Kerpauskas, Vilius

Nutukimas - viena aktualiausių dabartinės visuomenės problemų, neigiamai veikianti daugelį organizmo sistemų ir trikdanti sergančiojo šia liga gyvenimo kokybę, darbingumą bei trumpinanti gyvenimą. Tai - metaboliškai aktyvi ir recidyvuojanti liga, kurios metu kūno masė didėja riebalinio audinio sąskaita. Nutukimą kaip ligą Amerikos medicinos asociacija oficialiai pripažino 2013 metais. Nutukimas pastaruoju metu yra labiausiai aptarinėjama tema tiek medicinos, tiek plačiojoje visuomenėje. Kalbant apie nutukimą, dažnai ši būklė siejama su asmeniniu kaltės priskyrimu: „reikia tik noro“, „reikia suimti save į rankas“ ir t. t. Įvairiais istoriniais laikotarpiais požiūris į žmogaus kūno formas keitėsi nuo Rubenso tipo moterų iki anoreksinių mados manekenių formų. Menamų kūno formų standartų neatitinkantis žmogus gali būti pavadintas putliu, stambiu, apkūniu, didelio dydžio ar net storuliu ar apsileidusiu. Medicinos bendruomenėje vyrauja terminai: antsvoris, hipotalaminis, pilvinis, centrinio tipo, kušingoidinis, morbidinis nutukimas ir kt. Nutukimas turi kompleksines pasekmes - skatina lėtines ligas, galinčias sutrumpinti žmogaus amžių 10-15 metų. Per pastaruosius 5 dešimtmečius nutukimo paplitimas pasaulyje padidėjo daugiau nei 3 kartus, ir dabar tai įvardijama kaip nutukimo pandemija. Klinikinėje praktikoje nustatomos įvairiausios nutukimo priežastys - nuo genetinių (Prader-Willi sindromas, Aistrom sindromas, LEPR (leptino receptoriaus) ar LEP (leptino) geno mutacijos ir kt.), endokrininių (hipotirozė, hiperkorticizmas, hipogonadizmas ir kt.) iki valgymo priklausomybių. Skirtingos yra ir nutukusių kūno formos bei kūno kompozicija. Todėl kūno masės indeksas (KMI) klinikiniu požiūriu jau nebetenka prasmės. KMI tikslinga naudoti populiaciniams, palyginamiesiems tyrimams. Statistiniais duomenimis (HIS Lietuva, Eurostat, 2019-2022 m.), pagal KMI nutukusių suaugusių Lietuvoje buvo 21-23 proc. Skaičiuojama, kad apie 60 proc. suaugusiųjų Lietuvoje turi antsvorio ar yra nutukę. Tai - tik statistika, neatspindinti konkrečios individo būklės. 2025 m. pasaulio 58 ekspertų grupė, atstovaujanti įvairioms medicinos specialybėms ir šalims, išanalizavo turimus įrodymus ir, pritarus 75 medikų ir pacientų organizacijoms, rekomendavo klasifikaciją, kurioje išskiriamas ikiklinikinis ir klinikinis nutukimas. Pagal epidemiologinius ir klinikinius duomenis, nutukimas susijęs su daugiau nei 200 skirtingų ligų ir sveikatos sutrikimų. [...]

Gripas – dažna virusinė kvėpavimo takų infekcija, pasireiškianti karščiavimu, kosuliu, raumenų skausmu ir bendru silpnumu. Liga dažniausiai praeina savaime, tačiau rizikos grupėms gali sukelti komplikacijų. Diagnostika remiasi klinikiniais simptomais ir, jei reikia, laboratoriniais tyrimais. Gydymui taikomi antivirusiniai vaistai ir simptominis gydymas. Pagrindinė prevencijos priemonė – sezoninė vakcinacija.

