Machine-assisted interpretation of auramine stains substantially increases through-put and sensitivity of microscopic tuberculosis diagnosis.

Of all bacterial infectious diseases, infection by Mycobacterium tuberculosis poses one of the highest morbidity and mortality burdens on humans throughout the world. Due to its speed and cost-efficiency, manual microscopy of auramine-stained sputum smears remains a crucial first-line detection method. However, it puts considerable workload on laboratory staff and suffers from a limited sensitivity. Here we validate a scanning and analysis system that combines fully-automated microscopy with deep-learning based image analysis. After automated scanning, the system summarizes diagnosis-relevant image information and presents it to the microbiologist in order to assist diagnosis. We tested the benefit of the automated scanning and analysis system using 531 slides from routine workflow, of which 56 were from culture positive specimen. Assistance by the scanning and analysis system allowed for a higher sensitivity (40/56 positive slides detected) than manual microscopy (34/56 positive slides detected), while greatly reducing manual slide-analysis time from a recommended 5-15 min to around 10 s per slide on average.

Renal involvement in sarcoidosis--a report of 6 cases.

This report concerns 6 patients with renal involvement in sarcoidosis. Two of the patients had no clinical symptoms at all. In 3 patients, no extrarenal organ manifestation was found. All 6 patients had elevated levels of serum creatinine, 2 were hypercalcemic. Five patients manifested with mild proteinuria, but in none of the cases was a nephritic sediment with erythrocytes found. Kidney biopsies in 5 patients showed epitheloid cell granulomatous interstitial nephritis, and 1 patient presented with nephrocalcinosis. All patients were treated with corticosteroids. The serum creatinine levels decreased significantly in 4 patients (> 50% decrease), and slightly in 2 patients, elevated serum calcium levels were normalized. Thus, even in the absence of other organ manifestations, sarcoidosis can be the cause of renal insufficiency, and it responds well to corticosteroid treatment. These patients demonstrate the importance of kidney biopsy in the unexplained deterioration of renal function.

Inhibitory effect of uremic solutions on protein-DNA-complex formation of the vitamin D receptor and other members of the nuclear receptor superfamily.

Chronic renal failure is often associated with a resistance to the biologically active form of vitamin D(3), the nuclear hormone 1alpha, 25-dihydroxyvitamin D(3) (VD). The actions of VD are mediated by the vitamin D receptor (VDR), a ligand-dependent transcription factor that binds as a dimeric complex with the retinoid X receptor (RXR) to specific DNA binding sites in the promoter regions of primary VD responding genes, referred to as VD response elements (VDREs). It could be shown in this study that uremic solutions derived from ultrafiltrate from hemodialysis patients and dialysate from peritoneal dialysis patients had an inhibitory effect on the complex formation and ligand inducibility of VDR-RXR heterodimers on different VDRE types. This inhibition was attributed to the formation of Schiff bases between "reactive aldehydes" and lysine residues of the DNA binding domain (DBD) of the VDR, but point mutagenesis data of different lysine residues in this study could not confirm this idea. However, the inhibitory effect of uremic solutions could also be observed for the complex formation of other homo- or heterodimer forming nuclear receptors, whereas an as a monomer binding nuclear receptor did not appear to be affected. These results indicate that VDR is a target of substances in uremic solutions in vitro, but also to some extent other nuclear receptors (i.e., other endocrine signaling systems) may be affected by renal failure.

Point mutations of the human parathyroid calcium receptor gene are not responsible for non-suppressible renal hyperparathyroidism.

The calcium-dependent secretion of parathyroid hormone (PTH) is mediated through an extracellular G protein-coupled calcium receptor (CaR). Inactivating point mutations of this receptor have been found in familial hypocalciuric hypercalcemia and neonatal severe hyperparathyroidism. These diseases feature a decreased calcium sensitivity of the parathyroid glands, resulting in a rightward shift of the Ca2(+)-PTH relationship. Severe non-suppressible renal hyperparathyroidism (rHPT) is often characterized by similar setpoint shifts to the right. Thus, point mutations of the CaR gene could contribute to non-suppressible rHPT. We examined genomic DNA of hyperplastic or mainly nodular tissues of 39 parathyroids from 25 rHPT-patients with resistance to calcitriol therapy. Amplification of the six exons of the CaR gene was followed by single-strand conformation polymorphism (SSCP) analysis. DNA sequencing was performed where band shifts were observed. No point mutations in the coding sequence of the CaR gene were detected using the PCR-SSCP strategy. Point mutations in the coding regions of the CaR gene probably play no role in the evolution of renal HPT and are not responsible for the calcitriol resistance of PTH secretion.

