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PubMed2004

Colonic toxicity of administered drugs and chemicals.

Although uncommon, medication-induced colonotoxicity is important to recognize because medication cessation generally leads to prompt clinical improvement, while medication continuation results in disease exacerbation. This review categorizes the association between medications and colonotoxicity as "well-established" or "probable," according to the following criteria: total number of reported cases, number of different research groups reporting an association, experimental and pharmacologic evidence of an association, and validity of an association in each reported case. Cocaine, ergotamine, estrogen, sodium polystyrene, alosetron, amphetamines, pseudoephedrine, and vasopressin are associated with colonic ischemia. The mechanisms include vasospasm, thrombogenesis, and shunting of blood from mesenteric vessels. Narcotics, phenothiazines, vincristine, atropine, nifedipine, and tricyclic antidepressants are associated with colonic pseudo-obstruction. The mechanisms include antagonizing prokinetic neurotransmitters, stimulating antikinetic neurotransmitters, promoting dysmotility, relaxing smooth muscle, and injuring enteric neurons. Numerous antibiotics are associated with pseudomembranous colitis; ampicillin is associated with hemorrhagic colitis; chemotherapy is associated with neutropenic colitis; and deferoxamine is associated with Yersinia enterocolitis. Mechanisms of these toxicities include altering normal bowel flora, weakening immunologic defenses, promoting microorganism virulence, and mucosal injury. Gold compounds, nonsteroidal antiinflammatory drugs, alpha-methyldopa, salicylates, and sulfasalazine are associated with an inflammatory or cytotoxic colitis. The mechanisms include direct mucosal cytotoxicity, antimetabolite effects, or drug allergy. Nonsteroidal antiinflammatory drugs, cyclo 3 fort, flutamide, lansoprazole, and ticlopidine are associated with lymphocytic colitis. The mechanisms include immunologic activation or attenuated immunologic defenses. Chronic cathartic use leads to colonic hypomotility and abdominal distention. Intrarectally administered corrosive compounds can produce a toxic colitis.

Administration, Oral↗

PubMed1986

Evidence for oligoclonal B cell expansion in the peripheral blood of patients with rheumatoid arthritis.

Peripheral blood lymphocytes from patients with rheumatoid arthritis and osteoarthritis were examined for evidence of oligoclonal B cell expansion using the computer assisted flow cytometric technique of kappa-lambda (kappa-lambda) analysis. Eleven of 29 patients with rheumatoid arthritis but only one of 16 with osteoarthritis gave abnormal results (p less than 0.025). Abnormal kappa-lambda determinations did not correlate with age, duration of disease, presence of rheumatoid factor, or other clinical and laboratory parameters. Therapy with oral or intramuscular gold compounds appeared to diminish the incidence of kappa-lambda abnormality. These findings may indicate defective control of clonal B cell proliferation in rheumatoid arthritis.

Adult↗

PubMed1988

Anti-inflammatory drugs modulate histamine release from mast cells induced by fibrinogen degradation products.

The products resulting from proteolytic degradation of human fibrinogen (FDP) were found to induce the release of histamine from rat peritoneal mast cells. Low molecular weight, dialysable peptides (FDP) showed the highest dose dependent, histamine releasing activity. Histamine release induced by FDP was effectively inhibited by the gold compound auranofin at a concentration of 10(-5)-10(-7) mol/l and also by the non-steroidal anti-inflammatory drugs BW 755c, timegadine, medosan, naproxen, and aspirin at the higher concentration range of 10(-4)-10(-6) mol/l. It is concluded that the release of histamine from mast cells may be modulated to some extent by anti-inflammatory drugs, especially auranofin, BW 755c and timegadine, a functional property which may be beneficial in the management of joint disease.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗

PubMed1982

Effects of anti-inflammatory drugs on triple vaccine-induced pleurisy in rats.

