the pathogenic over-production of tumor necrosis factor-alpha (TNF-alpha). TNF-alpha is a cytokine that plays a central role in the regulation of the host immune and inflammatory response to infection. In the central nervous system, TNF-alpha is involved in induction of a fever response and triggers the release of other cytokines, and may also influence transport of compounds into the brain, leading to cerebrospinal fluid leukocytosis, increased protein influx, and lactate accumulation. Thalidomide has been shown to down-regulate the production of TNF-alpha. On the other hand, knowledge of the effects of thalidomide on granulocyte functions is limited. Thalidomide has been shown to attenuate neutrophil adhesion and chemotaxis. We present herein two cases of Streptococcus pneumoniae bacterial meningitis that developed soon after the initiation of thalidomide treatment, and discuss the effect of thalidomide on the immune system. Although, it is not clear whether thalidomide caused the development of the bacterial infections and meningitis, or what its pathogenetic mechanisms are, physicians should be alert for signs and symptoms of meningitis in patients with multiple myeloma who are treated with thalidomide, especially those in neutropenic states.

Clarifying the relationship between ABO/Rhesus blood group antigens and upper gastrointestinal bleeding.

BACKGROUND AND AIM: The relationship between blood group antigens and peptic ulcer disease has been widely evaluated in the past. Data concerning the same association with upper gastrointestinal bleeding are very limited. We aimed to evaluate this association and we thought it was worthwhile to try to determine whether these components take some part in this complication. METHODS: The study population consisted of 1,098 adults (364 patients and 734 volunteer blood donors as controls). Demographic features, comorbid illnesses, and use of aspirin/nonsteroidal anti-inflammatory drugs (NSAIDs) were recorded. Blood groups were examined by gel centrifugation method. We included only patients with bleeding from peptic ulcer disease and erosive gastropathy. Ulcers were classified by using Forrest's classification system in terms of rebleeding risk. Helicobacter pylori was examined by histology. RESULTS: The gender distribution was similar in both groups. The ABO blood group phenotype distribution in patients and controls (respectively) was as follows: 46.2% versus 34.9% for group O, 32.4% versus 39.5% for group A, 15.7% versus 18.4% for group B, and 5.8% versus 7.2% for group AB. Blood group O was found to have higher frequency in the patient group than in the control group (P=0.004). Rh positivity was also higher in patients than in controls (P=0.007). H. pylori positivity was similar between blood groups among patients. The rebleeding and mortality rates between blood groups were also similar. CONCLUSION: ABO blood group O had an important role in patients with upper gastrointestinal bleeding. The impact of blood group on rebleeding and mortality may be a focus for further studies.

The prevalence of primary and secondary Helicobacter pylori resistance to clarithromycin and probable contributing cofactors: data from southeastern Anatolia.

BACKGROUND/AIMS: Antibiotic resistance of Helicobacter pylori is the most important reason for failure in its eradication. We aimed to determine the prevalence of primary and secondary H. pylori resistance to clarithromycin in isolated H. pylori from dyspeptic patients in southeastern Anatolia and to evaluate the cofactors affecting this clinical problem. METHODOLOGY: The study involved adult patients who had already been diagnosed with symptomatic H. pylori infection based on rapid urease test, gastric histopathological examination and culture. H. pylori strains were isolated from antral biopsies taken during upper endoscopy in 142 dyspeptic patients with no previous therapy against the microorganism. MICs of clarithromycin were determined by E-test. Patients were treated for 14 days with standard triple-agent protocol. H. pylori eradication rate was assessed after 8 weeks. Each patient was re-interviewed to determine secondary resistance. Primary clarithromycin resistance was defined as pre-treatment resistance, while secondary as after treatment resistance. Strains were considered resistant to clarithromycin if the MIC > 1 microg/mL. RESULTS: In total 213-105 women and 108 men-patients was enrolled to the study. The mean age was 35.5+/-14.1 years. In 142 (66.7%) patients out of the total patients enrolled in the study, H. pylori was detected. H. pylori could be cultured from only 61 (43%) of them. In 16.4% of the cases, primary clarithromycin resistance was noted. After 8 weeks, seventy-seven (54.2%) of the 142 patients were reevaluated. Helicobacter pylori eradication could be achieved in 68.8% of them. The proportion of H. pylori eradication in clarithromycin-sensitive patients was 75.8% and the respective proportion was 10% for resistant cases. In the group where H. pylori was still positive the secondary resistance percentage was found to be 27.2%. CONCLUSIONS: The prevalence of primary clarithromycin resistance is relatively high in our geographical area. Secondary resistance rate was 27.2%. None of the criteria of age, gender, presence of endoscopic lesions, detected H. pylori concentration and gastritis activity showed any effect on the primary resistance.