Serum bone alkaline phosphatase is superior to plasma levels of bone matrix proteins for assessment of bone metabolism in patients receiving renal transplants.

The plasma concentrations of two bone matrix proteins (osteocalcin, osteonectin) were monitored in 56 samples from 14 patients receiving renal transplants and the values compared with serum bone alkaline phosphatase mass concentrations and osteotropic hormone levels (parathyroid hormone, calcitriol). There were no significant changes in the concentrations of plasma osteonectin at any time after transplantation, as compared with the values before transplantation (P > 0.1). None of the plasma samples showed osteonectin levels above the reference interval. There was a weak but significant relationship between platelet counts and plasma osteonectin levels (r = +0.322; P < 0.05). Osteocalcin showed a marked decrease of the values 1 week following transplantation as compared with the values before transplantation without further change of the values 1 and 3 months after transplantation (P > 0.5) whereas 3 months after transplantation bone alkaline phosphatase levels were higher than before transplantation (P < 0.05). Multiple regression analysis (performed with data from 42 samples obtained after transplantation) revealed serum creatinine as an independent predictor of plasma osteocalcin whereas serum calcitriol was an independent predictor of serum bone alkaline phosphatase (P < 0.05). No correlation was observed between serum calcitriol/plasma parathyroid hormone on the one hand and plasma osteocalcin on the other (P > 0.05). After transplantation there was a lack of correlation between serum bone alkaline phosphatase mass concentrations and plasma osteocalcin values (P > 0.05). In conclusion, serum bone alkaline phosphatase should be preferred to bone matrix proteins for the assessment of bone metabolism in patients receiving renal transplants: (a) bone alkaline phosphatase-but not osteocalcin-is significantly correlated with calcitriol and adequately reflects increased bone formation after renal transplantation; (b) interpretation of osteocalcin values is severely hampered by their strong correlation with serum creatinine concentrations; (c) plasma osteonectin determinations are not useful for monitoring bone formation.

Early detection of avascular necrosis of the femoral head following renal transplantation.

This prospective study included 43 patients undergoing renal transplantations. Magnetic resonance imaging (MRI) and X-rays of the hip joints were produced 3 and 12 months after transplantation. In 6 hip joints of 4 patients (9.3%), we discovered femoral head necroses just 3 months after transplantation. Three of the hip joints affected were symptomatic and 3 painless. The MR images taken 12 months after transplantation revealed no additional femoral head necrosis. A core decompression was performed on 3 joints. In contrast to those with core decompression, the femoral heads without core decompression showed a progression of the necrosis in 2 of 3 cases. All 4 patients with femoral head necroses were younger than 50 years and exhibited a premature conversion of the haematopoietic marrow to fatty marrow in the area of the proximal femoral metaphysis. A similar premature conversion to fatty marrow was seen in 6 of the 22 (27.2%) patients younger than 50 years and without femoral head necroses. The doses in long-term steroid medication and the steroid doses during the rejection periods of the patients with femoral head necroses were not significantly higher than those for the patients with premature conversion to fatty marrow. The latter had also not received significantly higher doses than the patients whose MRI findings were inconspicuous.

[Proton spin tomographic changes of the femoral shaft in patients with kidney transplantation]. / Kernspintomographische Veränderungen des Femurschaftes bei nierentransplantierten Patienten.

In a prospective study 43 patients were reviewed 3 and 12 months after renal transplantation. The patients had MRI examinations and plain x-rays of the hips as well as punch biopsies of the iliac crest. In 9 patients diffuse, inhomogeneous bilateral changes of the MRI-signal patterns of the femoral diaphysis were seen. They were hypointense in the T1-weighted images and hyperintense in the STIR-images. All plain x-rays were inconspicuous. These changes of the femoral shaft were significantly more frequent in patients with renal osteodystrophy of the histological type Delling Ila. We conclude that these changes of MRI-signals patterns might be connected with an osteoidosis.

Tubular dysfunction following kidney transplantation.