Geležies stokos anemija (GSA) yra dažniausia anemijos forma visame pasaulyje, ypač paplitusi tarp vaisingo amžiaus moterų, vaikų ir vyresnio amžiaus žmonių. GSA išsivysto dėl nepakankamo geležies kiekio organizme, kuris lemia sumažėjusią hemoglobino gamybą ir sutrikusią deguonies pernašą į audinius. Pagrindinės GSA priežastys – nepakankamas geležies suvartojimas su maistu, sutrikęs jos pasisavinimas, padidėjęs poreikis arba geležies netekimas dėl kraujavimo. Klinikiniai simptomai įvairūs – nuo nuovargio ir dusulio iki pažinimo sutrikimų. Diagnozė nustatoma remiantis laboratoriniais tyrimais, tokiais kaip hemoglobino ir feritino koncentracijų nustatymas. Gydymui taikomi geležies preparatai, kurie gali būti skiriami per burną arba intraveniniu būdu, atsižvelgiant į deficito sunkumą ir preparatų toleravimą. Ankstyva diagnostika ir tinkamas gydymas yra būtini siekiant išvengti komplikacijų ir pagerinti paciento gyvenimo kokybę.

Introduction. Combined Pituitary Hormone Deficiency (CPHD) is a condition characterized by deficiency in growth hormone and at least one other pituitary hormone. Affecting 1 in 4,000 to 10,000 births, it may result from trauma, tumours, or genetics. In over 80% of cases, no genetic cause is identified. The most common genetic cause is pathogenic variants in the PROP1 gene, while pathogenic variants in the HESX1 gene may be the rarest. Nevertheless, we present three apparently unrelated patients with this variant. Case description. Three patients were diagnosed with CPHD: patients A (11 y.o. male), B (17 y.o. male) and C (13 y.o. female). Patients A and C were diagnosed in infancy, while patient B was diagnosed in 2021. Lab results for A and C showed deficiencies in somatotropin, adrenocorticotropin, thyrotropin, and gonadotropins, while patient B had low somatotropin, gonadotropins, and later thyrotropin. All patients showed pituitary hypoplasia on brain MRI. Patients A and C had hypoglycemia while B and C experienced prolonged jaundice. Patient A also had cryptorchidism and micropenis. Whole exome sequencing revealed homozygous pathogenic HESX1 gene variant NM_003865.3:c.326G>A, p.Arg109Gln in all three patients. Summary. HESX1 encodes a conserved homeobox protein that represses transcription in the developing forebrain and pituitary. HESX1-related CPHD causes growth hormone deficiency in all described patients in literature, along with additional hormonal deficiencies in about 50% and septo-optic dysplasia in 30%. Pituitary hypoplasia occurs in 80% of cases. In our cases, all patients have multiple hormonal deficiencies and pituitary hypoplasia, but no septo-optic dysplasia. As the condition is inherited in an autosomal recessive manner, genetic testing enables sibling screening and planning for future children, with a 25% chance of inheritance. Conclusion. Whole exome sequencing can identify the causes of CPHD, improving understanding of disease mechanisms and potentially improving future therapies.

Introduction. IgA nephropathy (IgAN) is a common cause of glomerulonephritis and kidney failure. Transplantation is the main treatment for progressive failure, but recurrence, both histologically and clinically, is common. For patients with rapidly progressing native kidney failure, recurrence often occurs early post-transplant. Case description. Our patient in 2010 at 14 years old presented with persistent proteinuria and hematuria, biopsy revealed IgAN. Renal function remained stable, condition was managed with AH medication under family physician supervision. No pathogenetic treatment was administered, the patient was not referred to a nephrologist until end stage CKD. In 2017.09 patients kidney function critically declined, biopsy revealed advanced IgAN. On 2018.04.30 patient received live donor (father) kidney transplant. Post transplant laboratory results showed impaired graft function. 2 months post transplant, biopsy revealed a relapse of IgAN. In 2021.08 patient was hospitalised due to exacerbation of chronic transplanted renal insufficiency, laboratory results showed significant decline in graft function. Biopsy showed mixed damage to the transplanted kidney - aggressive IgAN and humoral rejection. Immunosuppresive and human IgC treatment was administered. Further post transplant period was complicated by active CMV infection, secondary diabetes mellitus and ongoing transplant rejection. In 2023.02 hemodialysis was resumed. On 2023.11.23 patient was hospitalised for live donor (grandmother) kidney transplantation. Surgery was complicated by bleeding from ruptured kindey, kidney thrombosis and clotting in the renal vein, which lead to graft nephrectomy. In 12.04 arteriovenous fistula was formed. On 2024.11.20 patient received a cadaveric kidney transplant. Summary. This case highlights the complexities of IgAN in a young patient with recurrent disease and multiple transplant failures. Conclusions. Early and close management of IgAN is crucial to prevent disease progression to end-stage kidney failure. Recurrence post-transplant is common, requiring close monitoring to preserve graft function and improve long-term outcomes.

