scholarly journals COVID-19 IN A PATIENT WITH HIV AND KAPOSI SARCOMA

2021 ◽  
Vol 24 (2) ◽  
pp. 118-123
Author(s):  
Maria-Andrada Corodeanu ◽  
◽  
Sorina Vasile ◽  
Anca-Cristiana Oprea ◽  
◽  
...  

A 53 year old male diagnosed with HIV, SARS-CoV-2 and Kaposi sarcoma developed a purple-brown maculopapular rash on the left calf approximately 6 months before hospitalization and was diagnosed with venous ulcer. The lesions grew in size, spread on the whole body and also appeared on the palate. During this time the patient did not ask for a second opinion and was not monitored by a medical specialist. In December 2020, he developed a severe form of COVID-19 with acute respiratory failure and was admitted to the hospital. He was simultaneously diagnosed with HIV and severe immunosuppression. The skin biopsy confirmed Kaposi sarcoma in the nodular stage. Antiretroviral therapy (ART) was initiated and the patient later received liposomal doxorubicin chemotherapy. The patient slowly recovered whilst showing improvement of his clinical condition and immunological status.

2021 ◽  
Vol 32 (3) ◽  
pp. 286-289
Author(s):  
I-Fan Lin ◽  
Jiun-Nong Lin ◽  
Tsung-Heng Tsai ◽  
Chao-Tien Hsu ◽  
Yu-Ying Wu ◽  
...  

Coexistence of multicentric Castleman disease and Kaposi sarcoma is rare and might be missed without an experienced pathologists’ interpretation. A 46-year-old man had been diagnosed with HIV infection and treated with combination antiretroviral therapy of dolutegravir/abacavir/lamivudine (Triumeq) for one year. The latest viral load was 49 copies/mL and CD4 T-cell count was 192 cells/uL. He was admitted due to fever off and on, splenomegaly, general lymphadenopathy, and severe thrombocytopenia for two months. Biopsy of a purplish skin lesion and gastric tissue showed Kaposi sarcoma. The pathology of inguinal lymph nodes revealed coexistence of Kaposi sarcoma and multicentric Castleman disease. The plasma Kaposi sarcoma herpesvirus viral load was 365,000 copies/mL. During hospitalization, progressive pancytopenia and spiking fever persisted, and he died of multi-organ failure before completion of chemotherapeutic treatments with rituximab plus liposomal doxorubicin.


2021 ◽  
Author(s):  
Fumihiro Ogawa ◽  
Yasufumi Oi ◽  
Kento Nakajima ◽  
Reo Matsumura ◽  
Tomoki Nakagawa ◽  
...  

Abstract Background: Coronavirus disease (COVID-19) pneumonitis associated with severe respiratory failure has a high mortality rate. Based on recent reports, the most severely ill patients present with coagulopathy, and disseminated intravascular coagulation (DIC)-like massive intravascular clot formation is frequently observed. Coagulopathy has emerged as a significant contributor to thrombotic complications. Although recommendations have been made for anticoagulant use for COVID-19, no guidelines have been specified.Case presentation: We describe four cases of critical COVID-19 with thrombosis detected by enhanced CT scan. The CT findings of all cases demonstrated typical findings of COVID-19 and pulmonary embolism or deep venous thrombus without critical exacerbation. Two patients died of respiratory failure due to COVID-19.Discussion: Previous reports have suggested coagulopathy with thrombotic signs as the main pathological feature of COVID-19, but no previous reports have focused on coagulopathy evaluated by whole-body enhanced CT scan. Changes in hemostatic biomarkers, represented by an increase in D-dimer and fibrin/fibrinogen degradation products, indicated that the essence of coagulopathy was massive fibrin formation. Although there were no clinical symptoms related to their prognosis, critical COVID-19-induced systemic thrombus formation was observed. Conclusions: Therapeutic dose anticoagulants should be considered for critical COVID-19 because of induced coagulopathy, and aggressive follow-up by whole body enhanced CT scan for systemic venous thromboembolism (VTE) is necessary.


2018 ◽  
Vol 1 (1) ◽  
pp. 10-17
Author(s):  
V. Yu. Artemenko ◽  
E. V. Plotna

The purpose of this article was to systematize available literary data and to provide general recommendations for respiratory therapy in patients with spinal muscular atrophy. Spinal muscular atrophy (SMA) is a severe neuromuscular disease with autosomal recessive inheritance with degeneration of alpha motor neurons in the anterior horns of the spinal cord, leading to progressive proximal muscle weakness and paralysis. SMN 1–2 genes potentially encode identical proteins, although most of the transcripts of the SMN1 genes are halfsized, whereas most transcripts of the SMN2 genes do not contain the seventh exon. Therefore, the SMN2 gene is only partially functional, and a low-level SMN protein is produced in SMA patients. Moreover, the number of copies of the SMN2 can not be considered an exact predictive factor for any particular patient. The main causes of mortality and deterioration in the quality of life are the development of secondary respiratory failure. Type 1 (a, b, c) is the heaviest: early onset and lack of motor abilities, usually patients with a disease of this type survive no more than 2 years. Type 2 – an intermediate type characterized by a later onset, the patient may take a sedentary position, survival may reach the adult height. Type 3 is the softest form that manifests itself at the age of 1 year, the patient can walk and stand. The forecast is more favorable. Type 4 “adult form” manifests itself at the age from 10 to 20 or from 20 to 30 years and has a favorable outlook. The main causes of respiratory failure in patients with neuromuscular diseases are weakness of the respiratory muscles, unproductive cough and sleep disturbances. The weakness of the respiratory muscles, defined as the inability of resting respiratory muscles in the state of rest to create a normal level of pressure and air flow velocity when entering and exhaling, is common. Patients with neuromuscular diseases are susceptible to sleep disruption, especially in the REM sleep phase, with the most frequent form of this disorder being hypoventilation. Over time, hypoventilation in a dream can become more prolonged, resulting in the development of a severe form of hypoxia, an increase in the level of carbon dioxide in the blood and the suppression of the activity of the respiratory center. Thus, as a result of the review of literary data, a strategy of respiratory support in patients with CMA was proposed.