After transplantation the kidney is subjected to rejection and other deleterious factors including ischemic damage, acute tubular necrosis, rejection and the use of cyclosporine A (CsA) or FK506. As a result, kidney damage may be generalized with azotemia as its hallmark. These tubular syndromes may cause profound changes in the acid base balance and in the level of certain blood electrolytes and minerals. As a general rule, the renal tubular acidosis (RTA) that appears early following transplantation disappears spontaneously and is predominantly a sequela to acute renal failure. On the other hand, defects occurring in the late posttransplant period are often due to chronic rejection or CsA-induced nephrotoxicity. Secondary hyperparathyroidism, urinary tract infection and obstructive uropathy may also play a contributory urinary role in the pathogenesis of RTA. Chronic RTA following transplantation may interfere with bone metabolism and at times lead to nephrocalcinosis and nephrolithiasis. Therefore, if the condition is prolonged, a supplement of bicarbonate should be given if for no other reason that to protect the skeleton. As these patients may develop either hyperkalemia or hypokalemia, treatment with potassium supplements or potassium-sparing diuretics should be carried out with caution and under constant surveillance. Furthermore, magnesium replacement may be advisable if hypomagnesemia by decreased proximal reabsorption becomes clinically evident. Tubular dysfunction may occur following renal transplantation even in patients with maintained glomerular filtration rate and may induce a number of clinical problems including deterioration of renal graft function.

Evaluation of a radioimmunoassay for determination of calcitriol in human sera employing a 125I-labelled tracer.

The performance characteristics of a radioimmunoassay employing a 125I-labelled tracer for determination of calcitriol in human sera are reported. The assay is based on an immunoextraction step employing a monoclonal antibody against calcitriol followed by a radioimmunoassay (using 125I-labelled calcitriol and sheep antiserum against calcitriol). Bound/free separation is performed with an anti-sheep IgG antibody bound to cellulose. Within-run imprecision (n = 20) was 12.8% (mean = 9.4 ng/l) and 11.1% (mean = 48.8 ng/l), between-day imprecision (n = 11) was 27.1% (mean = 9.6 ng/l) and 17.2% (mean = 47.2 ng/l). Linearity of dilution as investigated by mixing pooled sera containing 62.0 ng/l and 4.7 ng/l calcitriol, respectively. The relationship between measured and expected concentrations was characterized by a linear correlation coefficient of r = +0.990. The values obtained with the 125I-based radioimmunoassay were compared with those obtained with a radioreceptor-assay using a 3H-labelled tracer; the regression line was y = 1.091 x -4.545 (n = 84; r = +0.935), where y = calcitriol [125I] [ng/l] and x = calcitriol [3H] [ng/l]. Mixing 9 volumes of sera from patients with renal insufficiency (n = 7) with 1 volume of 'calibrator F' (assigned value: 227 ng/l) yielded recovery rates of 90 +/- 8% (mean +/- SD). The detection limit was 3.0 ng/l. The cross-reactivity of cholecalciferol metabolites was found to be < 0.00003 for 25-hydroxycholecalciferol, 24R,25-dihydroxycholecalciferol and 25S,26-dihydroxycholecalciferol. A preliminary reference interval (5th to 95th percentile) was established in 40 apparently healthy persons (17 males and 23 females; age range: 20-61 [mean: 32] years) (19-74 ng/l). The method presented shows high practicability and may therefore be considered as a useful alternative to cumbersome assays using 3H-labelled tracers.

Comparison between serum levels of bone alkaline phosphatase and the carboxy-terminal propeptide of type I procollagen as markers of bone formation in patients following renal transplantation.

The serum concentrations of the carboxy-terminal propeptide of type I procollagen (PICP) were monitored in 52 serum samples from 13 patients receiving renal transplants and the values compared with bone alkaline phosphatase (BAP) concentrations and intact parathyrin levels. There was a significant correlation between BAP and PICP values in all 52 serum samples examined (r = +0.770; P < 0.0001). Before transplantation BAP (P < 0.0001), but not PICP (P > 0.1), was correlated with intact parathyrin levels. BAP concentrations increased from 7.3 +/- 1.2 micrograms/l (median +/- S.E.M.) before transplantation to 13.3 +/- 1.2 micrograms/l 3 months after transplantation (P < 0.01). There was a concomitant rise in PICP levels from 95 +/- 19 micrograms/l to 166 +/- 27 micrograms/l (P < 0.05). No correlation was found between BAP or PICP levels on the one hand and intact parathyrin concentrations on the other at any time following renal transplantation (P > 0.5). In conclusion, PICP may be a useful parameter for monitoring bone formation following renal transplantation.

Monitoring of bone resorption after renal transplantation by measuring the urinary excretion of pyridinium cross-links.