Effects of various anti-inflammatory drugs on triple vaccine-induced pleurisy, a model of delayed hypersensitivity, were examined and compared with those on carrageenin-induced pleurisy in rats. Steroidal drugs depressed markedly the volume of exudate and the number of leucocytes in both types of pleurisy. Gold compounds also depressed both types of pleurisy. Non-steroidal anti-inflammatory drugs were apt to show depressive effects on carrageenin-induced pleurisy, especially on increased exudate volume. BW755C produced a depressive effect on carrageenin-induced pleurisy, but on triple vaccine-induced pleurisy, BW755C produced only a slight depressive effect. Cyproheptadine produced a slight depressive effect on carrageenin-induced pleurisy, but not on triple vaccine-induced pleurisy. Promethazine had a slight depressive effect on both types of pleurisy. D-penicillamine and levamisole did not show any depressive effects on triple vaccine-induced pleurisy. The results show that reported mediators in carrageenin-induced pleurisy (prostaglandin, serotonin, leukotriene B, etc.) are not relevant to triple vaccine-induced pleurisy. Specific lymphokines and/or degradated products of complement may participate in the latter. This triple vaccine-induced pleurisy seems to be a good model for screening non-steroidal anti-inflammatory drugs which have steroidal-like activity.

Animals↗

PubMed2004

Purification, characterization, and immunolocalization of a thioredoxin reductase from adult Fasciola hepatica.

Thioredoxin reductase (TrxR), an enzyme belonging to the flavoprotein family of pyridine nucleotide-disulfide oxidoreductases, was isolated from the deoxycholate-soluble extract of the common liver fluke, Fasciola hepatica. Purification to homogeneity of the 60-kDa enzyme from the adult worm was achieved by a combination of ammonium sulfate fractionation, anion exchange, and affinity chromatography on 2',5'-adenosine diphosphate-Sepharose. Using the 5,5'-dithiobis(2-nitrobenzoic acid) assay, the purified TrxR showed a specific activity of 7,117 U min(-1) mg(-1). The enzyme activity was completely inhibited by the presence of the gold compound aurothioglucose (IC50 = 120 nm), indicating that F. hepatica TrxR is a selenoenzyme. Also, the enzyme was capable of reducing disulfide bonds in insulin and was activated by the presence of the reduced form of flavin adenine dinucleotide, properties shared with mammalian TrxRs. Furthermore, the isolated enzyme showed very low glutaredoxin (Grx) activity (0.47 U mg(-1)), but no glutathione reductase activity was detected. Affinity-purified IgGs (20 microg ml(-1)) from the antisera produced against the purified TrxR inhibited its activity about 80% with respect to the control. The enzyme was immunolocalized in cells located within the parenchyma and in the testes, but it was not found in the tegument of the adult fluke.

Animals↗

PubMed1998

Treatment of inflammatory rheumatic disorders in pregnancy: what are the safest treatment options?

The interaction of pregnancy and the rheumatic diseases varies, ranging from life-threatening conditions such as thromboembolic events and progressive renal disease in some autoimmune disorders, to minor flares of peripheral arthritis in inflammatory rheumatic disease. As a consequence, treatment strategy will vary according to the maternal or fetal compromise expected. All nonsteroidal anti-inflammatory drugs (NSAIDs), including high dose aspirin (acetylsalicylic acid), can cause adverse effects during pregnancy related to the inhibition of prostaglandin synthesis. Prolongation of gestation and labour, constriction of the ductus arteriosus, persistent fetal circulation, impairment of renal function and bleeding are risks of third trimester exposure of pregnant women to all inhibitors of cyclo-oxygenase. Most of these adverse effects can be prevented by discontinuing NSAIDs 8 weeks prior to delivery. Low dose aspirin has not been associated with fetal or neonatal toxicity. Some corticosteroids such as prednisone and prednisolone do not readily cross the placenta and can be safely used during pregnancy as immunosuppressive drugs. Maternal complications related to corticosteroids may occur and close monitoring is therefore mandatory. There is limited information on the safety of disease-modifying antirheumatic drugs including gold, antimalarials, penicillamine (D-penicillamine), sulfasalazine and cyclosporin. Of these agents, sulfasalazine has the best record for tolerability and can be used by pregnant patients. Gold compounds and penicillamine should be discontinued when pregnancy is recognised. Hydroxychloroquine has not been associated with congenital malformations and seems preferable to chloroquine in patients requiring treatment with antimalarials. Use of cyclosporin may be an alternative to other therapy in pregnant patients with severe rheumatic disease. Indications for treatment with colchicine during pregnancy are few, except for familial Mediterranean fever. Azathioprine can be used when the maternal condition requires a cytotoxic drug during the first trimester. Cyclophosphamide, chlorambucil and methotrexate are contraindicated during pregnancy because of their teratogenic potential. Their use may be considered in late pregnancy if the mother has a life-threatening condition.

