acquired immunodeficiency syndrome

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AIDS

(ādz),
A deficiency of cellular immunity induced by infection with the human immunodeficiency virus (HIV-1) and characterized by opportunistic diseases, including Pneumocystis jiroveci (formerly carinii) pneumonia, Kaposi sarcoma, oral hairy leukoplakia, cytomegalovirus disease, tuberculosis, Mycobacterium avium complex (MAC) disease, candidal esophagitis, cryptosporidiosis, isoporiasis, cryptococcosis, non-Hodgkin lymphoma, progressive multifocal leukoencephalopathy (PML), herpes zoster, and lymphoma. HIV is transmitted from person to person in cell-rich body fluids (notably blood and semen) through sexual contact, sharing of contaminated needles (as by IV drug abusers), or other contact with infected blood (as in accidental needlesticks among health care workers). Maternal-fetal transmission also occurs. The primary targets of HIV are cells with the CD4 surface protein, including principally helper T lymphocytes. Antibody to HIV, which appears in the serum 6 weeks to 6 months after infection, serves as a reliable diagnostic marker but does not bind or inactivate HIV. Gradual decline in the CD4 lymphocyte count, typically occurring over a period of 10-12 years, culminates in loss of ability to resist opportunistic infections. The appearance of one or more of these infections defines the onset of AIDS. In some patients, generalized lymphadenopathy, fever, weight loss, dementia, or chronic diarrhea occurs much earlier in the course of the infection. Untreated AIDS is uniformly lethal within 2-5 years after the first appearance of an opportunistic infection. Besides prophylaxis against opportunistic infection, standard therapy of HIV infection includes use of nucleoside analogues (for example, didanosine, lamivudine, ribavirin, stavudine, zipovudine), nonnucleoside reverse transcriptase inhibitors (for example, delavirine, efavirenz, nevirapine) and protease inhibitors (for example, atazanavir, crixivan, indinavir, ritonavir, saquinavir).
See also: human immunodeficiency virus, plasma viral load.
[acronym, acquired immunodeficiency syndrome]

Each year about 5 million people contract AIDS worldwide, and 3 million die of it. Some 40-50 million are estimated to be living with the disease. The gender incidence is approximately equal. The highest prevalence is in some African countries, where as many as 25% of the adult population may test HIV positive; about 70% of the world's infected population lives in sub-Saharan Africa. The first cases of AIDS were reported in the U.S. in June 1981. During the succeeding 2 decades an estimated 1.4 million people in this country were infected with HIV and 816,149 cases of AIDS and 467,910 deaths were reported to the U.S. Centers for Disease Control and Prevention (CDC). The numbers of new AIDS cases and deaths declined substantially after introduction of combination antiretroviral therapy in the late 1990s. The annual number of new cases of AIDS in the U.S. has remained stable at about 40,000, with 16,000 deaths since 1998. The number of people infected with HIV continues to increase, and of an estimated 1 million, one fourth are unaware that they are infected. In the U.S., AIDS is the leading cause of death among men 25-44 years old, and the fourth leading cause of death among women in the same age group. The development of effective antiretroviral agents (for example, reverse transcriptase inhibitors and protease inhibitors) and of quantitative plasma HIV RNA assays that can monitor progression of disease and response to treatment has shifted the goal of management in AIDS from prophylaxis and treatment of opportunistic infections to achievement of remission through suppressive therapy. Immune compromise is monitored by serial CD4 counts, viral replication by plasma HIV RNA assay (that is, plasma viral load, PVL). Indications for starting antiretroviral therapy are the appearance of symptoms of opportunistic infection, decline of the CD4 count below 350/mm3, or viral load exceeding 30,000 copies/mL. The CD4 count is considered a more sensitive predictor of disease progression than viral load. Empiric treatment may be begun early (within 6 months after conversion to HIV-positive status) in an effort to preserve immune function and mobilize the patient's own defenses against the virus. But current guidelines advise deferring treatment as long as possible so as to limit induction of drug resistance. Protease inhibitors have been shown to be highly effective antiretroviral agents and standard treatment regimens combining 2 reverse transcriptase inhibitors with 1 protease inhibitor ("triple therapy") have clearly demonstrated superiority over monotherapy. These drugs are expensive. Regimens are often complex, with varying requirements for fasting and timing of doses, and adverse effects and drug interactions are common. Protease inhibitors have been associated with elevation of cholesterol and triglycerides, insulin resistance, and disfiguring lipodystrophy. In one large study, more than one half of HIV-infected adults under treatment were found to be infected with strains of virus resistant to one or more antiretroviral drugs, and strains of HIV that are resistant to all available protease inhibitors have appeared. The rationale for current AIDS regimens is an effort to eradicate HIV infection by inhibiting spread of virus to new cells until all infected cells have died. However, actual cure seldom if ever occurs. A small number of resting CD4 memory cells in treated patients with undetectable plasma HIV RNA levels harbor HIV proviral DNA capable of replication, and these cells may survive for months or years. Macrophages and CNS neurons may serve as an anatomic sanctuary for HIV into which antretroviral drugs cannot penetrate in adequate concentration. When antiretroviral therapy is initiated early, CD4 helper cell counts rise, CD4 cell activity is preserved, and HIV RNA levels may remain undetectable for long periods. But in about 50% of patients with advanced disease, even multidrug regimens fail to suppress plasma viral RNA to undetectable levels. Many treatment failures result from poor compliance with multidrug regimens. Failure of one therapeutic regimen often precludes success with others because of the high degree of cross-resistance among antiretroviral drugs. After failure of an initial regimen, genotypic testing can be used to identify mutations in the HIV genome that confer resistance to one or more classes of HIV drugs. Many patients remain vulnerable to opportunistic infections despite restoration of CD4 counts to normal, probably because some subpopulations of T cells have been annihilated and cannot be recovered even after HIV has been suppressed. Moreover, even HIV-infected patients with undetectable viral loads must still be considered infectious. In a small set of those infected with HIV, impairment of immunity progresses to AIDS slowly or not at all. CD8 T-cells from such nonprogressors have been found to produce proteins called α-defensins. Evolving standards of treatment in HIV disease include aggressive prophylaxis in pregnancy and after accidental needle stick and sexual assault. Administration of antiretroviral agents to HIV-positive mothers before birth and during labor and delivery, and to newborns for the first 6 weeks of life, markedly decrease the risk of vertical transmission of HIV infection. The risk of HIV infection after occupational parenteral exposure to blood from an HIV-infected patient is approximately 0.3%. Postexposure prophylaxis with antiretroviral agents continued for 28 days have been shown to reduce the risk by 80%. The selection of agents depends on the source patient's therapeutic history. Efforts to develop a vaccine against HIV have been hampered by the unique properties of the virus and the long incubation period of AIDS. Early in the 21st century, public health authorities sought to make HIV testing a routine part of medical care, to facilitate diagnosis outside formal clinical settings, to prevent new infections by educating people and their sexual partners, and to decrease perinatal HIV transmission through routine HIV testing of pregnant women and of infants whose mothers were not screened.

