Serum sickness-like reaction to D-supplement: a case report.

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. CASE PRESENTATION: 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.

Serum sickness induced by alemtuzumab in a kidney-pancreas transplant recipient.

Serum sickness is an immune-complex-mediated hypersensitivity reaction that was first noted in the early 1900s in patients receiving heterologous antisera, such as horse antitetanus or antidiphtheria serum. This condition is primarily self-limited; however, in its acute state, it can cause severe symptoms of fever, rash, polyarthritis, or polyarthralgias. In solid organ transplantation, this condition is frequently reported in association with the use of rabbit anti-thymocyte globulin and chimeric murine monoclonal antibodies such as rituximab. Alemtuzumab, designed as a humanized monoclonal antibody against CD52, is expected to be less immunogenic. Here, we report a case of serum sickness associated with alemtuzumab induction therapy in a kidney-pancreas dual-organ recipient.

Efficacy and safety of etanercept for postoperative pyoderma gangrenosum after infliximab serum sickness.

Non-peristomal postoperative pyoderma gangrenosum (PPG) is a rare subtype of pyoderma gangrenosum that occurs in the early postoperative period at surgical incisions, most commonly after breast surgery. Early diagnosis and treatment is essential to prevent severe scaring. TNF-alpha inhibitor infliximab was reported to be efficient in treatment of PPG refractory to systemic corticosteroids. However infliximab can be not well tolerated. We report the first case of etanercept efficacy in post-plastic breast surgery pyoderma gangrenosum after infliximab serum sickness.

Urticaria mimickers in children.

Acute urticaria is a self-limited cutaneous condition marked by transient, erythematous, and pruritic wheals. It is a hypersensitivity response that is often secondary to infection, medications, or food allergies in children. In contrast, the urticarial "mimickers" described in this review article are often seen in the context of fever and extracutaneous manifestations in pediatric patients. The differential diagnosis ranges from benign and self-limited hypersensitivity responses to multisystem inflammatory diseases. Establishing the correct diagnosis of an urticarial rash in a pediatric patient is necessary to both prevent an unnecessary work up for self-limited conditions and to appropriately recognize and evaluate multisystem inflammatory disorders. Herein, we describe two cases to illustrate the clinical manifestations, laboratory findings, histopathology and differential diagnoses for several mimickers of acute urticaria including: urticaria multiforme, serum sickness like reaction, Henoch-Schönlein purpura, acute hemorrhagic edema of infancy, systemic onset juvenile idiopathic arthritis, cryopyrin associated periodic syndromes, and urticarial vasculitis.

Serum sickness-like reaction in children due to cefditoren.

We describe the case of a 7-year-old boy with urticaria, fever, and arthritis that appeared 10 days after starting cefditoren therapy for acute tonsillopharyngitis, which was diagnosed as a serum sickness-like reaction due to this medication.

Case Report: Use of Obinutuzumab as an Alternative Monoclonal Anti-CD20 Antibody in a Patient With Refractory Immune Thrombocytopenia Complicated by Rituximab-Induced Serum Sickness and Anti-Rituximab Antibodies.

Management of refractory immune thrombocytopenia frequently involves rituximab, a chimeric anti-CD20 monoclonal antibody, to target B cells and induce remission in most patients. However, neutralizing antibodies to rituximab that nullify therapeutic response and may lead to serum sickness have been rarely reported. Here, we present a case of a young adult woman with Evans syndrome treated with rituximab, complicated by the development of serum sickness, acute respiratory distress syndrome, and platelet refractoriness presumed secondary to neutralizing antibodies to rituximab. She was successfully treated with the humanized anti-CD20 monoclonal antibody, obinutuzumab, with subsequent symptom resolution. Additionally, a review of 10 previously published cases of serum-sickness associated with the use of rituximab for idiopathic thrombocytopenic purpura (ITP) is summarized. This case highlights that recognition of more subtle or rare symptoms of rituximab-induced serum sickness is important to facilitate rapid intervention.

Serum sickness and severe acute renal failure after rabbit antithymocyte globulin treatment in aplastic anemia: a case report.

Serum sickness is an immune-complex-mediated illness that frequently occurs in patients after polyclonal antibody therapy (thymoglobulin). Although serum sickness has been described secondary to thymoglobulin therapy in adults, there are no reports in children on thymoglobulin-induced acute renal failure. We report a case of serum sickness in a 10-year-old girl who was treated for severe aplastic anemia using rabbit antithymocyte globulin (ATG). Eleven days after being started on antithymocyte globulin treatment, she developed fever, gross hematuria, arthralgia, rash, and acute renal failure. Laboratory results showed decreased complement levels, hypergammaglobulinemia, serum creatinine of 4.8 mg/dL (0.6 mg/dL at baseline), and blood urea nitrogen of 79 mg/dL (28 mg/dL at baseline). Peritoneal dialysis was required for 14 days. The patient's symptoms resolved after 13 days on treatment with a short course of high-dose steroids for 3 days, followed by a prednisolone taper. Early recognition and accurate diagnosis is the key for managing thymoglobulin-induced serum sickness, as treatment is highly effective at achieving good outcomes.

