Paraphenylenediamine (PPD), the principal ingredient of oxidative hair dyes, is a growing cause of acute poisoning in developing nations. This paper provides a comprehensive overview of published case reports, observational studies of PPD poisoning, clinical manifestations, current management strategies, analytical methods for PPD detection, and offers key clinical and post-mortem toxicology considerations. A literature search related to PPD poisoning was conducted from 1991 to 2025 across PubMed, Scopus, Web of Science, and Google Scholar. Publications encompassing 6,843 individual cases were reviewed, and data on demographics, dose, route, clinical features, laboratory parameters, treatment modalities, outcomes, and analytical approaches were analyzed. Angioedema, rhabdomyolysis, and acute renal failure form a characteristic clinical triad that is almost universal in moderate-to-severe cases, with mortality rates ranging up to 55.5% in hospital cases. Cardiac and hepatic injury are also common. PPD has no specific antidote, and treatment is completely supportive. Analytical methods ranging from colorimetric screening to confirmatory tandem mass spectrometry for PPD detection in biological and non-biological matrices are discussed. This review strongly suggests that PPD poisoning represents a significant public health concern in the developing world. Young women with low socioeconomic and rural backgrounds predominantly ingested PPD with suicidal intent. The highest fatality rates were observed in cases where treatment was delayed due to late diagnosis, primarily because no point-of-care test is currently available for the rapid detection of PPD. The combination of lethality, availability, and accessibility makes PPD an ideal agent for suicidal poisoning in populations with high rates of impulsive suicidal behavior. Early diagnosis can improve survival rates in PPD poisoning cases.

Drug-induced lupus erythematosus is an autoimmune condition that resembles systemic lupus erythematosus and occurs after exposure to specific medications, including tumor necrosis factor alpha inhibitors. We report a rare case of golimumab-induced lupus erythematosus complicated by macrophage activation syndrome, angioedema, and severe dysphagia with anti-galactocerebroside antibodies detected. A 57-year-old woman with ulcerative colitis developed facial swelling, malar rash, arthritis, pancytopenia, hyperferritinemia, hypocomplementemia, and proteinuria after long-term treatment with tumor necrosis factor alpha inhibitors, most recently golimumab. Bone marrow examination demonstrated hemophagocytosis, confirming macrophage activation syndrome. Computed tomography and endoscopy revealed soft tissue and esophageal edema consistent with angioedema. Despite improvement of systemic inflammation following high-dose glucocorticoids and intravenous cyclophosphamide, severe dysphagia persisted. A videofluoroscopic swallowing study demonstrated pharyngeal muscle dysfunction, and serum testing detected anti-galactocerebroside immunoglobulin G antibodies. Neurological imaging and electrophysiological studies were unremarkable. Swallowing function gradually recovered after discontinuation of golimumab. This case highlights that golimumab-induced lupus erythematosus may trigger multiple autoimmune complications, including macrophage activation syndrome, angioedema, and antibody-associated neuromuscular dysphagia. Awareness of these potentially life-threatening manifestations is essential for early recognition and appropriate management in patients receiving tumor necrosis factor alpha inhibitors.

Influenza remains a major cause of morbidity and mortality worldwide, particularly among elderly patients with comorbidities. Oseltamivir (Tamiflu), a neuraminidase inhibitor, is the most widely prescribed antiviral therapy for influenza A and B. Although oseltamivir is associated with increased nausea and vomiting, it is generally well tolerated. On rare occasions, oseltamivir has been associated with rare hypersensitivity reactions, including angioedema. Angiotensin-converting enzyme (ACE) inhibitors are also well known to cause angioedema, sometimes years after therapy initiation. We present the case of a 73-year-old man with influenza A who developed acute lip swelling after starting oseltamivir while on long-term lisinopril therapy. Oseltamivir was discontinued, and the swelling subsided. This raised important diagnostic and therapeutic considerations in differentiating viral illness, drug reaction, and medication-induced angioedema.

