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Stevens‐Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are acute, life‐threatening and rare severe cutaneous adverse reactions induced by drugs in most cases. The drugs most often reported to be implicated in inducing TEN/SJS are allopurinol, antibacterial sulfonamides, antiepileptic drugs and oxicam. Pristinamycin is an oral streptogramin antibiotic with bactericidal activity against Gram‐positive bacteria that is rarely linked to TEN. Typically, this condition develops 4‐28 days after drug exposure, Herein, we report a case of a 71‐year‐old female who developed TEN within 3 days of administration of pristinamycin and was managed successfully with supportive care, including intravenous fluids, pain control, prophylactic antibiotics and intravenous methylprednisolone. This case of rapidly developing SJS/TEN after administration of pristinamycin highlights the possibility that these complications can develop within only a few days following ingestion of drugs thought to be probably safe. [ABSTRACT FROM AUTHOR]

Antipsychotics can cause hematologic disorders, and they can have life-threatening consequences. Risperidone, less commonly associated with hematologic adverse effects, is an atypical antipsychotic medication used to treat conditions such as schizophrenia, bipolar disorder and irritability associated with autism. While risperidone primarily affects the central nervous system, it can have some hematologic adverse effects, although these are relatively rare. It is crucial to note that these side effects are not common, and most people taking risperidone do not experience hematologic disorders. The reporting of such disorders may be more frequent with clozapine compared to other atypical antipsychotics because clozapine treatment necessitates regular hematological monitoring 1. [ABSTRACT FROM AUTHOR]

Globularia alypum L. (GA) belonging to the Globulariaceae family is a Mediterranean plant which is widely used in traditional Tunisian medicine. The aim of this study was to investigate the phytochemical composition, antioxidant, anti-arthritic, antiproliferative, antibacterial and antibiofilm potential of aqueous GA leaf extracts (AGAL). Quantitative analyses of the different constituents of extracts were evaluated by high-performance liquid chromatography with photodiode-array detection (HPLC-DAD). Spectrophotometric methods and chemical tests were used for antioxidant and anti-arthritic activities. The antiproliferative study was evaluated using colorectal cancer SW620 cells, while the antibacterial assessment and analysis of the antibiofilm effects were determined by the microdilution method and the crystal violet assay, respectively. AGAL extracts presented several components, mainly Nepetin-7-Glucoside and trans-ferrulic acid. The results showed that they had an important antioxidant (IC50 = 0.34; 0.38 and 1.20 mg/mL) and anti-arthritic (IC50 = 2.94 mg/mL) properties, and these effects are displayed in a dose-dependent manner. In addition, this extract demonstrated significant antiproliferative (IC50 = 50 µg/mL), antibacterial (MIC = 6.25 mg/mL and MBC = 6.25 mg/mL), and antibiofilm (59.70% at 25 mg/mL) properties especially against S. aureus. The results achieved confirm the important role of this plant as a source of therapeutic activities. [ABSTRACT FROM AUTHOR]

Ureteral double-J stents are frequently used to prevent urinary obstruction. They can develop bacterial colonization and encrustation, which leads to persistent infections that seldom respond to antibiotic treatment. Thus, the goal of this study was to evaluate the local spectrum of bacterial pathogens and their susceptibility to natural compounds. A total of 59 double-J ureteral stents from 59 consecutive patients were examined. The samples were inoculated on agar culture mediums. Extracts of Globularia alypum L. were evaluated for their antibacterial activity with the diffusion and broth dilution methods; for antibiofilm activity, the crystal violet assay was used. The identification and the quantification of the different constituents of extracts were determined by reverse-phase high-performance liquid chromatography (RP-HPLC). Bacterial growth was found in three patients (5.1%). Enterococcus faecalis (1.7%), Acinetobacter baumanii (1.7%), and Pseudomonas putida (1.7%) strains were more commonly detected. They were resistant to several common antibiotics. All extracts presented several components, mainly nepetin-7-glucoside and trans-ferulic-acid, and they had antibacterial activity (MIC = 6.25 mg/mL and MBC = 6.25 mg/mL), and antibiofilm (59.70% at 25 mg/mL) properties, especially against Acinetobacter baumanii. The results achieved confirm the important role of this plant as a source of therapeutic activities. [ABSTRACT FROM AUTHOR]

The article presents a case study of a 68-year-old woman who developed atropine-induced allergic periocular dermatitis, confirmed through patch testing after treatment for uveitis. It highlights the symptoms of pruritus, erythema, and edema around the eyes, emphasizing the significance of identifying and eliminating the causative agent to prevent further complications.

The article presents a case study involving the concomitant use of carbamazepine and acetazolamide and its potential association with severe liver injury. It explore the possible mechanisms of this drug interaction and highlight the importance of monitoring both free and bound drug concentrations to assess drug efficacy and toxicity. It further emphasize the need for further research to better understand this interaction.