Adrenal Cortex Hormones↗

PubMed2003

Methotrexate intolerance in elderly patients with rheumatoid arthritis: what are the alternatives?

Rheumatoid arthritis (RA) in the elderly may be mild or severe, with features that are similar to those seen in younger patients. As such, the treatment regimen in the elderly is almost the same as in younger patients. Methotrexate is the most popular disease-modifying antirheumatic drug (DMARD) for the treatment of RA in the US and Europe. It has excellent efficacy and an acceptable toxicity profile. However, a number of patients do not tolerate methotrexate and an alternative DMARD should be chosen. In the elderly, choice of an alternative DMARD should be made after careful consideration of several age-related factors including concomitant diseases, existing medication, drug compliance, and altered age-related physiology and pharmacokinetics. In elderly patients with RA who are unable to tolerate methotrexate, the alternatives are hydroxychloroquine or sulfasalazine for mild-to-moderate disease and cyclosporin or leflunomide for severe disease, given in combination with low-dose oral corticosteroids. This is primarily due to their efficacy combined with a relatively low toxicity profile compared with other DMARDs, such as gold compounds, penicillamine, azathioprine and alkylating agents. Where the above DMARDs are contraindicated, anticytokine therapy should be considered. The therapy of RA is a dynamic process and requires a delicate balance of benefits and risks. Experience and familiarity with the currently available agents, and knowledge of the nature of the disease are necessary in order to make better therapeutic decisions.

Aged↗

PubMed1994

Optimisation of antirheumatic drug treatment in pregnancy.

Active rheumatic disease during pregnancy may require drug treatment to ensure the mother's health is maintained and that there is a good outcome for the fetus. However, knowledge on the use of antirheumatic drugs during pregnancy is limited, rendering decision making difficult both for the patient and the physician. The effect of nonsteroidal anti-inflammatory drugs (NSAIDs) in the treatment of rheumatoid arthritis has been investigated in depth for aspirin (acetylsalicylic acid) and indomethacin only. Information about the use of ibuprofen, sulindac, ketoprofen and diclofenac during pregnancy is scanty and there is no such information for newer agents such as the fenemates and oxicams. There is no evidence for teratogenicity of any NSAID in humans. However, due to the shared property of inhibition of prostaglandin synthesis, adverse effects such as constriction of the ductus arteriosus in utero, persistent pulmonary hypertension in the neonate and prolongation of pregnancy and labour are possible. When administered to pregnant patients, NSAIDs should be given in the lowest effective dose, and should be withdrawn within the 8 weeks prior to expected delivery. Transplacental passage varies for different corticosteroids. Because of the inability of the fetal liver to convert prednisone to its active metabolite and the ability of the placenta to convert prednisolone to the inactive prednisone, both prednisolone and prednisone are drugs of choice in pregnant patients requiring corticosteroid treatment. Corticosteroids do not increase the risk of congenital malformations. Possible adverse effects are perinatal infection and adrenal insufficiency in the newborn. Both events are only rarely reported in the literature, which comprises information on more than 1000 pregnancies. The clinical experience on the effect of slow-acting antirheumatic drugs (SAARDs) on pregnancy is insufficient to draw substantial conclusions. Available data from the literature give no clear evidence of an increased risk of teratogenicity for any of these drugs. Rheumatologists differ in their view on the advisability of using SAARDs during pregnancy. Hydroxychloroquine, which is regarded as less toxic than chloroquine, is recommended by some rheumatologists for the treatment of pregnant patients with active systemic lupus erythematosus (SLE) or rheumatoid arthritis. Sulfasalazine can be continued during pregnancy. Data on gold compounds and penicillamine are sparse and inconclusive. A reasonable approach is to stop these agents as soon as pregnancy is confirmed. The limited experience with cyclosporin has been obtained when the drug was used to prevent allograft rejection. Further data regarding the use of this drug in pregnant patients with rheumatic diseases are needed.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenal Cortex Hormones↗

PubMed2001

A clinical and economic review of disease-modifying antirheumatic drugs.