Familial Mediterranean fever gene mutations in the Southeastern region of Turkey and their phenotypical features.

Familial Mediterranean fever (FMF) is an autosomal recessive disease characterized by recurrent inflammatory attacks of serosal membranes. Several studies have focused on the differences between frequency of the mutations and their phenotypical manifestations. The aim of this study was to evaluate whether or not this phenotypical variation is associated with the existence of particular mutations. Twelve MEFV (Mediterranean fever) gene mutations were investigated in 119 patients suffering from FMF. Heterozygote M694V (21/119), heterozygote E148Q (21/119), homozygote M694V (17/119) and heterozygote V726A (12/119) mutations were the most common mutations. Patients were grouped according to the presence of the M694V mutation: group I was M694V/M694V, group II was M694V/others, and group III was other/other. Mean severity scores for the groups were 13.94 +/- 4.10, 10.79 +/- 3.01 and 8.31 +/- 2.26, respectively. There were statistically significant differences between the mean severity scores of groups I and II (p = 0.029), groups I and III (p < 0.0001), and groups II and III (p < 0.0001). Diagnosis of amyloidosis was established in four (23%) patients of group I, and three (8%) patients of group II, but in none of the patients in group III. There was also a statistically significant difference between groups I and III (p = 0.046), but not between groups II and III (p = 0.083) and groups I and II (p = 0.317) in terms of amyloidosis development. In conclusion, we found a higher disease severity score and higher prevalence of amyloidosis in FMF patients who were M694V mutation carriers. Many ethnic groups live in Anatolia and more ethnic origin-based studies are needed to determine the real effect of these mutations on disease severity and amyloidosis.

Pseudoxantoma elasticum, as a repetitive upper gastrointestinal hemorrhage cause in a pregnant woman.

Pseudoxantoma elasticum is a rare, hereditary, multisystemic disease affecting the skin, eye, and cardiovascular system. A twenty-eight-year-old female has presented to emergency unit with the complaint of gastrointestinal hemorrhage. This patient, who had been monitored in the gastroenterology clinic more than 10 times in the past 8 years, noted a repetitive hemorrhage during her previous pregnancy in her history. The examination of the patient revealed the following signs and symptoms: atrophy in the epithelium of the retina pigment; typical angioid streaks and peau d'orange finding in the fundus; thinning of the retinal nerve fiber in OCT (optic coherence tomography); bilateral and reticular papillary lesions with yellowish-color in the neck region (plucked chicken appearance); presence of bleeding foci in fundus; and nephrocalcinosis in kidneys. In light of these symptoms, the patient was diagnosed with pseudoxantoma elasticum. Skin biopsy confirmed the pseudoxantoma elasticum diagnose. PXE is an uncommon, hereditary disease. Early diagnosis of pseudoxantoma elasticum cases, is important for minimalizing systemic complications and informing the other family members through genetic counseling.

Does adding misoprostol to standard intravenous proton pump inhibitor protocol improve the outcome of aspirin/NSAID-induced upper gastrointestinal bleeding?: a randomized prospective study.

