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Biomedical subjects

H H Hirsch

Publications and source records attributed to H H Hirsch.

At least 19 recordsLinked to original sources
PubMed2006

[Respiratory syncytial virus infections: measures in immunocompromised patients].

RSV infections are an annually recurring problem of significant morbiditiy and mortality in the immunocompromised host, especially after lung and stem cell transplantation. The effectiveness of hygienic (isolation) and therapeutic (ribavirin, immunoglobulin, pavilizumab) measures depends of high index of suspicion and rapid diagnostic confirmation by the antigen test, PCR and/or culture. Allocation of resources require stratification of measures according to the known or estimated risk for complications.

Adult↗
PubMed2006

Hearing loss after discontinuing secondary prophylaxis for cryptococcal meningitis: relapse or immune reconstitution?

Relapse and immune reconstitution syndrome are difficult to distinguish in HIV-infected patients treated with antiretroviral therapy (ART). We report on a 26-year-old HIV-infected male (CDC C3) with hearing loss on the right side 2 months after discontinuing secondary prophylaxis for cryptococcal meningitis. CD4 cell counts had increased from 32/microl to stable counts > 200/microl for the preceding 6 months on ART but HIV replication was not fully suppressed (7,000 copies/ml). Magnetic resonance imaging identified lesions at the origin of the right cranial nerve VIII. Lumbar puncture revealed monocytic pleocytosis, slightly increased protein, but normal glucose and lactate levels, negative microbiological studies. Fluconazole was restarted and a new ART regimen was started in order to fully suppress HIV replication. Clinical and radiological signs were reversible during follow-up, and secondary prophylaxis was stopped after 6 months without adverse events. We review 26 published cases of cryptococcal infections with immune reconstitution syndrome and highlight the distinguishing features.

AIDS-Related Opportunistic Infections↗
PubMed2006

Polyomavirus-associated nephropathy: update of clinical management in kidney transplant patients.

Over the last decade, polyomavirus-associated nephropathy (PVAN) has occurred with increasing frequency after renal transplantation, leading to significant renal dysfunction and graft loss. More than 95% of all cases are caused by the human polyomavirus type 1 called the BK virus. The primary treatment for PVAN is immunosuppression reduction, which must be carefully balanced against increased risks of rejection. Although no validated protocols exist, a first step commonly involves reduction of calcineurin inhibitors with antiproliferative agents by more than one-third, e.g., reaching trough levels of tacrolimus <6 ng/mL, of cyclosporine <150 ng/mL, dosing of mycophenolate mofetil to <1 g/day, and azathioprine <75 mg/day. When rejection is diagnosed together with PVAN, a transient pulse treatment is recommended before subsequent reduction in immunosuppression. No antiviral treatments for PVAN have been approved by the United States Food and Drug Administration. The antiviral drug cidofovir has shown in vitro activity against murine polyomaviruses, and has been used in some patients in lower doses in an effort to minimize the nephrotoxic effects of cidofovir while treating PVAN. Small series of PVAN patients treated with leflunomide, intravenous immune globulin therapy, and fluoroquinolones have also been reported recently.

BK Virus↗
PubMed2006

Polyomavirus-associated nephropathy: update on BK virus-specific immunity.

The human polyomavirus type 1, also called BK virus (BKV), causes polyomavirus-associated nephropathy (PVAN) in 1-10% of renal transplant recipients, with graft loss in over 50% of cases. The risk factors for PVAN are not conclusively defined and likely involve complementing determinants of recipient, graft, and virus. A central element seems to be the failing balance between BKV replication and BKV-specific immune control, which can result from intense triple immunosuppression, HLA-mismatches, prior rejection and anti-rejection treatment, or BKV-seropositive donor/seronegative recipient pairs. Consistent with this general hypothesis, the timely reduction of immunosuppression in kidney transplant recipients reduced graft loss to less than 10% of cases. However, the BKV-specific humoral and cellular immune response is not well characterized. Recent work from several groups suggest that changes in antibody titers and BKV-specific CD4+ and CD8+ T cells may help to better define the risk and the course of PVAN in renal transplant patients.

BK Virus↗
PubMed2005

[Infections after organ transplantation].

Early postoperative infections after transplantation vary according to the transplanted organ. During the subsequent course opportunistic infections such as cytomegalovirus reactivation, Pneumocystis jiroveci pneumonia, invasive pneumococcal infection and mould infections predominate. Reactivated tuberculous infection appears to become more prevalent. Some of the opportunistic infections are preventable by chemoprophylaxis; others can be managed very effectively by monitoring and early preemptive therapy. Physicians caring for patients after organ transplantation need to early consider in the differential diagnosis rare pathogens which are often overlooked with standard diagnostic procedures.

Bacterial Infections↗
PubMed2005

Genotypic and phenotypic resistance testing of HIV-1 in routine clinical care.

Data on genotypic and phenotypic resistance testing of HIV-1 in the routine clinical setting are lacking. In a retrospective single-center study, all patients (n = 102) for whom genotypic resistance typing (GRT) and phenotypic resistance typing (PRT) were performed during the calendar year 2002 were examined. GRT and PRT results were concordant for 79% of the drugs, being highest for nevirapine (92%) and lowest for didanosine (57%). Concordance of results for protease inhibitors was lowest for lopinavir (78%) and highest for indinavir (88%). Discordant results for lamivudine were observed in 16% of patients; 90% of these results corresponded to high-level resistance by PRT and susceptibility by GRT. Overall, HIV loads were lower and CD4+ cell counts higher after therapy following resistance testing, but a significant association with the number of active drugs as predicted by GRT or PRT could not be identified. In a subgroup of 43 patients with virological failure under antiretroviral therapy and sufficient follow-up data, HIV loads were significantly lower after 3 and 6 months. More patients with HIV loads <400/ml had 2 or more active drugs according to PRT (21/29 [75%]) than according to GRT ([15/29 [52%]; p = 0.109. This was also found for HIV loads <50/ml (PRT 16/22 [72%], GRT 10/22 [42%]; p = 0.103), although the differences were not statistically significant. There was no discernable difference between GRT and PRT in the clinic-based population, but the numbers of resistance tests performed are not sufficient to draw definitive conclusions.