acquired immunodeficiency syndrome (AIDS)

a syndrome involving a defect in cell-mediated immunity that has a long incubation period, follows a protracted and debilitating course, is manifested by various opportunistic infections, and without treatment has a poor prognosis. The disorder originally was found in homosexual men and IV drug users but now occurs increasingly among heterosexual men and women and children of those with the disease. More than 1 million cases of AIDS have appeared in the United States, where in 1993 it was the leading cause of death among men between 25 and 44 years of age and the fourth leading cause of death among women of the same age group. Worldwide, an estimated 25 million had died from the epidemic by the end of 2006, 2.9 million of those in 2006 alone. Approximately 40 million people are estimated to be living with HIV/AIDS, 37.2 million adults and 2.3 million children under the age of 15. The disease is particularly prevalent in sub-Saharan Africa.
observations AIDS is caused by either of two varieties of the human immunodeficiency virus, designated HIV-1 and HIV-2. HIV is a retrovirus that attracts and kills CD4+ helper T lymphocytes, weakening the immune system's ability to prevent infection. The virus may also invade macrophages, in which it replicates freely, undetected by the immune system. HIV is not spread by casual contact but rather by sexual intercourse or exposure to contaminated blood, semen, breast milk, or other body fluids of infected persons. A patient may be diagnosed as having AIDS if he or she is infected with HIV, has a CD4+ count below 200 to 500/mL, and exhibits one or more of the following signs and symptoms: extreme fatigue, intermittent fever, night sweats, chills, lymphadenopathy, enlarged spleen, anorexia and consequent weight loss, severe diarrhea, apathy, and depression. As the disease progresses, characteristics are a general failure to thrive, anergy, and any of a variety of recurring infections, most commonly Pneumocystis pneumonia, tuberculosis, meningitis, and encephalitis caused by aspergillosis, candidiasis, cryptococcosis, cytomegalovirus infection, toxoplasmosis, or herpes simplex. Some patients with AIDS are susceptible to malignant neoplasms, especially Kaposi's sarcoma, Burkitt's lymphoma, and non-Hodgkin's lymphoma, that both cause and result from immunodeficiency. Psychological complications of AIDS may include chronic anxiety, depression, substance dependence, organic mental disorders, and suicidal ideation.
interventions Treatment consists primarily of chronic symptom management and combined chemotherapy to counteract the opportunistic infections. There is no known cure. Drugs used to treat AIDS include reverse transcriptase inhibitors, such as zidovudine and dideoxyinosine, which interfere with the virus' ability to synthesize DNA within host cells, and HIV protease inhibitors, such as ritonavir and indinavir, which cause the production of noninfectious HIV particles. These drugs are given in combinations (often called cocktails); one commonly used combination is made up of two reverse transcriptase inhibitors and a potent HIV protease inhibitor. Vaccines routinely recommended for AIDS include those directed against pneumococcal influenza, hepatitis B, and general childhood infections, as well as infections that may be endemic in countries where the patient may travel, such as typhoid and yellow fever.
nursing considerations Nursing care of the patient with AIDS varies with the patient's symptoms. These may include dyspnea, nutritional wasting, fatigue, pain, and incontinence. Intervention is directed at providing education to prevent the spread of disease and infection, promoting self-care and optimal nutrition, and providing emotional support for patients and their families. Patients with tumors, hematologic abnormalities, and infections require routine treatment for these disorders along with care for their HIV-related complaints. See also AIDS-dementia complex, AIDS-wasting syndrome.

AIDS

Acquired Immunodeficiency Syndrome. An immunosuppressing condition which is intimately linked to infection by a retrovirus, human immunodeficiency virus (HIV-1). 
Bangui definition A points-based system used to define AIDS in countries where HIV testing is not available. It was developed by workers from the CDC and WHO at a conference held in Bangui, Central African Republic, in 1985, and gives the most points for severe weight loss, protracted asthenia, recalcitrant fever and diarrhoea. AIDS is diagnosed with scores of 12 or more.
Clinical findings Weight loss exceeding 10% of body weight, protracted asthenia, continuous fever for >1 month, diarrhoea >1 month, persistent cough, oropharyngeal candidiasis, relapsing cutaneous herpes, generalised pruritic dermatosis, generalised lymphadenopathy, Kaposi's sarcoma.
Management Long-term survival after HIV infection is possible, but requires aggressive multi-agent therapy; once clinical AIDS develops, it is fatal, despite temporary response to various therapies.
AIDS is also an abbreviation for:
Academy of International Dental Studies
Accident/Incident Data System
Accretive Industrial Development Syndrome. A non-medical term used in real estate.
All Individuals Deserve Support. A slogan used by an AIDS support group.

acquired immunodeficiency syndrome

See AIDS.

