Fanconi syndrome (FS) is a complex disorder characterized by a reabsorption defect in the proximal renal tubule (PT), leading to urinary loss of molecules such as glucose, phosphate, calcium, amino acids, bicarbonate, potassium, and low-molecular-weight proteins. Its etiology can be genetic or acquired, with drug toxicity being a significant cause of the acquired forms. The heterogeneous manifestations of FS, whether in its partial or complete form, can pose challenges in the emergency department; nevertheless, it should be considered in certain patients, as understanding its cause is crucial for initiating effective treatment. We present the case of a 59-year-old female patient with FS who was treated with lenalidomide in the context of stage III IgG kappa multiple myeloma according to the Salmon Durie classification. We highlight the recurrent nature of this syndrome in this patient.

In developing countries like India, Linezolid is widely used for the treatment of Multi drug resistant tuberculosis (MDR-TB) and extensively drug resistant tuberculosis (XDR-TB). Long-term administration of Linezolid is reported to cause toxic optic neuropathy causing bilateral, progressive visual loss in patients. We report case details of three patients on anti-tubercular therapy presented to us with sudden, progressive, painless blurring of vision of both eyes the cause of which was confirmed to be toxic optic neuropathy due to linezolid. Subsequently, cessation of the drug resulted in complete visual recovery in two patients whereas one patient had minimal visual improvement due to secondary optic atrophy. Clinicians and health care workers need to be aware of sight threatening complications of Linezolid.

Linezolid plays a clinically important role; however, it is responsible for severe pharmacological interactions and side effects, such as myelosuppression, serotonin syndrome, and lactic acidosis. We report a case of an 80-year-old man treated with venlafaxine for depression. He was admitted with a right femur fracture and submitted to surgical intervention, complicated by local infection. In collected pus was identified multiple microorganisms including Enterococcus faecium resistant to vancomycin. The therapeutic was adjusted to linezolid. On the 36th day of treatment, he developed hypertension, poor peripheral perfusion, and generalized tremor. He was disoriented, with marbled skin, myoclonus, and sinus tachycardia; and apyretic, with no signs of respiratory distress or joint/surgical wound inflammatory signs. Blood tests showed hyperlacticemia and discrete elevation of C-reactive protein but in a decrescent trend, with no other relevant alterations. The diagnosis of lactic acidosis and probable serotonin syndrome secondary to linezolid was made, supported by improvement after the drug suspension.

A 59-year-old male with a history of alcohol abuse presented with altered mental status. Upon examination, he was hypertensive and lethargic, and laboratory results revealed severe transaminitis, coagulopathy, and lactic acidosis, despite having normal serum alcohol levels. Additionally, his urine drug screen tested positive for methamphetamine. Following the exclusion of infectious, autoimmune, and other common causes of acute hepatitis, a diagnosis of methamphetamine-induced acute hepatitis was established. A non-acetaminophen toxicity N-acetylcysteine (NAC) protocol was initiated, resulting in a positive response with improvement in mentation and a decrease in liver enzyme levels. This case emphasizes the potential effectiveness of NAC in treating amphetamine-induced liver injury, supported by the limited available literature on the subject.

Hydroxychloroquine (HCQ) induced cardiotoxicity is a rare diagnosis and is often associated with chronic use of the medication. It has been shown that chronic HCQ use is associated with a drug-induced cardiomyopathy mainly driven by acquired lysosomal storage defects leading to hypertrophy and conduction abnormalities. As the only proven treatment is the discontinuation of the offending agent, prompt recognition is required to avoid further exposure to the drug and potential progression of disease. History, physical examination and advanced imaging modalities are useful diagnostic tools, but more invasive testing with an endomyocardial biopsy is required for definitive diagnosis. We present a descriptive case series of ten patients that were diagnosed with biopsy proven HCQ cardiotoxicity.

Diagnosing hyperferritinemia can be challenging due to the nonspecific nature of symptoms and various potential causes. This case report discusses the intricacies faced when diagnosing an elderly individual with hyperferritinemia, which eventually led to a specific diagnosis. An elderly patient presented with two months of fatigue, fever, and malaise, initially receiving several diagnoses. Despite some treatments, the patient\'s condition worsened, prompting further evaluation. Further investigation revealed a rare diagnosis. The progression of the disease led to the decision of palliative care. This case emphasizes the challenges in diagnosing elderly individuals and the importance of comprehensive follow-up and broad differential diagnosis. The need for a thorough investigation in the face of specific indicators is underscored. The patient\'s non-response to certain treatments required the consideration of less common conditions in the differential diagnosis. The case offers insights into addressing treatment suitability and making necessary adjustments. The situation underscores the need for careful evaluation, especially in unusual presentations, and the importance of timely conversations about care options. Lessons from this case assist healthcare professionals in understanding and managing intricate presentations in the elderly.

