Blaženka Miškić

Background/Objectives: BCR::ABL1-negative myeloproliferative neoplasms (MPNs), including essential thrombocythemia (ET), polycythemia vera (PV), and myelofibrosis (MF), are clonal hematopoietic stem cell disorders characterized by chronic systemic inflammation and elevated thrombotic risk. Osteoarthritis (OA), the most prevalent joint disease globally, is common in MPNs and shares a common proinflammatory cytokine milieu with MPNs. However, whether symptomatic OA may independently impact MPN-related symptom burden and thrombotic outcomes remains unexplored. Methods: In this prospective two-center study conducted in Croatia (2021–2023), 107 consecutive MPN patients diagnosed by 2016 World Health Organization criteria underwent orthopedic evaluation and completed the MPN Symptom Assessment Form (MPN-SAF) at enrolment. Symptomatic OA was defined as radiographic grade ≥1 (Kellgren–Lawrence) with concordant symptoms. Patients were subsequently followed for thrombotic events. Multiple linear regression and Cox proportional hazards regression were used for multivariable analyses. Results: Symptomatic OA was identified in 64 patients (59.8%). The total symptom score (TSS) was significantly higher in OA patients (p < 0.001), and in multivariable analysis, OA independently predicted higher TSS (β 10.12, 95% confidence interval-CI 5.38–14.86, p < 0.001), alongside female sex and arterial hypertension. Over a median follow-up of 44 months, 10 thrombotic events occurred. Patients with symptomatic OA had significantly worse time to thrombosis (hazard ratio-HR 3.61, 95% CI 1.02–12.8, p = 0.046). In multivariable Cox regression, OA remained associated with thrombosis (HR 15.55, p = 0.002), while female sex (HR 0.17, p = 0.042) and aspirin use (HR 0.15, p = 0.019) were protective. Conclusions: Symptomatic OA may be associated with higher symptom burden and, in this preliminary analysis, with higher thrombotic risk in MPNs. These findings support systematic OA evaluation in MPNs and multidisciplinary management strategies targeting this frequent and burdensome comorbidity.

Background: Nearly 10% of all community-acquired pneumonias are caused by Chlamydia pneumoniae. This is a Gram-negative intracellular coccus that poses a significant challenge for routine diagnostics due to its poor growth in tissue culture and non-specific clinical presentations. Case Report: This study presents the case of a 61-year-old man whose initial disease manifestation included a non-specific upper respiratory tract infection and reactive pericarditis. A diagnostic work-up of the etiology of pericarditis, with stepwise exclusion of other causative agents, led to confirmation of a possible chronic, recurrent C. pneumoniae infection, with good clinical and laboratory responses to azithromycin across multiple hospitalizations. However, upon initiation of prolonged doxycycline therapy, the disease course was complicated by the development of Guillain–Barré syndrome. With appropriate treatment, the neurological deficit regressed, with near-complete resolution of the syndrome’s clinical picture. Discussion and Conclusions: The development of reactive pericarditis and the patient’s neurological symptoms stemmed from an immune response to bacterial antigens that resemble antigens of the central nervous system and the pericardium. Prolonged doxycycline therapy, together with symptomatic management of the neurological condition and concomitant pericarditis, represents good clinical practice and is one potential management approach for patients with similar presentations.

Given in reperfusion, the use of stable gastric pentadecapeptide BPC 157 is an effective therapy in rats. It strongly counteracted, as a whole, decompression/reperfusion-induced occlusion/occlusion-like syndrome following the worst circumstances of acute abdominal compartment and intra-abdominal hypertension, grade III and grade IV, as well as compression/ischemia-occlusion/occlusion-like syndrome. Before decompression (calvariectomy, laparotomy), rats had long-lasting severe intra-abdominal hypertension, grade III (25 mmHg/60 min) (i) and grade IV (30 mmHg/30 min; 40 mmHg/30 min) (ii/iii), and severe occlusion/occlusion-like syndrome. Further worsening was caused by reperfusion for 60 min (i) or 30 min (ii/iii). Severe vascular and multiorgan failure (brain, heart, liver, kidney, and gastrointestinal lesions), widespread thrombosis (peripherally and centrally) severe arrhythmias, intracranial (superior sagittal sinus) hypertension, portal and caval hypertension, and aortal hypotension were aggravated. Contrarily, BPC 157 therapy (10 µg/kg, 10 ng/kg sc) given at 3 min reperfusion times eliminated/attenuated venous hypertension (intracranial (superior sagittal sinus), portal, and caval) and aortal hypotension and counteracted the increases in organ lesions and malondialdehyde values (blood ˃ heart, lungs, liver, kidney ˃ brain, gastrointestinal tract). Vascular recovery promptly occurred (i.e., congested inferior caval and superior mesenteric veins reversed to the normal vessel presentation, the collapsed azygos vein reversed to a fully functioning state, the inferior caval vein–superior caval vein shunt was recovered, and direct blood delivery returned). BPC 157 therapy almost annihilated thrombosis and hemorrhage (i.e., intracerebral hemorrhage) as proof of the counteracted general stasis and Virchow triad circumstances and reorganized blood flow. In conclusion, decompression/reperfusion-induced occlusion/occlusion-like syndrome counteracted by BPC 157 therapy in rats is likely for translation in patients. It is noteworthy that by rapidly counteracting the reperfusion course, it also reverses previous ischemia-course lesions, thus inducing complete recovery.