Acquired immunodeficiency syndrome (AIDS)

A group of diseases resulting from infection with the human immunodeficiency virus (HIV). A person infected with HIV gradually loses immune function, becoming less able to resist aliments and cancers, resulting in eventual death.
Mentioned in: Autopsy

syndrome

aggregated objective signs, subjective symptoms and specific pathologies that typify specific conditions
  • acquired immunodeficiency syndrome; AIDS severe reduction in numbers of T4 lymphocyte helper (CD4) cells (due to infection with human immunodeficiency virus [HIV]) and resultant compromise of humoral and cell-mediated immunity; patients show lymphadenopathy, opportunistic infections (e.g. tinea and verrucae) and unusual infections (e.g. histoplasmosis, gastrointestinal tract candidiasis, Pneumocystis carnii pneumonia [PCP]), unusual malignancies (e.g. Kaposi's sarcoma), wasting diseases and presenile dementia

  • acute compartment syndrome; ACS increased lower-limb intracompartmental pressure on exercise (exercise expands muscles, increases intracompartmental pressures, inducing pain); treated initially by rest, immobilization, non-steroidal anti-inflammatory drugs; severe cases may require surgical decompression (fasciotomy)

  • anterior tarsal syndrome; ATS deep peroneal nerve entrapment at anterior ankle/dorsal talonavicular joint, due to restriction of ankle dorsiflexion (e.g. tight boots; ski boots), or local soft-tissue trauma (e.g. dorsal tarsal exostoses); characterized by extensor hallucis longus weakness, dorsal foot paraesthesia and numbness of first intermetatarsal space (symptoms can be induced by deep peroneal nerve percussion as crosses the anterior aspect of the ankle joint, or by ankle joint plantarflexion whilst simultaneously dorsiflexing toes)

  • anterior tibial compartment syndrome ischaemic necrosis of anterior compartment muscle fibres, due to local arterial compression by engorged muscles, after unaccustomed exertion

  • anterior tibiotalar impingement syndrome anterior ankle pain at ankle dorsiflexion (e.g. at midstance, just before heel lift) due to inferior tibial/neck of talus exostosis

  • Apert's syndrome type Ia acrocephalosyndactyly, characterized by features of Carpenter's syndrome, with lesser digital (2-5) fusion into one mass, usually with a common mega-nail

  • Apert-Crouzon syndrome type IIa acrocephalosyndactyly characterized by features of Carpenter's syndrome with additional craniofacial dysostosis, maxillary hypoplasia, and 2-4 digit fusion

  • Bazex syndrome; acrokeratosis paraneoplastica keratoderma (i.e. erythema, scaling and irritation) of skin of ears, nose, hands and feet and later generalized hyperkeratosis in men with underlying internal malignancy; condition regresses when underlying malignancy is resolved

  • Behçet's syndrome chronic vasculitic disease of unknown cause; characterized by seronegative arthritis of knees and ankles, elbows and wrists, mouth ulcers, erythema nodosum, visual impairment and cerebrovascular accident

  • benign familial joint hypermobility syndrome; BFJHS generalized joint hypermobility, diagnosed as 2 major/1 major + 2 minor/4 minor criteria (see Table 1) in the absence of Ehlers-Danlos syndrome, Marfan's syndrome and osteogenesis imperfecta

  • Brocq-Lyell syndrome; toxic epidermal necrolysis severe, acute, systemic drug reaction characterized by hyperpigmented skin lesions and epidermal detachment

  • Brown-Séquard syndrome hemiparaplegia and hyperaesthesia, with ipsilateral loss of stereognosis and contralateral hemianaesthesia; due to unilateral spinal cord lesion

  • carpal tunnel syndrome pain, paraesthesia and loss of power of palmar muscles; associated with rheumatoid arthritis

  • Carpenter's syndrome; acrocephalopolysyndactyly oxycephaly, bradysyndactyly and polydactyly of the feet, with learning difficulties

  • Charcot's syndrome see intermittent claudication

  • chronic compartment syndrome; CCS; chronic exertional compartment syndrome exercise-induced fascial compartment pain; caused by compromised circulation and relative ischaemia of intracompartmental tissues, with long-term muscle and nerve dysfunction and damage; recalcitrant cases require surgical decompression through fasciotomy (see syndrome, acute compartment)

  • compartment syndrome see syndrome, acute compartment; syndrome, chronic compartment

  • complex regional pain syndrome; CRPS; chronic regional pain syndrome neuroinflammatory dysfunction, due to ion interaction of nociceptive C-fibre nerve endings, the sympathetic nervous system and spinal cord efferent motor nerves; characterized by vasomotor instability, hyperalgesia and impaired motor function; diagnosed from clinical presentation, symptoms reduction on administration of sympathetic nerve blockade, and intense, focal periarticular uptake of contrast medium in a delayed imaging-phase bone scan; treated by early, aggressive physical therapy to prevent contracture and muscle wasting, symptomatic relief by sympathetic nerve blockade, non-steroidal anti-inflammatory drugs, tricyclic antidepressants and anticonvulsant medication; immobilization is contraindicated

  • complex regional pain syndrome type 1; CRPS 1; reflex sympathetic dystrophy; Sudek's atrophy; allodynia sympathetic nervous system-mediated acute pain and vasomotor instability, triggered by minor or surgical trauma without obvious nerve injury; affects women more than men; pain is excessive and out of proportion to severity of initiating injury; diagnosis is based on clinical symptoms aided by bone scan, laser Doppler studies and thermography; patients may show anxiety, depression and disturbed sleep; condition is difficult to manage; patients suspected of CRPS 1 should have early referral to a pain clinic (see Table 2); presents in three stages:

    • stage 1 acute phase, lasting 2-3 months, with regional severe burning pain, warmth and swelling triggered by stress/light touch, bone demineralization, skin trophic changes

    • stage 2 dystrophic phase/Sudek's atrophy; lasting for several months; characterized by constant unrelenting pain, exacerbated by any stimulus, and tissue cyanosis, coolness and induration, and diffuse osteoporosis