Rheumatoid arthritis is one of the most common chronic systemic inflammatory diseases, affecting approximately 1% of the adult population. Disease-modifying antirheumatic drugs (DMARDs) have been the mainstay of treatment for rheumatoid arthritis when combined with physical therapy and aspirin (acetylsalicylic acid) or nonsteroidal anti-inflammatory drugs. Recently, a number of new biological therapies have been introduced for the treatment of this condition and will have a major impact on the future management of this disabling disease. In this review, we summarise data on the efficacy and tolerability of the currently available DMARDs, including gold compounds, antimalarials, penicillamine, cytotoxic drugs (azathioprine and cyclophosphamide), sulfasalazine, methotrexate, leflunomide, cyclosporin, anti-tumour necrosis factor agents, combination therapy and apheresis. A literature review and quality assessment of economic evaluations of DMARDs is presented, illustrating that there has been a paucity of economic evaluations on these agents and showing the variable quality of those studies that are available. The manuscript also addresses the pharmacoeconomic implications of the new agents for rheumatoid arthritis; the need for formal long term economic evaluations in order to determine the cost effectiveness of these costly, but highly effective, new treatments is emphasised.

Antirheumatic Agents↗

PubMed1990

Upper gastrointestinal manifestations in rheumatoid arthritis patients: intrinsic or extrinsic pathogenesis?

Apart from the complication of gastrointestinal vasculitis it is not known whether the upper gastrointestinal (UGI) tract has any special disease characteristics in rheumatoid arthritis (RA). However, oesophageal motility disorders have been reported in 30% of RA patients. Hypergastrinaemia has been found in 23-43% of RA patients, usually in combination with a decreased gastric acid output. Another finding suggestive of a decreased secretory state, namely a decreased level of pepsinogen A, was found in RA patients with the sicca syndrome and in patients with active disease. The risk for peptic ulcer disease with regard to nonsteroidal anti-inflammatory drugs (NSAID) is possibly higher in RA patients than in patients with other rheumatic diseases. These findings suggest that in RA patients intrinsic factors play a role in the pathogenesis of the oesophageal motility disorders, in hypergastrinaemia and hypopepsinogenaemia and the related decreased gastric secretory state, and possibly in the increased susceptibility to NSAID-related ulcers. However, there are also indications that oesophageal motility disorders, hypergastrinaemia, and NSAID-related ulcers in RA are the result of extrinsic factors, mainly the use of NSAIDs. The effects of NSAIDs and gold compounds on infection with Helicobacter pylori, a possible pathogenetic factor in ulcer disease, is discussed. It is clear that the discussion about intrinsic and extrinsic factors as a cause of the UGI manifestations in RA remains an intriguing but difficult subject for further studies.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed1999

Nuclear factor kappaB (NF-kappaB) pathway as a therapeutic target in rheumatoid arthritis.

Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by persistent joint swelling and progressive destruction of cartilage and bone. Current RA treatments are largely empirical in origin and their precise mechanism of action is uncertain. Increasing evidence shows that chronic inflammatory diseases such as RA are caused by prolonged production of proinflammatory cytokines including tumor necrosis factor (TNF) and interleukin 1 (IL-1). The nuclear factor kappaB (NF-kappaB) plays an essential role in transcriptional activation of TNF and IL-1. NF-kappaB is induced by many stimuli including TNF and IL-1, forming a positive regulatory cycle that may amplify and maintain RA disease process. NF-kappaB and enzymes involved in its activation can be a target for anti-inflammatory treatment. Aspirin and sodium salicylate inhibit activation of NF-KB by blocking IkappaB kinase, a key enzyme in NF-kappaB activation. Glucocorticoids suppress expression of inflammatory genes by binding glucocorticoid receptor with NF-kappaB, and increasing expression of inhibitory protein of NF-kappaB, IkappaBalpha. Sulfasalazine and gold compounds also inhibit NF-kappaB activation. Continuing advances in our understanding of action mechanism of antirheumatic agents will benefit the future development of RA regimens with greater efficacy and less toxicity.

Animals↗

PubMed2003

[Kidney involvement in rheumatoid arthritis].

