Toenail onychomycosis in patients with acquired immune deficiency syndrome: treatment with terbinafine

The samples of blood freshly taken from healthy men were gamma-irradiated with a dose of 10 Gy. It was shown that after the treatment the blood gained the capacity to emit secondary biogenic radiation. Emission lasted for some hours, passed through quartz-glass cuvette and was revealed by stimulating influence on biological detector (sprouting seeds).     

Cytomegalovirus preemptive therapy with ganciclovir in renal transplant patients treated with OKT3

In an attempt to decrease the prevalence and severity of cytomegalovirus (CMV) disease, preemptive therapy with ganciclovir was administered to all renal transplant patients treated with OKT3 between February 1993 and December 1994 (26 patients). The results were compared with those of a historical group treated with OKT3 but not with ganciclovir (29 patients). Both groups were similar in age, sex, number of previous transplants, number of rejections, serological status of donor and recipient and OKT3 dose. Ganciclovir was administered during the period of treatment with OKT3. Only 2 (7.7%) treated patients developed CMV disease versus 11 (37.9%) of the control group (p = 0.01). In the control group the intensity of the disease was severe in 7 (63.6%) cases, whereas in the treated patients it was always of slight intensity (p = 0.01). In conclusion, preemptive therapy with ganciclovir during treatment with OKT3 decreases the prevalence and severity of CMV disease.     

The role of endoscopic sinus surgery in patients with acquired immune deficiency syndrome

Pseudofolliculitis barbae, commonly referred to as "razor bumps" or "ingrown hairs," is a papular and pustular, foreign body inflammatory reaction that can affect any individual who has curly hair and who shaves. This condition is a particular nuisance to African-Americans. This report will discuss the causes of pseudofolliculitis barbae and present a systematic approach to treatment.     

Pleural disease and acquired immune deficiency syndrome

Patients with acquired immune deficiency syndrome (AIDS) do not frequently have pleural complications. However, pneumothorax is a troublesome complication of patients with AIDS. At some medical centres, more than 50% of patients with spontaneous pneumothorax have AIDS. Most patients with spontaneous pneumothorax and AIDS have Pneumocystis carinii infection and necrotic subpleural blebs. The pneumothoraces in these patients usually cannot be managed with tube thoracostomy alone. Patients who do not respond to tube thoracostomy are best managed with a Heimlich valve or with thoracostomy with stapling of blebs and pleural abrasion. Approximately 2% of human immunodeficiency virus (HIV)-positive individuals will have a pleural effusion. Parapneumonic effusions or empyema, tuberculosis and Kaposi's sarcoma are the three leading causes. P. carinii infection is frequently responsible for pulmonary infections, but is only occasionally responsible for a pleural effusion. Pleural effusions may also develop from non-Hodgkin's lymphoma (NHL). There is one relatively rare NHL that is associated with the Kaposi's sarcoma associated virus that produces a lymphoma confined to the body cavity.     

Varicella zoster virus retrobulbar optic neuritis preceding retinitis in patients with acquired immune deficiency syndrome

A 10-year-old girl with lupus vulgaris following single BCG vaccination is reported. She had a 15 x 20 cm painless lesion covering her left shoulder, axilla, triceps and biceps region. PPD test was positive. Histopathological picture was identical to lupus vulgaris.     

Quantitative cytomegalovirus DNA level in the blood and its relationship to cytomegalovirus retinitis in patients with acquired immune deficiency syndrome