Rituximab-induced serum sickness in refractory immune thrombocytopenic purpura.

Serum sickness may occur in patients treated with chimeric monoclonal antibody. Rituximab, an anti-CD20 chimeric monoclonal antibody, is used with increasing frequency in chronic immune thrombocytopenic purpura (ITP). Rituximab is relatively safe; however, serum sickness is reported in 1-20% of patients, more commonly among those with autoimmune conditions. We describe a case of serum sickness in a patient with ITP and review the literature of rituximab-induced serum sickness.

Fever, urticaria, lymphadenopathy, and protracted arthralgia and myalgia resistant to corticosteroid therapy.

Allergen immunotherapy is commonly incorporated in the management of allergic rhinoconjunctivitis, allergic asthma, and insect sting hypersensitivity. It is generally safe, but systemic reactions occasionally occur, mainly of the immediate type and rarely of the delayed type. We report a case of a 50-year-old man with allergic rhinoconjunctivitis on immunotherapy for 3 years and then received an injection from another patient's extract. The latter contained a higher concentration of house-dust mite and pollens of grasses, trees, and weeds. It also contained molds that the patient's correct extract did not have. Within half an hour, he developed a systemic reaction that resolved with symptomatic treatment. Two weeks later, he received one-half of his usual immunotherapy dose. Within a week, he developed urticaria, arthralgia, myalgia, fever, and lymphadenopathy. Laboratory abnormalities included leukocytosis, elevated erythrocyte sedimentation rate, hematuria, and elevated liver enzymes. Oral corticosteroid therapy for 3 weeks was ineffective. He developed significant myalgia and apparent mood changes, attributable to corticosteroid intake. After a single plasmapheresis, he felt remarkable improvement within <24 hours. Corticosteroid therapy was gradually withdrawn over 10 weeks without relapse of symptoms. This is a rare case of probable serum sickness after the administration of a wrong allergy immunotherapy extract. However, a causal relationship could not be proven. The response was poor to prolonged corticosteroid therapy but was remarkable to one plasmapheresis.

Serum sickness reaction to obinutuzumab in a patient with chronic lymphocytic leukaemia.

Serum sickness (SS) is a known phenomenon; however, it is commonly missed due to vague symptoms, and is usually confounded by other aetiologies that present similarly. Obinutuzumab is a novel anti-CD20 antibody agent that has been approved for chronic lymphocytic leukaemia (CLL) treatment. At the time of approval, it was not linked to SS; however, this phenomenon has been recognised with other anti-CD20 agents like rituximab. SS remains a rare entity, but it is important to be recognised accurately and quickly in the appropriate circumstances, so that effective treatment with corticosteroids can be initiated to alleviate inflammatory symptoms. Here we present a patient with CLL who developed maculopapular rash, fever and polyarthritis and elevated inflammatory markers consistent with serum sickness triggered by obinutuzumab and was effectively treated with corticosteroids.

Rituximab-induced serum sickness and anaphylaxis in a child with nephrotic syndrome.

BACKGROUND: Rituximab is effective for treatment of children with refractory nephrotic syndrome (NS). However, the drug may cause serum sickness characterized by fever, rash, and arthralgia 10-14 days after primary antigen exposure or within a few days after secondary antigen exposure. Rituximab may also lead to anaphylaxis. It is important to recognize rituximab-induced serum sickness (RISS) clinically, as it may mimic various infectious or vasculitic diseases. CASE: A six-year-old male with NS treated with rituximab presented with diffuse arthralgia and myalgia eight days after the first dose. He developed an urticarial rash and arthralgia one week after the second dose, while he had swelling of lips and periorbital regions, choking sensation and erythematous rash in whole body within minutes after the third dose of rituximab. The first two reactions resemble typical serum sickness whereas the third reaction seem to be an anaphylaxis/anaphylactoid reaction. CONCLUSIONS: Although rituximab-induced serum sickness is typically self-limited, further infusions of rituximab should be avoided as it may provoke more severe symptoms. Most of the previous reported cases of RISS are patients with autoimmune or hematologic disorders. We present the first pediatric case with membranous nephropathy and RISS. The patient also developed anaphylactoid reaction during the third rituximab infusion.