Is leptin associated with hypertensive retinopathy?

Previous studies have demonstrated that elevated plasma leptin concentrations are associated with essential hypertension. It has also recently been shown that leptin plays a promoting role in angiogenesis, and the vascular endothelium expresses the long form of leptin receptor. Those data led us to hypothesize that leptin might contribute to end-organ damage in hypertension. Thus, in the present study we evaluated the relationship between plasma leptin concentrations and hypertensive retinopathy (HR). One hundred and eleven patients newly diagnosed with essential hypertension [EHT; mean age, 43.5 +/-10.7 yr; body mass index (BMI), 28.1 +/- 4.4 kg/m2; male/female ratio, 71/40] and 79 healthy normotensive control subjects (NT; mean age, 43.6 +/- 9.2 yr; BMI, 28.2 +/- 3.3 kg/m2; male/female ratio, 50/29) were enrolled in the study. For the assessment of retinopathy according to the Keith-Wagener classification, direct and indirect ophthalmoscopy were performed in all subjects after dilatation of the pupils. Plasma leptin levels were significantly higher in EHT (11.8 +/- 11.1 ng/mL) than in NT (7.2 +/- 5.1 ng/mL) (P = 0.003). Plasma leptin concentrations were strongly correlated with BMI in both EHT (r = 0.45; P = 0.001) and NT (r = 0.38; P = 0.001) groups. Plasma leptin in patients with grade 2 HR (24.8 +/- 15.8 ng/mL; n = 22) was significantly higher than that in patients with grade 1 HR (16.1 +/- 4.9 ng/mL; n = 29; P = 0.001), grade 0 HR (5.1 +/- 3.1 ng/mL; n = 60; P = 0.001), and NT (P = 0.001). Plasma leptin in patients with grade 1 HR was also significantly higher than that in patients without retinopathy (P = 0.001) or in NT (P = 0.001). The estimated threshold of plasma leptin concentration for HR was 10.2 ng/mL. This critical leptin level served largely to separate patients with retinopathy from those without retinopathy. In summary, our results show that plasma leptin concentrations increase progressively with higher grades of hypertensive retinopathy even after correction for BMI, suggesting that a critical leptin level is needed for the development of retinopathy. Elevated concentrations of plasma leptin might be secondary to release of leptin by the vascular endothelium damaged by high blood pressure, as an epiphenomenon. However, a pathogenic role for leptin in hypertensive retinopathy cannot be excluded.

Inhibition of inducible nitric oxide synthase reduces bacterial translocation in a rat model of acute pancreatitis.

INTRODUCTION: Translocation of bacteria from the gut into pancreatic necrosis is an important factor in the development of septic complications and mortality in acute pancreatitis. S-methylisothiourea (SMT) is an inducible nitric oxide synthase inhibitor that has been shown to decrease bacteria] translocation in sepsis and thermal injury. AIM: To investigate whether SMT could affect bacterial translocation in acute necrotizing pancreatitis. METHODOLOGY: Forty-five Sprague-Dawley rats were studied. Acute pancreatitis was induced in Group I and Group II by injection of taurocholate and trypsin into the common biliopancreatic duct. Group III underwent laparotomy with the manipulation (but not cannulation) of the pancreas and received saline injection. Group I rats received normal saline as a placebo, and Group II rats received SMT after surgery for 2 days. At 48 hours, blood was drawn for serum amylase determinations. Bacterial translocation to mesenteric lymph nodes and distant sites (pancreas, liver, and peritoneum) were examined. A point scoring system of histologic features was used to evaluate the severity of pancreatitis. RESULTS: Plasma amylase levels and pancreatic histologic score were significantly reduced in Group II rats given SMT compared with those in Group I rats given saline (p < 0.01, p < 0.05, respectively). All Group I rats had bacterial translocation to mesenteric lymph nodes compared with 7 of 12 rats in Group II (p < 0.05). There was no difference in bacterial translocation to distant organs between the two groups, although rates tended to be lower in Group II compared with Group I (p > 0.05). Bacterial counts in the pancreas were significantly reduced in Group II rats compared with those in Group I rats (p < 0.05). CONCLUSION: Treatment with SMT appears to have ameliorated the course of acute pancreatitis; however, mortality was not affected.

Fulminant hepatic failure as the initial manifestation of primary hepatocellular carcinoma.

A 20-year-old male, with no history of chronic liver disease, presented with fulminant hepatic failure. The cause was not established until post mortem when it was found that he had a primary hepatocellular carcinoma in a non-cirrhotic liver. To our knowledge, this is the third report of hepatocellular carcinoma presenting in this manner. Although rare, primary malignancies of the liver should be considered in the differential diagnosis of fulminant hepatic failure, especially when other more common causes are excluded.

CA-125; a new marker for diagnosis and follow-up of patients with tuberculous peritonitis.