OBJECTIVE: A pilot study was performed to determine whether relationships exist between changes in a quantitative solution hybridization assay for cytomegalovirus (CMV) DNA in the blood and development of CMV retinitis, development of nonocular CMV disease, or reactivation of pre-existing CMV retinitis lesions. DESIGN: Observational case series. PARTICIPANTS: Two groups of human immunodeficiency virus-infected patients: 10 CMV antibody-positive patients with CD4+ T-lymphocyte counts of less than 50 ml and no CMV disease at baseline and 11 patients with CMV retinitis but no extraocular CMV disease at baseline. INTERVENTION: Quantitative changes in leukocyte-associated CMV DNA levels were observed over time. Anti-CMV therapies were based on clinical findings only. MAIN OUTCOME MEASURES: Development of CMV end-organ disease or change in activity of pre-existing CMV retinitis lesions was measured. RESULTS: Among patients with no CMV disease at baseline, four had CMV disease develop during follow-up (three cases of CMV retinitis, one case of presumed CMV esophagitis); all had CMV DNA levels greater than 5000 genomes/ml before the onset of CMV disease. The remaining six patients had levels less than 5000 genomes/ml throughout follow-up (P = 0.05). Among patients with CMV retinitis at baseline, all whose CMV DNA blood levels rose more than tenfold had extraocular CMV disease or reactivation of CMV retinitis develop. Raised CMV DNA blood levels were not seen in every patient with clinical reactivation of CMV retinitis. CONCLUSION: Elevated or rising CMV DNA blood levels appear to be associated with the development of CMV disease in individuals with low CD4+ T-lymphocyte counts. In patients with CMV retinitis, rising levels appear to be associated with the development of extraocular CMV disease or reactivation of CMV retinitis. Conversely, reactivation of CMV retinitis also may occur in the absence of changes in CMV DNA blood levels. Further studies are warranted to determine whether changes in CMV blood levels can be used as a guide for preemptive therapy to prevent reactivation of CMV retinitis lesions or to help choose between local and systemic therapy for management of reactivations.     

Social stress results in altered glucocorticoid regulation and shorter survival in simian acquired immune deficiency syndrome

From early in the AIDS epidemic, psychosocial stressors have been proposed as contributors to the variation in disease course. To test this hypothesis, rhesus macaques were assigned to stable or unstable social conditions and were inoculated with the simian immunodeficiency virus. Animals in the unstable condition displayed more agonism and less affiliation, shorter survival, and lower basal concentrations of plasma cortisol compared with stable animals. Early after inoculation, but before the emergence of group differences in cortisol levels, animals receiving social threats had higher concentrations of simian immunodeficiency virus RNA in plasma, and those engaging in affiliation had lower concentrations. The results indicate that social factors can have a significant impact on the course of immunodeficiency disease. Socially induced changes in pituitary-adrenal hormones may be one mechanism mediating this relationship.     

Induction of feline acquired immune deficiency syndrome by feline leukemia virus: immuno- and neuroendocrine dysfunctions

Young cats, when chronically infected with feline leukemia virus (FeLV), developed feline acquired immune deficiency syndrome (FAIDS). The syndrome was associated with a sequence of dysfunctions in the hypothalamic-pituitary-gonadal (HPG) and the immune system, manifested in the reduction of luteinizing hormone-releasing hormone (LHRH), follicle stimulating hormone (FSH), luteinizing hormone (LH), and testosterone in blood plasma. The average FSH and LH (in plasma or lymphocyte), testosterone, and LHRH concentrations in the 20 FeLV-infected cats were measured by radioimmunoassay. The results were compared with those of the 12 control cats that were not FeLV-infected. Four weeks after infection, the plasma LHRH concentration in the infected cats showed a 43% reduction. Five to six weeks after infection, the content of FSH and LH in lymphocyte was reduced by 50% and 28%, respectively, whereas, the plasma FSH and LH was reduced by 52% and 42%, respectively. A significant reduction in testosterone content was detected at Week 11 of infection. The onset of the immuno- and neuroendocrine dysfunctions in FAIDs cats followed this sequence: hypothalamus, lymphocyte, pituitary, adrenal gland, and gonads. Indirect immunofluorescence assay showed the presence of FeLV cytoplasmic antigens in the fibers of the hypothalamic preoptic region and the Leydig cells. The possible causal relationship between the dysfunction of the lymphocyte and HPG systems and the presence of FeLV was discussed.     

Systemic meningococcal infections in patients with acquired complement deficiency

Congenital deficiency of the late components of the complement may predispose the individual to systemic meningococcal infection. Assuming that patients with acquired complement deficiencies may also have an increased risk of contracting meningococcal infections, a retrospective and prospective study to assess this association was conducted. Over 20 years (1970-1989), 30 patients with meningococcemia or meningococcal meningitis, proven by blood or CSF culture, were treated at the Beilinson Medical Center. Only one patient died of the infection. Risk factors were found in three patients (10%). One had a congenital deficiency of C7, and two had acquired complement deficiency due to systemic lupus erythematosus (SLE) and membranoproliferative glomerulonephritis (MPGN). These latter two patients had low serum concentration of C3 and C4 and reduced complement hemolytic activity before onset of the infection. Since the incidence of culture-proven systemic meningococcal infection in the Jewish population in central Israel is 1/100,000, and the prevalence of SLE and MPGN is, at most, 250/100,000, the finding of two patients with meningococcal infection and these rare disorders is over 100 times the expected incidence. We conclude that patients with acquired complement deficiency are at significant risk of meningococcal infection.     