    • stage 3 atrophic phase, characterized by reduced/absent/intractable pain, irreversible atrophy of skin/subcutaneous tissues, flexion contractures of foot, advanced osteoporosis with a 'ground-glass' appearance on X-ray of affected bone

  • complex regional pain syndrome, type 2; CRPS 2; causalgia; sympathetic pain syndrome persistent and severe skin paraesthesia/burning sensations; caused by trauma to peripheral sensory nerve fibres; symptoms, progress and treatment are similar to that of CRPS 1

  • Conn's syndrome primary aldosteronism; characterized by headaches, thirst, nocturia, polyuria, hypovolaemia, fatigue, hypertension, alkalosis, and potassium depletion

  • constrictive band syndrome intrauterine development of deep, tight, circumferential folds around leg/foot, and compromised limb development distal to band (e.g. autoamputation; marked oedema of distal tissues); thought to relate to strands of amniotic membrane enwrapping the developing limb

  • Cushing's syndrome raised blood cortisol (e.g. due to pituitary tumour; long-term steroid therapy); characterized by central obesity, moon-like facies, acne, skin striae, hypertension, decreased carbohydrate tolerance and tendency to diabetes, female amenorrhoea and hirsutism

  • Down's syndrome chromosomal disorder (trisomy 21) characterized by congenital short stature, broad short hands/feet, characteristic facies (pronounced epicanthic skin folds, flat hypoplastic face, short nose, enlarged tongue), transverse palmar crease, very dry skin, learning difficulties; formerly termed mongolism

    Edwards' syndrome trisomy 18, with congenital characteristic facies (micrognathia, low-set ears), rocker-bottom feet, severe learning difficulties; affected children often die in early childhood

  • Ehlers-Danlos syndrome; Ehlers-Danlos diseases I-X hereditary connective tissue disorder characterized by collagen abnormality, marked generalized skin and blood vessel laxity, and joint hypermobility; skin is readily traumatized and heals slowly; see syndrome, hypermobility

  • Franconi's syndrome a form of anaemia associated with renal tubule dysfunction; adult Franconi's syndrome shows synostosis with osteomalacia, and acquired Franconi's syndrome is associated with multiple myeloma

  • Giles de la Tourette syndrome motor incoordination characterized by verbal, facial or limbic tics

  • Gorlin's syndrome multiple naevus-like basal cell carcinomata, causing small pits and depressions of palmar and plantar skin

  • Guillain-Barré syndrome; acute inflammatory polyneuropathy; acute idiopathic polyneuritis; infectious polyneuritis; postinfective polyneuropathy sudden-onset, acute, postviral polyneuritis; presents as distal pain, muscular weakness/flaccidity, paraesthesia; spreads proximally over 14-21 days; severe cases show spinal nerve involvement, with respiratory failure and limb paralysis (patient will require life support and anticoagulation to prevent deep-vein thrombosis); spontaneous recovery occurs over several weeks/months; some residual neuromotor effects may persist

  • Haglund's syndrome prominence of posterior superior lateral area of calcaneum, retrocalcaneal bursitis, Achilles tendon thickening and Achilles tendinitis; diagnostic rearfoot radiographic features include positive parallel pitch lines, loss of retrocalcaneal recess (indicating retrocalcaneal bursitis), Achilles tendon thickening, loss of distinct interface between Achilles tendon and pre-Achilles fat pad

  • heel pain syndrome see heel pain

  • heel spur syndrome see heel spur

  • Howel-Evans syndrome familial palmoplantar keratoderma, with increased risk of oesophageal cancer

  • Hurler's syndrome; lipochondrodystrophy; dysostosis multiplex autosomal-recessive inherited generalized lipid disturbance and mucopolysaccharoidosis, affecting cartilage, bone, skin, subcutaneous tissues, brain, liver and spleen; characterized by short stature, shortness of neck, trunk and digits, kyphosis, reduced joint mobility, learning difficulties, characteristic facies (so-called gargoylism) and visual impairment

  • hypermobility syndrome; joint hypermobility syndrome disordered collagen (types 1 and 3) structure, with associated decreased tensile strength of skin/structural tissues; characterized by generalized joint hypermobility, easy bruising, impaired healing, increasing incidence of joint/soft-tissue pain, joint dislocation and osteoarthritis; a presenting feature of benign familial joint hypermobility syndrome (BFJHS) (see Table 3), Ehlers-Danlos syndrome, Marfan syndrome and osteogenesis imperfecta

  • iliotibial band syndrome; ITBS; iliotibial band friction syndrome; ITBFS overuse-associated, friction-induced inflammation of ITB and associated bursa, where ITB moves over lateral femoral condyle (Gerdy's tubercle); due to repeated knee flexion and extension, especially in athletes/cyclists; presents as ITB pain at heel strike progressing to constant ITB pain; early-stage treatment includes a daily stretching programme (see Table 4) and application of heat (pre-exercise) and ice (postexercise) (see Table 5)

  • joint hypermobility syndrome see syndrome, hypermobility

  • lobster-claw syndrome extreme form of ectrodactyly; characterized by absence of third and fourth rays

  • Korsakoff's syndrome confusion and severe memory impairment with confabulation and Wernicke's syndrome, associated with chronic alcoholism

  • Lyell's syndrome drug-induced, acute skin sensitivity reaction; characterized by acute erythema, urticaria, vasculitis, purpura, marked exfoliation (peeling), flaccid bullae formation, subepidermal separation/detachment

  • Marfan's syndrome familial, autosomal-dominant, congenital changes in mesodermal and ectodermal tissues; characterized variably by musculoskeletal changes (e.g. increased height, excessive limb length, arachnodactyly; generalized tissue laxity and joint hypermobility), visual effects, and cardiovascular effects (e.g. aortic aneurysm)