Rheumatoid Arthritis (RA) is a widespread disease and its renal involvement, relatively common, is clinically significant because worsens course and mortality of the primary disease. There is still no agreement on the prevalence of renal disorders in RA: data analysis originates from different sources, as death certificates, autopsies, clinical and laboratory findings and kidney biopsies, each with its limitations. Histoimmunological studies on bioptical specimens of patients with RA and kidney damage, led to clarify prevalent pathologies. In order of frequency: glomerulonephritis and amyloidosis (60-65% and 20-30% respectively), followed by acute or chronic interstitial nephritis. Kidney injury during RA includes secondary renal amyloidosis, nephrotoxic effects of antirheumatic drugs and nephropathies as extra-articular manifestations (rheumatoid nephropathy). Amyloidosis affects survival, increases morbidity and is the main cause of end stage renal disease in patients with RA and nephropathy. Strong association between RA activity and amyloidosis needs the use of immunosuppressive and combined therapies, to prevent this complication and reduce risk of dialysis. Long-lasting and combined RA pharmacotherapy involves various renal side effects. In this review we describe NSAIDs and DMARDs (Disease-Modifying Antirheumatic Drugs) nephrotoxicity, particularly by gold compounds, D-penicillamine, cyclosporine A and methotrexate. Rare cases of IgA glomerulonephritis during immunomodulating therapy with leflunomide and TNF blocking receptor (etanercept) are reported; real clinical significance of this drug-related nephropathy will be established by development of RA treatment. In RA nephropathies, mesangial glomerulonephritis is the most frequent histological lesion (35-60 % out of biopsies from patients with urinary abnormalities and/or kidney impairment), followed by minimal change glomerulopathy (3-14%) and p-ANCA positive necrotizing crescentic glomerulonephritis.

Amyloidosis↗

PubMed1985

Efficacy of total lymphoid irradiation in intractable rheumatoid arthritis. A double-blind, randomized trial.

Twenty-six patients participated in a randomized, double-blind study of the efficacy of total lymphoid irradiation in the treatment of intractable rheumatoid arthritis. All 26 patients, for whom therapy with gold compounds and penicillamine had failed, would ordinarily have been considered candidates for cytotoxic or antimetabolite drug therapy. Thirteen patients randomly assigned to receive full-dose total lymphoid irradiation (2000 rad) and 11 patients assigned to receive control low-dose total lymphoid irradiation (200 rad) completed radiotherapy. Alleviation of joint disease activity was significantly greater in the high-dose group as judged by morning stiffness, joint tenderness, and functional assessment (global composite score) at 3 and 6 months after radiotherapy. The high-dose group had a marked reduction in both T-lymphocyte function and numbers, but this finding was not observed in the low-dose group. Complications seen in the high-dose but not low-dose group included transient neutropenia, thrombocytopenia, pericarditis, and pleurisy.

Adult↗

PubMed1999

Disappointing longterm results with disease modifying antirheumatic drugs. A practice based study.

OBJECTIVE: To evaluate the longterm effectiveness of disease modifying antirheumatic drugs (DMARD) in an inception cohort of patients with rheumatoid arthritis (RA) seen by rheumatologists. METHODS: We performed a retrospective audit of the records of patients with onset of RA between January 1985 and June 1994. Charts were reviewed from the time of diagnosis to the last consult. Survival analysis was performed using Kaplan-Meier and Cox proportional hazard regression to adjust for potential confounders. RESULTS: A total of 2296 DMARD therapies were analyzed. Roughly half were started within 2 years of disease onset. By 16 months, 50% of the DMARD therapy courses had been discontinued, and after 4.5 years 75% had been discontinued. Over all, methotrexate (MTX) had the highest probability of continuation. After roughly 3 years 50% of patients were still receiving MTX, compared to one-third of patients who received antimalarials or intramuscular gold, 30% D-penicillamine, 25% sulfasalazine, and 18% oral gold. After 6 years, when considering all DMARD together, only 20% of the therapies had not been discontinued, with no substantial differences between drugs. Toxicity from gold compounds occurred within the first 18 months of therapy and stabilized thereafter. For MTX, withdrawals due to toxicity continued throughout therapy. CONCLUSION: This is the largest observational study examining the longterm termination rates of DMARD in patients followed from the time of their initial consult. Our results confirm previous reports of short therapeutic times, even for patients treated early in the course of their disease. MTX appears to be the best drug within the first 5 years of disease. These differences, however, decrease in the longer term. It is unclear whether the results observed for MTX within the first years of therapy translate to better health status in the longer term when compared to other DMARD.

Antirheumatic Agents↗

PubMed2000

[Drug-induced oral ulcerations].