Neurogenic bladder in patients with acquired immunodeficiency syndrome

We have performed a urodynamic study on 3 patients with acquired immunodeficiency syndrome (AIDS), presenting with a neurogenic bladder. The first patient had an ascending myelitis of probable herpetic origin, the second patient had a cerebral abscess caused by Toxoplasma gondii, and the third patient had an AIDS dementia complex. The urodynamic study showed an areflexic detrusor in the first 2 patients, and a hyperreflexic detrusor in the third patient.     

Pulmonary cryptosporidiosis in patients with acquired immunodeficiency syndrome

Several reports have showed Cryptosporidium species as a cause of intractable diarrhea and malabsorption in patients with acquired immunodeficiency syndrome (HIV). A case of chronic diarrhea in a drug addict woman associated with a symptomatic interstitial pulmonary infection due to Cryptosporidium parvum is described. This unusual C. parvum spread into the bronchial tree is underlined and a survey of the literature is made.     

Mycobacteremia in patients with the acquired immunodeficiency syndrome

BACKGROUND: Bacillemia is a key event in the pathogenesis of tuberculosis. Although current evidence indicates that Mycobacterium tuberculosis bacteremia is rare in patients seronegative for the human immunodeficiency virus, it has been increasingly reported in patients with the acquired immunodeficiency syndrome (AIDS). OBJECTIVE: To determine clinical and laboratory characteristics of patients with AIDS and tuberculosis with and without bacillemia. METHODS: Fifty patients with AIDS with clinical suspicion of disseminated mycobacterial disease were prospectively selected. Three consecutive blood samples were collected for culture using a standardized protocol. RESULTS: Mycobacterium was isolated from any body site in 42 patients (84%). Bacillemia was detected in 30 (71.4%) of these 42 patients: 11 (28.2%) caused by Mycobacterium avium-intracellulare complex and 19 (71.8%) caused by M tuberculosis. Blood culture was the only method used to confirm the diagnosis in 5 (15%) of the 33 tuberculosis cases. Tuberculosis in patients with AIDS developed with nonspecific insidious symptoms, a remarkable elevated alkaline phosphatase level, and without the classic miliary radiological pattern. We could demonstrate 2 previously unrevealed clinical characteristics of bacteremic tuberculosis in patients with AIDS: a shift to the left in the white blood cell count and abdominal lymph node enlargement. In patients with tuberculosis, the in-hospital mortality rate was higher among patients with bacillemia, although the posttreatment survival rate was comparable. CONCLUSIONS: Blood culture is a valuable tool to confirm the clinical diagnosis of disseminated tuberculosis in patients with AIDS and can distinguish patients with characteristic clinical findings and outcome. Abdominal ultrasonography may be an additional helpful tool to identify these patients.     

A case of acquired immune deficiency syndrome presenting acute lumbosacral polyradiculopathy due to opportunistic infection of cytomegalovirus

The binding of antiphospholipid antibodies to circulating platelets and the potential association with thrombocytopenia and platelet activation was investigated in 25 patients with primary antiphospholipid syndrome (APS). Fourteen patients had a platelet count above 150 x 10(9)/l, and 11 patients had mild to moderate thrombocytopenia of 50-150 x 10(9)/l. The presence of platelet autoantibodies was investigated by immunofluorescent binding. No correlation between the presence of autoantibodies on platelets and thrombocytopenia was found. The binding of antibodies in patients' serum and platelet eluates was investigated by performing enzyme-linked immunosorbent assays with phospholipids as antigens. In seven patients antibodies to negatively charged phospholipids were present in platelet eluates. Platelet activation was measured by flow cytometry using a fluorescein isothiocyanate (FITC) labeled monoclonal antibody to P-selectin (CD62). The binding of anti-P-selectin to patients' platelet surface P-selectin was not increased, compared with the binding to platelets obtained from normal donors. Platelet serotonin concentration in APS patients was significantly lower than that found in the platelets of normal controls. More studies are necessary to determine the exact role of antiphospholipid antibodies in the pathogenesis of thrombocytopenia, and to elucidate the cause of low serotonin levels in platelets of APS patients.     

