A case of thrombocytopenia developing during the course of haemophilius influenza pneumonia

Sistemik infeksiyöz hastalıkların seyri sırasında trombositopeni gelişimi oluşabilir.Hemofilus influenza'ya bağlı solunum yolu enfeksiyonu seyrinde trombositopeni gelişimi rapor edilmemiştir. Burada Hemofilus influenza pnömonisi seyrinde gözlenen ve pnömoni için uygulanan antibiyotik tedavisine cevap veren trombositopenili bir olgusunulmaktadır.Thrombocytopenia may develop during the course of systemic infection. Thrombocytopenia development has not been reported in course of respiratory infections due to Haemophilius influenza. We present a case of thrombocytopenia seen in course of Haemophilius influenza pneumonia and its respond to the antibiotic treatment of pneumonia

The prevalance of thyroid autoantibodies in patients with rheumatoid arthritis

Giriş: Romatoid artrit (RA) toplumun yaklaşık %1'ini etkileyen inflamatuar karakterde sistemik otoimmün bir hastalıktır ve genellikle sistemik otoimmün hastalıklarla organa özgü otoimmün hastalıkların bir arada görülme sıklığının az olduğu kabul edilir. Biz çalışmamızda RA'li hastalarda, organa özgü otoimmün hastalıkların en sık görülenlerindenbiri olanotoimmün tiroid hastalığı varlığını ve tiroidotoantikor sıklığını belirlemeyi amaçladık. Materyal ve Metod: Çalışmaya 1987 ARA sınıflama kriterlerine göre RAtanısı konulan ve yaş ortalaması 484 olan, 82 aktif hasta (67 kadınve 15 erkek) kabul edildi.Kontrol grubuolarak 31 kadın ve 16 erkek olmak üzere 47 sağlıklı birey çalışmaya dahil edildi. Hasta ve kontrol grubunda serbest tiroksin (sT4), serbest triiodotironin (sT3), tirotropin(TSH), anti-tiroglobulin antikoru (Anti-T) ve anti-peroksidaz antikor (anti-TPO) bakıldı ve iki gruparasında sonuçlar karşılaştırıldı. Sonuçlar: Serum tiroid otoantikor seviyeleri RA'li hasta grubunda anti-TPO:85.69±106.83 IU/ml ve anti- TG:58.2±83.9 IU/ml olarak bulunurken, kontrol grubunda anti-TPO:43.16± 132.23 IU/ml ve anti- TG:24.19±36.74 IU/ml olarak bulundu. İki grup arasında tiroid otoantikorlarının serum seviyeleri arasında istatiksel olarak anlamlı fark saptandı (sırasıyla p=0.008 ve p=0.0004). Tiroid hormon seviyeleri (sT3, sT4 ve TSH) açısından2 gruparasında istatistiksel farkyoktu(p>0.05). Tartışma: Burada elde edilen bulgulara göre RA'li hastalarda otoimmün tiroid hastalığının sıklığı normal populasyona göre daha sıktır. Bu da sistemik veya organa özgü olduğuna bakmaksızın, otoimmün hastalıklarda immün yanıtın tümden etkilendiğini düşündürmektedir. RA'li hastalarda başta otoimmün tiroid hastalığı olmak üzere diğer organa özgüotoimmün hastalıkların gelişimi açısından da dikkatli olunmalıdır.Background: Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disorder that affectsapproximately 0.5-1% of the population and according to general opinion the frequency of systemic autoimmune disorders to be seen together with organ specific autoimmune disorders is not very common. The aim of this study was to evaluate the thyroid functions and thyroid autoantibodies in patients with RA and to determine the frequency of autoimmune thyroid disorders in these patients. Materyal and Method: 82 active patients (67 females and 15 males) witha diagnosis of RA according to 1987 ARA classification criteria were included in the study. 47 healthy individuals (31 females and 16 males) were included in the study as the control group. In all participants free thyroxine (fT4), free triiodothyronine (fT3), thyrotropin (TSH), thyroglobulin antibody (anti-Tg) and anti-peroxidase (anti-TPO) antibody titres were measured. Results of the RApatients were compared with the controls. Results: In the RAgroup thyroid autoantibody values were as follows: anti-TPO 85.69±106.83 IU/ml and anti-Tg 58.2±83.9 IU/ml. These values were: anti-TPO 43.16±132.23 IU/ml and anti-Tg 24.19±36.74 IU/ml in the control group. There was a statistically significant difference between two groups with regards to thyroid autoantibodies (p=0.008, p=0.0004, respectively). There was not any statistically significant difference between two groups with regards to fT3, fT4 and TSH values (p > 0.05). Conclusion: As there was not an apperent finding specific for a thyroid disorder in patients with RA in our study, the thyroid antibody positivity identified here might be due to a pathologic autoimmune response rather than demonstrating a thyroid disease.Thyroid function and TPO Ab tests should be performed as part of the biochemical and immunological profile in RApatients