UNASSIGNED: To present a case of irreversible corneal edema after 10 years of amantadine use. A literature review was carried out to describe the clinical characteristics and outcomes of amantadine-induced corneal edema.
UNASSIGNED: A 36-year-old woman presented with a 6-week history of gradually progressive bilateral painless visual loss with visual acuity (VA) of 20/350 and 20/300 in the right and left eye, respectively. Examination showed bilateral diffuse central corneal edema with multiple Descemet membrane folds without endothelial guttata, keratic precipitates or intraocular inflammation. This did not respond to hypertonic saline drops and empirical treatment for presumed herpetic endotheliitis with oral acyclovir. Medication review revealed the use of amantadine 100mg daily for the past 10 years, prescribed by her neurologist for fatigue. Despite discontinuing amantadine, corneal edema was irreversible due to a markedly reduced endothelial cell count of 625 (right) and 680 cells/mm2 (left).
UNASSIGNED: This case highlights the need to consider amantadine as a cause of unexplained bilateral non-guttae corneal edema. A literature review of 33 case reports revealed broadly similar features of amantadine-induced corneal edema; whilst most cases had favorable outcomes with median VA 20/25 (interquartile range IQR 20/20-20/30) and complete resolution of corneal edema within 30 days (IQR 14-35) of amantadine discontinuation, most experienced low endothelial cell density 759 cells/mm2 (IQR 621-1078). Taken together, screening specular microscopy ought to be considered for those in whom amantadine is likely required long-term.

Acute renal failure in elderly patients can be caused by a wide spectrum of diseases that usually have a cause outside the kidney. The most common causes include renal impairment as part of ANCA vasculitis, another category includes clonal plasmatic cell disease with light chain cast nephropathy; and there also exists an increasing number of drug-induced tubulointerstial damage. We present a case of iatrogenic less common form of acute failure in a 73-year-old woman, who did not suffer from any serious disease until then. Although the biopsy helped to determine the cause of the failure and thus affect subsequent therapy, the function did not return to the previous state and the patient progressed to CKD G3bA1 with serum creatinine values of around 170-140 μmol/l.

BACKGROUND: RAD140 (Testalone) is a novel selective androgen receptor modulator with very limited data currently available on adverse effects related to this compound. The first-in-human phase 1 trial was recently published and did report a significant proportion of elevated aspartate aminotransferase, alanine transaminase, and total bilirubin among the test subjects. RAD140 may be associated with an idiosyncratic drug-induced liver injury. It is easily purchased online as a workout supplement. Given its ease of use from being an oral formulation, and not requiring a physician\'s prescription, its use among the young male population will likely rise. Clinicians should ask about the use of RAD140, and other workout supplements, in young men presenting with acute liver injury.
METHODS: We present the case of a 26-year-old Caucasian male without any significant past medical history who presented with nausea, vomiting, severe right upper quadrant abdominal pain, and jaundice from acute liver injury. Extensive inpatient workup did not reveal a definite cause for his liver injury other than the use of a novel selective androgen receptor modulator called RAD140 (Testalone). He was treated with supportive care and discharged after short hospitalization. He was instructed to stop RAD140, which he reported compliance with, and on 2-month follow-up his liver function panel had normalized without recurrence of any symptoms.
CONCLUSIONS: Novel selective androgen receptor modulators such as RAD140 may be associated with idiosyncratic drug-induced liver injury. Workup of new liver injury in young and middle-aged males should involve asking about use of these novel compounds, for if missed and use continues, it can likely lead to fulminant liver failure or decompensated liver cirrhosis.

BACKGROUND: To report the first case of bull\'s eye maculopathy associated with veterinary niclosamide.
METHODS: A 27-year-old Iranian female presented with a history of reduced vision and photopsia since 3 years, after accidental ingestion of four boluses of veterinary niclosamide. Fundus examination showed atrophy in parafoveal retinal pigmentary epithelium, appearing as bilateral bull\'s-eye maculopathy. Optical coherence tomography revealed disruption of the parafoveal ellipsoid zone and outer retinal thinning, appearing as a flying saucer sign. Electroretinography displayed decreased scotopic and photopic amplitudes with normal waveform in both eyes. The causality score was 4, showing \"possible\" retinopathy due to niclosamide according to Naranjo\'s causality assessment algorithm. Based on clinical and ancillary findings, a diagnosis of niclosamide-induced maculopathy was made.
CONCLUSIONS: Veterinary niclosamide is an anthelmintic drug that in higher doses could be detrimental to the human retina. Awareness about its side effects and appropriate drug labeling could prevent accidental toxicity.