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Presents photographs taken of a man with a history of cutaneous mastocytosis. Symptoms experienced by the patient, including skin lesions; Methods of diagnosis, including bronchoscopy; Treatment of mast cells with prednisolone and interferon 2α.

Tissues often experience hypoxia at sites of inflammation due to malperfusion, massive immune cell recruitment, and increased oxygen consumption. Organisms adapt to these hypoxic conditions through the transcriptional activation of various genes. In fact, there is significant crosstalk between the transcriptional responses to hypoxia and inflammatory processes. This interaction, named inflammatory hypoxia, plays a crucial role in various diseases including malignancies, chronic inflammatory lung diseases, and sepsis. To further elucidate the crosstalk between hypoxia and inflammation in vivo and assess its potential for innovative therapies, our study aimed at investigating the impact of acute hypoxic conditions on inflammation-induced immune responses. To this end, we exposed healthy human subjects to hypoxia either before (hypoxia priming) or after a single intravenous (i.v.) injection of 0.4 ng/kg LPS. Our data show that hypoxia exposure prior to LPS injection (hypoxia priming) amplified the proinflammatory response. This was reflected by an increase in body temperature, plasma noradrenaline levels, and the production of proinflammatory cytokines (i.e., IL-6 and TNF-α), compared with LPS control conditions. These effects were not observed when participants were exposed to hypoxia after LPS administration, demonstrating that the interaction between hypoxia and inflammation highly depends on the timing of both stimuli. Our findings suggest that acute hypoxia (i.e., hypoxia priming) modulates transient inflammation, leading to an enhanced proinflammatory response in healthy human subjects. This highlights the need for further investigations to understand the pathology of various hypoxia-inducible factor (HIF)-associated inflammatory diseases and to develop suitable, innovative therapies. NEW & NOTEWORTHY To our knowledge, this is the first in vivo study investigating the effects of hypoxia preceding (hypoxia priming) or following LPS administration on the endotoxin-induced inflammatory response in healthy human subjects. The data show that hypoxia priming amplified the proinflammatory response, reflected by an increased body temperature, increased plasma noradrenaline levels, and higher production of proinflammatory cytokines (i.e., IL-6 and TNF-α) compared with LPS control conditions.

Cells of the immune defence, especially leukocytes, often have to perform their function in tissue areas that are characterized by oxygen deficiency, so-called hypoxia. Physiological hypoxia significantly affects leukocyte function and controls the innate and adaptive immune response mainly through transcriptional gene regulation via the hypoxia-inducible factors (HIFs). Multiple pathogens including components of bacteria, such as lipopolysaccharides (LPS) trigger the activation of leukocytes. HIF pathway activation enables immune cells to adapt to both hypoxic environments in physiological and inflammatory settings and modulates immune cell responses through metabolism changes and crosstalk with other immune-relevant signalling pathways. To study the mutual influence of both processes in vivo, we used a human endotoxemia model, challenging participants with an intravenous LPS injection post or prior to a 4-h stay in a hypoxic chamber with normobaric hypoxia of 10.5% oxygen. We analysed changes in gene expression in whole blood cells and determined inflammatory markers to unveil the crosstalk between both processes. Our investigations showed differentially altered gene expression patterns of HIF and target genes upon in vivo treatment with LPS and hypoxia. Further, we found evidence for effects of hypoxic priming upon inflammation in combination with immunomodulatory effects in whole blood cells in vivo. Our work elucidates the complex interplay of hypoxic and inflammatory HIF regulation in human immune cells and offers new perspectives for further clinical research., (© 2024. The Author(s).)

