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It is responsible for con- 17ß-Hydroxysteroid dehydrogenase type 2 verting the weak androgen androstenedione into the more 5·-Reductase type 1 potent androgen testosterone discount hydrea 500 mg mastercard. It can also interconvert weak and potent estrogens such as estrone and estradiol order hydrea 500mg with visa. Testosterone in turn can be produced from androstene- dione effective hydrea 500mg. To date discount 500 mg hydrea fast delivery, seven types of human 17ß-HSDs have been cloned generic hydrea 500 mg, sequenced purchase hydrea 500mg with visa, and characterized, designated active within the sebaceous gland and in keratinocytes types 1–7 in the chronological order of their isolation [20– derived from the infrainfundibular region of piloseba- 23]. Recently, the type 8 17ß-HSD also known as Ke6 ceous follicle (from the base of the epidermis to the point gene was shown to efficiently transform estradiol to estro- of insertion of the sebaceous duct) [3, 29]. The type 2 iso- gen in transfected HEK-293 cells. The type 2 isozyme zyme is most active in the prostate gland where it can be of 17ß-HSD appears to be the most active within the seba- inhibited by drugs such as finasteride. While the type 1 ceous gland where it prefers to oxidize testosterone back 5·-reductase has a broad alkaline pH optima of 6. In this regard, the 17ß-HSD and demonstrates relatively moderate affinity for steroid enzyme may play a protective role in the skin by metabo- substrates (Km = 1–5 ÌM), the type 2 5·-reductase has a lizing testosterone back to the less potent precursor, narrow acidic pH optimum of 5. It may also represent a regulatory point high affinity for substrates (Km = 4–50 nM) [30, 31] in androgen and estrogen metabolism within the skin. Activity of 5·-reductase and 17ß-HSD exhibits region- Dihydrotestosterone is produced from testosterone al differences depending upon the source of the sebaceous within peripheral tissues such as the skin by the action of glands [25, 29] (fig. In skin that is prone to acne, such the 5·-reductase enzyme. Recently, two isozymes of 5·- as facial skin, activity of the type 1 5·-reductase in seba- reductase have been identified. The type 1 isozyme is ceous glands is greater than in sebaceous glands obtained Update and Future of Hormonal Therapy Dermatology 2003;206:57–67 59 in Acne from nonacne-prone skin. Enzymes involved in lipogenesis in human sebaceous being produced in sebaceous glands from facial skin com- glands pared to other areas of the body that are not prone to Enzymes involved in Enzymes involved in develop acne. In contrast, the oxidative activity of the cholesterol synthesis fatty acid synthesis type 2 17ß-HSD enzyme is greater in sebaceous glands from nonacne-prone areas compared to sebaceous glands Acetoacetyl CoA thiolase Acetyl CoA carboxylase obtained from facial skin. Since the predominant activity HMG CoA synthetase Fatty acid synthetase HMG CoA reductase of this isozyme is to transform testosterone back to its less Mevalonic acid kinase active precursor, it may be inferred that facial skin is less Mevalonate decarboxylase able to metabolize testosterone to its less potent precur- Isopentenyl pyrophosphate isomerase sor. The net effect of the activity of these two enzymes is Geranyl transferase the greater production of potent androgens such as T and Squalene synthetase Squalene oxidocyclase DHT within sebaceous glands of facial areas that may in part account for the development of acne in these areas. Site of Androgen Action in Acne The sebaceous gland is known to be a site of androgen regulating the production of growth factors by dermal action within the pilosebaceous unit. The stromal/epithelial interaction of sex ste- hypothesized that androgens may play a role in follicular roid hormones and growth factors is an important phe- hyperkeratinization in acne in addition to their effects on nomenon in the local regulation of other endocrine- stimulating sebum secretion [1, 2]. Indirect evidence in responsive tissues such as the prostate, breast, endometri- support of this hypothesis includes the finding of andro- um and ovary. Evidence exists for the importance of these gen receptors in the outer root sheath of sebaceous folli- autocrine and paracrine effects of androgens and growth cles, the clinical observation that antiandrogens may factors in the regulation of sebaceous glands. In addition reduce follicular casts and the finding of activity of andro- to androgen receptors, sebocytes also possess receptors for gen-metabolizing enzymes such as 3ß-HSD, 17ß-HSD growth factors such as epidermal growth factor (EGF) and and 5·-reductase in follicles. Furthermore, the activity of insulin-like growth factor I (IGF-I). Evidence exists 17ß-HSD and 5·-reductase is significantly greater in for the role of EGF, IGF-I and keratinocyte growth factor infrainfundibular keratinocytes compared to keratino- (KGF) in modulating sebaceous gland growth. For exam- cytes obtained from the interfollicular epidermis, suggest- ple, growth of sebocytes is enhanced by supplementation ing that follicular keratinocytes have a greater propensity of cell culture medium with EGF and insulin. Direct evidence in sup- of experimental animals with KGF stimulates growth of port of the effects of androgens on follicular keratiniza- hair and sebaceous glands [34, 35].
