Cocaine is an illegal drug; its abuse and toxicity are a public health problem due to its high morbidity and mortality. Cocaine can affect the cardiovascular, central nervous and respiratory systems. The case of a 42-year-old male without history of chronic or degenerative diseases, but previous cocaine consumption is presented in this report. The patient is admitted to the Emergency Department given that the clinical presentation included hemoptysis and dyspnea with mild to minimal activity, which evolved to orthopnea. Advanced airway management was required and supportive care at the Intensive Care Unit was provided. Imaging studies showed evidence compatible with alveolar hemorrhage diagnosis. In search of an autoimmune etiology, an antibody-screening panel was requested, reporting negative results for autoimmune disorders. The patient management was based on corticosteroid therapy and plasmapheresis to counter the persistent hemoptysis and hemoglobin serum level decline. The management strategy was based on the clinical suspicion of vasculitis and a torpid clinical evolution. Pulmonary sepsis ensued, resulting in patient's death. The necropsy report describes the primary cause of death as diffuse alveolar hemorrhage secondary to diffuse alveolar injury. This case report presents the detailed clinical, imagining and histopathological findings of a patient with alveolar hemorrhage secondary to cocaine consumption, as well as a review of the literature.

Conditions, where the patient's immune system is compromised are the main risk factor for mucormycosis. Approximately 23% of the world's population is estimated to have a latent Mycobacterium tuberculosis infection and more than 10 million new cases were estimated in 2017. Pulmonary mucormycosis and tuberculosis co-infections are very rare. We present the case of a 56-year-old insulin-dependent diabetic patient with a pulmonary mucormycosis and tuberculosis co-infection. While the patient did not suffer from ketoacidosis, she had poor glycemic control. A chest X-ray and a computed tomography showed nodular and cavitary lesions in both lungs. The patient was diagnosed through a biopsy of the bronchial mucosa and an RT-PCR for M. tuberculosis from bronchoalveolar lavage. The patient was treated with the recommended 4-drug regimen for TB (i.e. isoniazid, rifampin, pyrazinamide, and ethambutol); concurrently, amphotericin B deoxycholate was administered to treat the mucormycosis infection. Thirty days after initial hospital admission the patient underwent a lobectomy on the right lung. The case described here is only the sixth case reported in the literature of concomitant pulmonary tuberculosis and mucormycosis and the third case associated with a TB and mucormycosis co-infection involving an uncontrolled DM patient to survive.

Cancer patients with spinal metastases are a diagnostic and treatment challenge for the clinician. This challenge must be addressed through a multidisciplinary, multimodal, and individualized management. The presence of tumor cells in bone metastases results in homeostatic disruption between bone formation and remodeling. Bone destruction is a late event in the formation of lytic bone metastasis, starting when tumor cells proliferate; this in turn activates osteoclasts, seen as trabecular destruction in imaging studies. There may be excessive bone destruction and increased bone formation, which produce blastic lesions. Bone scintigraphy is currently the most widely used diagnostic method and is considered as the reference test for the diagnosis of spinal bone metastasis. However, we believe that in the near future positron emission tomography associated to computed tomography with 18F-NaF, or magnetic resonance using diffusion-weighted whole-body imaging with background body signal suppression, will replace bone scintigraphy due to their improved diagnostic accuracy. These new diagnostic tools will help prevent bone metastasis complications such as: intractable pain; spinal cord or cauda equina compression; hypercalcemia; pathological fractures; and spinal instability. With regards to the treatment, it can be uni- or multimodal, depending on the type and number of bone metastases. Among the types of treatment available for bone metastasis are chemotherapy, radiotherapy, and invasive procedures. The prognosis of patient survival depends on the histopathology of the primary tumor, the presence of bone metastasis, and the presence of neurological deficits.

