Envenomation from snakebites is a significant public health concern in the Southeast Asian region resulting in considerable mortality and morbidity. Anti-snake venom (ASV) despite being the only rescue can bring forth several acute and delayed adverse effects. Among them, serum sickness is a late manifestation after treatment with ASV that presents after 5-14 days of treatment. However, there is no specific definition to diagnose serum sickness or proven treatment. Here, we present a case of serum sickness to provide an insight into this unventured zone, briefing the presentation, treatment and probable reason for serum sickness and its prevention after common krait envenomation and treatment with polyvalent ASV in India.

UNASSIGNED: Rituximab-induced serum sickness (RISS) is a rare complication of Rituximab (RTX) in immunobullous disorders. Clinicians should be aware of the occurrence of serum sickness symptoms during RTX administration, and prompt initiation of corticosteroid therapy is crucial in these patients. Additionally, RISS may occur with subsequent RTX doses and patients should be counseled accordingly.
UNASSIGNED: Rituximab (RTX) is a chimeric monoclonal anti-CD20 antibody which has gained approval for the treatment of various autoimmune and lymphoproliferative disorders. While RTX-induced minor reactions, including immediate infusion-related reactions, are common, serum sickness is rare. Limited data exist regarding rituximab-induced serum sickness (RISS) in pemphigus vulgaris (PV) and mucous membrane pemphigoid (MMP). We report two cases of RISS following RTX administration in PV and MMP patients. Both patients presented with typical symptoms of serum sickness after RTX infusion, necessitating drug cessation and corticosteroid therapy for resolution. RISS represents a rare complication of RTX therapy. Clinicians should maintain awareness of serum sickness presentations during and post-RTX administration.

BACKGROUND: Serum Sickness-Like Reaction (SSLR) is an immune response characterized by rash, polyarthralgias, inflammation, and fever. Serum sickness-like reaction is commonly attributed to antibiotics, anticonvulsants, and anti-inflammatory agents.
METHODS: A 16-year-old female with a history of overactive bladder and anemia presented with a diffuse urticarial rash, headaches, joint pain, and swelling for three days. Her medications included oral contraceptive pills, iron, mirabegron, UQora, and a probiotic. Physical examination revealed a diffuse urticarial rash, and her musculoskeletal exam revealed swelling and tenderness in her wrists. She was evaluated by her pediatrician and started on a 7-day course of prednisone, as well as antihistamines. Her CBC, basic metabolic panel, liver function panel, Lyme titers, and urinalysis were all within normal limits. With concern for hypersensitivity reaction to medication, all medications were discontinued. Nine days after symptom onset, the patient was evaluated by an allergist, who confirmed her presentation was consistent with serum sickness-like reaction. Her symptoms resolved, and her medications were re-introduced sequentially over several months. Restarting UQora, however, triggered a recurrence of her symptoms, and it was identified as the culprit medication. Consequently, UQora was permanently discontinued, and the patient has remained symptom-free.
CONCLUSIONS: This case report describes the first documented case of serum sickness-like reaction caused by UQora (active ingredient D-mannose). D-mannose is a monosaccharide, and it is frequently promoted to prevent urinary tract infections. While the clinical features and timeline in this case were typical of serum sickness-like reaction, UQora as the trigger was highly unusual. Clinicians should be aware of the diverse triggers of serum sickness-like reaction and the importance of prompt identification and management to enhance patient safety. Further research is necessary to better understand the potential therapeutic applications of D-mannose, as well as the potential risks and interactions.

Although lymphoma is the most frequent malignancy in common variable immunodeficiency (CVID), solid tumors, especially affected by oncogenic viruses, are not considered. Furthermore, in vitro genetic studies and cell cultures are not adequate for immune system and HBV interaction. We adopted a previously introduced clinical model of host-virus interaction (i.e., infectious process in immunodeficiency) for analysis of B cells and the specific IgG role (an observational study of a CVID patient who received intravenous immunoglobulin (IVIG). Suddenly, the patient deteriorated and a positive results of for HBs and HBV-DNA (369 × 106 copies) were detected. Despite lamivudine therapy and IVIG escalation (from 0.3 to 0.4 g/kg), CT showed an 11 cm intrahepatic tumor (hepatocellular carcinoma). Anti-HBs were positive in time-lapse analysis (range 111-220 IU/mL). Replacement therapy intensification was complicated by an immune complex disease with renal failure. Fulminant HCC in CVID and the development of a tumor as the first sign is of interest. Unfortunately, treatment with hepatitis B immune globulins (HBIG) plays a major role in posttransplant maintenance therapy. Anti-HB substitution has not been proven to be effective, oncoprotective, nor safe. Therefore, immunosuppression in HBV-infected recipients should be carefully minimized, and patient selection more precise with the exclusion of HBV-positive donors. Our clinical model showed an HCC pathway with important humoral host factors, contrary to epidemiological/cohort studies highlighting risk factors only (e.g., chronic hepatitis). The lack of cell cooperation as well as B cell deficiency observed in CVID play a crucial role in high HBV replication, especially in carcinogenesis.