BACKGROUND: Most malignancies with peritoneal infiltration, especially ovarian cancers and chronic liver diseases associated with ascites give rise to high serum CA-125 levels. Tuberculous peritonitis is another cause for high serum CA-125 levels. AIM: To investigate the relation between serum CA-125 level and response to treatment in tuberculous peritonitis patients. PATIENTS: Ten patients with tuberculous peritonitis were enrolled in the study. METHOD: Definite diagnosis of tuberculous peritonitis was made by acid-fast smears, specific culture, and polymerase chain reaction. Serum CA-125 levels were measured before and at the fourth month of treatment. RESULTS: Before antituberculous treatment, serum CA-125 levels of all patients were very high (mean+/-SD: 475. 80+/-106. 19 U/ml) and comparable with those of patients with ovarian cancers. At the end of the fourth month of treatment, serum CA-125 levels in all patients decreased to within normal limits (<35 U/ml)(20.80:+/-5.18 U/ml) in parallel with the clinical improvement. The differences in CA125 levels before and after treatment were statistically significant (p<0.001). CONCLUSIONS: Results of our study suggest that serum CA-125 levels in patients with tuberculous peritonitis are as high as ovarian cancers associated with peritoneal infiltration. By the end of the fourth month of antituberculous therapy, serum CA-125 levels have returned to normal. We, therefore, suggest that serum CA-125 can be used to evaluate the efficacy of therapy in tuberculous peritonitis.

Insulin resistance in non-alcoholic steatohepatitis.

BACKGROUND: Non-alcoholic steatohepatitis is a chronic liver disease that is capable of progressing to end-stage liver disease, but generally has a benign course. Obesity, non-insulin-dependent diabetes mellitus and hyperlipidaemia are the most common associations of the disease. AIMS: To investigate the insulin resistance in patients with non-alcoholic steatohepatitis who have no other causes of insulin resistance such as obesity, diabetes mellitus, and hyperlipidaemia. PATIENTS: Thirteen patients (7 male, 6 female) with non-alcoholic steatohepatitis and 12 (6 male, 6 female) healthy volunteers. METHODS: All patients and healthy volunteers were submitted to biochemical tests and hyperinsulinaemic euglycaemic insulin clamp technique. RESULTS: Basal insulin levels and C-peptide levels were significantly higher in non-alcoholic steatohepatitis group than in controls (p<0.001 and p<0.001, respectively). Hyperinsulinaemic euglycaemic insulin clamp technique revealed lower glucose utilization in the non-alcoholic steatohepatitis group and the difference was statistically significant (p<0.001). CONCLUSIONS: Our study revealed marked hyperinsulinaemia and insulin resistance in patients with non-alcoholic steatohepatitis. Hyperinsulinaemia and insulin resistance may contribute to pathogenesis of nonalcoholic steatohepatitis.

Effects of losartan treatment on T-cell activities and plasma leptin concentrations in primary hypertension.

Recent evidence shows that leptin may contribute to elevated blood pressure (BP) and interact with the renin-angiotensin-aldosterone and cellular immune systems. Altered T-cell activities and changes in T-cell subset ratios have also been reported in hypertension. However, little is known about the effects of AT1-receptor antagonism on T-cell activities and plasma leptin concentrations in primary hypertension. We have, therefore, investigated the relationship between leptin and T-cell activities and the effect of an AT1-receptor antagonist, losartan, in primary hypertension. Twenty recently-diagnosed and untreated young adults (11 males and 9 females, age; 39.9+/-7.6 years, range 23-49 years, BMI; 27.6+/-3.7kg/m2) and 20 normotensive healthy, age-, sex- and BMI-matched controls were studied. The [3H]-thymidine uptakes of cultured lymphocytes were determined, both spontaneously and after stimulation with phytohaemagglutinin. The tests were performed before and after three months of treatment with losartan. The results indicate that the blastogenic responses of T-cells to phytohaemagglutinin are significantly higher in the patient group compared with controls (p=0.02). After normalisation of BP, T-cell responses were significantly reduced and were lower than in the controls (p=0.01). Pretreatment plasma leptin levels were significantly higher in hypertensives than in controls (p=0.01). However, losartan treatment had no significant effect on leptin concentrations; moreover, no correlation between leptin levels and T-cell activity was found. Our data show that plasma leptin levels and T-cell activity are markedly enhanced in untreated essential hypertension and that the alteration of T-cell activity is not related to plasma leptin levels. Antihypertensive treatment with losartan decreases T-cell activities but does not influence plasma leptin levels. We conclude that leptin levels are not affected by AT1-receptor blockade and are not related to T-cell activity.

Erythropoietic protoporphyria with antinuclear antibody positivity: avoiding misdiagnosis of systemic lupus erythematosus.