Background: Inflammation and depressed mood constitute clinically relevant vulnerability factors for enhanced interoceptive sensitivity and chronic visceral pain, but their putative interaction remains untested in human mechanistic studies. We tested interaction effects of acute systemic inflammation and sad mood on the expectation and experience of visceral pain by combining experimental endotoxemia with a mood induction paradigm., Methods: The double-blind, placebo-controlled, balanced crossover fMRI-trial in N = 39 healthy male and female volunteers involved 2 study days with either intravenous administration of low-dose lipopolysaccharide (LPS, 0.4 ng/kg body weight; inflammation condition) or saline (placebo condition). On each study, day two scanning sessions were conducted in an experimentally induced negative (i.e., sad) and in a neutral mood state, accomplished in balanced order. As a model of visceral pain, rectal distensions were implemented, which were initially calibrated to be moderately painful. In all sessions, an identical series of visceral pain stimuli was accomplished, signaled by predictive visual conditioning cues to assess pain anticipation. We assessed neural activation during the expectation and experience of visceral pain, along with unpleasantness ratings in a condition combining an inflammatory state with sad mood and in control conditions. All statistical analyses were accomplished using sex as covariate., Results: LPS administration led to an acute systemic inflammatory response (inflammation X time interaction effects for TNF-α, IL-6, and sickness symptoms, all p <.001). The mood paradigm effectively induced distinct mood states (mood X time interaction, p <.001), with greater sadness in the negative mood conditions (both p <.001) but no difference between LPS and saline conditions. Significant main and interaction effects of inflammation and negative mood were observed for pain unpleasantness (all p <.05). During cued pain anticipation, a significant inflammation X mood interaction emerged for activation of the bilateral caudate nucleus and right hippocampus (all p FWE  < 0.05). Main effects of both inflammation and mood were observed in multiple regions, including insula, midcingulate cortex, prefrontal gyri, and hippocampus for inflammation, and midcingulate, caudate, and thalamus for mood (all p FWE  < 0.05)., Conclusions: Results support an interplay of inflammation and sad mood on striatal and hippocampal circuitry engaged during visceral pain anticipation as well as on pain experience. This may reflect a nocebo mechanism, which may contribute to altered perception and interpretation of bodily signals. At the interface of affective neuroscience and the gut-brain axis, concurrent inflammation and negative mood may be vulnerability factors for chronic visceral pain., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Author(s). Published by Elsevier Inc. All rights reserved.)

Background: CD19+CD24hiCD38hi transitional immature B-lymphocytes have been demonstrated to play an important role in regulating the alloimmune response in transplant recipients. Here, we analyzed the effect of calcineurin inhibition on these peripherally circulating regulatory B-cells (Breg) in renal transplant recipients receiving cyclosporine A (CsA) or tacrolimus., Methods: PBMCs from healthy subjects (HS) (n = 16) and renal transplant recipients (n = 46) were isolated. Flow cytometry was performed for CD19, CD24, CD38 and IL-10 either after isolation or after 72 hours of co-culture in presence of PMA/Ionomycin and TLR9-ligand in presence or absence of increasing concentrations of tacrolimus or CsA., Results: The amount of CD19+ B-cells among lymphocytes was ∼9.1% in HS, ∼3.6% in CsA (n = 11, p<0.05) and ∼6.4% in TAC (n = 35, p<0.05) treated patients. Among B-cells, a distinct subset of Breg was found to be 4.7% in HS, 1.4% in tacrolimus treated patients and almost blunted in patients receiving CsA. Similarily, ∼4% of B-cells in HS and even fewer in CsA or tacrolimus treated patients produced IL-10 (0.5% and 1.5%, p<0.05) and this was confirmed both in non-transplanted CsA-treated healthy subjects and in in vitro co-culture experiments. Among 29 patients with <1% of Breg, 9 cases (31%) displayed an allograft rejection in contrast to only one case of rejection (6%) among 17 patients with >1%., Conclusion: Calcineurin inhibitors reduce number and IL-10 production of Bregs in the peripheral circulation of both renal transplant recipients and non-transplanted healthy subjects. CNI induced Breg reduction is not restricted to a solid organ transplant setting and is not mediated by co-medication with steroids or MPA. A low proportion of Breg cells is associated with an elevated frequency of allograft rejection events.

Background: Immunosuppressive therapy with mammalian target of rapamycin inhibitors (mTORi) requires maintenance of an effective inhibition of the alloimmune response, whereas reducing drug-related nephrotoxicity. Therapeutic monitoring is based on mTORi trough levels, which do not necessarily reflect biologic effects on the PI3K-Akt-mTOR pathway and hence may often result in under-immunosuppression or over-immunosuppression., Methods: Phosphorylation of p70S6 kinase was studied by phosphoflow cytometry and by Western blot in both peripheral blood monocyte cells and CD3+ T cells of renal transplant recipients (RTX) receiving tacrolimus (n=34) or cyclosporine A (CsA) (n=24) or an mTORi (n=26). 16 healthy age-matched volunteers served as a control group. To clarify whether p70S6K activity is varying among CD4(+) T-cell subsets, cell sorted CD4(+)CD25(hi) regulatory T cells (Tregs) and CD4(+)CD25- T cells were analyzed for p70S6K phosphorylation., Results: Simultaneous analysis of p70S6K phosphorylation by phosphoflow cytometry and Western blot showed high correlation in peripheral blood mononuclear cells of renal transplant patients (r=0.91, P<0.001). Mammalian target of rapamycin inhibition was associated with marked reduction of p70S6K phosphorylation compared to healthy volunteers or RTX patients receiving calcineurin inhibitors (all P<0.001) but did not correlate with mTORi trough levels. Interleukin-2 production in mitogen-stimulated CD3(+) T cells correlated with the degree of p70S6K phosphorylation in everolimus-treated patients. p70S6K phosphorylation in CD4+CD25(hi) Tregs was significantly lower compared to CD4(+)CD25- T cells (n=3). In mTORi treated RTX recipients, p70S6K phosphorylation was selectively reduced in CD4(+)CD25- T cells leaving CD4(+)CD25(hi) Tregs unimpaired., Conclusion: Phosphoflow cytometric quantification of p70S6K phosphorylation may play an adjunct role to pharmacodynamically guide an individualized mTORi therapy. It may have potential to be used in purity testing of Treg suspensions generated for adoptive tolerogenic therapies.

