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E Pedrol

Publications and source records attributed to E Pedrol.

At least 19 recordsLinked to original sources
PubMed2001

Mitochondrial involvement in antiretroviral therapy-related lipodystrophy.

OBJECTIVES: The management of HIV infection has greatly improved during recent years essentially because of the appearance of new antiretroviral drugs. Highly active antiretroviral therapy (HAART) has achieved important reductions of viraemia and significant recoveries of CD4(+) cell counts in HIV-infected patients. Nonetheless, cases of HIV-infected individuals experiencing lipodystrophy (LD) are being increasingly reported. The purpose of this work was to analyse whether the presence of mitochondrial abnormalities is a frequent feature in LD, since we previously detected mitochondrial abnormalities in an HIV-patient. The second main objective was to study whether LD could be associated with a specific drug. DESIGN: Seven HIV patients presenting LD and five HIV non-LD controls participated in the study. LD patients met the following criteria: (1) LD was their only clinical abnormality, (2) LD was clinically relevant, (3) compliance with antiretroviral treatment was higher than 90% and (4) patients did not have personal or familial history suggestive of mitochondrial disease or neuromuscular disorder. METHODS: Histological stainings, histo-enzymatic reactions, enzymatic and respiratory activities of mitochondrial respiratory chain complexes, and mitochondrial DNA (mtDNA) depletion and rearrangements were examined on muscle mitochondria. RESULTS: Structural muscle abnormalities, mitochondrial respiratory chain dysfunction or mtDNA deletions were detected in all HIV lipodystrophic patients. CONCLUSIONS: The mitochondrial abnormalities found suggest that mitochondrial dysfunction could play a role in the development of antiretroviral therapy-related lipodystrophy.

Adult↗
PubMed2000

[Changes in emergency visits of patients infected by human immunodeficiency virus since the widespread use of protease inhibitors].

OBJECTIVE: To evaluate the changes in the urgent visits made by HIV+ patients after generalisation of the protease inhibitors. PATIENTS AND METHODS: Comparison on the visits made during a period prior to and after use of protease inhibitor. RESULTS: After the generalisation of the protease inhibitors the visits rate decreased, the motives for consulting with the physician and complementary examinations changed, invasive therapeutic procedures, admissions from urgencies and death rates decreased. CONCLUSIONS: The protease inhibitors have changed the urgent visits profile of HIV+ patients.

Acquired Immunodeficiency Syndrome↗
PubMed1998

Clinical, histological and molecular reversibility of zidovudine myopathy.

The use of zidovudine in the treatment of human immunodeficiency virus infection has been associated with toxic mitochondrial myopathy. There are some reported cases of improvement after stopping the drug, but in only one were molecular studies performed. We therefore studied three patients with toxic AZT myopathy during AZT treatment and after drug withdrawal. Clinical complaints disappeared within the next three months after drug cessation. In all cases, histological data of mitochondrial abnormalities also disappeared. Molecular studies showed an initial depletion of the total amount of mitochondrial DNA with respect to healthy controls which was reversible after AZT withdrawal. This work demonstrates that AZT myopathy is reversible not only at a clinical and histological, but also at a molecular level.

Adult↗
PubMed1997

Skeletal muscle studies in patients with HIV-related wasting syndrome.

Previous reports have suggested that HIV-related wasting syndrome may be considered as a form of myopathy. The aim of the present study was to investigate histopathological muscle changes in HIV-related wasting syndrome in order to know if there is a common substrate and whether muscle plays a primary or secondary role in its development. Patients with wasting syndrome diagnosed by Centers for Disease Control (CDC) criteria were prospectively evaluated. Clinical, analytical, nutritional, anthropometrical and muscular data were recorded. The patients were subdivided into two groups: group A was constituted by patients in whom wasting syndrome was the AIDS-defining illness, and group B by patients in whom AIDS diagnosis was previously made. In all cases muscle biopsy was performed and processed for conventional stainings and histochemical reactions. Thirty patients were included (group A, 12; group B, 18). Clinical, analytical, nutritional and anthropometrical data did not essentially differ between the two groups. All patients were malnourished with respect to controls. Histopathological findings in muscle biopsy were heterogeneous and similar in both groups, except for HIV-related myopathies, which were more frequently seen in the patients from group A (P=0.05). In five cases (17%) an unsuspected and potentially treatable myopathy was diagnosed. Patients with polyarteritis nodosa (two) or polymyositis (one) were treated with prednisone, which improved their wasting syndrome. By contrast, patients with AZT-myopathy (two) did not improve when the drug was discontinued. We conclude that in most cases the wasting syndrome cannot be considered as a true myopathy, and probably metabolic and/or nutritional factors may account for wasting development. However, in a subset of patients muscle biopsy allows the diagnosis of a treatable myopathy leading to the improvement of wasting syndrome.

