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Biomedical subjects

D Lacomis

Publications and source records attributed to D Lacomis.

At least 37 records · Page 2Linked to original sources
PubMed1997

Percutaneous needle muscle biopsy in the evaluation of patients with suspected inflammatory myopathy.

OBJECTIVE: To determine the usefulness of a unique method of percutaneous needle muscle biopsy (NMB) in patients with suspected idiopathic inflammatory myopathy (IIM). METHODS: The yield of percutaneous NMB was studied in 55 patients who were found to have a combination of clinical, laboratory, or electromyographic features of IIM. RESULTS: A diagnosis of IIM was confirmed histopathologically in 29 patients (53%), other specific myopathies were found in 5 (9%), nonspecific myopathic changes were present in 11 (20%), and a neurogenic process was diagnosed in 3 (5%). Nonspecific changes or no abnormalities were present in 7 patients (13%). Followup of the 18 patients with nonspecific histopathologic findings disclosed that only 3 had a subsequent disease course compatible with IIM. CONCLUSION: Percutaneous NMB is a safe, convenient, and relatively inexpensive method of muscle biopsy, with a high diagnostic yield for the pathologic confirmation of IIM. It should be considered as a primary method of acquiring muscle for histopathologic examination in the evaluation of suspected IIM.

Adult↗
PubMed1997

Acute onset of colchicine myoneuropathy in cardiac transplant recipients: case studies of three patients.

Colchicine causes both muscle and peripheral nerve toxicity of subacute onset in patients with renal insufficiency. We report three cardiac transplant recipients, treated with colchicine for cyclosporin A (CyA)-induced gout, who developed acute weakness due to colchicine myoneuropathy. The onset of disabling weakness occurred over a 1-2 week period. All three patients had concomitant renal insufficiency and an elevated serum creatine kinase and two elevated CyA levels at the time of presentation. Electromyography revealed features of myopathy and motor axonal neuropathy in all three patients. Two underwent muscle biopsy which confirmed the presence of sarcoplasmic vacuoles characteristic of colchicine-induced myopathy. All patients rapidly improved with either colchicine dose reduction or drug discontinuation. In conclusion, cardiac transplant recipients treated with CyA and colchicine may be at increased risk of developing colchicine-induced myoneuropathy especially in the setting of concurrent renal insufficiency. In patients with post-transplantation gouty arthritis, other treatment modalities are suggested; and if colchicine is administered, the dose should be reduced, CyA levels should be monitored closely and patients should be assessed for signs of neuromuscular toxicity.

Acute Disease↗
PubMed1997

October 1996--rapidly progressive weakness.

One week after a flu-like illness, a 51-year-old woman developed rapidly progressive weakness. Within three weeks, she required mechanical ventilation. A neurological exam revealed severe motor involvement with normal sensory findings confirmed by nerve conduction studies. Five days after intubation a catastrophic brain hemorrhage occurred. Autopsy showed severe loss of axons in the motor roots with periaxonal macrophages and no lymphocytes. These findings are typical of acute motor axonal neuropathy, which is rare in the United States.

Acute Disease↗
PubMed1996

Acute myopathy of intensive care: clinical, electromyographic, and pathological aspects.

An acute myopathy of intensive care occurs in critically ill patients treated with intravenous corticosteroids and neuromuscular junction-blocking agents. The full clinicopathological spectrum is uncertain. We evaluated the clinical, electrodiagnostic, and histopathological features of 14 patients who developed acute myopathy of intensive care after organ transplantation or during treatment of severe pulmonary disorders and sepsis. Patients received high-dose intravenous corticosteroids, usually in conjunction with relatively low to moderate doses of neuromuscular junction-blocking agents. After discontinuation of the latter drugs, most had diffuse, flaccid weakness with failure to wean from mechanical ventilation. Electrodiagnostic findings were consistent with a necrotizing myopathy. Muscle histopathology revealed myopathy with loss of thick filaments in 79%, mild myopathic changes in 14%, and atrophy of type 1 and type 2 fibers in 7%. Loss of thick filaments was identified in muscle biopsy specimens obtained 30 +/- 11 days (mean +/- standard deviation) after intravenous corticosteroid treatment but not in those obtained earlier (12 +/- 2 days). Critically ill patients, including those receiving organ transplants, may develop acute myopathy of intensive care after exposure to intravenous corticosteroids and neuromuscular junction-blocking agents, although the exposure to the latter drugs may be minimal. Selective loss of thick filaments is common in acute myopathy of intensive care, especially if the muscle biopsy specimen is obtained 2 weeks or more after intravenous corticosteroid exposure.