Classical variants of specific cutaneous LE lesions are chronic discoid LE (CDLE) and subacute cutaneous LE (SCLE). CDLE and SCLE may appear at any age; however, the most common age of onset is between 20 and 40 years, with a female predominance of 3:1 in CDLE and 3-6:1 in SCLE. Nonspecific LE skin lesions such as generalized or acrolocalized vasculitis (4-30%), livedo reticularis (22-35%), and alopecia (38-78%) are frequently seen in patients with cutaneous LE. Other typical cutaneous LE subsets such as LE profundus/panniculitis, LE tumidus, urticaria vasculitis, hypertrophic LE, and bullous LE are rather rare variants. Butterfly rash and/or macular exanthema are characteristic skin lesions of systemic lupus erythematosus (SLE) rarely found in patients with cutaneous LE.

Background and Aim: Tea tree oil, a distillation product of the Australian tea tree (Melalence alternitolia) is increasingly used as an alternative remedy for various dermatological diseases. Tea tree oil contains several allergenic monoterpenes and sesquiterpenes. In this multicenter study it was evaluated, whether the increasing use of tea tree oil has lead to an increased frequency of sensitization in Germany and Austria which would justify its inclusion into the standard series., Patients and Method: For patch testing a standardized tea tree oil was used, dissolved 5% in diethylphtalate (DEP). Consecutive patients of 11 dermatological departments in Germany and Austria were tested. Readings were taken on day 2 and 3 according to the guidelines of the German Contact Dermatitis Research Group (DKG)., Results: 5% tea tree oil was positive in 36/3375 patients (1.1%). Sensitization frequencies showed great regional variations and ranged from 2.3% (Dortmund), 1.7% (Buxtehude), 1.1% (Essen), 0.7% (Graz), to 0% (Berlin, Vienna). 14/36 patients (38.9%) also showed a positive patch test reaction to oil of turpentine., Conclusion: Our results show that tea tree oil is an important contact allergen for some centers. It should be tested, if medical history suggests its previous use. Considering the great regional differences in frequencies of sensitization its inclusion into the standard series is not recommended yet.

Aquagenic urticaria is a rare disorder characterized by the occurrence of pruritus and wheals after temporary contact with water. The familial occurrence of aquagenic urticaria over 3 generations is reported here in association with familial lactose intolerance, a condition in which the enzyme lactase encoded on chromosome 2, is deficient. In two patients, a young man and his mother, we verified the appearance of pruritic hives 5 to 10 minutes after contact with water of any temperature. Other types of physical urticaria were absent, and mastocytosis was excluded by extensive laboratory investigations; lactose intolerance was confirmed in both patients by H(2)-exhalation test. In these patients the clinical symptoms did not respond to antihistamines or UV-radiation therapy. Four other members of the family had wheals from water contact, two of whom had lactose intolerance. Two other members had lactose intolerance only. Although the association of aquagenic urticaria with lactose intolerance may be coincidental, attention is drawn to the fact that the 2 conditions, known to be familial, may coexist in the same family, possibly based on an association of gene loci.

