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H Dega

Publications and source records attributed to H Dega.

13 recordsLinked to original sources
PubMed2003

[Dapsone-induced sensory peripheral neuropathy].

INTRODUCTION: Peripheral neuropathy is a rare complication of dapsone therapy. CASE-REPORT: A 74 year-old woman was treated with dapsone, 50 mg per day, for a linear IgA dermatosis. One month later, the disease was controlled but the patient complained of a sensory peripheral neuropathy, which was documented on electromyographic studies. Dapsone was stopped and symptoms resolved within 24 hours. Three months after the beginning of linear IgA dermatosis, a colic adenocarcinoma was revealed by an acute occlusive syndrome. After surgical resection of the tumor, remission of linear IgA dermatosis was obtained with salazopyrine. DISCUSSION: This is a rare side effect of dapsone therapy. Twenty-one cases have been previously reported. In most cases, there was a pure motor or mixed neuropathy. Dapsone therapy was then stopped or decreased. Recovery usually occurs within one year after dapsone therapy is discontinued.

Aged↗
PubMed2003

[Amyloidosis complicating psoriatic arthritis].

BACKGROUND: Secondary AA amyloidosis is a classical complication of rheumatismal or chronic infectious diseases. Psoriasis is a rare cause of secondary amyloidosis with only around thirty cases reported in the literature. CASE REPORT: A 62 year-old man exhibited cutaneous lesions of psoriasis for six years complicated by articular involvement over the past year. The occurrence of an isolated proteinuria revealed renal and hepatic AA amyloidosis. Treatment with methotrexate (Méthrotrexate), enalapril (Renitec) and colchicine (Colchicine) was initiated and led to a stabilization of the proteinuria for two years. DISCUSSION: In psoriatic patients, secondary amyloidosis mainly complicates the arthritic diseases of prolonged progression. Our case report is original in the rapid onset of amyloidosis after the first articular signs. The clinical manifestations of secondary amyloidosis are related to renal or gastrointestinal involvement. Prognosis is usually poor. Treatment of secondary amyloidosis is difficult and relies on systemic treatment. Colchicine may be helpful.

Amyloidosis↗
PubMed2001

Activities of new macrolides and fluoroquinolones against Mycobacterium ulcerans infection in mice.

Mice infected in the left hind footpad with 5 log(10) acid-fast bacilli of Mycobacterium ulcerans were divided into an untreated control group and 17 treatment groups that received one of the following regimens for 4 weeks (all doses in milligrams per kilogram): 100 mg of azithromycin (AZM), 100 mg of clarithromycin (CLR), or 50 mg of AZM for a duration of 5 days a week (daily), three times a week, or once weekly. In addition, the following regimens were administered daily: 100 mg of telithromycin (TLM), sparfloxacin (SPX), or moxifloxacin (MOX); 200 mg of levofloxacin (LVX); 100 mg of streptomycin (STR) or amikacin (AMK); 10 mg of rifampin (RIF); and the combination of 10 mg of RIF and 100 mg of AMK (RIF+AMK). After completion of treatment, mice were observed for 30 weeks. The effectiveness of treatment regimens was assessed in terms of the delay in median time to footpad swelling in treated mice compared with that in the untreated controls. Clear-cut bactericidal activity, i.e., an observed delay in footpad swelling that exceeded the period of treatment, was observed in the STR-, AMK-, and RIF+AMK-treated mice. However, all mice treated with either AMK or STR alone had swollen footpads before the end of the 30-week observation period, suggesting regrowth of M. ulcerans. In contrast, 50% of the mice treated with the RIF+AMK combination exhibited no lesion even after 30 weeks, suggesting cure. The remaining regimens could be assigned to one of three groups: (i) no activity (50 mg of AZM, 100 mg of AZM thrice weekly, TLM, and LVX); (ii) bacteriostatic activity, i.e., a delay in footpad swelling shorter than the 4-week treatment duration (100 mg of AZM daily or once weekly, CLR thrice or once weekly, and MOX); or (iii) weak bactericidal activity (CLR daily and SPX). The RIF+AMK combination and possibly RIF+STR warrant further study for the treatment of M. ulcerans infection in humans.

