Intralesional sodium stibogluconate alone or its combination with either intramuscular sodium stibogluconate or oral ketoconazole in the treatment of localized cutaneous leishmaniasis: a comparative study

Background Cutaneous leishmaniasis (CL) is a disease caused by leishmania species. Intralesional sodium stibogluconate (SSG) has been considered the first line therapy for localized cutaneous leishmaniasis. There is still a need for more effective and less time‐consuming therapeutic methods for this condition. Objective The aim of the present study was to investigate if the combination of intramuscular (IM) SSG or oral ketoconazole with intralesional (IL) SSG would be more effective than the intralesional SSG given alone in the treatment of localized cutaneous leishmaniasis. Patients and methods Thirty patients with confirmed diagnosis of cutaneous leishmaniasis were included in the study. They were randomly assigned to three groups. The first group (10 patients with 12 lesions) was treated with intralesional SSG alone. The second group (10 patients with 15 lesions) was treated with the combination of intralesional SSG + intramuscular SSG. The third group (10 patients with 13 lesions) was treated with the combination of intralesional SSG and oral ketoconazole. A follow‐up was performed every 4 weeks for a treatment period of 12 weeks, then monthly for a period of 6 months after the end of the treatment. Results Complete cure occurred in 58.3% of lesions in group 1, while 93.3% and 92.3% of lesions were cured in group 2 and 3 respectively. The difference between group 1 and the other groups was statistically significant (P < 0.05). Conclusion Combined intramuscular SSG or oral ketoconazole with intralesional SSG is more effective than intralesional SSG alone for the treatment of CL. Oral ketoconazole is much easier and safer therapy than intramuscular SSG in combination with intralesional SSG in the treatment of localized cutaneous leishmaniasis.     

Mitochondrial DNA 8993 (NARP) mutation presenting with a heterogeneous phenotype including 'cerebral palsy'

The mitochondrial DNA (mtDNA) mutation 8993 is an important cause of Leigh's encephalopathy. A family is reported where other affected members have presented with non-specific delayed development or cerebral palsy. The diagnosis should be considered not only in children with Leigh's encephalopathy, but also in those with mild neurological dysfunction (including cerebral palsy) if there is a pigmentary retinopathy or a family history of neurological or ophthalmological disease. There was some correlation in this family between the disease severity and the proportion of mutant mtDNA in the blood. This mutation appears to segregate to high levels of mutant mtDNA rapidly within pedigrees and the mother of a severely affected child has a high risk of having further children with a high proportion of mutant mtDNA and a severe phenotype.     

Deafness after bacterial meningitis

Seventeen children with previous bacterial meningitis and 17 sib controls were examined clinically and otoscopically. They were also tested with air-conduction and bone-conduction audiometry and evaluated by tympanometry. There were no major neurological abnormalities and few otoscopical signs of ear disease. 21% of the ears showed abnormalities on air-conduction audiometry but all were normal on bone-conduction audiometry. 30% had abnormal middle-ear pressures (more negative than 100 mm water) on tympanometry and 7% had abnormal compliance of the drum. There were no significant differences on any test between the postmeningitis children and the sib controls. Population studies have confirmed that minor hearing loss due to middle-ear dysfunction is common in children, but is probably temporary in most of them. We have found no excess of middle-ear dysfunction and no sensorineural deafness in these postmeningitis children, but other workers have shown that nerve deafness may occur in association with clinical neurological damage. However, much of the deafness attributed to bacterial meningitis in other studies may well reflect population variability.     

Dopa-responsive dystonia in British patients: new mutations of the GTP- cyclohydrolase I gene and evidence for genetic heterogeneity

Dopa-responsive dystonia (DRD) was originally described in a series of Japanese patients, but is now increasingly recognized in other countries. Recently the GTP cyclohydrolase I (GTPCH) gene was isolated as the first causative gene for dopa-responsive dystonia (DRD). Mutations were identified in three Japanese families with autosomal dominantly inherited DRD and in one sporadic Japanese patient. Characterisation of the exon-intron boundaries of this gene has now allowed the analysis of mutations at the level of genomic DNA. Amplifying all six exons, we analyzed the GTPCH gene in nine British families with 33 affected family members and in three sporadic cases and found six new mutations. Only point mutations were found, causing a stop codon in one family and an amino acid change in highly conserved regions of the gene in a further four families and in one sporadic case. None of these mutations were detected more than once and none of the mutations previously described were found in our patients. No mutations were identified in four families and in two sporadic cases.      

T and B lymphocyte markers in effusions of patients with non-Hodgkin's lymphoma

T and B cells were sought in effusion fluids of 13 patients with lymphoma. In T cell lymphomas (four cases) morphologically abnormal cells that formed E rosettes were present. In B cell lymphomas (nine cases) morphologically abnormal cells were present in only two cases, however immunological studies showed a reduction in T cells and monoclonal light chain immunoglobulin expression in six of nine cases.     

Comparison of microscopic epididymal sperm aspiration and intracytoplasmic sperm injection/in-vitro fertilization with repeat microscopic reconstruction following vasectomy: is second attempt vas reversal worth the effort?

Since 1986, we have performed microscopic reconstruction in 18 men following failed microscopic vasectomy reversal. Between 1994 and 1996, nine couples have undergone microscopic epididymal sperm aspiration (MESA)/ intracytoplasmic sperm injection (ICSI) treatment for male infertility due either to congenital absence of the vas deferens (CAVD) or inoperable excurrent duct obstruction. We compared the cost efficiency of repeat vasectomy reversal to that for MESA combined with ICSI/in-vitro fertilization (ICSI/IVF). The cost of male partner procedures (vasectomy reversal, MESA) was based on physician and hospital charges, while the cost of ICSI/IVF included preparation of the female partner (medications and physician charges) and procedures (physician and hospital charges including oocyte retrieval, micromanipulation, and embryo transfer). Our cost examination does not include charges related to follow-up visits, prenatal monitoring, complications of pregnancy (i.e. miscarriage) or delivery in either group. Overall patency and pregnancy rates in the repeat vasectomy reversal group were 78 and 44% respectively. The cost per delivered baby (including multiple metachronos deliveries per couple) was $14892. Fertilization of oocytes has been achieved in 37/72 (51%) and pregnancies have occurred in 6/9 (67%) attempts and 5/9 (56%) report delivery. The average cost per pregnancy was $25637 and the average cost per delivered baby (or ongoing pregnancy) was $35570. The cost per delivery by MESA/ ICSI/IVF is 2.4 times the charges per delivery obtained through repeat vasectomy repair. Couples attempting to overcome infertility caused by vasal obstruction should be informed that vas reconstruction remains a cost effective means of re- establishing fertility even in men who have previously failed vasectomy reversal.