Sulfonamide non-antibiotics have less risk of cross reactivity, but it remains possible.7 The rate of allergic reaction is likely not dependent on the medication, but rather an intrinsic predisposing factor to hypersensitivity reactions. Glimepiride is an antidiabetic sulfonylurea agent that is generally well tolerated. Skin adverse reactions related to glimepiride are rare and include rash, pruritis, photosensitivity and lichenoid eruption.1 However, severe cutaneaous adverse reactions may occur with glimepiride, including toxic epidermal necrolysis (TEN) and Stevens-Johnson syndrome.2 Several publications indicate that cross-reactivity between sulfonamide antimicrobials (sulfamethoxazole-trimethoprim [SMX-TMP]) and sulfonamide non-antimicrobials including antidiabetic sulfonylurea agent (glimepiride) is unlikely.3 Herein, we report a case of fatal TEN probably related to glimepiride in a patient with a previous medical history of hypersensitivity to SMX-TMP. [Extracted from the article]

The most commonly incriminated drugs inducing SJS are antibacterial sulphonamides, anticonvulsants, nonsteroidal anti-inflammatory drugs (NSAIDs), antimalarials and allopurinol.[2] We report here the first case of carbocisteine-induced SJS confirmed by inadvertent re-exposure. SJS is a life-threatening disease with mortality rates of 4.8-9%.[1] Drugs are considered the primary cause of SJS. Dear Editor, Stevens-Johnson syndrome (SJS), an immune-mediated type IV hypersensitivity reaction, is clinically characterized by intense erythema followed by painful dermal blistering lesions of the skin and mucosa. [Extracted from the article]

Hyperuricaemia is a common clinical condition that can be defined as a serum uric acid level >6.8 mg/dl (404 mmol/l). Gout, a recognized complication of hyperuricaemia, is the most common inflammatory arthritis in adults. Drug-induced hyperuricaemia and gout present an emergent and increasingly prevalent problem in clinical practice. Diuretics are one of the most important causes of secondary hyperuricaemia. Drugs raise serum uric acid level by an increase of uric acid reabsorption and/or decrease in uric acid secretion. Several drugs may also increase uric acid production. In this review, drugs leading to hyperuricaemia are summarized with regard to their mechanism of action and clinical significance. Increased awareness of drugs that can induce hyperuricaemia and gout, and monitoring and prevention are key elements for reducing the morbidity related to drug-induced hyperuricaemia and gout. [ABSTRACT FROM AUTHOR]

The article presents a 32-year-old woman with a history of fever with a generalized eruption of non-follicular pustules and erythema. Topics discussed include acute generalized exanthematous pustulosis caused by oxacillin, increased white blood cell count with neutrophilia, and appearance of lesional pattern after patch testing with oxacillin.

Drug-induced hyperglycaemia and diabetes is a global issue. It may be a serious problem, as it increases the risk of microvascular and macrovascular complications, infections, metabolic coma and even death. Drugs may induce hyperglycaemia through a variety of mechanisms, including alterations in insulin secretion and sensitivity, direct cytotoxic effects on pancreatic cells and increases in glucose production. Antihypertensive drugs are not equally implicated in increasing serum glucose levels. Glycaemic adverse events occur more frequently with thiazide diuretics and with certain beta-blocking agents than with calcium-channel blockers and inhibitors of the renin-angiotensin system. Lipid-modifying agents may also induce hyperglycaemia, and the diabetogenic effect seems to differ between the different types and daily doses of statins. Nicotinic acid may also alter glycaemic control. Among the anti-infectives, severe life-threatening events have been reported with fluoroquinolones, especially when high doses are used. Protease inhibitors and, to a lesser extent, nucleoside reverse transcriptase inhibitors have been reported to induce alterations in glucose metabolism. Pentamidine-induced hyperglycaemia seems to be related to direct dysfunction in pancreatic cells. Phenytoin and valproic acid may also induce hyperglycaemia. The mechanisms of second-generation antipsychotic-associated hyperglycaemia, diabetes mellitus and ketoacidosis are complex and are mainly due to insulin resistance. Antidepressant agents with high daily doses seem to be more frequently associated with an increased risk of diabetes. Ketoacidosis may occur in patients receiving beta-adrenergic stimulants, and theophylline may also induce hyperglycaemia. Steroid diabetes is more frequently associated with high doses of glucocorticoids. Some chemotherapeutic agents carry a higher risk of hyperglycaemia, and calcineurin inhibitor-induced hyperglycaemia is mainly due to a decrease in insulin secretion. Hyperglycaemia has been associated with oral contraceptives containing high doses of oestrogen. Growth hormone therapy and somatostatin analogues may also induce hyperglycaemia. Clinicians should be aware of medications that may alter glycaemia. Efforts should be made to identify and closely monitor patients receiving drugs that are known to induce hyperglycaemia. [ABSTRACT FROM AUTHOR]