Aspirin and nonsteroidal anti-inflammatory drug (NSAID)-induced gastrointestinal bleeding is recognized as an important health problem. We performed a single-center randomized clinical trial to compare the effect of high-dose intravenous proton pump inhibitor (omeprazole) alone (group 1) with omeprazole in combination with a low-dose prostaglandin analog (misoprostol; group 2) on clinical outcomes in patients with aspirin/NSAID-induced upper gastrointestinal bleeding. Additionally, we evaluated the contribution of Helicobacter pylori eradication therapy on the late consequences. Patients were recruited to the study if they had upper gastrointestinal bleeding with history of taking aspirin or other NSAIDs within the week before the onset of bleeding. All were evaluated in terms of probable risk factors. After the standard treatment protocol, patients with histologically proven H pylori infection were prescribed a triple eradication therapy for 14 days. The primary end points were recurrent bleeding, surgery requirement, and death rates before discharge and at the end of follow-up period. This study lasted for 2 years. A total of 249 patients with upper gastrointestinal bleeding were admitted, and 49.7% of these patients were users of aspirin/NSAIDs. There were 67 patients in group 1 and 56 in group 2. The distributions for gender, age, comorbidity, H pylori infection, and high-risk ulcer rate were similar in both groups. Among aspirin/NSAID users, endoscopy revealed duodenal ulcer in 47 (38.2%), gastric ulcer in 10 (8.1%), and erosive gastropathy in 33 (26.8%). The overall rebleeding occurred in 12.2%, death in 2.4% of the patients. The in-hospital death (P=.414), rebleeding (P=.925), and surgery (P=.547) rates were similar in both treatment groups. After the follow-up period of 3 months, overall rebleeding occurred in 4.1%, and death in 4.8% of the patients. The overall mortality rate was highest in those >65 years old, who were chronic low-dose aspirin users with comorbidity. One died of transfusion-related graft-versus-host disease. In this pilot study, we indicated that adding misoprostol (600 microg/day) to standardized proton pump inhibitor treatment did not improve or change the rebleeding or mortality rates of patients with upper gastrointestinal bleeding related to aspirin/NSAID use. Other prospective studies on higher doses of misoprostol are needed to establish the coeffect. One should bear in mind that all blood products must be irradiated before transfused to the host.

Epidemiological and clinical aspects of liver cirrhosis in adult patients living in Southeastern Anatolia: leading role of HBV in 505 cases.

BACKGROUND/AIMS: Liver cirrhosis is the terminal condition of liver disorders resulting from various causes. Literature lacks data on epidemiological and clinical aspects of liver cirrhosis in Turkey. We aimed to evaluate the main features of liver cirrhosis in this study. METHODOLOGY: We included in the study a total of 505 patients referred to Dicle University Hospital in the last five years and evaluated retrospectively. Demographic features, etiology, clinical findings, disease severity, complications and mortality rates were all recorded. RESULTS: Of the patients, 136 (27%) were female and 369 were (73%) male. Mean age was 50.4. The etiologic spectrum consisted of 368 HBV (72.9%), 41 HCV (8.1%), 12 alcohol (2.4%). Rate for cryptogenic cirrhosis (CC) was 11.1% with mean age of 45.4. HDV superinfection was present in 17.8%. Most of the patients were in Child-Pugh class B. Number of decompensated cirrhosis cases was 278 (55%). Hepatocellular cancer (HCC) was seen in 8.9% of patients and 88% had HBV with a mean age of 60. HCC was seen more commonly in HDV superinfected patients (p = 0.035). In-patient mortality was observed in 13.2%. CONCLUSIONS: HBV is the leading etiological factor of liver cirrhosis in Southeastern Anatolia and strict measures must be taken against perinatal or horizontal transmission of contagious pathogens. Alcohol had a marginal role in cirrhosis in our region. Although HDV superinfection is decreasing with time, it may increase HCC risk. Patients with cryptogenic cirrhosis were younger and had lower Child-Pugh scores.

A comprehensive analysis of 12 thrombophilic mutations and related parameters in patients with inflammatory bowel disease: data from Turkey.

BACKGROUND: Possible association of inflammatory bowel disease (IBD) with the most common inherited prothrombotic conditions has been the focus of many investigations. Advance in modern molecular biology is expanding the thrombophilia evaluation steadily. We tried to put forward a comprehensive thrombophilic profile in IBD and to see the probable role of this profile in pathogenesis. METHODS: A total of 60 adults (33 patients and 27 healthy controls) were included. We used the CVD-StripAssay which is based on the reverse-hybridization principle to identify a total of 12 thrombophilic gene mutations: Factor V R506Q, Factor V H1299R, prothrombin G20210A, Factor XIII V34L, beta-Fibrinogen-455 G-A, PAI-1 4G/5G, platelet GPIIIa L33P, MTHFR C677T, MTHFR A1298C, ACE I/D, Apo B R3500Q and Apo E2/E3/E4, respectively. Besides, we evaluated many related blood parameters such as protein C, protein S, AT-III, IL-6, TNF-alpha, Apo-A1, Apo-B100, homocysteine (tHcy) etc. using commercially available assays. RESULTS: The frequencies of genetic polymorphisms were found to be statistically insignificant among patients and controls, except for three: Beta-Fibrinogen-455G-A, MTHFR A1298C and ACE-I/D. Two patients with a history of deep venous thrombosis had more than one polymorphism. Patients with MTHFR C677T and MTHFR A1298C gene mutations had a similar mean tHcy levels with controls. Patients with Apolipoprotein B R3500Q and Apolipoprotein E4 gene mutations had similar mean LDL-cholesterol levels. Mean total cholesterol and triglyceride levels were similar in patients and controls of Apo E2, E3, E4 alleles. CONCLUSION: Predominantly, the presence of genetic mutations that predispose to hypercoagulable states does not appear to be in correlation with IBD. There was a statistical difference between the proportions of the mutated allele frequencies of Beta-Fibrinogen-455G-A, MTHFR A1298C and ACE-I/D in IBD.