Myoferlin (encoded by MYOF) is a highly expressed protein in myoblasts and endothelial cells; mutations in MYOF are linked to malignancies, skeletal and cardiac myopathy, and hereditary angioedema with normal C1-inhibitor (HAE-nl-C1-INH). We present a 31- year-old female with recurrent severe abdominal angioedema attacks since late childhood. Mucocutaneous angioedema attacks began in early adolescence, triggered by stress and mechanical stimuli, and hormonal changes, often proceded bya fatigue or chest discomfort. Assessment of C1INH level and function had not shown any deficiency C1-INH protein level and function. Because C1-INH protein level and function were normal, whole exome sequencing (WES) was performed, identifying a novel heterozygous missense mutation in MYOF. Family screening revealed the same mutation in her mother and brother. Her angioedema symptomswere partially controlled using daily tranexamic acid and weekly anti-androgenic agents, with fresh frozen plasma or Berinert reserved for severe attacks. Over the past two years, she developed slowly progressive weakness in her facial, proximal, and distal extremity muscles, causing fatigue, bilateral ptosis, and difficulty climbing stairs or rising from a chair. Neurological examination, EMG-NCV studies, and elevated serum creatine kinase (CK) and lactate dehydrogenase (LDH) levels confirmed reduced muscle strength and generalized myopathy. Additionally, she experienced palpitations and unprovoked sinus tachycardia, likely reflecting cardymyopathy secondary to myoferlin deficiency.

Hereditary angioedema (HAE) is a genetic disorder characterised by recurrent cutaneous or submucosal oedema. Most cases are caused by pathogenic SERPING1 variants (types I and II), while a smaller subset presents with normal C1-inhibitor (C1-INH) levels and function (HAE-nC1INH). Despite its potentially life-threatening attacks, HAE remains under-diagnosed owing to inconsistent screening practices, low clinical awareness, poor patient acceptance, and resource limitations, resulting in diagnostic delays and preventable morbidity. Although international guidelines recommend family screening to identify at-risk relatives, no standardised protocol exists for its systematic implementation. Cascade family screening offers a structured approach to trace and test all known at-risk relatives across generations. Complementing this strategy, dried blood spot (DBS) assays provide a less invasive, cost-effective alternative to conventional serological testing, with particular utility in resource-limited settings. In this review, we critically appraise current screening methodologies, synthesise emerging evidence on cascade family screening and DBS-based diagnostics, and propose an actionable clinical flowchart to standardise identification, testing, and patient education from index case detection through multi-generational family screening.

In the present study, an efficient reverse-phase high-performance liquid chromatography method was developed for the quantification of impurities of icatibant (IBT) injection in finished formulations. The stationary phase employed is Kromasil 100 C18 with dimension of (150 × 4.6) mm, 3.5 µm. A 0.05 M KH2PO4 (pH 2.5) and methanol in the ratio of (90:10%v/v) was used as eluent A and 0.05 M KH2PO4 (pH 2.5) and methanol in the ratio of (70:30%v/v) was used as eluent B pumped through 1.0 mL/min flow rate using photodiode array detector at 210 nm. The IBT injection was analyzed under various degradation conditions, including acid, base, peroxide, photolytic, and thermal, were evaluated using a present proposed developed method. The method validation was carried out based on International Conference on Harmonization guidelines, by evaluating several key parameters. The observed limit of detection values were 0.066, 0.165, 0.165, 0.197, 0.134, and 0.493 μg/mL, the observed limit of quantification values were 0.201, 0.501, 0.500, 0.598, 0.406, and 1.495 μg/mL for icatibant (7-10), Des-Pro-Impurity, Des-Arg-impurity, Des-D-Arg-impurity, D-Tic (O) 8-10 icatibant and icatibant (1-6), respectively. The average recovery percentages of impurities of IBT injection were found to be 87.4% to 108.2%. The established methodology demonstrated linearity across a concentration interval of 0.020 to 34.73μg/mL for IBT and its impurities. Specific unidentified "Impurity at RRT about 0.92" (D-Tic (O) 8-10 Icatibant), "Impurity at RRT about 1.15," "Impurity at RRT about 1.24," and "Impurity at RRT about 0.57" were identified and liquid chromatography-high resolution mass spectrometry technique was used for their characterization. This method was assessed and confirmed to be more reliable for quantifying impurities of IBT injections.