Different side effects of drugs have been described in the oral cavity, including oral ulcerations. Direct contact between drugs and oral mucosa may induce chemical burn or local hypersensitivity. Less frequently, these drug-induced oral ulcerations are part of a complex reaction with cutaneous or systemic manifestations. Sometimes, one or more oral ulcerations appear as the main side-effect of a drug, or exceptionally as solitary lesions. Solitary oral ulcerations usually appear after few weeks of treatment. In most of cases, these lesions resist to conventional treatments, with a rapid healing following the suppression of the responsible drug. This diagnosis is usually difficult, particularly with patients receiving multiple drug therapy. Besides, special attention must be paid to new drugs. Oral ulcerations following symptoms of burning mouth, metallic taste, dysgueusia or agueusia are strongly suggestive of a pharmacological origin. Most of the molecules able to induce solitary oral ulcerations are commonly prescribed in a) rheumatology: NSAI (diclofenac, flurbiprofen, indomethacin, naproxen), long-term rheumatoid arthritis therapy (azathioprine, methotrexate, penicillamine, gold compounds, tiopronin); b) cardiology: angiotensin-converting-enzyme inhibitors (captopril, enalapril), angiotensin 2-receptor antagonist (losartan), anti-angorous (nicorandil), c) psychiatry: antidepressants (fluoxetine, lithium), d) AIDS therapy (foscarnet, zalcitabine).

Anesthetics, Local↗

PubMed2002

[Thioredoxin reductase--a new target for molecular medical investigations].

Thioredoxin reductase (TrxR) is the first selenoenzyme containing selenocysteine in the active center and FAD as a second prosthetic group. TrxR catalyses the NADPH-dependent reduction of thioredoxin and of many other physiologically important substrates. TrxR exhibits a many-fold increase in the activity in tumor cells and stimulates their proliferation as well the phenotype changes. Some gold compounds and a number of other clinically and experimentally tested drugs have been shown to inhibit TrxR. The involvement of TrxR/Trx/NADPH system in a broad spectrum of cellular processes renders it a potential target for therapeutic approaches.

Animals↗

PubMed1991

Angiogenesis and its inhibition: potential new therapies in oncology and non-neoplastic diseases.

To summarise the key points: The ability to mount an angiogenic response is probably present in all tissues, and stimulation of endothelial cells by any one of a wide variety of factors initiates a cascade of events leading to angiogenesis. In most tissues the overall lack of angiogenesis in normal situations probably results from the interaction of a complex series of multifactorial systems, each of which maintained in a state of balance between stimulation and inhibition. An imbalance in any one of these systems, for example by an increase in the concentration of a growth factor, may lead to angiogenesis. Inhibition of angiogenic stimuli is unlikely to be effective as an approach to new angiostatic drugs, given the multiple stimulatory pathways available. Tumour cells for example may induce angiogenesis via release of numerous growth factors, prostaglandins etc, and by their attraction of inflammatory cells which in turn release multiple angiogenic stimuli. Inhibitory modulation of many of the individual steps of capillary growth which occur following an angiogenic stimulus can block the angiogenic response. This leads to the expectation that an effective inhibitor of a single key step in this cascade would be able to completely suppress angiogenesis. Inappropriate angiogenesis is an important factor in many diseases including cancer and arthritis. In particular angiogenesis is an absolute requirement for neoplastic growth of solid tumours, and the establishment of secondary growths. There is also a strong link between induction of angiogenesis by a tumour and its ability to metastasise. Several drugs with proven clinical effects in diseases involving angiogenesis have recently been found to be angiogenesis inhibitors, and this may be their primary mechanism of action. In particular the activities of methotrexate and gold compounds in arthritis, and alpha-interferon and medroxyprogesterone in cancer therapy may be due to inhibition of angiogenesis. In animal models, treatment with angiogenesis inhibitors has proven anti-tumour effects in vivo, and can both reduce metastases and lead to regression of the primary growth by necrosis following capillary retraction. In man the success of alpha-interferon and TNF alpha in AIDS related Kaposi's sarcoma may be due to inhibition of angiogenesis. Interferon has also been successfully used to treat pulmonary hemangiomatosis, in which angiogenesis in the lung may be the pathogenic basis of the disease.

Adult↗

PubMedDate not supplied

[Panhypogammaglobulinemia: a rare complication of parenteral gold therapy].

Secondary antibody deficiency is one of the rare adverse effects of chrysotherapy in rheumatoid arthritis. The plasma levels of all immunoglobulins fall into ranges significantly lower than the tolerable physiological minimum. The long-lasting panhypogammaglobulinemia can increase the risk of infection in the patient and, therefore, should be closely monitored. Hence, a record of immunoglobulin levels before and during therapy with gold compounds seems to be mandatory.

Agammaglobulinemia↗