Animals↗
PubMed2000

Activities of several antimicrobials against Mycobacterium ulcerans infection in mice.

Mycobacterium ulcerans inoculated into the footpads of mice at 6 x 10(3) CFU was shown to have a generation time of 6.5 days when estimated from weekly changes in microscopic counts of acid-fast bacilli (AFB) and 7.5 days when calculated from actual CFU enumerated on Lowenstein-Jensen egg medium incubated at 32 degrees C. Footpads became swollen at week 10 (W10) after infection, and all infected control mice were dead at W15 after infection. Daily (5 days/week) treatment with 100 mg of clarithromycin (CLR)/kg of body weight beginning the day after infection prevented swelling of footpads at W10. When initiation of treatment was delayed until obvious footpad swelling was observed, there was a reduction in both the increase in AFB counts and deterioration of swollen footpads and also a prolonged survival of the mice to W18. Mice infected in the hind footpads with 5 x 10(5) CFU of M. ulcerans were divided into an untreated control group and six treatment groups that received one of the following therapies for 8 weeks: 100 mg of CLR/kg, 25 mg of minocycline (MIN)/kg, 50 mg of sparfloxacin (SPX)/kg, 10 mg of rifampin (RIF)/kg, 10 mg of rifabutin (RBT)/kg, or 100 mg of amikacin (AMK)/kg. After completion of therapy, treated animals were observed for an additional 17 weeks. All control mice and mice treated with CLR, MIN, or SPX exhibited swollen footpads during the observation period. In contrast, of those animals treated with RIF, RBT, or AMK, none had footpad swelling and all inoculated cultures done after the W17 observation remained negative. These results suggest that RIF, RBT, and AMK may be effective in the treatment of human infection with M. ulcerans.

Animals↗
PubMed2000

[Mycobacterium ulcerans infection].

Mycobacterium ulcerans infection, or Buruli ulcer, is the third most common mycobacterial disease of the immunocompetent host in the tropical areas. M. ulcerans reservoir is aquatic. Infection occurs in children and young adults. The lesion begins with an indolent subcutaneous nodule, principally located on the limbs, that progressively changes into a deep indolent extensive ulcer. M. ulcerans produces a lipidic necrotic and immunosuppressive toxin, named mycolactone, that causes the clinical lesions. In endemic areas, clinical diagnosis is confirmed by microscopic examination. Spontaneous healing occurs after several months or years, causing retractile scars. Surgical excision and grafting is the treatment of choice. Antibiotic therapy is of limited value.

Adult↗
PubMed1998

[Pruritus and the hepatitis C virus. The MULTIVIRC Unit].