  • medial tibial stress syndrome; MTSS; tibial fasciitis; shin splint muscle fatigue, reduced shock absorption, traction enthesiopathy and periostitis along anterior and posterior medial lower one-third of tibia (see Table 6) secondary to overuse/underpreparation for exercise; exacerbated by exercising on hard surfaces, especially in individuals who pronate excessively; treated by muscle-strengthening exercises, pre-exercise flexibility programme, modification of overall sports exercise programme (see Table 7), in conjunction with gait analysis, orthoses and correct shoe selection

  • Morquio's syndrome; type IV mucopolysaccharoidosis severe skeletal dysplasia including spine/thorax deformity, irregular epiphyses but normal shaft length of long bones, enlarged joints, flaccid ligaments, waddling gait and urinary abnormalities, due to autosomal-recessive error of mucopolysaccharide metabolism

  • Morton's syndrome congenital shortening of first metatarsal with apparent shortening of hallux and associated metatarsalgia

  • Munchausen's syndrome repeated fabrication of illness/symptoms of illness

  • Munchausen's syndrome by proxy repeated reporting of spurious illness/symptoms of illness by one person about another

  • musculoskeletal pain syndrome see polymyalgia rheumatica

  • nail-patella syndrome; hereditary arthrodysplasia autosomal-dominant abnormality of finger/toenails, absent/hypoplastic patella, defects of head of radius and iliac horns, and iris discoloration

  • nephrotic syndrome peripheral oedema, albuminuria, reduced plasma albumin (hypoalbuminaemia), refractory bodies in urine and raised blood cholesterol

  • nerve entrapment syndromes local nerve trunk compression (e.g. tibial, medial calcaneal lateral, first lateral branch of calcaneal, lateral plantar, high tibial, popliteal, deep peroneal, superficial, saphenous, sural or medial common hallucal nerves), as in tarsal/carpal tunnel syndromes, plantar digital neuritis, Morton's neuroma; characterized by distressing distal dermatomal sensory (e.g. pain and paraesthesia) and/or motor symptoms (e.g. muscle atrophy) (see Table 8)

  • Nievergelt-Pearlman syndrome rare autosomal-dominant bone disease causing lower-limb 'rhomboidal' tibia/fibula (crura rhomboidei), joint dysplasias, genu valgum, club foot, deformed toes; more common in males

  • overlap syndromes see mixed connective tissue diseases

  • patellofemoral joint syndrome see syndrome, runner's-knee

  • peroneal cuboid syndrome loss of rearfoot eversion due to long-standing peroneal tendon dysfunction/tendinitis; characterized by plantar pain from cuboid to first metatarsal

  • polycystic ovary syndrome see syndrome, Stein-Leventhal

  • Raynaud's syndrome concomitant Raynaud's disease (always affecting hands, and frequently feet) in patients with connective tissue disorders, characterized by generalized digital cyanosis, localized painful vasculitic lesions of dorsal forefoot (30% of cases) and apices of toes (20-25% of cases); subcutaneous calcinosis (20% of cases) may masquerade as a seed corn

  • Reiter's syndrome urethritis, iridocyclitis, arthritis, plantar enthesiopathy and heel spur formation, often triggered by earlier gastrointestinal Escherichia coli infection or exposure to a sexually transmitted disease (e.g. Chlamydia trachomatis); more common in human leukocyte antigen (HLA) B27 tissue-type males; see keratoderma blenorrhagicum

  • restless-leg syndrome overwhelming need to move the lower limbs constantly; characteristic of chronic renal failure; thought to be triggered by accumulation of metabolites and uraemia

  • Reye's syndrome cerebral oedema and death (in 50% of cases, usually children), provoked by aspirin therapy; aspirin is proscribed for children less than 16 years old

  • Riley-Day syndrome; familial dysautonomia autosomal-dominant complete indifference to pain; also characterized by orthostatic hypotension, hyperhidrosis and hyporeflexic/absent deep tendon reflexes, pes cavus and trophic plantar ulceration

  • Roussy-Levy syndrome; hereditary areflexic dystasia; Charcot-Marie-Tooth (CMT) disease type II essential tremor, sensory ataxia, poor coordination and judgement of movement, kyphoscoliosis and distal muscle atrophy (especially peronei); autosomal-dominant inherited disease similar to CMT disease type 1, but developing in early childhood

  • runner's-knee syndrome mild lateral subluxation of patella in patellar groove; due to an increase in Q angle (i.e. >15°), often in association with excessive foot pronation, tibial varum, internal tibial torsion, weakened quadriceps group, malposition of vastus medialis, hard running surfaces or faulty sports shoes, leading to uneven pressure on anterolateral surface of femoral condyle and local pain; often affects female runners; treated by prescription orthoses to reduce torque, torsion and knee joint stress

  • scalded-skin syndrome scaled/peeling appearance of skin overlying areas of infection, or associated with adverse drug reactions

  • 'second-class travel' syndrome pulmonary thromboembolism due to prolonged periods of inactivity, e.g. passengers (who have been static for > 4 hours during long-haul intercontinental air flights) develop deep-vein thrombosis; the clot detaches, passing through venous circulation and heart, to block the pulmonary artery; characterized by sudden collapse and death; passengers on long-haul flights are advised to undertake leg muscle exercises regularly throughout the duration of the flight, wear 'antithrombotic' elasticated hosiery and consider medication with aspirin in the weeks before long-haul flight

  • sinus tarsi syndrome sensation of unsteadiness when walking on gravel/uneven ground and ongoing pain in lateral tarsal area just distal to and level with lateral malleolus, subsequent to inversion sprain/excess rearfoot pronation (e.g. as in rearfoot rheumatoid arthritis); local symptoms are exacerbated by heel inversion/eversion; treated by non-steroidal anti-inflammatory drugs, local immobilization, orthoses or steroid injection