Acute Disease↗
PubMed1996

Hepatic myelopathy. Case report with review of the literature.

Hepatic myelopathy is a rare complication of hepatic insufficiency, causing progressive spastic paraparesis. There are few reports detailing the clinical and diagnostic aspects of this uncommon cause of neurological deterioration in patients with liver disease. Early recognition of this disorder will become more important as patients with liver disease survive longer due to medical advances, including liver transplantation. We present an additional patient with hepatic myelopathy associated with infantile portal vein thrombosis and review the previous reports of hepatic myelopathy in the English literature.

Adult↗
PubMed1996

Case of the month. June 1996--anorexia nervosa.

A 32 year old woman with a history of anorexia nervosa began experiencing severe muscle weakness. Proximal weakness was worse than distal and she became unable to walk. Serum creatine kinase was elevated 15-fold and EMG was consistent with a myopathic process. Muscle biopsy showed focal areas of absent staining using NADH and ATPase enzyme histochemistry. Gomori trichrome revealed many positive inclusions which were positive using immunohistochemistry for actin. Electron microscopy revealed these areas to contain cytoid bodies with Z-band streaming and disorganization of the myofibrillar network. These findings are consistent with the myopathy associated with ipecac (emetine) toxicity. A urine toxicology screen demonstrated evidence of emetine abuse, which was later admitted by the patient. Following discontinuation of the drug, the patient recovered normal muscle strength.

Adenosine Triphosphatases↗
PubMed1995

Disseminated histoplasmosis presenting as myositis and fasciitis in a patient with dermatomyositis.

A 54-year-old man with dermatomyositis initially responsive to corticosteroids and methotrexate developed severe myalgias, increasing weakness, and fevers. Laboratory studies were suggestive of disseminated histoplasmosis, and muscle biopsy revealed myositis, fasciitis, and yeast in the perimysial connective tissue. Histoplasma capsulatum was cultured from skeletal muscle. Despite antifungal therapy, necrotizing fasciitis progressed to gluteal abscess formation. Disseminated histoplasmosis may present atypically in immunocompromised hosts as fasciitis and myositis. Patients with dermatomyositis could be particularly vulnerable to soft tissue invasion by fungi due to their underlying microangiopathy.

Abscess↗
PubMed1993

Acute myopathy and neuropathy in status asthmaticus: case report and literature review.

A 38-year-old woman developed acute, severe weakness during the treatment of status asthmaticus that included high-dose intravenous corticosteroids. A muscle biopsy and EMG indicated a myopathy, and nerve conduction studies disclosed a neuropathic component. In association with corticosteroid tapering, the clinical, EMG, and nerve conduction abnormalities resolved. In some patients, intensive treatment of status asthmaticus may cause a reversible, toxic disorder of muscle and nerve.

Acute Disease↗
PubMed1993

Myopathy in the elderly: evaluation of the histopathologic spectrum and the accuracy of clinical diagnosis.