Should recurrent Cytomegalovirus infections in patients with liver transplantation be treated?

Cytomegalovirus (CMV) is the single most important viral pathogen in organ transplantation. Treatment strategy for CMV infection and disease is not well established in transplantation. We report a case of primary CMV infection and two relapses in a woman with a liver transplant in whom spontaneous clearing of the second CMV relapse was seen. A 23 year-old CMV-seronegative woman received a liver transplant with a CMV-negative organ. Six weeks after transplantation she had her primary CMV infection proved by seroconversion and virus isolation. She had no clinical symptoms. Treatment with ganciclovir for five weeks resulted in declining CMV-antigen positive cells from 300/200.000 PMNs to CMV-antigen negativity. Only a slight antibody response was seen. At week 13 the first relapse occurred evidenced by antigenaemia. Ganciclovir was reinstituted for six weeks resulting in reduced antigenaemia. At week 22 liver biopsy was performed due to slightly elevated ALAT. The biopsy showed evidence of focal CMV hepatitis and blood analysis showed 120 CMV-antigen positive cells/200.000 PMNs. In spite of this, ganciclovir was not reinstituted, but the immunosuppressive treatment was reduced to a minimum to stimulate the patient's immune response to CMV. During the following months the patient gradually developed IgG antibody, cleared the antigen and levels of liver enzymes returned to normal. We suggest that ganciclovir treatment, may be omitted in cases of relapse with minimal clinical symptoms, slight antigenaemia and a beginning antibody response and that, the immunosuppressive treatment should be reduced instead. Such an approach requires careful clinical monitoring of the patient.     

Progressive ocular toxoplasmosis in patients with acquired immunodeficiency syndrome

We studied two patients, a 43-year-old Hispanic man with a one-year history of acquired immunodeficiency syndrome (AIDS) and a 34-year-old Hispanic man with newly diagnosed AIDS. Both had necrotizing retinitis that progressed to panophthalmitis and orbital cellulitis. Toxoplasmosis was not diagnosed in the first patient early in the course of the disease. The second patient had a history of toxoplasmic retinochoroiditis. Despite anti-toxoplasmosis therapy, visual acuity deteriorated to no light perception in both patients. Diagnostic biopsy of the eye wall was performed on the first patient and enucleation of the globe on the second. Toxoplasmic panophthalmitis and orbital cellulitis were diagnosed in each patient by light microscopy and confirmed by electron microscopy. When patients with AIDS develop necrotizing retinitis, toxoplasmosis must be considered in the differential diagnosis, along with cytomegalovirus retinitis, progressive outer retinal necrosis, and syphilitic retinitis. Unlike cytomegalovirus retinitis, progressive outer retinal necrosis, and syphilitic retinitis, however, toxoplasmosis can cause a progressive intraocular infection, panophthalmitis, and orbital cellulitis in patients with AIDS.     

Septic shock in patients with the acquired immunodeficiency syndrome

OBJECTIVE: To evaluate the prognosis of patients with septic shock admitted to an intensive care unit (ICU), according to their HIV serostatus. DESIGN: Retrospective study. SETTING: Medical ICU of a university hospital. PATIENTS: 76 patients with septic shock admitted to the same ICU, of whom 28 were HIV positive and 48 were HIV negative. MEASUREMENTS AND RESULTS: Severity scores, number and type of organ failures, and survival rates were assessed in the two groups of patients. Glasgow Coma Scale and general severity scores [Acute Physiology and Chronic Health Evaluation II and Simplified Acute Physiology Score (SAPS)] were significantly worse in HIV-infected patients. The total number of organ failures was also higher in the HIV-positive group: 3.7 +/- 0.2 vs 3.1 +/- 0.2 in the HIV-negative group (p < 0.001). On day 28, 21 (46%) HIV-negative patients were dead compared to 26 (93%) patients in the HIV-positive group (p < 0.001). In the multivariate analysis, HIV infection was an independent risk factor for mortality, as were the SAPS score, use of mechanical ventilation, and the McCabe score. CONCLUSIONS: This study reports a considerable excess mortality in HIV-infected patients with septic shock. Although severity of illness was clearly much more pronounced in HIV-positive patients, retroviral infection was independently associated with death. Improving survival in HIV-positive patients with septic shock may require earlier diagnosis and treatment of the causative infection.     