A reason for high liver function test results: celiac disease

Çölyak hastalığı (ÇH) çevresel faktörün (gliadin) oluşturduğu bilinen tek otoimmun bozukluktur. Son yıllarda olguların %40'ında transaminaz yüksekliklerinin görülebileceği bildirilmektedir. On yedi yasında bayan olgu 5 yıldır olan halsizliğinin son 6 aydır artması şikayeti ile başvurdu. Diyare ve dispeptik yakınmalar tariflemiyordu. Muayene, solukluk dışında normaldi. ALP: 1026 IU/L (kemik kaynaklı),AST: 50 IU/L,ALT: 71 IU/L, GGT: 52 IU/L, total bilirubin 1.93 mg/dL, direkt bilirubin 1,34 mg/dL, Anti HBs, HBsAg, Anti HCV, HAV Ig M negatif, hemoglobin: 7.7 gr/dl, ferritin: 2.92 ng/ml idi. Magnetik rezonans görüntüleme ile kolanjiopankreotikografisi normal, DEXA vertebral ölçümde T skoru: -5, Z skoru: -4.7 idi. Endomisial antikor (EMA) Ig A, anti Gliadin antikor IgA>200 RU/ml (>50 pozitif) veAnti-Gliadin antikor IgG 61.5 RU/ml pozitifti. Karaciğer biyopsisisinde parankimde fokal spoty nekroz ve kolestaz bulguları vardı. Endoskopik duodenal biyosisinde villuslarda atrofi, yüzey epitelyimunda yoğun intraepitelyal lenfosit varlığı, immunhisto kimyasal boyamada intraepitelyal lenfositlerin CD3 ve CD8 ile diffüz boyandıgı, CD4 ve CD20 ile az sayıda lenfositin pozitif boyandığı gözlendi. Bulgular ÇH modifiye Marsh klasifikasyonuna göre Tip 3B ile uyumluydu. Olguya biyopsi ve antikor değerlendirmesi ile ÇH tanısı kondu. Glutensiz diyet başlandı. Tedavinin birinci ayında ALP (büyüme çağında olgu) yüksekliği dışında AST,ALT, GGT, bilirubin değerleri normal sınırlarda saptandı. Sonuç olarak karaciğer fonksiyon testi yüksekliğinin ayırıcı tanısında diyare olmasa da ÇH düşünülmelidir.Celiac disease (CD) is the only autoimmune disorder caused by an environmental factor (gliadin). Recently it has been reported that transaminase increase was seen in 40% of the cases.A17 years old female patient was admitted for increased weakness in the last 6 months, which she has been complaining for 5 years. She didn't have diarrhea or dyspepsia. Except paleness, her examination was normal. Biochemical test results were as follows;ALP:1026 IU/L (originating from bone), AST:50 IU/L, ALT:71 IU/L, GGT:52 IU/L, total bilirubin: 1.93mg/L, direct bilirubin:1.34 mg/dL, Anti-HBs, HbsAg,Anti HCV,HAVIgM were negative, hemoglobin: 7.7g/dL, and ferritin: 2.92 ng/ml. Cholangiopancreaticography with magnetic resonance imaging was resulted normal. In DEXA, vertebral measurement T score was -5 and Z score was -4.7. Endomysial autoantibody (EMA) IgA, anti gliadin antibody IgA>200 RU/ml (>50 positive), and anti gliadin antibody IgG 61.5 RU/ml were positive. Liver biopsy showed focal spotty necrosis and cholestasis in parenchyma. Endoscopic duodenal biopsy showed villous atrophy, intense intraepithelial lymphocytes in surface epithelium. Intraepithelial lymphocytes were dyed diffusely with CD3 and CD8 in immunohistochemical staining but few were dyed positively with CD4 and CD20. Findings were in agreement with type 3B according to modified Marsh classification for CD. She was diagnosed with CD according to biopsy and antibody evaluation.Agluten free diet was started. In the first month of treatment except ALP increase (she was in puberty), AST, ALT, GGT, bilirubin values were normal. In conclusion, even if no diarrhea,CDmust be thought in differential diagnosis of increased liver function tests

Combined metabolic activators improve metabolic functions in the animal models of neurodegenerative diseases