2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Ayaka Ishihara ◽  
Shuji Hatakeyama ◽  
Jun Suzuki ◽  
Yusuke Amano ◽  
Teppei Sasahara ◽  
...  

Abstract Background Pegylated liposomal doxorubicin plays an important role in the treatment of patients with severe refractory human immunodeficiency virus (HIV)-associated Kaposi sarcoma (KS). High cumulative doses of conventional doxorubicin exceeding 500 mg/m2 are known to cause cardiac toxicity. However, the safe cumulative dose of pegylated liposomal doxorubicin is unclear. Case presentation A 40-year-old Japanese man with HIV infection presented with pain, edema, and multiple skin nodules on both legs which worsened over several months. He was diagnosed with HIV-associated KS. He received long-term pegylated liposomal doxorubicin combined with antiretroviral therapy for advanced, progressive KS. The cumulative dose of pegylated liposomal doxorubicin reached 980 mg/m2. The patient’s left ventricular ejection fraction remained unchanged from baseline during treatment. After he died as a result of cachexia and wasting, caused by recurrent sepsis and advanced KS, an autopsy specimen of his heart revealed little or no evidence of histological cardiac damage. We also conducted a literature review focusing on histological changes of the myocardium in patients treated with a cumulative dose of pegylated liposomal doxorubicin exceeding 500 mg/m2. Conclusions This case report and literature review suggest that high (> 500 mg/m2) cumulative doses of pegylated liposomal doxorubicin may be used without significant histological/clinical cardiac toxicity in patients with HIV-associated KS.


2020 ◽  
Vol 13 (1) ◽  
pp. e227570
Author(s):  
Emma Boertjes ◽  
Stefanie Hillebrand ◽  
Janneke Elisabeth Bins ◽  
Laurien Oswald

Leptospirosisis a zoonosis caused by spirochaetes from the species Leptospira. The more severe form of leptospirosis, known as Weil’s disease, is characterised by the triad of jaundice, renal impairment and haemorrhages. Pulmonary involvement occurs in 20%–70% of the patients, with severity ranging from non-productive cough to respiratory failure mainly due to pulmonary haemorrhage. Recognition of Weil’s disease in patients presenting with pulmonary symptoms can be difficult. This case illustrates a classic case of pulmonary haemorrhagic involvement in Weil’s disease.


2020 ◽  
Vol 38 (15_suppl) ◽  
pp. 11552-11552
Author(s):  
Ramya Ramaswami ◽  
Kathryn Anne Lurain ◽  
Anaida Widell ◽  
Priscila Hermont Goncalves ◽  
Irene Ekwede ◽  
...  

11552 Background: Kaposi sarcoma herpesvirus (KSHV, also known as human herpesvirus 8 [HHV-8]), is the causative agent of Kaposi sarcoma (KS), a multicentric angioproliferative tumor, a form of multicentric Castleman disease (KSHV-MCD), and KSHV inflammatory cytokine syndrome (KICS). KS can be difficult to treat when it occurs with KSHV-MCD or KICS; resulting in high mortality rates. Liposomal doxorubicin (LD) is an FDA-approved treatment for KS. Pomalidomide, an oral immunomodulatory drug, is safe and has demonstrated activity in KS, but the activity of the combination (pomalidomide+LD) in KS alone or with KSHV-associated diseases is unknown. Methods: The primary objective was to evaluate safety and tolerability of pomalidomide+LD in two groups of patients with KS requiring systemic therapy: Group I (GI)- KS alone; Group II (GII)- KS with concurrent KSHV-MCD or KICS. Patients received LD at 20 mg/m2 intravenously on day 1 of a 28-day cycle combined with pomalidomide once daily on days 1 to 21 at escalating dose levels (DL) (I - 2mg, II - 3mg, or III- 4mg) in a 3+3 design until plateau of response or other pre-specified criteria. Patients received 81mg of aspirin daily as thromboprophylaxis. KS responses were evaluated using the modified AIDS Clinical Trial Group criteria. Results: Thirty-four cisgender men, all with T1-stage KS [21 patients (62%) in GI and 13 patients (38%) in GII] were treated; 32 (94%) were HIV-infected and 22 (65%) had prior chemotherapy for KS (15/21 GI and 7/13 GII). There were no dose-limiting toxicities (DLTs) at DLIII for GI, and additional patients were treated at DLIII. In GII, grade 3 rash and pharyngeal edema were DLTs observed at 3mg of pomalidomide. Overall a median of 6 cycles were administered; the most common grade 3/4 toxicity was neutropenia. Among evaluable patients receiving >2 cycles,17/21 patients in GI had a response (all partial) (81% [95% confidence interval (CI) 58-95%]) and 5/10 patients in GII had a response (4 partial and 1 complete) (50% [95% CI 19-81%]). Conclusions: Pomalidomide+LD was well-tolerated and active in heavily pretreated patients with KS alone. In patients with KS and other KSHV-associated diseases, activity was noted but less well-tolerated. Clinical trial information: NCT02659930 .


Sign in / Sign up

Export Citation Format

Share Document