Hyperkalemia is a common clinical condition that can be defined as a serum potassium concentration exceeding 5.0 mmol/L. Drug-induced hyperkalemia is the most important cause of increased potassium levels in everyday clinical practice. Drug-induced hyperkalemia may be asymptomatic. However, it may be dramatic and life threatening, posing diagnostic and management problems. A wide range of drugs can cause hyperkalemia by a variety of mechanisms. Drugs can interfere with potassium homoeostasis either by promoting transcellular potassium shift or by impairing renal potassium excretion. Drugs may also increase potassium supply. The reduction in renal potassium excretion due to inhibition of the renin-angiotensin-aldosterone system represents the most important mechanism by which drugs are known to cause hyperkalemia. Medications that alter transmembrane potassium movement include amino acids, beta-blockers, calcium channel blockers, suxamethonium, and mannitol. Drugs that impair renal potassium excretion are mainly represented by angiotensin-converting enzyme inhibitors, angiotensin-II receptor blockers, direct renin inhibitors, nonsteroidal anti-inflammatory drugs, calcineurin inhibitors, heparin and derivatives, aldosterone antagonists, potassium-sparing diuretics, trimethoprim, and pentamidine. Potassium-containing agents represent another group of medications causing hyperkalemia. Increased awareness of drugs that can induce hyperkalemia, and monitoring and prevention are key elements for reducing the number of hospital admissions, morbidity, and mortality related to drug-induced hyperkalemia. [ABSTRACT FROM AUTHOR]

The article presents a case study of a 39-year-old woman with a history of psoriasis and was treated with acitretin. The patient receives lornoxicam for back pain and developed erythematous skin eruption without fever. The patient's skin biopsy shows irregular acanthosis, spongiosis, orthokeratosis associated with neutrophil cells. It also cites histological characteristics of the exanthematous pustulosis.

A letter to the editor is presented in response to the article "Drug reaction with eosinophilia and systemic symptoms due to lercanidipine" that was published in the previous issue.

Cross-reactivity between NSAIDs occurs frequently in patients with skin reactions and has been linked to NSAIDs with chemically related structures.3 Herein we describe a patient with FDE induced by mefenamic acid with unusually cross-reactivity to a chemically distinct NSAID diclofenac and has not been reported before. Fixed drug eruption (FDE) is a common drug side effect constituting about 10% of all skin drug eruptions.1 Nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most common causes of FDE.2 Mefenamic acid (anthracitic acid derivative) and diclofenac (phenylacetic acid) both have a chemically distinct structures. Fixed drug eruption (FDE) induced by mefenamic acid with unusually cross-reactivity to diclofenac: A case report. [Extracted from the article]

Enalapril-lercanidipine combination induced leukocytoclastic vasculitis: A case report Leukocytoclastic vasculitis (LCV) is a hypersensitivity vasculitis. It can occur in association with drugs, infection, collagen-vascular diseases, haematologic disorders, and malignancy.1 Drug-induced LCV accounts about 10% of all vasculitis cases.2 Several drugs are implicated as causes of drug-induced vasculitis.3 Herein we describe a case of LCV probably induced by enalapril-lercanidipine combination. [Extracted from the article]

Stevens-Johnson Syndrome is an uncommon life threatening disease generally induced by drugs. Antibiotics, mainly sulphonamides, are the most involved drugs in Stevens-Johnson Syndrome in children. Co-amoxiclav is a well tolerated antibiotic. It has never been reported to cause, lonely this syndrome in children. Herein, we report a co-amoxiclav-induced Stevens-Johnson Syndrome occurring in an 18-month-old child. The diagnosis of SJS is often challenging in children and other possible diseases should be ruled out. The etiology of this syndrome is not yet fully understood. It is thought to be mediated by an immunologic mechanism. Management involves early identification, withdrawal of the culprit drug and rapid initiation of supportive therapies. [ABSTRACT FROM AUTHOR]

Acetaminophen is a widely used analgesic drug. Its adverse reactions are rare but severe. An 89-year-old man developed an indurated edematous and erythematous plaque on his left arm 1 day after acetaminophen ingestion. Cellulitis was suspected and antibiotictherapy was started but there was no improvement of the rash; there was a spectacular extension of the lesion with occurrence of flaccid vesicles and blisters in the affected sites. The diagnosis of generalized-bullous-fixed drug eruption induced by acetaminophen was considered especially with a reported history of a previous milder reaction occurring in the same site. Acetaminophen was withdrawn and the rash improved significantly. According to the Naranjo probability scale, the eruption experienced by the patient was probably due to acetaminophen. Clinicians should be aware of the ability of acetaminophen to induce fixed drug eruption that may clinically take several aspects and may be misdiagnosed. [ABSTRACT FROM AUTHOR]

Allopurinol hypersensitivity syndrome (AHS) is a severe drug reaction. It is characterized by rash, fever, and internal organ involvement. It may present in different clinical forms. We present a case of acute generalized exanthematous pustulosis occurring as a manifestation of AHS. [ABSTRACT FROM AUTHOR]