We report a rare long-term case in which systemic polyarteritis nodosa (PAN) was ultimately diagnosed in adulthood after childhood-onset recurrent inflammatory disease with atypical Still-like features. A Japanese man had recurrent febrile episodes from infancy and was diagnosed with juvenile idiopathic arthritis at 9 years of age. In early adulthood, he developed recurrent fever, rash, polyarthralgia, splenomegaly, neutrophilia, and elevated inflammatory markers, and was considered to have Still-spectrum disease. However, ferritin elevation remained modest despite marked systemic inflammation, suggesting that the early phenotype may not have represented typical Still's disease and may instead have reflected a broader autoinflammatory process. At 25 years of age, he developed digital ischaemia with necrosis, palpable nodules, and erectile dysfunction. Angiography demonstrated narrowing of the ulnar and palmar arteries, and skin biopsy showed necrotising vasculitis involving medium-sized vessels, leading to the diagnosis of systemic PAN. He subsequently developed fever, rash, inner-ear involvement, hypertrophic pachymeningitis, and tortuosity/dilatation of a right intercostal artery. A subtle suspected lesion of the right testicular artery later became a definite enlarging aneurysmal lesion on serial imaging. Systemic inflammatory manifestations were subsequently controlled during treatment that included glucocorticoids, azathioprine, and tocilizumab. However, serial imaging demonstrated gradual enlargement of the right testicular artery aneurysmal lesion despite the absence of fever, rash, or C-reactive protein elevation for 5 years. This clinical course suggests that vascular progression may not always be adequately reflected by C-reactive protein levels during interleukin-6 blockade. This case illustrates the diagnostic difficulty of childhood-onset recurrent inflammatory disease with atypical Still-like features that was ultimately recognized as systemic PAN in adulthood. Occult or under-recognized medium-vessel vasculitis may have been present earlier in the disease course. Long-term diagnostic reappraisal, vascular imaging when indicated, and continued follow-up across paediatric and adult rheumatology care may therefore be important in similar patients, particularly in the current biologic era.

Acute paraplegia is a neurological emergency requiring prompt diagnosis to prevent irreversible neurological deficits and permanent disability. Although traumatic causes of acute paraplegia are well-characterized, non-traumatic acute paraplegia poses a diagnostic challenge because of its diverse etiologies. Leriche syndrome, also known as aortoiliac occlusive disease, typically presents with chronic lower-extremity claudication, diminished femoral pulses, and erectile dysfunction; however, it can rarely present with acute paraplegia and mimic a spinal cord emergency. We report the case of a 58-year-old woman with uncontrolled diabetes who presented to the emergency department with sudden-onset, non-traumatic flaccid paraplegia, accompanied by sensory loss below the level of L1 and urinary retention. Physical examination revealed cold bilateral lower extremities with absent bilateral femoral and distal pulses, raising suspicion for an acute vascular etiology. Computed tomography angiography revealed complete occlusion of the abdominal aorta and bilateral common iliac arteries at the L1-L2 level, consistent with acute Leriche syndrome. The patient was treated with intravenous heparin, followed by catheter-directed thrombolysis and aortic stent placement. Her motor function improved from 0/5 at admission to 3/5 at hospital discharge, with substantial neurological recovery during the three-month follow-up while undergoing physiotherapy. This case demonstrates that acute Leriche syndrome may present with acute paraplegia and mimic a spinal cord emergency. It highlights the critical importance of incorporating vascular assessment into the evaluation of non-traumatic acute paraplegia, as timely diagnosis and revascularization may improve neurological outcomes.

Diabetic autonomic neuropathy is a clinically important component of diabetic neuropathy involving the cardiovascular, gastrointestinal, genitourinary, sudomotor, pupillary, and glucose counterregulatory systems. Cardiovascular autonomic neuropathy (CAN) has been extensively studied and is clinically relevant because of its association with adverse cardiovascular and renal outcomes. Early CAN is frequently silent and may only be recognized by reduced heart rate variability or abnormal cardiovascular autonomic reflex testing. As CAN progresses, patients develop resting tachycardia, reduced exercise tolerance, orthostatic or postprandial hypotension, abnormal nocturnal blood pressure regulation, and perioperative hemodynamic instability. Non-cardiovascular manifestations include gastroparesis, bowel and bladder dysfunction, erectile dysfunction, sudomotor and pupillary abnormalities, and impaired hypoglycemic awareness. The underlying mechanisms involve chronic hyperglycemia, glycemic variability, dyslipidemia, insulin resistance, oxidative and mitochondrial stress, inflammation, microvascular injury, and impaired axon-glial support. Clinically, evaluation should begin with a systematic symptom review, neurological examination, supine and standing blood pressure measurements, and heart rate assessment, followed by organ-specific testing if indicated. Treatment was based on comprehensive risk factor control and symptom-directed management.