A head to head comparison of oral vs intravenous omeprazole for patients with bleeding peptic ulcers with a clean base, flat spots and adherent clots.

AIM: To compare the effect of intravenous and oral omeprazole in patients with bleeding peptic ulcers without high-risk stigmata. METHODS: This randomized study included 211 patients [112 receiving iv omeprazole protocol (Group 1), 99 receiving po omeprazole 40 mg every 12 h (Group 2)] with a mean age of 52.7. In 144 patients the ulcers showed a clean base, and in 46 the ulcers showed flat spots and in 21 old adherent clots. The endpoints were re-bleeding, surgery, hospital stay, blood transfusion and death. After discharge, re-bleeding and death were re-evaluated within 30 d. RESULTS: The study groups were similar with respect to baseline characteristics. Re-bleeding was recorded in 5 patients of Group 1 and in 4 patients of Group 2 (P = 0.879). Three patients in Group 1 and 2 in Group 2 underwent surgery (P = 0.773). The mean length of hospital stay was 4.6 +/- 1.6 d in Group 1 vs 4.5 +/- 2.6 d in Group 2 (P = 0.710); the mean amounts of blood transfusion were 1.9 +/- 1.1 units in Group 1 vs 2.1 +/- 1.7 units in Group 2 (P = 0.350). Four patients, two in each group died (P = 0.981). After discharge, a new bleeding occurred in 2 patients of Group 1 and in 1 patient of Group 2, and one patient from Group 1 died. CONCLUSION: We demonstrate that the effect of oral omeprazole is as effective as intravenous therapy in terms of re-bleeding, surgery, transfusion requirements, hospitalization and mortality in patients with bleeding ulcers with low risk stigmata. These patients can be treated effectively with oral omeprazole.

Changes in pulse oximetry levels and factors affecting oxygen saturation during routine upper gastrointestinal endoscopy with or without sedation.

BACKGROUND/AIMS: We aimed to investigate whether endoscopy or midazolam as premedication causes oxygen desaturation and to determine factors which may affect the occurrence of oxygen desaturation. METHODS: Totally 200 patients with various indications (103 men and 97 women), who presented to the Endoscopy Unit of Dicle University Hospital for upper gastrointestinal endoscopy examination, were included in the study. Anamnesis and anthropometric values of the patients were taken. Preoperative oxygen saturation, hemoglobin levels and heart rate per minute were recorded. Patients with initial oxygen saturation levels <90% were excluded. Patients were divided into two groups. The first group included 100 patients who underwent endoscopic examination without sedation and the second group included 100 patients who underwent endoscopic examination with sedation [midazolam (2-5 mg)]. At the end of endoscopy, intravenous flumazenil (0.2 mg) was administered to the premedication patients. Patients were monitored for oxygen saturation and heart rate starting before the sedation and oropharynx anesthesia and lasting until 1 min after the end of the procedure. During the endoscopic examination, minimum oxygen saturation and maximum heart rate values were recorded. The duration of the oxygen saturation <90% was recorded throughout the procedure and the relation of this time with the total time of the endoscopic examination was evaluated. RESULTS: The mean age of the 200 patients included in the study was 45 and 44 years for Group 1 and Group 2, respectively. No differences were found between the two groups in terms of body mass index, smoking, hemoglobin and basal maximum pulse rate, duration of endoscopy, minimum basal oxygen saturation, duration of hypoxia and time to hypoxia. No relation was determined between oxygen desaturation and gender, duration of the endoscopy, basal pulse rate or hemoglobin level. It was found that smoking made significant contributions to the oxygen desaturation. CONCLUSION: Midazolam premedication for upper gastrointestinal system endoscopy is a reliable procedure and does not contribute an additional risk in individuals without serious comorbidities. Smoking habits should be taken into account in endoscopy patients.