  • SjÖgren's syndrome; sicca syndrome; keratoconjunctivitis sicca oral mucous membranes dryness, loss of lacrimal secretion, facial telangiectasias (i.e. butterfly rash), bilateral parathyroiditis (in younger women), strongly associated with rheumatoid arthritis and Raynaud's phenomenon

  • Stein-Leventhal syndrome; polycystic ovary syndrome multiple ovarian cyst formation, with associated menstrual abnormalities, infertility, enlarged ovaries, insulin resistance, obesity, acne, evidence of masculinization (e.g. hirsuitism) and increased tendency to type 2 diabetes mellitus; responds to treatment with oral contraceptive pill and/or metformin

  • Stevens-Johnson syndrome widespread bullous erythema multiforme of skin/mucous membranes; due to hypersensitivity/drug reaction

  • talar compression syndrome posterior ankle pain when foot is maximally plantarflexed at ankle joint; due to compression of posterior tubercle of talus on posterior margin of distal end of tibia; note: similar condition occurs with os trigonum, which impinges on posteroinferior margin of tibia (see Table 9)

  • tarsal tunnel syndrome; TTS pain, paraesthesia and numbness in sole of foot; due to tibial nerve compression within tarsal tunnel; associated with excess foot pronation or rearfoot rheumatoid arthritis; symptoms reproduced by tapping the skin overlying distal medial malleolar area (Tinel's sign positive); conservative treatment includes valgus filler pads, cobra pads and medial heel wedges, or control of excessive rearfoot pronation with moulded cushioned orthoses worn with bespoke shoes, together with non-steroidal anti-inflammatory drugs and/or disease-modifying antirheumatic drugs; surgical treatment includes decompression procedures to free posterior tibial nerve and excise local fibrous structures (see tarsal tunnel)

  • distal tarsal tunnel syndrome isolated entrapment of medial/lateral plantar nerves; medial plantar nerve is compressed between navicular tuberosity and belly of abductor hallucis longus, causing 'jogger's foot'; first branch of lateral plantar nerve (Baxter's nerve) may be entrapped as it courses laterally between bellies of abductor hallucis and quadratus plantae (flexor accessories) muscles (see Table 10)

  • proximal tarsal tunnel syndrome entrapment of posterior tibial nerve/its branches deep to flexor retinaculum; due to excessive subtalar joint pronation (with narrowing of tarsal tunnel, e.g. in rheumatoid foot) due to entrapment within attachments of flexor retinaculum, compression by an enlarged abductor hallucis muscle belly, enlarged navicular tuberosity, accessory navicular, presence of os tibialis externum, ischaemic compromise of posterior tibial nerve, or varicosities within tarsal tunnel

  • trisomy 21 syndrome see syndrome, Down's

  • Turner's syndrome sex-chromosome (XO) abnormality affecting 1:2500 females, with characteristic morphology (web neck, short stature), infantilism and amenorrhoea, coarctation of aorta and peripheral oedema; feet are oedematous, short and broad, show excess subtalar joint pronation and hyperextended halluces; nails tend to involution, and affected subjects are prone to ingrowing nails

  • Werner's syndrome autosomal-recessive condition characterized by scleroderma-like skin, cataracts, progeria (premature senility), hypogonadism and diabetes mellitus

  • Wernicke's syndrome; Wernicke-Korsakoff syndrome; Wernicke's encephalopathy brainstem ischaemia causing nystagmus and other ocular effects, tremors and ataxia, mental confusion, hypothermia and hypotension; more common in chronic alcoholics

  • Wolff-Parkinson-White syndrome congenital atrioventricular interconnection causing tachycardia and characteristic electrocardiogram pattern

  • yellow-nail syndrome see nail, yellow

Table 1: The major and minor diagnostic criteria of benign familial joint hypermobility syndrome (BFJHS)
Major criteria
Current/historic Brighton score of 4/9
Arthralgia for >3/12 in four or more joints
Minor criteria
Current/historic Brighton score of 1, 2 or 3/9 (0, 1, 2, 3/9 if >50 years old)
Arthralgia for minimum of 3 months in 1-3 joints, or back pain for minimum of 3 months, or spondylosis/spondylolysis/spondylolisthesis
Dislocation/subluxation of > one joint, or one episode of simultaneous dislocation/subluxation of more than one joint
Three or more lesions of soft-tissue rheumatism (e.g. spondylitis, tenosynovitis, bursitis)
Marfanoid habitus (i.e. tall, slim physique, span:height ratio >1.3, upper:lower segment ratio <0.89, arachnodactyly [+Steinberg/wrist signs])
Abnormal skin: striae, hyperextensibility, thin skin, papyraceous scarring
Eye signs: drooping eyelids, myopia, antimongoloid slant
Varicose veins or hernia or uterine/rectal prolapse

Note: BFJHS is diagnosed in the presence of two major criteria, or one major and two minor criteria, or four minor criteria (adapted from Grahame R, Bird HA, Child A, Dolan AL, Fowler-Edwards A, Ferrell W, Gurley-Green S, Keer R, Mansi E, Murray K, Smith E. The British Society Special Interest Group on Heritable Disorders of Connective Tissue Criteria for the Benign Joint Hypermobility Syndrome. "The Revised (Brighton 1998) Criteria for the Diagnosis of the BJHS". Journal of Rheumatology 2000; 27:1777-1779).