OBJECTIVE: Determine the characteristics of pruritus in a selected population of patients with positive hepatitis C virus serology. PATIENTS AND METHODS: In a retrospective study, we re-examined outpatient reports for patients who consulted for pruritus from January 1993 to April 1996 and were followed in a hepatology unit for hepatitis C infection. The following data were collected: age, sex, risk factors, HIV and HBV serologies, duration of pruritus and diagnosis, ALAT, gamma GT and total bilirubin, METAVIR score, HCV RNA PCR, search for cryoglobulins, antiviral and dermatology treatments. There were 1,060 patients followed in the hepatology unit during this period, including 327 with cirrhosis. RESULTS: Twenty-seven patients were retained for study, 16 men and 11 women, mean age 53 years. None of the patients had HIV infection, 7 had a past history of hepatitis B infection (positive for anti-Hbc antibodies). Median duration of pruritus prior to consultation was 3 months (95 p. 100 CI: 3 months-2 years). Pruritus was associated with non-specific lesion in 19 cases (70 p. 100: 95 p. 100 CI: 51-85 p. 100). There were excoriated eczema-like lesions in 11 cases (41 p. 100: 95 p. 100 CI: 15-49 p. 100). Other causes were urticaria in 5 cases (18 p. 100: 95 p. 100 CI: 7-36 p. 100), including 1 case of urticarial vasculitis with cryoglobulinemia, 2 cases with atopic dermatitis, and 1 case of primary biliary cirrhosis. In four cases, lichen planus was associated. Skin biopsies were obtained in 10 patients and showed eczema-like alterations in 9 and urticarial vasculitis in 1. Mean ALAT and gamma GT levels were 2.6 N (95 p. 100 CI: 1.9 N-3.3 N) and 2.2 N (95 p. 100 CI: 1.4 N-3 N) respectively, including 11 cases without cholestasis (normal gamma Gt). PCR was positive in 13 cases out of 15. Cryoglobulinemia was found in 10 cases out of 24. At consultation, 3 patients were given ursolvan, 7 interferon, 1 ursolvan with ribavirin, and 3 an interferon-ribavirin combination. Dermatology treatment associated antihistamine agents, emollients, and corticosteroids. This population of hepatology patients referred for pruritus comprised 2.5 p. 100 of all patients (95 p. 100 CI: 1.7-3.6 p. 100). Among them, 1.8 p. 100 (95 p. 100 CI: 1.1-2.7 p. 100) had eczema-like lesions associated with cutaneous xerosis. DISCUSSION: Pruritus in our patient population was generally associated with non-specific excoriations, prurigo or xerosis in 19 cases (70 p. 100). As only ambulatory patients were retained for analysis, this is not a comprehensive population and the percentage of non-specific pruritus, evaluated at 1.8 p. 100, is probably an underestimation. Cholestasis cannot explain alone these manifestations since 11 patients had normal gamma GT levels. Several etiologies could be involved: a direct effect of HCV, interferon. A prospective study should allow an estimation of frequency, risk factors and possible impact on quality of life.

Female↗
PubMed1996

Infections associated with totally implantable venous access devices (TIVAD) in human immunodeficiency virus-infected patients.

We report on a retrospective study evaluating infectious morbidity associated with totally implantable venous access devices (TIVAD) (Port-A-Cath) in HIV-infected patients. This study of 84 consecutive HIV-infected patients requiring 89 TIVAD between January 1990 and October 1993 was performed in the Department of Infectious Diseases Hôpital de l'Institut Pasteur, Paris, France. The total number of catheter days was 11,595. Eighteen of 89 patients with TIVAD (20%) were infected, causing 25 infectious events (25/89: 28%) among 17 different patients (17/84: 20%). The infection rate was 0.22 per 100 catheter days. Mean onset of infection was 82 days. Twenty microorganisms were isolated: Staphylococcus aureus in eight cases (40%), coagulase-negative Staphylococcus in six cases (30%), Streptococcus D faecalis in one case; Gram-negative bacilli were found in five cases (25%). All patients received an intravenous antibiotherapy combined with a local lock treatment in eight cases. Nine TIVAD removals were performed. One death was related to the TIVAD infection. No additional predisposing factor for infection was identified other than the implied condition of the HIV infection. The population and material in this study were homogeneous. The TIVAD infection rate was comparable to other published reports. Prospective evaluation comparing tunneled catheter and TIVAD in HIV-infected patients is needed.

Adult↗
PubMed1995

Brain stem encephalitis due to varicella-zoster virus in a patient with AIDS.

We describe a patient infected with human immunodeficiency virus (HIV) who had localized brain stem encephalitis due to varicella-zoster virus (VZV) and no cutaneous eruption. Diagnosis of the infection was based on the presence of Cowdry type A intranuclear inclusions in neurons, astrocytes, and oligodendrocytes positive for VZV (as shown by immunochemical staining). Although this infection is rare, we demonstrate the need for clinicians to include VZV infection in the differential diagnosis of rapidly progressive multiple cranial nerve palsies in HIV-infected patients, particularly because specific treatment for VZV infection is effective and relatively safe.

Acquired Immunodeficiency Syndrome↗