The use of glucagon-like peptide-1 receptor agonists (GLP1-RAs) and sodium-glucose cotransporter 2 inhibitors (SGLT2is) resulted in weight loss and long-term cardiovascular (CV) and renal safety preservation. Their role in male sexual hormones and behavior is still not sufficiently investigated. This paper aims at summarizing the effects of GLP1-RA and SGLT2i on obesity-associated hypogonadism and sexual dysfunctions. Both GLP1-RA and SGLT2i resulted in an improvement of body composition and metabolic profile, supporting erectile function amelioration. Only GLP1-RA showed a weight loss dependent increase in total and calculated free testosterone with lower effects on gonadotropin levels, while for SGLT2i, the data are contradictory. Finally, the use of testosterone replacement therapy showed better results as compared to GLP1-RA when orgasm and sexual satisfaction domains were investigated. In conclusion considering the beneficial effects of GLP1-RA on long-term CV mortality and morbidity, compared to the substantially neutral effects derived from the use of testosterone replacement therapy, we support the use of this class of medications for improving sexual dysfunction and its underlying CV problems in overweight and obese patients with erectile dysfunction.

Diabetes mellitus (DM) related erectile dysfunction (ED) is a common complication in males. We aim to explore the specific regulatory mechanisms of TEA domain family member 1 (TEAD1) in DMED rats. Diabetic ED in rats was induced by streptozotocin and evaluated by the intracavernosal pressure response to electrical stimulation and the apomorphine test. Corpus cavernosum smooth muscle cells (CCSMCs) were isolated to explore the role of TEAD1 in phenotypic transformation. TEAD1 knockdown was performed in DMED rats and CCSMCs using the CRISPR/Cas9 technology. Hematoxylin-Eosin and Masson staining were applied to observe the penile tissue pathology. The CCSMC function was evaluated by detecting viability and apoptosis. Protein and gene expression levels were examined by Western blot and real-time quantitative polymerase chain reaction. The TEAD1 gene knockdown ameliorated erectile function in DMED rats. Knockdown of TEAD1 in CCSMCs of DMED rats enhanced their viability and inhibited their apoptosis, promoting the transformation of CCSMCs from a synthetic to a contractile phenotype. Furthermore, bioinformatics analysis identified the calcium signaling pathway as a candidate pathway warranting further experimental investigation. TEAD1 knockdown was associated with altered expression of calcium-related proteins and elevated intracellular Ca[2+] levels. The calcium channel blocker Nimodipine could reverse the improvement of erectile function in DMED rats and the transformation of CCSMC phenotype caused by TEAD1 knockdown. TEAD1 knockdown promotes the transformation of CCSMCs from a synthetic to a contractile phenotype and is associated with modulation of calcium signaling-mediated contractile machinery, contributing to the relief of DMED.

New-onset sexual dysfunction in men, particularly erectile dysfunction, should not be regarded merely as an isolated sexual complaint. It may represent an early manifestation of endothelial dysfunction, atherosclerotic disease, diabetes mellitus type 2, obesity, arterial hypertension, dyslipidemia, hypogonadism, hyperprolactinemia, thyroid disorders, or adverse drug effects. The aim of this review is to summarize current evidence on the relationship between sexual dysfunction and cardiometabolic risk and to provide a practical outpatient approach for primary care, internal medicine, diabetology, urology, and sexual medicine. This narrative review is based mainly on the current European Association of Urology recommendations, the Princeton IV Consensus, and selected systematic reviews and meta-analyses. Particular attention is paid to focused history taking, physical examination, basic laboratory work-up, risk stratification, and the differential diagnosis of vasculogenic, endocrine, iatrogenic, and psychogenic causes. The review also incorporates the Czech clinical context and proposes a pragmatic referral framework for situations requiring further evaluation or specialist care.