[Anti-PD1 immunotherapy followed by tuberculosis infection or reactivation]. / Tuberculose pulmonaire sous traitement par immunothérapie type anti-PD1.

INTRODUCTION: Immunotherapy is now a standard of care in oncology. There is a need to improve our knowledge about immune-related adverse events, especially infectious diseases. CASE REPORT: We describe the case of a 49-year old male who received anti-PD1 therapy, to treat metastatic melanoma with pulmonary metastasis. After 3 cycles of nivolumab, computed tomography scanning showed a decrease of the pulmonary metastasis in the upper left lobe, but revealed new pulmonary lesions such as tree-in-bud and a lung cavity in the same lobe. This was diagnosed as pulmonary tuberculosis with no antibiotic resistance identified. The patient continued the immunotherapy and was initiated onto a standard anti-tuberculosis therapy. In the absence of an initial positive IFN-γ release assay (Quantiferon) test, but as there might have been a history of primary infection during childhood, a reactivation of tuberculosis was considered to be likely. CONCLUSIONS: This is the ninth case of tuberculosis infection under immunotherapy and it underlines the need to consider infection risks in patients undergoing immunotherapy. An INF-γ release assay screening test should be considered an essential part of the pre-treatment work-up.

[Severe pulmonary tuberculosis in the ICU, diagnosis and treatment]. / Diagnostic et traitement d'une pneumonie tuberculeuse grave en réanimation.

INTRODUCTION: Pulmonary tuberculosis can rarely lead to acute respiratory distress syndrome and anti-tuberculous therapy initiation depends on this difficult diagnosis in ICU. CASE REPORT: A 50-year-old man presented a septic shock and acute respiratory distress syndrome with bilateral infiltrates mainly in the upper lobes on chest radiography. Diagnosis of pulmonary tuberculosis was made 10days after admission on examination of cavitary and diffuse infiltrates on a second CT scan, in addition to presence of acid-fast bacilli on smear examination of bronchial aspirates. Amikacin, with four first-line anti-tuberculous drugs, was started in the case of a resistant strain and seriousness of the illness. After 14weeks, he left on rifampicin and isoniazid treatment. CONCLUSIONS: There are no specific recommendations concerning pulmonary tuberculosis in ICU but a delay in initiation of anti-tuberculous therapy is a factor of poor prognosis. Using a second-line anti-tuberculous drug, like amikacin or/and fluoroquinolones, within initial treatment may accelerate improvement of sepsis and immediately treat resistant strains, when genomic methods for detection of resistance are not available in routine.

[Disseminated aspergillosis with pulmonary and cardiac localization in an HIV-infected patient]. / Aspergillose disséminée avec localisations pulmonaires et cardiaques chez un sujet infecté par le VIH.

The authors report a case of invasive aspergillosis with pulmonary and cardiac involvement revealed by a pericarditis in a seropositive patient (VIH1). Clinical findings, differential diagnosis and outcome underly the issues encountered in the management of aspergillosis in AIDS patients. Indeed, the low prevalence of aspergillosis in AIDS and the insidious features of aspergillosis locations make the early diagnosis difficult. It is though essential for a favourable outcome under specific treatment. The risk factors, clinical characteristics and diagnostic procedures are mentioned as well as the various available treatments.

[Pulmonary artery hypertension in HIV seropositive drug addicts. Apropos of 10 cases]. / Hypertension artérielle pulmonaire chez le toxicomane VIH+. A propos de 10 cas.

Pulmonary hypertension (PH) is a classic complication associated with intravenous drug addiction. Various pathogenic mechanisms may be involved but HIV infection now appears to be the main etiologic factor. We report herein 10 case of PH occurred in HIV+ intravenous drug abusers. Each patient had several pathogenic factors: HIV infection, pills crushed and intravenously injected (6 cases), heavy and repeated consumption of amphetamines and cocaine (6 cases), cirrhosis with portal hypertension (2 cases), anticardiolipid antibodies (2 cases). The clinical findings were similar to those reported for PH in HIV seronegative patients; however, in 5 cases, opiates could have alleviated dyspnea, which became perceptible only at the time of drug withdrawal. Because drug addicts usually exhibit a weak support for medical prescriptions, long term therapy needing regular follow-up such as anticoagulation appears to be hazardous and even dangerous. The prognosis remains poor, since the progression of PH led to the death of one third patients within the year following the diagnosis.

[A rare cause of cyanosis: Sulphaemoglobinaemia related to thiocolchicoside (Miorel)]. / Une cause rare de cyanose: sulfhémoglobinémie imputable au thiocolchicoside (Miorel).

INTRODUCTION: An acquired abnormality of haemoglobin is among the many causes of cyanosis, especially in patients with no identified cardiorespiratory cause. CASE REPORT: A 50-year-old woman, suffering from amyotrophic lateral sclerosis, was hospitalised for dyspnoea. Physical examination revealed cyanosis that persisted despite oxygen therapy. Discordance between the reduced arterial oxygen saturation and normal arterial oxygen tension led to a search for a dyshaemoglobinaemia as a possible cause. Use of co-oxymetry with spectrophotometry revealed sulphaemoglobinaemia. Sulphaemoglobinaemia is due to irreversible incorporation of a thiol radical into the porphyrin ring of a haem group. This decreases the affinity of haemoglobin for oxygen and thus reduces oxygen carrying capacity. A drug-induced cause is often identified. However, no previously described cause for sulphaemoglobinaemia was identified in our patient. The patient was currently being treated with thiocolchicoside (Miorel((R))). Thiocolchicoside was suspected as the cause because its chemical structure contains an easily hydrolysable thiol radical. Withdrawal of thiocolchicoside led to regression of the sulphaemoglobinaemia. CONCLUSIONS: This report underlines the importance of searching for an acquired abnormality of haemoglobin (methaemoglobinaemia or sulphaemoglobinaemia) in patients with cyanosis resistant to oxygen, in the absence of any cardiorespiratory abnormality. This case is the first to suspect thiocolchicoside as a possible cause of sulphaemoglobinaemia.