This case highlights a rare instance of severe anemia requiring multiple blood transfusions in a young male due to chronic, undiagnosed hemorrhoidal bleeding, despite thorough investigation ruling out other potential sources. A 28-year-old male construction worker presented with extreme fatigue and dizziness. Laboratory investigations revealed severe anemia with a hemoglobin level of 56 g/L. Multiple blood transfusions were administered to stabilize the patient, followed by a course of intravenous iron therapy. During hospitalization, a comprehensive diagnostic workup, including gastroscopy, colonoscopy, and abdominal ultrasound, was conducted to identify the source of bleeding. No gastrointestinal pathology was found; however, the presence of enlarged hemorrhoids was noted. Given the absence of other causes, hemorrhoidal bleeding was determined to be the likely source of chronic blood loss leading to transfusion dependent anemia. Chronic hemorrhoidal bleeding is a common condition but is rarely reported to cause severe anemia necessitating blood transfusion. The gradual nature of blood loss from hemorrhoids can lead to iron deficiency anemia, which may go undetected until it reaches a critical stage. This case underscores the importance of considering hemorrhoids as a potential cause of unexplained anemia, particularly when standard investigations fail to reveal an alternate source. While conservative treatments such as iron supplementation and dietary adjustments are typically effective for mild hemorrhoidal bleeding, cases with severe anemia may require more definitive interventions such as rubber band ligation, sclerotherapy, or even surgical hemorrhoidectomy. This case emphasizes the need for heightened awareness regarding chronic hemorrhoidal bleeding as a potential cause of severe anemia. In cases where routine investigations fail to identify a source of gastrointestinal bleeding, persistent hemorrhoidal disease should not be overlooked. Early recognition and appropriate management are crucial to preventing life threatening complications and reducing the need for recurrent transfusions.

This case highlights an uncommon extrapulmonary complication of Mycoplasma pneumoniae: acute pancreatitis. It underscores the importance of considering the systemic effects of respiratory infections. A 36-year-old previously healthy male presented with a five-day history of cough, fever, and malaise. A chest X-ray confirmed pneumonia, and he was started on antibiotics for atypical pneumonia. On the third day of hospitalization, he developed sudden, severe epigastric pain radiating to his back, accompanied by nausea and vomiting. On examination, he was febrile, tachycardic, and exhibited epigastric tenderness. Laboratory results showed significantly elevated amylase (432 U/L) and lipase (1,056 U/L), confirming acute pancreatitis. A CT scan demonstrated pancreatic edema but no gallstones or biliary obstruction. Serologic testing revealed elevated M. pneumoniae IgM antibodies, supporting a recent infection and its potential association with pancreatitis. The patient was managed conservatively with intravenous fluids, analgesia, and bowel rest. His condition gradually improved, and he was discharged in stable condition after seven days. Acute pancreatitis is a rare but recognized extrapulmonary manifestation of M. pneumoniae infection. The exact pathophysiology remains unclear, but proposed mechanisms include immune-mediated inflammation, direct bacterial invasion, and immune complex deposition in pancreatic tissue. This case highlights the need for clinicians to remain vigilant for atypical presentations in patients with M. pneumoniae infections. Early recognition of such complications can guide appropriate management and improve patient outcomes. This case underscores the potential for M. pneumoniae to cause extrapulmonary complications, including acute pancreatitis. Clinicians should consider this rare association in patients with M. pneumoniae who develop unexplained abdominal symptoms. Awareness of these complications is essential for timely diagnosis and effective management.