Adult↗
PubMed1997

["Multicore" myopathy: report of 5 cases].

Five cases (three of them from a same family) of multicore myopathy are presented. The age at diagnosis ranged from 4 to 38 years. In 2 cases muscle complaints developed early in childhood while in the remaining 3 cases raised CK serum levels lead to perform a muscle biopsy. Malignant hyperthermia occurred in a young boy among the three affected relatives. Other family members are probably affected, suggesting an autosomal dominant inheritance. In none of the patients progressive disabling myopathy has occurred after a long term follow-up. A review of the bibliography is included, and clinical and evolutive characteristics of this myopathy are commented.

Adolescent↗
PubMed1997

[Chronic fatigue syndrome: study of the clinical course of 28 cases].

BACKGROUND: Chronic fatigue syndrome (CFS) is an entity of unknown etiopathogenesis without specific markers. The diagnosis is based on clinical criteria. There are few studies evaluating the natural evolution and prognosis-related factors in CFS. OBJECTIVES: a) to evaluate the outcome of patients suffering from CFS, and b) to detect predictive factors associated with a better prognosis. MATERIAL AND METHODS: Clinical records of all patients diagnosed of CFS between January 1986 and December 1992 were retrospectively reviewed. Of these patients, we included those fulfilling the CDC criteria for CFS, with a follow-up period greater than one year. We evaluated epidemiological, clinical and evolutive data recorded by their usual physicians. Moreover, the patients were interviewed in order to know their own appreciation with respect to their current clinical status, as well as their present working situation. RESULTS: Twenty-eight patients were included in the present study. Their mean age was 38 +/- 7. Seventy-five percent of them were women. The mean time of clinical follow-up was of 3.2 +/- 1.8 years. According to evaluation, 21% of patients improved or became asymptomatic. A similar percentage (28%) of improvement was obtained from the interview. Forty-eight percent of cases had transitory or definitive laboral incapacity. Regarding to prognostic factors, we could not find any statistical differences among the analyzed variables except for marital status. In this variable, married patients had better outcome than unmarried patients. CONCLUSION: CFS is an entity with a poor outcome, since it evolves towards to chronicity in an important number of cases. In addition, strong functional disability may be present, leading frequently to laboral incapacity.

Adult↗
PubMed1996

Lack of muscle toxicity with didanosine (ddI). Clinical and experimental studies.

Currently, 2',3'-dideoxyinosine (ddI) is used in AIDS therapy. To investigate the possible myotoxicity of ddI in patients infected with human immunodeficiency virus (HIV), we examined the effect of ddI in vitro in tissue cultures of skeletal muscles of rats exposed to ddI at doses equivalent to plasma ddI levels obtained in the treatment of HIV patients. Control cultures were exposed to normal saline and zidovudine (AZT). After 4 weeks no changes were noted in the ddI and normal saline cultures, but AZT cultures showed abnormal accumulation of mitochondria. The creatine kinase values in culture supernatants were all normal. We also reviewed the clinical, nutritional and biological parameters, AZT and ddI dosage, and histochemical findings in muscle specimens of 14 HIV patients receiving ddI therapy. All patients had previously received AZT. The mean cumulative dose of ddI was 91.6 gm. Two patients had myalgia, 9 muscle atrophy, and 13 weakness. All patients were malnourished. Five patients had mitochondrial myopathy related to AZT, 4 had ddI-associated neuropathy and 2 patients had only selective type 2 fiber atrophy. One patient had necrotizing vasculitis, one had scattered necrotic fibers and type 2 fiber atrophy and 2 had a normal muscle biopsy. On the basis of the results, we have been unable to implicate ddI as a cause of skeletal myopathy.

