Biomedical subjects
Thomas M Roy
Publications and source records attributed to Thomas M Roy.
Pasteurella multocida respiratory infection: an important cat-associated zoonosis.
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Delay in diagnosis among hospitalized patients with active tuberculosis--predictors and outcomes.
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Magnesium: its proven and potential clinical significance.
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Mycobacterium xenopi pneumonia in the southeastern United States.
Mycobacterium xenopi (M. xenopi) is a slow-growing, nontuberculous mycobacterium (NTM). This organism is found in fresh water and has been isolated in water samples collected from water systems in homes and hospitals. Before the acquired immunodeficiency syndrome epidemic, M. xenopi infection was infrequent and occurred in clusters; however, M. xenopi is now a recognized cause of pulmonary infection in immunocompetent patients with preexisting lung disease. The classic chest x-ray appearance is cavitary apical pulmonary disease, which mimics tuberculosis. M. xenopi is currently one of the most common NTM pathogens in parts of England and Canada and has been reported in parts of the northeastern United States. Whether the isolation of M. xenopi from our patient in Tennessee represents a new geographic distribution of this organism or technologic advancements that now allow for reliable identification is debatable. This case serves as a reminder to clinicians that the incidence of NTM infection is rising in the United States and that unusual NTM are capable of causing disease even in patients who are not immunocompromised.
Atypical Pott's disease: localized infection of the thoracic spine due to Mycobacterium avium-intracellulare in a patient without human immunodeficiency virus infection.
Mycobacterium avium-intracellulare (MAI) rarely causes disease of the spine in healthy individuals. We describe an elderly woman who had isolated skeletal involvement with MAI, mimicking Pott's disease. She responded well to surgical excision of the inflamed tissue and antibiotic therapy. Osteomyelitis due to MAI must be differentiated from that due to Mycobacterium tuberculosis because the treatment regimens are different.
Methotrexate-induced pulmonary lymphoma.
Methotrexate has proven to be effective in treating rheumatoid arthritis (RA), and is believed to be nononcogenic in the low weekly dose typically employed in the patients with RA. We report, however, a patient with RA in whom a rapidly enlarging diffuse large B-cell lymphoma developed in the left upper lung after weekly treatment with methotrexate for 5 years. The patient had a positive serum IgG for Epstein-Barr virus but a negative in situ hybridization of the resected specimen. Methotrexate therapy was discontinued, and the patient elected for clinical observation instead of chemotherapy or radiation therapy. There has been no clinically detectable recurrence of the lymphoproliferative disorder for 2 years. We believe that methotrexate has an oncogenic potential even in low weekly dosing in a subset of patients with RA and latent Epstein-Barr virus infection. The strongest causal link is demonstrated by the persistent tumor remission after stopping treatment with methotrexate.
Anaerobic blood cultures: useful in the ICU?
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Acquired methemoglobinemia: a rare but serious complication.
Topical and local anesthetics are employed during minor invasive procedures to increase patient tolerance and to reduce the need for intravenous sedation. A potentially fatal complication of these anesthetics is methemoglobinemia (Met-Hgb). Met-Hgb should be suspected in patients with cyanosis that does not respond to administration of oxygen and who have a discrepancy in oxygen saturation measured by pulse oximetry compared with the arterial partial pressure of oxygen (PaO2) determined by blood gas analysis. We present a patient who developed life-threatening Met-Hgb from the local anesthesia required during percutaneous endoscopic gastrostomy tube placement.
Spontaneous negative pressure changes: an unusual cause of noncardiogenic pulmonary edema.
The principal physiologic mechanism underlying the formation of negative pressure pulmonary edema (NPPE) is thought to be the creation of excessive negative intrathoracic force from inspiration against a critical obstruction of the upper airway. The increased subatmospheric transpulmonary pressures result in transudation of fluid from the pulmonary capillaries to the interstitium and alveoli. The clinical picture is that of pulmonary edema. Aggressive diagnostic and therapeutic intervention can be avoided if the syndrome is recognized early. This report highlights the clinical features of NPPE and serves as a reminder to the clinician that although NPPE can cause significant morbidity, conservative supportive therapy typically results in a good outcome.
Acinetobacter baumannii pneumonia: a case report and review of the literature.
Bacteria that constitute the genus Acinetobacter were originally identified in the first decade of the 20th century. However, it was not until the last decade that its role as an opportunistic pathogen was fully appreciated. It is now clear that Acinetobacter is an important cause of nosocomial infection and contributes significantly to the patient's morbidity and mortality. The prevalence of infection with A. baumannii has increased significantly during the last decade. At the same time, A. baumannii has developed one of the most impressive patterns of antibiotic resistance ever observed, establishing it as an important nosocomial pathogen. It has been nicknamed the "Gram-negative MRSA" because of its frequent resistance to commonly used antibiotics. Infection with A. baumannii should be suspected in hospitalized patients who are not responding to initial empiric antibiotic treatment, and the therapeutic approach should be customized according to when the pathogen is isolated.