Cardiovascular disease (CVD) remains a leading cause of death worldwide, making early risk assessment crucial. Body Mass Index (BMI) has long been used as a primary indicator of obesity and cardiovascular risk. However, BMI doesn’t distinguish between fat and lean mass, which can reduce its effectiveness in assessing true health risk. Waist Circumference (WC), a measure of abdominal fat, is becoming recognized as a more accurate predictor of cardiovascular risk due to its link to visceral fat. This review compares BMI and WC in predicting cardiovascular risk based on recent studies. A systematic review was conducted following PRISMA guidelines. Studies published between 2014 and 2024 were retrieved from PubMed and Google Scholar. Keywords like “BMI and cardiovascular risk,” “waist circumference and cardiovascular disease,” and “obesity and heart disease” were used. After screening 253 articles, 37 studies met the criteria and were included in this review. This review aims to compare the effectiveness of BMI and WC in predicting cardiovascular risk, focusing on how each correlates with metabolic syndrome, hypertension, and other cardiovascular conditions. BMI has been a standard tool for assessing obesity, but it has its limitations. While it correlates with conditions like hypertension, diabetes, and hyperlipidemia, it doesn’t reflect how fat is distributed in the body. This can lead to misclassifications, especially for individuals with normal BMI but high abdominal fat. Waist Circumference, on the other hand, directly measures central obesity, which is strongly linked to metabolic syndrome and CVD. Studies show that WC is a stronger predictor of cardiovascular risk, especially for those with normal BMI but high WC. However, there are challenges, including inconsistent measurement methods and the need for population-specific thresholds. In summary, Waist Circumference offers a more accurate assessment of cardiovascular risk compared to BMI, particularly in those with normal BMI but high abdominal fat. Including WC alongside BMI in clinical practice could improve cardiovascular risk evaluation. Future research should focus on standardizing WC measurement and establishing population-specific thresholds for better clinical application.

Introduction Tuberculous meningoencephalitis (TBM) is a rare form of tuberculosis. Despite advances in diagnostics and treatment, TBM has a high mortality rate and requires timely intervention to reduce long term neurological complications [1,2]. This clinical case highlights the challenges of diagnosing and treating TBM, particularly in the context of drug resistance . Case Presentation An 18 year old male presented with fever, nausea, vomiting, dizziness and headache. Initial workup including cerebrospinal fluid (CSF) analysis and brain CT, was inconclusive. Since the cause of meningoencephalitis could not be determined, empirical treatment with acyclovir, ceftriaxone, and vancomycin was initiated. This treatment had no positive effect and the patient's neurological condition continued to deteriorate. Considering the family history, CSF analysis, clinical progression, and radiological imaging, treatment for tuberculous meningoencephalitis was initiated following the HRZE regimen with addition of dexamethasone. However, the patient's condition continued to deteriorate, eventually reaching a Glasgow Coma Scale score of 5. Therefore, despite negative results from GeneXpert MTB/RIF and AFB microscopy, the diagnosis of multi drug resistant tuberculosis was made based on family history. Subsequently, treatment following a a bedaquiline-levofloxacin-linezolid-clofazimine-terizidone (BdqLfx-Lzd-Cfz-Tzd) regimen was initiated. Following this treatment the patient improved significantly and soon regained consciousness. The clinical course was complicated by hydrocephalus requiring formation of an intraventricular drain and later a ventriculoperitoneal shunt was formed. The case was also complicated by bacterial and fungal sepsis. After 18 months of treatment, the patient was discharged in a stable condition with minimal residual effects. Discussion This case highlights the diagnostic challenges of TBM, when initial tests may be inconclusive. Advanced diagnostic tools like GeneXpert MTB/RIF are crucial for early detection, but drug-resistant tuberculosis can complicate diagnosis and treatment [2,3]. Conclusions Consider TBM in patients with meningitis, especially when initial treatments fail. Rapid diagnostics and aggressive treatment are vital for better prognosis.