Background: Neurodegenerative diseases (NDDs), including Alzheimer's disease (AD) and Parkinson's disease (PD), are associated with metabolic abnormalities. Integrative analysis of human clinical data and animal studies have contributed to a better understanding of the molecular and cellular pathways involved in the progression of NDDs. Previously, we have reported that the combined metabolic activators (CMA), which include the precursors of nicotinamide adenine dinucleotide and glutathione can be utilized to alleviate metabolic disorders by activating mitochondrial metabolism. Methods: We first analysed the brain transcriptomics data from AD patients and controls using a brain-specific genome-scale metabolic model (GEM). Then, we investigated the effect of CMA administration in animal models of AD and PD. We evaluated pathological and immunohistochemical findings of brain and liver tissues. Moreover, PD rats were tested for locomotor activity and apomorphine-induced rotation. Findings: Analysis of transcriptomics data with GEM revealed that mitochondrial dysfunction is involved in the underlying molecular pathways of AD. In animal models of AD and PD, we showed significant damage in the high-fat diet groups' brain and liver tissues compared to the chow diet. The histological analyses revealed that hyperemia, degeneration and necrosis in neurons were improved by CMA administration in both AD and PD animal models. These findings were supported by immunohistochemical evidence of decreased immunoreactivity in neurons. In parallel to the improvement in the brain, we also observed dramatic metabolic improvement in the liver tissue. CMA administration also showed a beneficial effect on behavioural functions in PD rats. Interpretation: Overall, we showed that CMA administration significantly improved behavioural scores in parallel with the neurohistological outcomes in the AD and PD animal models and is a promising treatment for improving the metabolic parameters and brain functions in NDDs.PoLiMeR Innovative Training Network ; SNIC ; ScandiBio Therapeutics ; ScandiBio Therapeutics and Knut ; Knut och Alice Wallenbergs Stiftels

Combined metabolic activators improve cognitive functions in Alzheimer's disease patients: A randomised, double-blinded, placebo-controlled phase-II trial

Background: Alzheimer’s disease (AD) is associated with metabolic abnormalities linked to critical elements of neurodegeneration. We recently administered combined metabolic activators (CMA) to the AD rat model and observed that CMA improves the AD-associated histological parameters in the animals. CMA promotes mitochondrial fatty acid uptake from the cytosol, facilitates fatty acid oxidation in the mitochondria, and alleviates oxidative stress. Methods: Here, we designed a randomised, double-blinded, placebo-controlled phase-II clinical trial and studied the effect of CMA administration on the global metabolism of AD patients. One-dose CMA included 12.35 g L-serine (61.75%), 1 g nicotinamide riboside (5%), 2.55 g N-acetyl-L-cysteine (12.75%), and 3.73 g L-carnitine tartrate (18.65%). AD patients received one dose of CMA or placebo daily during the first 28 days and twice daily between day 28 and day 84. The primary endpoint was the difference in the cognitive function and daily living activity scores between the placebo and the treatment arms. The secondary aim of this study was to evaluate the safety and tolerability of CMA. A comprehensive plasma metabolome and proteome analysis was also performed to evaluate the efficacy of the CMA in AD patients. Results: We showed a significant decrease of AD Assessment Scale-cognitive subscale (ADAS-Cog) score on day 84 vs day 0 (P = 0.00001, 29% improvement) in the CMA group. Moreover, there was a significant decline (P = 0.0073) in ADAS-Cog scores (improvement of cognitive functions) in the CMA compared to the placebo group in patients with higher ADAS-Cog scores. Improved cognitive functions in AD patients were supported by the relevant alterations in the hippocampal volumes and cortical thickness based on imaging analysis. Moreover, the plasma levels of proteins and metabolites associated with NAD + and glutathione metabolism were significantly improved after CMA treatment. Conclusion: Our results indicate that treatment of AD patients with CMA can lead to enhanced cognitive functions and improved clinical parameters associated with phenomics, metabolomics, proteomics and imaging analysis. Trial registration ClinicalTrials.gov NCT04044131 Registered 17 July 2019, https://clinicaltrials.gov/ct2/show/NCT04044131

ÜRİNER OBSTRÜKSİYONLARIN DOKU SERBEST OKSİJEN RADİKALLERİNE ETKİLERİ

Üriner obstrüksiyonların ortadan kaldırılmasının takiben serum serbest oksijen radikallerindeki artış, çeşitli çalışmalarla saptanmıştır

Karaciğer kist hidatik olgularımız (Yazarın yanıtı)

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