Thiamine deficiency as a cause of metabolic acidosis.
Since its introduction in the 1970s, total parenteral nutrition (TPN) has gained popularity as a means of nutritional support for patients who cannot orally ingest sufficient calories and nutrients to promote wound healing or recovery from debilitating illness. As this treatment modality is employed among heterogenous groups of patients, a number of potential problems have been identified. Fortunately, most of these difficulties can be eliminated or minimized by understanding the metabolic goals of TPN and by employing proper catheter management. One of the unusual complications, a high anion gap metabolic acidosis refractory to bicarbonate therapy, occurred in one of our patients who was receiving TPN without adequate thiamine supplementation. The casual relationship between thiamine deficiency and metabolic acidosis has been well described in the literature, but remains under-recognized by many physicians.
Malnutrition and pulmonary tuberculosis.
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Simvastatin-induced lactic acidosis: a rare adverse reaction?
Simvastatin, a hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, is a commonly used cholesterol-lowering agent. The long-term safety profile of simvastatin, established over 10 years of clinical use, is excellent. HMG-CoA reductase inhibitors block 3-hydroxy-3-methylglutaryl coenzyme A reductase, the rate-limiting enzyme in cholesterol synthesis. However, other important nonsterol compounds, such as coenzyme Q10 (CoQ10), are also derived from the same synthetic pathway. CoQ10 is an essential carrier in the mitochondrial respiratory chain that participates in oxidative phosphorylation. Simvastatin and other HMG-CoA reductase inhibitors have been documented to lower serum concentrations of CoQ10. It has been suggested that the adverse effect of myopathy caused by HMG-CoA reductase inhibitors is due to CoQ10 deficiency in the tissue mitochondria. Documentation of this cause-and-effect phenomenon, however, has been lacking. We offer evidence that lactic acidosis may develop as a complication of simvastatin therapy. Our patient also manifested the well-known HMG-CoA reductase inhibitor drug toxicities of rhabdomyolysis and hepatitis. The occurrence of these known adverse events with lactic acidosis in our patient suggests that interference of the mitochondrial respiratory chain may play a role in the toxicity of this class of drugs.
Rhabdomyolysis of infectious and noninfectious causes.
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Acute respiratory distress syndrome following treatment for babesiosis.
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Rhabdomyolysis associated with pneumococcal pneumonia: an early clinical indicator of increased morbidity?
Rhabdomyolysis most commonly results from crushing injuries, the toxic effects of drugs and alcohol, seizures, and strenuous physical activity. Though rhabdomyolysis has been rarely identified with bacterial pneumonia, it has recently been recognized that in the setting of Legionella pneumophila pneumonia it has important prognostic implications. In the English literature, there are 12 well-documented cases of rhabdomyolysis associated with Streptococcus pneumoniae pneumonia. Interestingly, in the majority of these patients, including ours, S. pneumoniae grew from their blood. Bacteremia in patients with S. pneumonia doubles the death rate. Nine of the 12 patients, ours included, with S. pneumoniae pneumonia associated rhabdomyolysis developed renal dysfunction, as evidenced by an elevation in their blood urea nitrogen (BUN) and serum creatinine. Uremia also indicates a poor prognosis in patients with pneumococcal pneumonia. Serum creatinine phosphokinase (CPK) is a simple test that may allow early recognition of S. pneumoniae pneumonia in patients who are at an increased risk for a poor outcome, and permit timely therapeutic intervention.
Reactive airways dysfunction syndrome following metal fume fever.
Metal fume fever (MFF) is an acute response to the inhalation of heavy metals used in industry. The patient typically experiences symptoms of cough, fever, chills, malaise, and myalgia that are self-limited and of short duration. Wheezing may occur and pulmonary function may be acutely impaired with a decrease in lung volumes and diffusing capacity of carbon monoxide. Nevertheless, respiratory function quickly returns to normal, and persistent pulmonary insufficiency is unusual. Irritant-induced asthma is a non-immunogenic form of airway injury that may be associated with industrial inhalation exposure. In this situation, the direct toxic effect on the airways causes persistent airway inflammation and bronchial hyperreactivity. The two conditions are considered distinct entities, but we report a previously healthy worker who had classic MFF and was left with irritant-induced asthma or reactive airways dysfunction syndrome (RADS).