The urinary excretion of pyridinium cross-links was measured in 70 second morning urine samples from 49 patients following renal transplantation. One and three months after renal transplantation, the urinary excretion of pyridinium cross-links was higher (p < 0.05) than at one week after transplantation. At all times after transplantation, the values for the excretion of pyridinium cross-links were correlated with the bone alkaline phosphatase concentrations (p < 0.001). However, there was no correlation between parathyrin concentrations and the values for the excretion of pyridinium cross-links (p > 0.05). This rise in the excretion of pyridinium cross-links is probably due to an increase of bone resorption caused by cyclosporin A and/or glucocorticoids. In the case of 17 urines with excretion values of pyridinium cross-links above the upper reference limit (pyridinoline equivalents, 93 mumol/mol creatinine), only 2 (12%) of the corresponding sera showed increased bone alkaline phosphatase values. In patients following renal transplantation simultaneous assessment of bone formation and bone resorption (determined from bone alkaline phosphatase serum concentrations and the excretion of pyridinium cross-links) may therefore enhance the diagnostic sensitivity for detecting effects on bone metabolism.

[A hemolytic crisis with liver failure as the first manifestation of Wilson's disease]. / Hämolytische Krise mit Leberversagen als Erstmanifestation eines Morbus Wilson.

An 18-year-old woman developed an acute haemolytic anaemia, acute transient renal failure and progressive hepatic failure. Coeruloplasmin and serum copper concentration were normal; a Kayser-Fleischer ring and any neurological symptoms were absent initially. Liver biopsy was contraindicated because of increased bleeding tendency. Wilson's disease was diagnosed only after the acute renal failure had regressed, on the basis of the urinary copper excretion (2890 micrograms/d, rising to 7330 micrograms/d after D-penicillamine administration). Progressive liver failure required transplantation. After it the patient quickly recovered and is now, two years later, free of disease. -This case demonstrates that Wilson's disease may be difficult to diagnose at the time of initial acute manifestation. But it can be recognized early from the pathognomonic low alkaline phosphatase and by calculation of free serum copper.

Monitoring of osteoblast activity with an immunoradiometric assay for determination of bone alkaline phosphatase mass concentration in patients receiving renal transplants.

We examined the diagnostic validity of an immunoradiometric assay for determination of mass concentration of bone alkaline phosphatase (EC 3.1.3.1) in 134 sera from 35 patients receiving renal transplants. Comparison between bone alkaline phosphatase concentration and total alkaline phosphatase activity yielded a strong correlation (r = +0.860; P < 0.001). Nine (17%) of 54 sera which were characterized by a total alkaline phosphatase activity between 100 units/l and the upper reference limit (178 units/l (males) and 160 units/l (females), respectively) showed an increased bone alkaline phosphatase concentration (> 21.3 micrograms/l (males) and > 15.0 micrograms/l (females), respectively). There was also a correlation between bone alkaline phosphatase values and parathyroid hormone levels both before (r = +0.640 (n = 23), P < 0.001) and after renal transplantation (r = +0.528 (n = 111), P < 0.0001). A follow-up of 15 patients after renal transplantation revealed that the median of bone alkaline phosphatase values increased from 5.5 micrograms/l before transplantation to 14.9 micrograms/l 3 months after transplantation (P < 0.0001). Nevertheless no correlation could be observed between parathyroid hormone concentrations and bone alkaline phosphatase values at any time following renal transplantation in these 15 patients (P > 0.1). Rise of bone alkaline phosphatase concentration following renal transplantation is most probably due to an activating effect of cyclosporin A upon osteoblasts.

[Does the captopril test improve the diagnosis of primary hyperaldosteronism?]. / Verbessert der Captopril-Test die Diagnostik des primären Hyperaldosteronismus?

Plasma concentrations of renin and aldosterone were measured before and 60 min after taking 25 mg captopril in 242 patients with arterial hypertension (124 men, 118 women, aged 51.9 +/- 12.7 years; unilateral aldosterone-producing adrenal adenoma in 8, idiopathic hyperaldosteronism in 16 and essential hypertension in 189). Basal plasma aldosterone levels were twice as high in those with adenoma or hyperaldosteronism (216.9 +/- 99.1 pg/ml and 256 +/- 123 pg/ml, respectively) as in those with essential hypertension (117.7 +/- 115 pg/ml). Basal renin levels in adenoma and idiopathic hyperaldosteronism (1 +/- 0.8 microU/ml and 2.6 +/- 1.9 microU/ml, respectively) were decreased compared with those in essential hypertension (13.1 +/- 14.2 microU/ml). The basal aldosterone/renin ratio was higher in adenoma (436 +/- 370 pg/microU) and idiopathic hyperaldosteronism (615 +/- 950 pg/microU) than in essential hypertension (52.9 +/- 151.3 pg/microU). The sensitivity of this ratio in combination with the aldosterone concentration was 100% for recognizing an adrenal adenoma, its specificity 92.7%. The mean plasma aldosterone level after captopril administration did not change in adenoma patients, but fell to 162 +/- 85 pg/ml (P less than 0.001) in those with idiopathic hyperaldosteronism. These data indicate that the captopril test contributes to distinguishing primary from idiopathic hyperaldosteronism.