The proapoptotic potential of tumor necrosis factor-alpha (TNF-alpha) has been demonstrated for various cell types, whereas nuclear factor-kappaB (NF-kappaB) is known to support the transcription of prosurvival genes. In the present study, investigation of normal human melanocytes revealed induction of apoptosis after TNF-alpha treatment (100 U/ml) in only 3 out of 11 cultures analyzed, whereas 8 cultures remained largely resistant. In sensitive cultures, NF-kappaB binding activity was found increased after TNF-alpha treatment; apoptosis-resistant cells were characterized by relatively high basic NF-kappaB binding activities and did not show NF-kappaB activation after TNF-alpha treatment. Inhibition of NF-kappaB by a specific inhibitor, Bay-11, either induced apoptosis itself or resistant melanocyte cultures became sensitive to TNF-alpha treatment. No correlation was found between apoptosis sensitivity and the expression of TNF receptor-1 or the expression of Bax, Bcl-2 and Bcl-X(L). A strong correlation, however, was found regarding the pigmentation degree, as high pigmentation correlated with apoptosis resistance and sensitive melanocyte cultures were weakly pigmented. These data may indicate that in cultured melanocytes, high levels of melanogenesis lead to an increase in oxidative stress which itself causes NF-kappaB activation. NF-kappaB mediates the transcription of antiapoptotic factors which may block TNF-alpha-induced apoptosis at early steps of the signal cascade., (Copyright 2002 S. Karger AG, Basel)

Nuclear factor-kappaB (NFkappaB) is a pleiotropic transcriptional activator, which is a sensitive transcriptional factor for free radicals and activates multiple target genes. UVA is very efficient in inducing free radicals in human skin cells. L-ascorbic acid is regarded as a scavenger of UVA-induced free radicals in human keratinocytes. In epidermis, melanocytes and keratinocytes play an important protective role against skin photodamage. In the present study, we aimed to investigate the role of NFkappaB on photodamage in melanocytes and keratinocytes. Normal human melanocytes (NHM) and HaCaT keratinocytes were treated with UVA (500 mJ/cm(2), 1,000 mJ/cm(2)) and/or L-ascorbic acid (100 microM, 250 microM). NFkappaB binding activity was analysed by electrophoretic mobility shift assay. NFkappaB binding activity was increased by UVA irradiation in HaCaT keratinocytes, but it was not affected in NHM. On the other hand, L-ascorbic acid decreased NFkappaB binding activity both in UVA-irradiated and in non-irradiated NHM. In contrast, NFkappaB binding activity in HaCaT keratinocytes was increased after treatment with L-ascorbic acid. In addition, L-ascorbic acid synergistically induced NFkappaB binding activity with UVA irradiation. The contrary response on NFkappaB binding activity in NHM and HaCaT keratinocytes indicated that the redox regulation might be different on photoprotective action in melanocytes and keratinocytes., (Copyright 2002 S. Karger AG, Basel)

Schnitzler's syndrome (SS) is characterized by the association of generalized chronic urticaria, osteocondensation and monoclonal IgM gammopathy. Nonsteroidal anti-inflammatory drugs and systemic steroids are the most promising treatments. In our patient, they were ineffective. By contrast, during the follow-up period of 18 months, interferon alpha(2b) therapy (IFN-alpha) relieved the patient from its urticarial lesions and bone pain. IFN-alpha was tried to be stopped twice: each time, relapse of urticaria was noticed and, each time, the cutaneous lesions disappeared after IFN-alpha had been reintroduced. Furthermore, our observation supports the idea of the interleukin (IL)-1-mediated pathogenesis of SS as IFN-alpha induces high levels of IL-1 receptor antagonists. IFN-alpha could be an alternative treatment in disabling SS resisting other drugs., (Copyright 2002 S. Karger AG, Basel)

Reactive oxygen species can cause harmful effects in keratinocytes and fibroblasts if antioxidative defence mechanisms are exhausted. Therefore, it seems to be reasonable to prove if oral supplementation with various nutrient antioxidants is useful in prevention or treatment of skin disorders especially in those mediated by UV irradiation. Betacarotene, ascorbic acid and tocopherol have been tested alone or in combination for prevention of sunburn, photodermatoses and photocarcinogenesis with divergent results. Other candidates for oral antioxidative supplementation in humans are selenium and polyphenols. However, clinical data are limited or missing up to date., (Copyright 2001 S. Karger AG, Basel)

Objective: How can patients and staff participate in redesigning psychiatric procedures through survey research?, Methods: Using interviews with circular-hypothetical questioning, 58 patients and 30 staff members of a psychiatric department of a general hospital were interviewed about their preferences for change and continuity in clinical practices, and results were feedbacked., Results: Suggestions for change concerning doctors' rounds, the integration of music therapy, the number of individual sessions and the postdischarge care initiated real change., Conclusions: Surveys planned cooperatively with staff and without competitive benchmarking can be effective tools in psychiatric organization development.