Table 2: Features of complex regional pain syndrome
PhaseFeatures
Acute phase (duration: 2-3 months)
Reversible
Severe burning pain, warmth, swelling and joint stiffness within a limb: not confined to a dermatome or myotome
Bone demineralization
Symptoms (exacerbated by limb dependence, contact or stress) persist for 2-3 months
Chronic phase (duration: several months)
Reversible
Pain continues
The limb becomes cool, firm and cyanotic
Radiographs show diffuse osteoporosis
Digits develop flexure contractures
Persists for several months
Atrophic phase
Irreversible
Pain diminishes or becomes intractable
Skin and subcutaneous tissues become atrophic
Flexion contractures in foot become fixed
Osteoporosis becomes advanced; bone has a 'ground-glass' appearance
Table 3: The major and minor diagnostic criteria of benign familial joint hypermobility syndrome (BFJHS)
Major criteria
Current/historic Brighton score of 4/9
Arthralgia for >3/12 in four or more joints
Minor criteria
Current/historic Brighton score of 1, 2 or 3/9 (0, 1, 2, 3/9 if >50 years old)
Arthralgia for minimum of 3 months in 1-3 joints, or back pain for minimum of 3 months, or spondylosis/spondylolysis/spondylolisthesis
Dislocation/subluxation of > one joint, or one episode of simultaneous dislocation/subluxation of more than one joint
Three or more lesions of soft-tissue rheumatism (e.g. spondylitis, tenosynovitis, bursitis)
Marfanoid habitus (i.e. tall, slim physique, span:height ratio >1.3, upper:lower segment ratio <0.89, arachnodactyly [+Steinberg/wrist signs])
Abnormal skin: striae, hyperextensibility, thin skin, papyraceous scarring
Eye signs: drooping eyelids, myopia, antimongoloid slant
Varicose veins or hernia or uterine/rectal prolapse

Note: BFJHS is diagnosed in the presence of two major criteria, or one major and two minor criteria, or four minor criteria (adapted from Grahame R, Bird HA, Child A, Dolan AL, Fowler-Edwards A, Ferrell W, Gurley-Green S, Keer R, Mansi E, Murray K, Smith E. The British Society Special Interest Group on Heritable Disorders of Connective Tissue Criteria for the Benign Joint Hypermobility Syndrome. "The Revised (Brighton 1998) Criteria for the Diagnosis of the BJHS". Journal of Rheumatology 2000; 27:1777-1779).

Table 4: Iliotibial band-stretching regime
Muscle groupAction (hold for 5-10 seconds; repeat ×5, three times a day)
Hip abductorStand erect, legs straight, feet together; stretch trunk (on frontal plane) towards the unaffected leg
Iliotibial bandLie on a bench on the unaffected side, with the unaffected hip and knee slightly flexed, in order to maintain balance; flex the affected hip and straighten the affected knee so that the affected leg hangs off the bench; allow the iliotibial band of the affected leg to be stretched by gravitational pull
Lie on a bench on the affected side with the affected leg in line with the body and the hip and knee locked; flex the unaffected (upper) leg; place the hands on the bench immediately under the shoulder and push the trunk upwards as far as possible to apply stretch to the lateral area of the affected leg
Upper iliotibial bandStand erect; with affected leg behind normal leg; stretch trunk (on frontal plane) towards unaffected side
Lower iliotibial bandStand erect as above, with the knee of the affected leg slightly flexed and hips rotated (on transverse plane) towards affected leg; stretch trunk (on frontal plane) towards the unaffected side
Iliotibial band and hamstringsStand erect, with the affected leg behind the normal leg so that the knee of the affected leg rests on the posterior aspect of the non-affected knee; rotate the trunk (on transverse plane) away from the affected leg and attempt to touch the heel of the affected leg
Table 5: Treatment regime for iliotibial band syndrome
VisitAction
1Examination
Including Nobel's and Ober's tests, and excluding other causes of knee joint pain
Gait analysis - walking and running
Check for presence of tibial varum, tibial torsion, uncompensated rearfoot varus and limb length discrepancy (include shoe wear pattern)
Instigate the iliotibial band stretching regime (see Table 11), with a quadriceps- and adductor-strengthening programme
Ice massage to painful area at lateral aspect of knee Advise reduction in athletic activity
2Commence physical therapies, e.g. cortisone iontorphoresis or ultrasound and ice massageStabilizing orthoses and/or foot and ankle taping, ± heel lift
Continue stretching programme ± massage
Non-steroidal anti-inflammatory (10-day course of 400 mg ibuprofen qds)
Stop all athletic activity if pain does not resolve
3Magnetic resonance imaging/computed tomographic scan to knee joint areaRefer to orthopaedics

Most cases will resolve with one treatment; more severe cases will require a second visit and some will require orthopaedic referral.