Subclinical hypothyroidism may be associated with elevated high-sensitive c-reactive protein (low grade inflammation) and fasting hyperinsulinemia.

UNLABELLED: The association between coronary heart disease and subclinical hypothyroidism (SCH) is unclear. We aimed to determine hs-CRP concentrations in patients with SCH. Seventy-seven patients (age 34.6 +/- 13.7 yr) with SCH (TSH > 4.2 microIU/ml and serum free thyroxine level between 0.932-1.71 ng/dL), and 80 control subjects (age 33.9 +/- 13.3 yr) were studied. Thyroid hormones, C-reactive protein, insulin, glucose, total, HDL, LDL and VLDL-cholesterol levels and HOMA-IR index were also determined. TSH levels of SCH group were higher than control (7.4 +/- 2.9 and 1.55 +/- 0.78 microIU/ml, respectively, p = 0.0001). However, FT4 levels were lower than control subjects (1.18 +/- 0.22 ng/dL and 1.38 +/- 0.26, respectively, p = 0.001). Serum hs-CRP levels of subjects with SCH were higher than control subjects (4.2 +/- 0.8 mg/l and 1.05 +/- 0.3 mg/l respectively, p = 0.0001). Insulin levels of SCH group were higher than control (8.5 +/- 4.3 microU/ml and 7.1 +/- 3.1 microU/ml respectively, p<0.02) but, Homa-IR levels of the two groups were not different. Mean total and LDL-cholesterol levels of SCH group were higher than control (p = 0.01 and p<0.02). We also found a positive correlation between hs-CRP levels and insulin (r = 0.362, p = 0.002 in men, r = 0.358, p = 0.0001 in women), TSH (r = 0.611, p = 0.0001 in men, r = 0.411 p = 0.0001 in women), and prolactin (r = 0.340, p = 0.01 in men r = 0.553, p = 0.0001 in women). CONCLUSIONS: Patients with SCH, irrespective of gender, have higher serum hs-CRP, insulin, total and LDL-cholesterol levels than healthy subjects. 2- High hs-CRP level, and thereby low grade inflammation may be associated with fasting hyperinsulinemia before insulin resistance becomes evident in patients with SCH.

Serum C-reactive protein (CRP) levels and insulin resistance in non-obese women with polycystic ovarian syndrome, and effect of bicalutamide on hirsutism, CRP levels and insulin resistance.

BACKGROUND/AIMS: Insulin resistance is associated with serum C-reactive protein (CRP) levels. We aimed to evaluate the effect of bicalutamide on insulin resistance and serum CRP levels in non-obese polycystic ovarian syndrome (PCOS) patients. METHODS: 40 non-obese patients (BMI < or =25 kg/m2) with PCOS and, 40 age- and BMI-matched healthy women were studied. Patients received bicalutamide orally at the dose of 25 mg/day. Serum CRP levels were measured with immunometric assay. Homeostasis model assessment (HOMA-IR) index was used for insulin resistance. RESULTS: Mean Ferriman-Gallwey score (FGS) (p = 0.001), insulin (p = 0.001), serum glucose (p = 0.001), prolactin (p < 0.003), total (p < 0.04) and free testosterone (p = 0.001) and free androgen index (FAI) levels (p = 0.001) of PCOS subjects were higher than in the control group. Mean HOMA-IR of PCOS patients was higher than in control subjects (2.43 +/- 1.2 and 0.94 +/- 0.37, p = 0.001). CRP levels in subjects with PCOS was also higher than in control subjects (4.27 +/- 1.33 and 0.98 +/- 0.19, p = 0.001). After bicalutamide treatment, FGS, free and total testosterone and FAI decreased (p = 0.001). HOMA-IR, prolactin and CRP levels did not show any statistical difference with bicalutamide treatment. CONCLUSIONS: PCOS patients had insulin resistance and a high CRP level. Bicalutamide treatment did not influence insulin resistance and CRP level in PCOS, and this ineffectiveness of bicalutamide on CRP levels may be the result of insulin resistance and/or high prolactin levels at this time.