Radiation-induced acne is a rare, clinically and pathogenetically ill-defined acneiform dermatosis with special features that may occur in irradiated skin areas especially after high doses of deeply penetrating radiation. We report on a patient with an oropharyngeal carcinoma who developed severe radiation-induced acne including comedones and cysts as well as few inflammatory papules and pustules in a skin area irradiated with up to 63 gray of a 6 MeV photon beam. Acnegenic drugs may precipitate the disease; our patient was on longterm therapy with carbamazepine whose acnegenic potency is less well documented than that of testosterone or glucocorticoids. Treatment of radiation-induced acne is comedolytic; topical retinoids are especially valuable.

During the past few years, bath PUVA has become established as an effective treatment for various dermatoses and especially for psoriasis. Using 3,4,5 trimethylpsoralen (TMP) in combination with subsequent UVA irradiation, a shower PUVA has been developed as an alternative in local PUVA therapy. This involves moistening the patient's skin - with the exception of the head and neck area - in a shower using water containing psoralen (TMP concentration 0,27 mg/l). The advantages of shower PUVA method are that time, space and cost savings are possible and that only a slight amount of physical exertion is required by the patient standing in the shower compared to immersing the whole body during bath PUVA therapy. The efficacy and practicability of shower PUVA were evaluated using the minimal phototoxic dose (MPD) for healthy volunteers assessing water temperature (33-38 degrees C), shower time (5-10 min), and UVA dose (0,06-1,0 J/cm(2)). Additionally, the time course of TMP-induced photosensitivity was observed over a period of 4 hours after the shower. Using a TMP concentration of 0,27 mg/l, the MPD for skin type I-II lay between 0,125-0,375 J/cm(2) and for skin type III-IV between 0,375-1,0 J/cm(2). Photosensitivity was induced by shower PUVA within 5-10 minutes shower time and at 33-38 degrees C water temperature. MPD exhibited an inverse correlation to temperature but no differences were apparent for shower times between 5 and 10 minutes. Photosensitivity completely disappeared within 2 hours. Minimal phototoxic doses using TMP in shower PUVA are comparable with classical bath PUVA when taking skin type into account. These results support the therapeutic use of shower PUVA using TMP.

Acute infection with hepatitis C virus (HCV) is often clinically inapparent, but may affect several organ systems in its chronic course. In dermatology, common diseases such as lichen planus, cryoglobulinemic vasculitis and porphyria cutanea tarda have been described in association with HCV infection. A number of other dermatologic disorders, e.g., psoriasis, chronic urticaria, chronic pruritus, pseudo-kaposi sarcoma, necrolytic migratory erythema and Behçet disease, have been associated in case reports with HCV-induced liver disease. In this study we summarize the recent literature reports, present three patients observed by our group and update the topic.

Acute neutrophilic dermatosis, also referred to as Sweet's syndrome according to the first description in 1964, occurs not only as an isolated phenomenon but also in the context of neoplastic and inflammatory diseases, occasionally including arthritides. Recently Sweet's syndrome has been reported in a small number of patients with chronic inflammatory bowel disease, mostly in advanced stages of the disease. Here, we describe the sudden outbreak of acute neutrophilic dermatosis in coincidence with the onset of severe Crohn's disease (CD) in a patient with long-standing ankylosing spondylitis (AS). This condition has not been described before and therefore Sweet's syndrome should be added to the spectrum of skin manifestations the rheumatologist has to think about in the context of the spondylarthropathies (SpA). Furthermore, this case report is of interest because the skin lesions of Sweet's syndrome are somewhat similar to psoriasis, which is a rather frequent feature of the spondylarthropathies. This article intends to clarify the clinical and histological differentiation between Sweet's syndrome, psoriatic skin lesions and erythema nodosum for the rheumatologist and stresses that these conditions must each be treated in a completely different manner.

A 76-year-old female patient developed severe manifestations of a kaposi-like acroangiodermatitis (so-called Mali's disease) due to chronic venous insufficiency of the lower extremities. The patient presented with large areas of confluent, violaceous or brown-black papules on both lower legs. Histologically, proliferation of thick-walled capillaries was seen in the upper dermis consisting of fully differentiated endothelial cells, as shown by immunohistochemistry. In contrast to true Kaposi's sarcoma, human-herpes-virus-8 DNA could not be detected by polymerase-chain-reaction in this condition. We review the diagnostic criteria used to distinguish between acroangiodermatitis, also called pseudo-Kaposi's sarcoma, and the true Kaposi's sarcoma.