Table 6: Iliotibial band-stretching regime
Muscle groupAction (hold for 5-10 seconds; repeat ×5, three times a day)
Hip abductorStand erect, legs straight, feet together; stretch trunk (on frontal plane) towards the unaffected leg
Iliotibial bandLie on a bench on the unaffected side, with the unaffected hip and knee slightly flexed, in order to maintain balance; flex the affected hip and straighten the affected knee so that the affected leg hangs off the bench; allow the iliotibial band of the affected leg to be stretched by gravitational pull
Lie on a bench on the affected side with the affected leg in line with the body and the hip and knee locked; flex the unaffected (upper) leg; place the hands on the bench immediately under the shoulder and push the trunk upwards as far as possible to apply stretch to the lateral area of the affected leg
Upper iliotibial bandStand erect; with affected leg behind normal leg; stretch trunk (on frontal plane) towards unaffected side
Lower iliotibial bandStand erect as above, with the knee of the affected leg slightly flexed and hips rotated (on transverse plane) towards affected leg; stretch trunk (on frontal plane) towards the unaffected side
Iliotibial band and hamstringsStand erect, with the affected leg behind the normal leg so that the knee of the affected leg rests on the posterior aspect of the non-affected knee; rotate the trunk (on transverse plane) away from the affected leg and attempt to touch the heel of the affected leg
Table 7: Grades and characteristics of medial tibial stress syndrome (MTSS)
GradeCharacteristic
1Pain on palpation of the anteromedial (or posteromedial) area of tibial crest
No pain during activity or exercise
2Pain after activity or exercise
No pain during activity or exercise
3Pain during activity or exercise
Pain after activity or exercise
4Pain and discomfort during normal walking
Continual pain during activity or exercise
Table 8: Phased treatment approach to medial tibial stress syndrome (MTSS)
PresentationTreatment
Phase 1: acute phaseCessation of exercise activity until all pain resolves RICE(P)
Phase 2: rehabilitation phaseDeep compartment muscle exercise to strengthen the deep fascial-bone interface and reduce tension on the deep fascial insertion, in order to decrease pain and swelling and prevent fascial scarring
Phase 3: functional phaseUse of antipronatory/functional orthoses, strapping or taping in order to strengthen the fascial-bone interphase and prevent further excessive tension on the tibia
Phase 4: return to activityPhased and gradual return to normal levels of activity
Table 9: Presentations of nerve trunk irritation in the foot
Neuroma/lesionInvolved nerveLocation
Proximal tarsal tunnel syndromeBranches of the posterior tibial nerveMedial ankle area
Distal tarsal tunnel syndrome Jogger's footMedial plantar nerveBetween navicular tuberosity and belly of abductor hallucis
Distal tarsal tunnel syndrome Baxter's neuritisLateral plantar nerveBetween bellies of abductor hallucis, quadratus plantae and abductor digiti quinti minimi
Joplin's neuromaMedial plantar nerve properMedial area of first metatarsal head
Houser's neuromaFirst plantar intermetatarsal nerveBetween 1 and 2 metatarsals
Heuter's neuromaSecond plantar intermetatarsal nerveBetween 2 and 3 metatarsals
Morton's neuromaThird plantar intermetatarsal nerveBetween 3 and 4 metatarsals
Islen's neuromaFourth plantar intermetatarsal nerveBetween 4 and 5 metatarsals
Table 10: Accessory bones in the foot
Accessory bone in the footLocation
Os tibiale externum (accessory navicular)Within tibialis posterior tendon, adjacent to proximal part of navicular tuberosity
Os trigonumPosterior margin of talus
Os peroneumWithin peroneus longus tendon, adjacent to inferior lateral border of cuboid/calcaneocuboid joint
Os vesalianumAdjacent to fifth metatarsal base
Os intermetatarseumBetween bases of first and second metatarsals
Os interphalangeusWithin insertion of flexor hallucis longus tendon, adjacent to plantar area of hallux interphalangeal joint
Table 11: Presentations of nerve trunk irritation in the foot
Neuroma/lesionInvolved nerveLocation
Proximal tarsal tunnel syndromeBranches of the posterior tibial nerveMedial ankle area
Distal tarsal tunnel syndrome Jogger's footMedial plantar nerveBetween navicular tuberosity and belly of abductor hallucis
Distal tarsal tunnel syndrome Baxter's neuritisLateral plantar nerveBetween bellies of abductor hallucis, quadratus plantae and abductor digiti quinti minimi
Joplin's neuromaMedial plantar nerve properMedial area of first metatarsal head
Houser's neuromaFirst plantar intermetatarsal nerveBetween 1 and 2 metatarsals
Heuter's neuromaSecond plantar intermetatarsal nerveBetween 2 and 3 metatarsals
Morton's neuromaThird plantar intermetatarsal nerveBetween 3 and 4 metatarsals
Islen's neuromaFourth plantar intermetatarsal nerveBetween 4 and 5 metatarsals

acquired immunodeficiency syndrome (AIDS),

n a disease caused by a retrovirus known as human immunodeficiency virus type 1 (HIV-1). A related but distinct retrovirus (HIV-2) has recently appeared in a limited number of patients in the United States. Patients are considered to have AIDS when one or more indicator diseases, as defined by the Centers for Disease Control and Prevention (CDC), are present. See also human immunodeficiency virus (HIV). The CDC has classified stages of the disease as follows:
Group I: acute HIV infection,
n a group who within one month of exposure develops the first clinical evidence of HIV infection, which may appear as an acute retroviral syndrome. This is a mononucleosis-like syndrome with symptoms including fever, rash, diarrhea, lymphadenopathy, myalgia, arthralgia, and fatigue. Development of antibodies usually follows.
Group II: asymptomatic HIV infection,
n a group in which most persons develop antibodies to the HIV within 6 to 12 weeks after exposure. Although individuals may remain asymptomatic for months or years, they can transmit the virus.
Group III: persistent generalized lymphadenopathy (PGL),
n a group who develops persistent generalized lymphadenopathy that lasts longer than 3 months. See also lymphadenopathy, persistent generalized.
Group IV: HIV-associated diseases,
n a group who is clinically variable and has signs and symptoms of HIV infection other than or in addition to lymphadenopathy. Based on clinical findings, patients in Group IV may be assigned to one or more of the following subgroups: (A) constitutional disease, also known as wasting syndrome. This subgroup is characterized by fever that lasts more than one month, involuntary weight loss of greater than 10% for baseline, or diarrhea persisting for more than one month, (B) neurological disease, (C) secondary infectious disease, (D) secondary cancers, and (E) other conditions resulting from HIV infections.

Patient discussion about acquired immunodeficiency syndrome

Q. Why AID spred? and How?

A. if you mean AIDS- it spread mostly because people don't practice safe sex or sharing needles when injecting drugs. here is a nice tutorial about HIV, it is also specify the ways of infection-
http://www.nlm.nih.gov/medlineplus/tutorials/aids/htm/lesson.htm

Q. The HIV test came back POSITIVE! My very close friend 'Demonte'. One day in December as he was returning from a business trip, his wife met him at the airport with terrible news. During a routine pregnancy check up, her doctor had administered an HIV test along with other blood-work. The HIV test came back POSITIVE! The doctor wanted to begin administering drugs immediately but the cost of these drugs here when compared to their family income was prohibitive. I helped him with some of my savings. He already sold his favorite sentimental car to save his precious wife. Now i want to know is there any NATURAL medicine to cure this? Hope it costs less and available.

A. there are no effective natural remedy for HIV. the medications are very hard ones that try to control the virus from spreading (cannot eliminate it though). no herbal remedy or nutrition change will do that.

More discussions about acquired immunodeficiency syndrome
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