[Anti-basal membrane glomerulonephritis after homologous kidney transplantation in hereditary Alport's nephropathy]. / Antibasalmembran-Glomerulonephritis nach Verwandtennierentransplantation bei hereditärer Nephropathie Alport.

A patient, born in 1968, was found at the age of 9 years to have Alport's syndrome. In his 20th year, when in terminal renal failure, his father's kidney was transplanted into him. 14 months later there was a sudden worsening of his renal function after a varicella infection; for the first time antibodies against the glomerular basal membrane (GBM) were detected. Despite an increase in prednisolone dosage and 6 plasmaphereses chronic haemodialysis again became necessary. Renal biopsy revealed necrotizing intra- and extracapillary glomerulonephritis. Simultaneously there was a raised anti-NC-1-antibody titre (1:80) in the serum. After removal of the transplant the titre fell to normal. The NC-1 antigen, a component of the GBM in healthy persons, may be absent in Alport's syndrome. An analysis of the few cases of anti-GBM glomerulonephritis in renal transplants of patients with Alport's syndrome may make it possible to recognize factors which precipitate or favour this form of glomerulonephritis.

[The effect of hemodynamic changes in 24-hour milrinone infusion on sympathetic activity and the renin-angiotensin-aldosterone system in patients with severe heart failure]. / Auswirkung der hämodynamischen Veränderungen unter 24stündiger Milrinon-Infusion auf die sympathische Aktivität und das Renin-Angiotensin-Aldosteron-System bei Patienten mit schwerer Herzinsuffizienz.

The hemodynamics of 18 patients (subgroup A) with severe heart failure (baseline Cl less than or equal to 1.55 l.min-1.m-2), including three patients with cardiogenic shock, and another 22 patients (subgroup B) with moderate heart failure (baseline Cl from 1.55 to 2.5 l.min-1.m-2) were investigated during a 24 h milrinone infusion, combined with investigation of the response of the sympathetic tone (plasma catecholamine levels) and the renin-angiotensin-aldosterone system to the hemodynamic improvement in both subgroups. Cl increased (p less than or equal to 0.001) to 162.7% after 5 min and further to 206.4% of baseline after 30 min of milrinone therapy in subgroup A, and in B to 139.3% and further to 146.4% after 15 min. PCWP decreased (p less than or equal to 0.001) to 83.8% and further to 65.5% of baseline after 30 min in subgroup A, and to 58.4% in subgroup B. Heart rate decreased (p less than or equal to 0.05) from 99.4 to 94.7 bpm in A and showed a decreasing tendency in B. MAP rose in A from 75.5 to 79.4 after 1 h and further to 83.3 mm Hg (p less than or equal to 0.01) after 24 h; in subgroup B, MAP did not change. Plasma noradrenaline level decreased (p less than or equal to 0.001) in A from 1419.5 (B: 782.9) to 838.2 (B: 529.6) after 1 h and further to 655.1 (B: 467.9) pg/ml after 24 h. Plasma renin decreased (p less than or equal to 0.01) in A from 1047.6 (B: 460.2) to 597.4 (B: 222.5) and further to 392.6 (B: 191.7) microU/ml.(ABSTRACT TRUNCATED AT 250 WORDS)

[Cardiac involvement within the scope of HIV-1 infection: preliminary results of echocardiography study]. / Kardiale Beteiligung im Rahmen der HIV-1-Infektion: Vorläufige Ergebnisse einer echokardiographischen Untersuchung.