Perforating disorders represent a heterogenous group of dermatoses characterized by transepithelial elimination of dermal structures. Primary perforating disorders should be distinguished from secondary perforating disorders in which perforation with transepithelial elimination is a rare component of a variety of dermatoses. The primary perforating disorders are hyperkeratosis follicularis et parafollicularis in cutem penetrans (Kyrle's disease), elastosis perforans serpiginosa and perforating folliculitis. Acquired reactive perforating dermatosis (also known as acquired reactive perforating collagenosis) together with the hereditary variant of the reactive perforating collagenosis represent further examples of the primary perforating disorders. We report on 84 year old and 96 year old female patients with an acquired perforating dermatosis. Both of the patients additionally showed diabetes and hyperuricemia. Oral administration of allopurinol (100 mg daily) led to a healing of the disseminated skin lesions in 1-2 weeks. After a follow-up period of 6 months, both patients were in complete remission. On one hand, these results prove again the existence and the severity of this disease, and on the other hand suggest an immunomodulating or differentiation-promoting action in addition to the uricostatic effect of allopurinol.

Pseudoscabies, i.e. infestation of human skin with animal mites may occasionally occur and should be considered in the differential diagnosis of pruritic and papular skin disease. We report here on a 52-year-old woman with pseudoscabies or canine scabies (Sarcoptes scabiei var. canis), transmitted by indirect contact with a red fox in the urban area of Berlin. Red foxes may live in unhabited areas of metropolitan large cities, i.e. in garages, car wrecks and cellars. Full remission of the prolonged and pruritic rush was seen after topical administration of lindane together with systemic corticosteroids.

Fibromyalgia has been reported to occur with high prevalence in systemic lupus erythematosus. Data on fibromyalgia in other subsets of lupus erythematosus are not available. Risk factors for fibromyalgia have not been defined. We investigated 60 patients with different subsets of lupus erythematosus for the presence of fibromyalgia, association with clinical and laboratory parameters and disease activity. Our data were compared with the multicentre lupus erythematosus registry at the Free University of Berlin. Ten out of 60 patients with more than 11 tender points and widespread pain for more than 3 months were classified as positive for fibromyalgia. All of them were female. Fibromyalgia-positive patients suffered significantly more often from headache, morning stiffness, diffuse alopecia, muscle pain, arthralgia, renal involvement, and disclosed peripheral blood cell cytopenia, rheumatoid factor, hypergammaglobulinaemia and intake of corticosteroids and azathioprine. Fibromyalgia was more frequent in systemic lupus than in other lupus subsets. Evaluation of fibromyalgia symptoms and lupus disease activity was performed in 30 patients in a 1-year (range 9-13 months) follow-up. These 30 patients consisted of 9 fibromyalgia-positive and 21 fibromyalgia-negative patients. Both groups were characterized by stable clinical features such as number of tender points and ECLAM index. Fibromyalgia did not show a correlation with lupus activity. We suggest that fibromyalgia and lupus erythematosus are distinct complaints. Patients with lupus are at risk of developing secondary fibromyalgia. The clinical features of fibromyalgia-positive patients may contribute to misinterpretation of lupus activity.

The pathogenesis of Kaposi's sarcoma (KS) is often attributed to an infectious agent. In particular, the human herpesvirus 8 (HHV-8) was currently shown to be closely related to all known KS types, including HIV-associated KS, European classic KS, African endemic KS and iatrogenic KS. We report here on an HIV-negative, German patient of neither Jewish nor Mediterranean descent with disseminated classic KS showing unusual rapid progression into the tumour stage. After systemic administration of interferon alpha-2a over 4 weeks all tumour lesions cleared completely. Interestingly, HHV-8 DNA sequences detected by nested polymerase chain reaction in KS lesions before the onset of treatment were still present in lesional skin after complete remission of the tumour. No recurrence was seen after a follow-up period of 6 months.

An HIV-1 infected immunosuppressed patient (CD4+ cell counts: 382 cells/microL; viral load 94,000 copies/mL) with recurrent perianal herpes simplex virus type 2 (HSV-2) infections is described, showing an unusual exophytic tumour resembling a squamous cell carcinoma in the lateral part of the tongue. He also had persistent facial herpes infection, oral candidosis, oral hairy leukoplakia and lymphadenopathy. The presence of HSV-2 was detected by polymerase chain reaction both in smears and in a tissue biopsy taken from the involved tongue area. Treatment with brivudin, a new oral virustatic drug, led to rapid regression of the tumour.