A young eunuchoid man was referred to our hospital with suspected erythropoietic protoporphyria. Serum antinuclear antibody (ANA) was found to be positive immediately after the porphyria attack and disappeared 30 days later. Many authors have mentioned the coexistence of systemic lupus erythematosus (SLE) and porphyria. As these two disorders have similar clinical features, the clinician must be alert and use strict diagnostic criteria in determining the presence of SLE with porphyria. In the past, elevation of ANA was reported in the cases of acute intermittent porphyria. However, there have been no reports in the cases of erythropoietic protoporphyria. In addition, the patient was found to have hypogonadotropic hypogonadism consistent with Kallmann's syndrome. To our knowledge, this report is the first case showing the coexistence of Kallmann's syndrome and erythropoietic protoporphyria. As yet, the clinical importance of this association remains unknown.

[Lyme disease]. / Lyme hastaligi.

Lyme disease, which is caused by the tick-borne spirochete Borrelia burgdorferi, usually begins with a characteristic skin lesion erythema chronicum migrans (ECM), that may be followed by neurological or cardiac abnormalities and is accompanied by malaise, fatigue, fever, myalgia, headache, lymphadenopathy and is often followed by arthritis. The disease takes its name from Lyme, Connecticut, where the full spectrum of illness was first described in 1975. It is known to be a multisystemic infectious disease. Because culture and direct visualisation of spirochetes are often negative in Lyme disease, serological testing has been the only practical laboratory aid in diagnosis and primarily clinical findings.

[Viral encephalitis]. / Viral ansefalitler.

Acute viral and other infectious causes of encephalitis usually produce fever, headache, stiff neck and alterations in consciousness, focal neurologic signs and seizures. A large number of viral and nonviral agents can cause encephalitis. Arthropod-borne viruses peak in summer, the tick-borne infections occur in early summer, enterovirus infections in later summer and mumps in the winter and spring.

[HIV infections among Turkish citizens who have lived in foreign countries]. / Yurt disinda yasayan vatandaslarimizin HIV enfeksiyonu yönünden incelenmesi.

AIDS or HIV infection, since 1981 when the first description was made because of showing epidemic characteristics, present increasing in number of patients, go along with high mortality, the disease become an event not only medically but also for any parts of the society. There is a danger of AIDS in risky groups and also danger of spreading by those persons. Among the 10985 Turkish citizens who came Turkey from foreign countries to fulfill military duty, antibody research against HIV was made and one positive anti-HIV case was observed.

[Botulism: a case report]. / Botulizm: bir olgu raporu.

Botulism is an acute form of poisoning that results from ingestion of a toxin produced by Clostridium botulinum. Botulism toxin causes their major effect by blocking neuromuscular transmission in autonomic and motor nerve terminals. Guillain Barre Syndrome, Myasthenia Graves, Lambert Eaton Myasthenic Syndrome, acute poliomyelitis and diphtheria must be considered in the differential diagnosis. Electrodiagnostic studies have been shown to be of value in differentiating botulism from other paralytic diseases. Identification of the toxin in the patients serum is diagnostic. The treatment of botulism is mainly supportive. In this study we have discussed a patient who was treated in our clinic as a botulism from unknown source, the differential diagnosis from other paralytic diseases.

Plasma leptin levels strongly correlate with plasma renin activity in patients with essential hypertension.

Previous studies demonstrated elevated plasma leptin and angiotensinogen (PRA) levels in essential hypertension. However, a few studies investigated the relationship between leptin and angiotensinogen levels in both lean and overweight/ obese hypertensives. The aim of the present study was therefore to examine the relationship between blood pressure, leptin and plasma renin activity in normotensives and in both lean and overweight/obese patients with essential hypertension. Two groups of subjects who were carefully matched for age, gender, waist:hip ratio and body mass index (BMI) were studied: 28 normotensives (NT) (age: 40.1+/-9.1 years old, BMI: 28.1+/-3.6 kg/m2, male/female: 18/10) and 33 newly diagnosed mild to moderate essential hypertensives (EHT) (age: 38.9+/-10 years old, BMI: 27.9+/-4.8 kg/m2, male/female: 22/11). No significant differences in age, gender, waist:hip ratio, fasting blood glucose and BMI were detected between EHT and NT groups. However, systolic and diastolic pressures, mean arterial blood pressures, plasma leptin levels and PRA were significantly higher in EHT group than in NT group (P = 0.001). Plasma leptin levels were strongly correlated with BMI in EHT (r=0.67, P = 0.001) and NT groups (r=0.44, P = 0.001). Plasma leptin levels were correlated with plasma PRA levels in both EHT and NT groups (r = 0.66 and r = 0.44; both P < 0.05, respectively). There was no correlation between leptin or PRA and systolic, diastolic pressures, or mean arterial blood pressures. Furthermore, the patients were divided as lean (n=16) and overweight/obese (n = 17) and compared with BMI-matched controls. In both subgroups, plasma leptin and PRA levels were also higher than those of controls. Our results showed that elevated plasma leptin and PRA are associated with hypertension in both lean and overweight/obese hypertensives. Moreover, plasma leptin was significantly correlated with plasma angiotensinogen levels. These findings suggest that adipose mass is an important determinant of blood pressure, although the mechanism is not clear.