Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Retroperitoneal bleeding is one of the most serious, potentially lethal complications of anticoagulation therapy. Although well documented in fully heparinized and coumadinized patients, there are only few reports of life-threatening hemorrhages in low-molecular-weight heparin (LMWH)-treated patients. We present a case of almost fatal spontaneous retroperitoneal bleeding in a 71-year-old woman with pneumonia and acute coronary syndrome. After receiving combination therapy with Lovenox (enoxaparin), aspirin, and Plavix for 5 days, she developed acute hemorrhagic shock and possible intra-abdominal compartment syndrome. Urgent computed tomography scan of the abdomen and pelvis was performed and showed a left retroperitoneal hematoma. The patient's condition continued to deteriorate, which prompted emergent exploration. After evacuating 3 L of free blood from the peritoneal cavity, we managed to stabilize the patient. Our case of spontaneous retroperitoneal bleeding adds to the growing number of cases in which enoxaparin has been associated with severe bleeding. A high index of suspicion is necessary if the patient displays any of the signs and symptoms that suggest major hemorrhage. It appears that those at highest risk receive doses approaching 1 mg/kg subcutaneously every 12 hours, have renal impairment, are of advanced age, and receive concomitant medications that can affect hemostasis. On average, a retroperitoneal hematoma occurs within 5 days of therapy with enoxaparin. In high-risk patients, enoxaparin activity (anti-factor Xa) should be carefully monitored.
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PMID:A retroperitoneal bleed induced by enoxaparin therapy. 1598 76

Mycoplasma pneumoniae infection is frequent but generally mild or self-limiting. Approximately 10% of cases develop clinical signs of pneumonia with "atypical" radiographic pattern. However, mycoplasma pneumoniae can be responsible for a variety of extrapulmonary manifestations, potentially involving all systems and apparatuses. Although exact pathophysiological mechanisms are not completely known, these could be secondary to direct invasion of the target organ, immunological damage due to molecular mimicry or vascular obstruction. A 45-year-old man was admitted to Internal Medicine Unit because of fever, dry cough and fatigue lasting 15 days. Fever disappeared after starting clarithromycin. About 72 h after admission the patient complained of right calf pain and tachypnea. The presence of anti-mycoplasma antibodies suggested mycoplasma pneumoniae infection. Moreover, a diagnosis of venous thrombo-embolism was performed. Given the absence of classical risk factors for thrombosis, patient was investigated for inherited and acquired thrombophilia and tested positive for antiphospholipid antibodies. A review of the English literature on the association between m. pneumoniae and pulmonary embolism will be provided in order to underline the possible pathogenetic role of antiphospholipid antibodies in this setting. Clinicians should outweigh risk and benefits for LMWH prophylaxis case by case considering these adjunctive pro-thrombotic mechanisms in patients m. pneumoniae infection.
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PMID:Venous thromboembolism during mycoplasma pneumoniae infection: case report and review of the literature. 3309 Apr 13