Chronic idiopathic urticaria (CIU) is a dermatologic condition characterized by recurrent wheals, angioedema, or both for more than six weeks in the absence of an identifiable trigger. It is driven by spontaneous mast cell activation and the release of inflammatory mediators in the skin. Given its poorly understood pathogenesis, significant morbidity, and limitations of available treatment modalities, studies have suggested a link between diet and CIU. The primary objective of this study was to evaluate the literature published from 2015 to 2025 on this link, with an emphasis on dietary interventions, patient-reported outcomes, and gaps in the existing knowledge base. We conducted a scoping review following PRISMA guidelines, utilizing databases such as EMBASE, OVID Medline, and Web of Science. Search terms related to urticaria included "chronic idiopathic urticaria," "chronic spontaneous urticaria," "chronic idiopathic/spontaneous urticaria," "CIU/CSU," "CSU/CIU," "spontaneous chronic urticaria," and "idiopathic chronic urticaria," combined with terms related to diet, including "diet," "diet influence," "diet regimen," and "dietary effect." The initial database search identified 121 records, of which nine met the eligibility criteria and eight were included after critical appraisal. The eight included studies examined the Mediterranean diet, a low-pseudoallergen diet, a pseudoallergen-free diet, a histamine-free, low-pseudoallergen diet, and a low-histamine diet, as well as micronutrient levels and inflammatory markers. The dietary interventions lasted from seven to slightly more than 39 days. The studies evaluated the effects of these diets on CIU disease activity, disease control, and quality of life using measures such as the Urticarial Activity Score, Urticarial Control Test, and Chronic Urticaria Quality of Life score. Outcomes tended to improve in the short term following the implementation of these diets, particularly in studies of diets limiting histamine and pseudoallergen intake. Additional findings included an association between CIU and a higher BMI. One study also reported higher vitamin D levels and lower vitamin B12 levels in patients with CIU than in the general population. The current body of literature is limited by small sample sizes, short intervention durations, and limited immunologic exploration. However, the consistency of patient-reported improvements across diverse geographic and dietary contexts underscores the potential role of diet as an adjunctive approach to CIU management. Future research should prioritize larger sample sizes, more balanced representation of the sexes, longer-term trials, and better control of participant-level confounding variables.

Spironolactone is a widely used mineralocorticoid receptor antagonist with a well-established adverse-effect profile; however, angioedema is uncommon and a poorly recognized adverse reaction. We report a case of suspected isolated lip angioedema associated with spironolactone therapy in a 74-year-old woman. The patient presented with a two-week history of persistent upper-lip swelling and facial heaviness without urticaria, pruritus, tongue or oropharyngeal involvement, or symptoms of airway compromise. Although spironolactone had been prescribed approximately one year earlier, the patient had been poorly adherent and had resumed consistent daily use approximately one month before the onset of symptoms. She continued spironolactone despite the development of swelling. Clinical evaluation and laboratory investigations did not identify an alternative cause, and serum complement C4 was within the normal range. C1-esterase inhibitor antigenic and functional assays were unavailable. Spironolactone was discontinued, resulting in substantial improvement by Day 7 and complete resolution by Day 14 without recurrence. The Naranjo Adverse Drug Reaction Probability Scale yielded a score of 6, consistent with a probable adverse drug reaction. This case highlights isolated lip angioedema as a potential, although rare, adverse reaction to spironolactone and underscores the importance of establishing actual medication exposure when assessing suspected drug-related reactions. Recognition of uncommon medication triggers may facilitate timely withdrawal of the offending agent and prevent potentially more severe recurrence.

Acute supraglottic edema is an uncommon but potentially fatal cause of upper-airway obstruction. Although dengue infection is associated with diverse systemic manifestations, isolated upper-airway involvement is exceedingly rare and may pose a significant diagnostic challenge. We report an elderly woman who initially presented with features of acute stroke but was subsequently found to have life-threatening airway edema as a manifestation of acute dengue infection. Neuroimaging excluded acute cerebrovascular disease. Within six hours, she rapidly developed inspiratory stridor, hypoxemia, and hypercapnic respiratory failure requiring emergency endotracheal intubation. Flexible fiberoptic laryngoscopy demonstrated diffuse supraglottic and laryngopharyngeal edema, leading to compromised airway. Initial blood investigations revealed thrombocytopenia and a positive dengue NS1 antigen (sent in view of the ongoing dengue endemic), establishing the diagnosis of acute dengue infection. Conservative management comprising mechanical ventilation, corticosteroids, antibiotics, electrolyte correction, and serial fiberoptic airway assessment resulted in complete recovery without tracheostomy. This case highlights the evolving diversity of presenting clinical features associated with dengue infections. The pathophysiology of isolated airway edema in dengue is quite unknown and is beyond the scope of this article, but prompt pharmacological management, along with airway protection, reflects the reversible nature of this symptom and the likelihood of an underlying non-IgE-mediated hypersensitivity-related pathophysiological process. Early recognition of evolving airway compromise and prompt multidisciplinary intervention are essential for favorable outcomes.