Pemphigus is a bullous autoimmune disease that affects the skin and mucous membranes. It is very difficult to establish the etiology and the triggering factors that influence reactivations in pemphigus vulgaris (PV). The case of a 33-year-old male with chronic history of intranasal cocaine consumption is presented in this report. We present the clinical case of the patient, followed for a total of 86 weeks, with ten relapses secondary to probable cocaine use. The patient was admitted to the emergency department after presenting polymorphic dermatosis characterized by blisters, vesicles, and excoriations extending from the oral cavity to the thorax, and to the inguinal and genital regions, affecting approximately 35 % of the body surface area with a score of 56 on the Pemphigus Skin Disorder Index. Skin biopsies were compatible with PV diagnosis. The patient had clinical improvement with a combination of methylprednisolone 500 mg intravenously (IV) and cyclophosphamide 500 mg IV every 15 days, along with prednisone 50 mg orally (PO) q24 h and mycophenolic acid 500 mg PO q6 h. Persistent cocaine use is highly likely to be the factor triggering lesion reactivation and responsible for the torpid evolution. We cannot definitively conclude whether the change from azathioprine to mycophenolic acid after the tenth relapse was the adjuvant medication responsible for the end of the consolidation phase and complete remission on therapy. This case study could potentially serve as a guide for management of patients who continuously persist with cocaine use, leading to a clinical picture refractory to multiple therapeutic schemes.

Introduction: Opsoclonus-myoclonus syndrome (OMS) is an inflammatory neurological disorder, often requiring a prompt medical evaluation. Among the diverse etiologies associated with OMS are autoimmune, infectious, paraneoplastic, and systemic diseases, and drug intoxication. Clinical Summary: The case of a 36-year-old female with a disabling holocranial headache, sudden loss of consciousness, aggressive behavior, vertigo, and a personal history of somatoform disorder and major depression is presented here. After hospital admission, the patient developed sudden stereotyped movements in all four extremities and oculogyric crises compatible with OMS. Cerebrospinal fluid analysis, viral and autoimmune assays, as well as blood, urine, and bronchial secretion cultures, drug metabolite urinalysis, and tumor markers were all negative. Furthermore, brain computed tomography (CT) and brain magnetic resonance imaging, along with thoraco-abdominopelvic CT and electroencephalography, were also all negative. The patient suffered type one respiratory insufficiency after 72 h of hospitalization, requiring an endotracheal tube. After 13 days the patient suffered cardiac arrest. Necropsy was performed reporting lymph nodes with a poorly differentiated malignant neoplastic lesion, HMB-45, melan-A, vimentin, and S-100 positive, compatible with melanoma metastasis from an occult primary cancer. Discussion: While the incidence of melanoma of unknown primary is between 2.6 and 3.2%, with a median overall survival ranging between 24 and 127 months, when melanoma patients develop OMS their survival is markedly decreased. Although only 5 cases of paraneoplastic OMS secondary to melanoma have been reported in the literature, all had a poor prognosis, dying within 8 months of OMS onset.

Encephalitis is a heterogeneous syndrome that is diagnosed through clinical assessment and the assistance of laboratory, neuroimaging and electroencephalographic workup. Over the past 10 years, autoimmune encephalitis has been more frequently recognized; however, most reports come from highly specialized hospital settings. Anti-N-methyl-D-aspartate receptor (NDMAR) encephalitis has been associated with paraneoplastic encephalitis syndromes and was first recognized in 2005. We present the case of a 34-year-old male patient who debuted clinically with a headache associated with neuropsychiatric symptoms (i.e., visual and auditory hallucinations, anxiety, aggressiveness) and memory deficits, progressing to autonomic dysfunction (i.e., tachycardia and hypertension), seizures, and stupor with catatonic features. Initially, infectious, metabolic, and toxicological etiologies were excluded; followed by the assessment of immunological and paraneoplastic etiologies, yielding positive IgG levels for anti-NMDAR antibodies. The patient was treated successfully with systemic steroid therapy and therapeutic plasmapheresis, while mutism was the only sequela. Although large case series reporting on paraneoplastic and autoimmune anti-NMDAR encephalitis have been reported in the literature in recent years, this case is of particular importance due to the stepwise differential diagnosis and treatment management procedure that was used in a regional but not highly specialized hospital setting.