Adult↗
PubMed2005

[Diagnostic tests of Lyme borreliosis].

The diversity of Borrelia burgdorferi subspecies (sensu lato) in Europe does not allow to simply adopt the US definitions and tests which were established for B. burgdorferi sensu stricto. Routine detection of Borrelia-specific antibodies now includes specific antigens of the subspecies B. afzelii and B. garinii. Thus, the 2-step serology of screening by ELISA and confirmation by immunoblot remains the most important diagnostic test of lyme borreliosis. The detection of borrelia by PCR or culture is of lesser importance due to the limited sensitivity, despite of the high specificity. In clinical practice, the risk of exposure to ticks and the stage of the clinical presentation guide the choice of appropriate diagnostic procedures and their interpretation.

Bacterial Typing Techniques↗
PubMed2004

[Cutaneous coagulase-negative staphylococci--always harmless?].

Staphylococcus lugdunensis belongs to the group of coagulase-negative staphylococci, but share many clinical and microbiological characteristics with Staphylococcus aureus. We report two cases of chronic recurrent purulent skin infections in two females (one immunocompetent, the other HIV-infected with CD4 cell counts of 438/microl) who were treated repeatedly with antibiotic and surgical interventions, but only became free of recurrences after this was combined with a decontamination strategy.

AIDS-Related Opportunistic Infections↗
PubMed2004

Improved outcome of polyoma virus allograft nephropathy with early biopsy.

Polyoma virus allograft nephropathy often results in accelerated graft loss despite reduction of immunosuppression and/or treatment with antiviral agents. Irreversible renal fibrosis due to late diagnosis is likely to be one of the important causes of treatment failure. Early biopsy in 14 patients resulted in stable graft function after a mean follow-up of 22 months.

Biopsy↗
PubMed2004

Cost efficiency in the prospective diagnosis and follow-up of polyomavirus allograft nephropathy.

Evaluation of urine cytology (UC) for decoy cells and quantitative determinations of viruria (urine viral load [UPCR])and viremia (viral load in blood [VLB]) have been proposed as surrogate markers of polyomavirus allograft nephropathy (PVAN). In this study, we present the experience with the concurrent evaluation of UC, UPCR, and VLB in 349 patients (940 sets of samples). Results were correlated with each other and with a previous, concurrent, or subsequent biopsy diagnosis of PVAN. Patients were followed up for a mean of 27 months posttransplantation. We conclude that both UC and UPCR are useful for screening of renal transplant recipients. Simultaneous performance of both UC and UPCR does not add useful clinical information. In patients with positive UC, performance of UPCR, however, can allow for the distinction between BK and JC polyoma viruses. Quantitative measurement of viremia is not indicated in patients lacking viruria because no patients with PVAN present with this combination of findings. In patients with viruria, a positive viremia strongly correlates with PVAN. Rationale selection of screening protocols based on the current knowledge of the infection and tailored to the available laboratory capabilities in each transplantation center can optimize the use of resources.

Biopsy↗
PubMed2003

[HIV-infection, HAART (highly-active antiretroviral therapy) and hyperlipidemia].

HISTORY AND ADMISSION FINDINGS: A 42-year-old man with long-standing HIV-infection (CDC C3) and multiple treatment failures was seen for follow-up 6 months after starting a new HAART (zidovudine, efavirenz, indinavir, ritonavir). The medical history is remarkable for a hypersensitivity reaction to abacavir, past smoking (10 pack years) and a family history of coronary heart disease of the patient's mother. Physical examination revealed discrete signs of lipoatrophy of the face, arms and legs, but no lipoaccumulation (hip-waist ratio 0.94; body mass index 22 kg/m2). Blood pressure measured 156/92 mmHg. LABORATORY FINDINGS: A rise in CD4 cell count from 24/ microL to 60/ microL was noted. For the first time, the HIV viral load decreased to < 50 copies/mL. Concentrations of triglycerides and cholesterol were found to be increased to 26 mmol/L (2275 mg/dL) and 15 mmol/L (580 mg/dL), respectively, compared previously normal readings. Other parameters were in the normal range. DIAGNOSIS AND THERAPY: Continuation of HAART resulted in rising CD4 counts to > 200/ microL and HIV viral load suppression to < 50 copies/mL. Neither dietary measures nor treatment with pravastatin significantly changed the drug-induced mixed hyperlipidemia. Treatment with fenofibrate (200 mg qd), however, was followed by a significant reduction of triglyceride and cholesterol concentrations to 12 mmol/L (1050 mg/dL) and 10 mmol/L (387 mg/dL). Addition of pravastatin did not result in further improvement. Arterial hypertension was diagnosed by ambulatory 24-h blood pressure monitoring (systolic 157+/-11 mmHg; diastolic 97+/-10 mmHg). CONCLUSION: HAART-induced mixed hyperlipidaemia is likely to increase the cardiovascular risk. According to first estimates, the 3-year risk of myocardial infarction amounts to 1.29 - 2.09 % for our patient. The 3-year risk of HIV progression to AIDS or death is > 30 % if HAART is stopped or fails upon switching due to unknown archived drug resistance. Thus, despite unsatisfactory lipid profiles, a modification of HAART seems only acceptable, if new, equally potent, but less lipidaemic drug combinations are available.

Adult↗