Extracorporeal lithotripsy in patients with acquired or congenital coagulopathies

Post ESWL haemorragic complications are frequent and most patients experience temporary haematuria and focal intrarenal bleeding or perirenal haematoma are detected by NMR or US imaging. By tradition coagulation troubles have been a contraindication for ESWL but literature describes cases of coagulopathic patients treated with ESWL. From January 1992 to July 1993, 4 of our patients with severe haemostatis troubles (severe haemophilia A in two cases, acquired deficit of coagulation factors and mild thrombocytopenia secondary to post-necrotic hepatitis in 1 case and Glanzmann's thrombasthenia in 1 case) underwent ESWL using Dornier HM3 mod. or MPL 9000. An extensive haematological and clinical evaluation pre and post-ESWL with an adequate haematological prophylaxis (transfusion of blood derivatives) has been performed depending on the coagulation disorder. In our patients we did not observe any haemorragic complication and we propose a reappraisal of the contraindications of ESWL in subjects with coagulation disorders: careful evaluation of haemorragic risk factors, by suitable correction measures and close clinical and instrumental monitoring, allows a reduction of the risk of haemorragic complications in coagulopathic patients who undergo ESWL treatment.     

Evaluation of solvent/detergent treated plasma in the management of patients with hereditary and acquired coagulation disorders

Haemostatic efficacy and pharmacokinetic analysis of solvent/detergent (S/D) treated, virus inactivated plasma (Octaplas, Germany) was evaluated in eight patients with hereditary factor VII, X and XI deficiency and in three patients with acquired coagulation disorders due to liver disease. The patients received the S/D plasma for treatment of haemarthrosis, menorrhagia or before surgical procedures. In all the patients the S/D plasma was sufficient to prevent or stop bleeding. Side effects included urticaria (one patient) and moderate anaphylactoid reaction (one patient). No evidence of plasma-born viral infections was observed up to 12 months after the treatment (95% confidence limits 0-22%). Calculated mean half-life of coagulation factors VII, X and XI was 4.36 h, 49.21 h and 44.5 h, respectively, similar to that observed with fresh-frozen plasma. Because of retained coagulation factor integrity and improved viral safety, S/D plasma could be considered a superior alternative to standard fresh-frozen plasma.     

Intraoral non-Hodgkin''s lymphoma in seven patients with acquired immunodeficiency syndrome

Transcranial Doppler sonography (TCD) of the middle, anterior and posterior cerebral arteries and of the basilar artery was used to evaluate the mean blood velocity (V mean) and the pulsatility index [PI = (V systolic-V diastolic)/V mean] as a vascular resistance index in 63 patients (male 40, female 23, mean age 43 +/- 19 y) with bacterial meningitis (n = 33, including 2 patients with fungal meningitis) and viral meningitis (n = 30) within 12 h after admission of the patients. The findings were similar for all intracranial arteries. Compared with reference values of 69 healthy volunteers [V mean of middle cerebral artery [MCA] 57 +/- 13 cm/s, MCA-PI 0.83 +/- 0.15], MCA-V mean was increased in patients with Glasgow coma scale (GCS) scores of 14 and 15 (71 +/- 18 cm/s; t-test: p < 0.001), not significantly different in the patients with GCS scores of 10-13 (55 +/- 21 cm/s) and decreased in those with GCS scores of 3-9 (42 +/- 21 cm/s, p < 0.01). The MCA-PI increased from 0.93 +/- 0.22 in the patients with GCS scores of 14-15 to 2.81 +/- 2.06 in those with GCS scores of 3-9 (p < 0.001 vs. controls). By regression analysis, MCA-V mean decreased and MCA-PI increased with decreasing GCS scores (p < 0.001). Only in patients with bacterial meningitis was the Glasgow outcome scale (GOS) score lower the more the MCA-PI was increased (regression analysis p < 0.001). We conclude that in patients with bacterial and viral meningitis, and in a good clinical state, the cerebral blood flow seems increased by hyperemia; with clinical deterioration the cerebral haemodynamics worsen. However, the early assessment of the cerebral blood flow by TCD seems useful for predicting outcome in bacterial meningitis only.