A 30-year-old, previously healthy adult male received equine rabies immunoglobulins (Ig) (ERIG) along with anti-rabies vaccinations as per protocol for postexposure prophylaxis after an unprovoked rabid dog bite of grade three wound over the shin of the left lower limb. On the 8th day, he developed urticarial rashes beginning from the site of the wound, which gradually became a widespread maculopapular rash. Development of the rash was followed by low-grade fever, nonspecific arthralgias and soreness in the throat. A diagnosis of serum sickness-like illness was made based on history, temporal correlation of administration of ERIG and development of symptoms. He responded well to antihistaminic and a short course of injectable steroids. The purpose of this article is to increase awareness regarding the clinical presentation and management of this rare yet potentially curable adverse event if identified timely.

2例原发性肾病综合征患儿使用利妥昔单抗（RTX）诱发血清病，诊断为利妥昔单抗诱导血清病（RISS）。例1，男，8岁，确诊原发性肾病综合征5年余，病理为局灶节段性肾小球硬化，应用第2剂RTX治疗6 d后，出现急性皮疹、关节肿痛、高热及休克等血清病表现，经激素等治疗5 d逐渐好转。例2，女，9岁，确诊原发性单纯型肾病综合征3年2个月，病理诊断微小病变，应用第2剂RTX治疗11 d后，出现急性皮疹、关节肿痛表现，2 d后自行好转。2例儿童肾病综合征RISS均发生在学龄期患儿重复使用RTX时，症状出现在再次应用1~2周内，主要表现为皮疹、关节痛、发热。严重者出现休克。激素为RISS的主要治疗方法，轻者自行缓解。.

BACKGROUND: Serum-sickness like reactions (SSLRs) to amoxicillin have been documented in the medical literature. Beta-lactams are important and commonly used medications especially in the pediatric population. Often, SSLRs present within days of and during first exposure/ingestion to the offending agent. We described a unique case of a 4-year-old boy who presented with symptoms of amoxicillin SSLR following his second course of amoxicillin with only 2 months and 10 days between his second and first course.
METHODS: A 4-year-old boy presented to hospital with a pruritic rash on day 7 of a 10-day course of amoxicillin for otitis media accompanied by fever (38.7 degrees Celsius). On day 7 of his second course of amoxicillin, which was separated from his first course by only 2 months and 10 days, his mother noticed erythematous, raised, pruritic lesions with central clearing on his sternum. He presented to the ED with emesis, progression of the rash to his torso, back, legs, and face, hypotension, angioedema, and joint pain. His bloodwork demonstrated a leukocytosis of 18.6 × 109 g/L with neutrophilic predominance and thrombocytosis with a platelet count of 653 × 109 g/L. He was treated with 5 mg oral cetirizine daily and 1 mg/kg oral prednisone which improved his rash and angioedema. He was managed with up to 4 times the usual dose of cetirizine. He was assessed in our outpatient clinic as an outpatient and penicillin skin testing was unremarkable. A diagnosis of a probable SSLR to amoxicillin was made.
CONCLUSIONS: We report an unusual presentation of SSLR following re-exposure to amoxicillin. Our case highlights that patients with previous asymptomatic exposure to amoxicillin can develop SSLR with repeat exposure. Although it is not uncommon for children to develop amoxicillin SSLRs after previous exposure to the drug, this case is unique because of its short time course of 2 months and 10 days months between drug courses. Penicillins are commonly used in the pediatric population. Therefore, it is important to correctly characterize adverse drug reactions to broaden our understanding of SSLRs, prevent unnecessary avoidance of the triggering agent, and improve patient management.

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