The results of one- and two-dimensional echocardiography in 128 patients (117 males, 11 females; median age 37 years) who were seropositive for HIV-1 were analyzed in addition to clinical, electrocardiographic, and laboratory data. Follow-up controls are available for 51 patients over an observation period of 1 to 24 months, median 9.5 months. Probably HIV-related echocardiographic abnormalities were identified in 36 patients (28%): small to moderate pericardial effusions (n = 34) and left ventricular dilation (n = 5). Pericardial effusions resolved in seven patients during follow-up, in three cases after tuberculostatic chemotherapy. Compared to patients without cardiac involvement patients with HIV-related echocardiographic abnormalities showed lower CD4-lymphocyte counts (143 +/- 138 vs 289 +/- 219/microliters, p less than or equal to 0.01), and left ventricular endsystolic dimensions were increased (34.2 +/- 4.5 vs 32.6 +/- 3.0 mm, p less than or equal to 0.05). Cardiac involvement occurred predominantly in the advanced stages of the HIV-1 infection with unclear etiology in the majority of cases, even though active concomitant diseases could be frequently demonstrated. The clinical course of some patients might be consistent with intercurrently completed perimyocarditis, probably of viral genesis. CD4-lymphocyte counts less than or equal to 100/microliters could be identified as a risk factor for the development of cardiac manifestations. The significance of a demonstrated involvement of the heart with regard to therapeutic consequences and prognosis appeared to be slight. Use of echocardiography as a routine method for the detection of cardiac involvement in HIV-1 infection has proved to be valuable, since indicative clinical symptoms were lacking in almost all cases.

High-dose intravenous immunoglobulins in HIV-1-infected adults with AIDS-related complex and Walter-Reed 5.

The influence of high-dose intravenous immunoglobulins (HD-IVIG) on the clinical status and T4 cell count of adults with AIDS-related complex (ARC) and Walter-Reed 5 (WR5) was evaluated in a randomized double-blind longitudinal study. Inclusion criteria were: (1) T4 cells less than 400/microliters and (2a) oral thrush or cutaneous anergy or (2b) two clinical ARC criteria (fever, diarrhea, weight loss, fatigue, night sweats). Thirty patients [28 males, 2 females, median age 41 (24-64) years] with ARC (n = 8), WR5 (n = 12) and both (n = 10) were stratified according to their T4 cell count (greater than or equal to vs. less than 300/microliters). Fifteen patients received 0.4 g/kg body weight IVIG and 15 placebo (albumin 0.03%) every other week for 26 weeks with follow-up for another 26 weeks. The clinical status was defined as a score consisting of fever, diarrhea, night sweats, fatigue, weight loss, oral candidiasis and mucosal or cutaneous herpes simplex. Clinical examination and routine laboratory assessments were performed before initiation of the study and before each administration, lymphocyte phenotyping every 4 weeks and cutaneous reaction, serology and lymphocyte stimulation every 12 weeks. Both groups were comparable in initial clinical symptoms and laboratory values. Seven patients developed AIDS (treatment group: 3, placebo group: 4), 1 patient died by homicide. After 26 weeks, the clinical score (particularly fatigue and fever) was significantly improved in the treatment group, while the T4 cell count and other clinical and immunological parameters remained unaltered. This limited effect was still evident at termination of the study after 52 weeks. In conclusion, HD-IVIG can improve the clinical status of patients with advanced HIV-1 infection without obviously correcting the underlying impaired cellular immunity. The substitution of intact antibodies in the state of functional hypogammaglobulinemia is suggested as possible therapeutic mechanism.

[AIDS-related complex: a superfluous concept?]. / Der AIDS-related complex: Ein überflüssiger Begriff?

The clinical value of different classification systems of HIV-infection has been examined in a cohort of 99 HIV-infected individuals. AIDS-related complex (ARC), Walter-Reed (WR) stage 5 and Centers for Disease Control (CDC) group IV without AIDS cases were equally capable of identifying patients with bad prognosis: Out of 12 patients progressing to AIDS, 9 WR 5, 7 CDC IV and 7 ARC. Prognostic parameters (Erythrocyte sedimentation rate, Haemoglobin, Leucocytes, CD4-lymphocytes and Beta 2-Microglobulin) did not differ in the three groups. However, there were great differences in the frequency of patients infected by homosexual contacts and of intravenous drug-abusers. Drug-abusers were more often seen in the ARC-group, whereas there was a slight dominance of homosexuals in the WR 5-group (and a marked preponderance in the AIDS-group). Using 3 different ARC-definitions we found an ARC-frequency of 10%, 24% and 41% in our cohort. Thus the great variability of the ARC-concept could be demonstrated. In conclusion we believe that for the purpose of clinical documentation and studies the ARC-concept is unnecessary. Further studies have to evaluate other classification systems (Walter-Reed, CDC) or to establish new ones.