Adult↗
PubMed1996

Muscle involvement in rheumatoid arthritis: clinicopathological study of 21 symptomatic cases.

The aim of the current study was to analyze the frequency and characteristics of symptomatic myopathies occurring in rheumatoid arthritis (RA) patients, to correlate these findings with clinical data, and to evaluate their therapeutic implications. All RA patients from a cohort of 350 RA patients from a single institution who developed muscular symptomatology during an 8-year period were included in the study (n = 21). Clinical and laboratory data and electromyographic results were recorded in all cases, and an open muscle biopsy was performed. Weakness and muscle atrophy were the most common symptoms. Serum creatine kinase was increased in 8 cases (38%). Histopathologic study showed type 2 atrophy in 12 cases. In 13 cases, a treatable disease was diagnosed: dermatomyositis (n = 2), d-penicillamine-related dermatomyositis (n = 2), polymyositis (n = 1), muscular mononuclear cell infiltration (n = 3), polyarteritis nodosa (n = 1), glucocorticoid myopathy (n = 3), and toxic chloroquine myopathy (n = 1). In all but 1 patient, muscular clinical response to new therapy and/or drug withdrawal was satisfactory. Although symptomatic muscular involvement in RA is low (6% in the current series), we have found that nearly two thirds of cases were caused by potentially treatable conditions, mainly myositis or toxic myopathies.

Adult↗
PubMed1996

The effect of zidovudine on skeletal muscle mtDNA in HIV-1 infected patients with mild or no muscle dysfunction.

Zidovudine (ZDV), a nucleoside analogue which inhibits viral replication, is currently used in the treatment of type 1 human immunodeficiency virus (HIV-1) infection. It has been considered to be the cause of an acquired form of myopathy associated with a depletion of mitochondrial DNA (mtDNA) in muscle fibres, although the fact that the patients previously studied were clearly symptomatic, and the theoretical difficulty in differentiating on HIV-related myopathy from the effects of ZDV, led to a controversy on the possible deleterious effect of ZDV on muscle fibres. We studied the muscle biopsy taken from 42 HIV-1 infected patients, regardless of their medical complaints, and two series of controls: 12 HIV-negative patients suffering from diverse neuromuscular diseases and 10 normal patients who underwent orthopaedic surgery. Whole DNA was extracted following standard procedures and analysed by means of Southern blotting and polymerase chain reaction (PCR). We found that mtDNA was only depleted in HIV-1 infected patients treated with ZDV, but not in controls or patients untreated with this antiretroviral drug. Moreover, the depletion was more marked in patients who either presented weakness, myalgia, raised serum creatine kinase (CK), or ragged-red fibres. Mitochondrial DNA deletions were found in low proportion in all groups of patients, regardless of their HIV infection or ZDV status, but not in normal controls. We conclude that ZDV treatment in HIV-1 positive patients produces depletion of muscle mtDNA. The depletion can be demonstrated even in asymptotic patients, but is more marked in patients with clinical symptoms or abnormalities in their muscle biopsies. Other mtDNA abnormalities such as deletions seemed to be more related to other circumstances concurring in HIV-1 infected patients than to the effects of ZDV.

Adult↗
PubMed1996

Polyarteritis nodosa in human immunodeficiency virus infection: report of four cases and review of the literature.

Four patients with HIV infection were diagnosed as having panarteritis nodosa type vasculitis in muscle samples taken by biopsy. Fever, weight loss and neuromuscular symptoms were the major complaints. All but one were successfully treated with a low dose of prednisone. The other patient refused treatment, but her muscular complaints did not worsen during 9 months of follow-up. Previously reported cases in the literature are reviewed.

Adult↗