We undertook a retrospective clinicopathologic study to ascertain the spectrum of histopathologic muscle biopsy changes in the elderly thought to have a myopathy, and to determine the accuracy of clinical diagnosis of myopathy in the elderly compared with a younger control population. We compared muscle histology and case histories, as well as EMG and creatine kinase (CK) data, obtained over 10 years from 77 consecutive patients aged 65 years or older (75 +/- 6, mean +/- SD; group 1) with those from 104 patients aged 30 to 50 years (group 2). Prominent myopathic features were present in 42% (group 1) versus 51% (group 2) of all biopsies. Neurogenic changes (17% versus 9%, p < 0.04) and type II fiber atrophy (22% versus 6%, p < 0.0005) were more common in the elderly, whereas normal findings tended to be less frequent (19% versus 35%). In at least 68% of patients in both groups with the histologic diagnosis of myopathy, either the CK was elevated or the EMG was consistent with that diagnosis. Our study indicates that (1) the spectrum of histopathologic changes in the two groups differs because of a higher frequency of neurogenic change and type II atrophy in the elderly, and (2) the accuracy of clinical diagnosis of myopathy in the elderly approximates that in a younger population.

Aged↗
PubMed1992

Angiotropic lymphoma (intravascular large cell lymphoma) presenting with cauda equina syndrome.

A 50-year-old man developed cauda equina syndrome of unknown etiology that was stable for 20 months. Two months prior to sudden death, he experienced new back pain, confusion, seizures, and multiple cranial nerve palsies. Neuropathologic examination revealed angiotropic lymphoma without parenchymal involvement or infarcts in the brain, spinal cord, and muscle. In addition, nerve roots in the cauda equina contained angiotropic lymphoma and infarcts of various ages. Angiotropic lymphoma should be considered as a cause of cauda equina syndrome and of disorders that affect the central and peripheral nervous systems concurrently.

Brain Neoplasms↗
PubMed1988

Magnetic resonance imaging in pituitary apoplexy.

The diagnosis of pituitary apoplexy, an often-fatal disorder, is frequently delayed. Computed tomographic (CT) scanning has been shown to be useful in the detection of pituitary apoplexy; however, the value of magnetic resonance imaging (MRI) is yet to be determined. The MRI and CT scans of three consecutive and histopathologically proved cases of pituitary apoplexy were reviewed. The MRI scans obtained at least five days after the onset of symptoms suggested pituitary apoplexy (hemorrhage) in all three cases, while CT scanning indicated pituitary hemorrhage in only one case. Increased signal on the T1-weighted image was the hallmark on MRI scans in all three cases. These findings suggest that MRI scanning may be superior to CT scanning in identifying pituitary apoplexy, at least in the subacute phase.

Adult↗
PubMed1986

Spin-lattice relaxation (T1) times of cerebral white matter in multiple sclerosis.

Magnetic resonance imaging was used to evaluate the cerebral white matter of three subject groups: (1) 22 patients with known multiple sclerosis (MS) (11 with disease of shorter duration (0-5 years) and 11 with disease of longer duration (greater than 5 years]; (2) 9 patients with suspected MS; and (3) 12 normal volunteers. Transverse spin-echo (SE) 30/500 and 120/1000 radiofrequency pulse sequences were used for anatomic localization and plaque identification, respectively, while combined spin echo-inversion recovery was used for T1 determination. T1 values were calculated for grossly normal cerebral white matter in the frontal, parietal, and occipital lobes of normal volunteers and MS patients, and for plaques in MS patients. When compared with normals, the T1 values of plaque-free areas from definite MS patients (shorter and longer duration disease groups combined) were significantly longer in the frontal lobe (MS = 374 +/- 34 ms, Normal = 352 +/- 39 ms, P less than 0.05) and in the occipital lobe (MS = 414 +/- 37, Normal = 378 +/- 40, P less than 0.02). Although the T1 values of the shorter duration MS group were longer than those of normals, the difference was not statistically significant. Thus, the significant difference between the definite MS group (both shorter and longer duration) is more heavily weighted by the longer duration MS group. T1 values in patients with suspected MS without plaques were not significantly different from those of normals. In diagnosed MS patients, T1 values of plaques were significantly longer than T1 values of corresponding normal areas (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