Compared to younger In the ﬁrst large studies to follow the same group of normal rats generic 500mg hydrea, the older rats have less growth of the new blood vessels healthy humans for many years order hydrea 500mg with mastercard, scientists have uncovered unex- that nourish neurons purchase hydrea 500mg on line. They report declines in some mental functions While much has been learned about the aging brain trusted 500mg hydrea, many and improvements in others discount hydrea 500mg free shipping. In one study cheap hydrea 500mg on-line, the speed of carry- questions remain to be answered. For instance, does the pro- ing out certain tasks became slower, but vocabulary improved. In a Several studies found less severe declines in the type of intelli- given neuron, does atrophy cause a higher likelihood of death? Are there gender This research is supported by animal studies in which sci- di∑erences in brain aging that may be due to hormonal changes entists found that changes in mental function are subtle. By understanding igating to ﬁnd food, tend to become more di≈cult with age. Scien- be able to inﬂuence the survival and degeneration of neurons. This neurologic disorder af- troubled by the development of drug-related involuntary move- ﬂicts one million individuals in the U. The past decade has also seen further attempts to treat majority of whom are older than 50. Parkinson’s such patients with surgical implantation of cells, such as fetal is characterized by symptoms of slowness of cells, capable of producing dopamine. Replacement therapy movement, muscular rigidity and tremor. P The discoveries in the late 1950s that the level of dopamine was decreased in the brains of patients was followed Pain in the 1960s by the successful treatment of this disorder by If there is a universal experience, pain is it. Each year, more than administration of the drug levodopa. This drug is changed to 97 million Americans su∑er chronic, debilitating headaches or dopamine in the brain. The successful treatment of Parkinson’s a bout with a bad back or the pain of arthritis—all at a total by replacement therapy is one of the greatest success stories in cost of some $100 billion. Levodopa is now combined with another drug, coveries about how chemicals in the body transmit and inter- carbidopa, that reduces the peripheral breakdown of levodopa, cept pain have paved the way for new treatments for both thus allowing greater levels to reach the brain and reducing side chronic and acute pain. Also playing an important role are newer drugs such as Until the middle of the 19th century, pain relief during pergolide that act directly upon dopamine receptors and other surgery relied on natural substances, such as opium, alcohol and inhibitors of dopamine breakdown. Not until 1846 Genetic studies have demonstrated several inheritable gene did doctors discover the anesthetic properties of ether, ﬁrst in abnormalities in certain families, but the vast majority of cases animals and then in humans. Soon afterwards, the usefulness of Parkinson’s occur sporadically. It is believed that heredity fac- of chloroform and nitrous oxide became known and heralded a tors may render some individuals more vulnerable to environ- new era in surgery. The dozens of drugs used today during mental factors such as pesticides. The discovery in the late 1970s surgery abolish pain, relax muscles and induce unconsciousness. MPTP was accidently synthesized by illicit drug to prevent pain during examinations, diagnostic procedures, designers seeking to produce a heroin-like compound. The most famous of these was found to be converted in the brain to a substance that agents, which temporarily interrupt the action of pain-carrying destroys dopamine neurons. Parkinson’s is now being inten- nerve ﬁbers, is Novocain.
The loca- stant and asymptomatic periods are frequent cheap 500 mg hydrea free shipping. It is tion of pain can indicate which structure is difficult for the patient with anterior knee pain to injured buy cheap hydrea 500mg online, which is extremely helpful to make the pinpoint the area of pain safe 500mg hydrea, placing his or her hand diagnosis and plan the treatment hydrea 500mg online. Both legs over the anterior aspect of the knee when we ask should be examined purchase 500mg hydrea with visa. However hydrea 500 mg with mastercard, the pain can The lateral retinaculum ought to be felt and also be medial, lateral, or popliteal. Tenderness somewhere over patients have multiple painful sites with different the lateral retinaculum, especially where the reti- pain intensity. Pain related to extensor mecha- naculum inserts into the patella, is a very frequent nism is typically exacerbated by physical activity, finding (90%) in patients with anterior knee descending stairs (which requires eccentric pain. This ting, for instance during a long trip by car or pro- test is performed with the knee flexed 30˚, and the longed sitting in a cinema (“movie sign” or quadriceps relaxed. The patella is divided into “theater sign”), and improves by extending the four longitudinal quadrants. A constant and severe pain far out of pro- placed in a medial direction. A medial translation portion to physical findings must make us think of one quadrant or less is suggestive of excessive of psychological issues or reflex sympathetic dys- lateral tightness. In a normal One must not forget the possibility of pain knee, the patella can be lifted from its lateral edge secondary to a posterior cruciate ligament (PCL) farther than the transepicondylar axis, with a fully deficiency when there has been a knee trauma- extended knee. This is a well-known cause for anterior 0˚ or less indicates a tight lateral retinaculum. Patients sometimes report locking of the knee, which usually is only a catching sensation, but they are able to actively unlock the knee and therefore this type of locking should not be mixed up with the one experienced by patients with meniscal lesions. Another symptom is the crepitus, which should not be mistaken from the snapping sensation more consistent with a pathologic plica. The patellofemoral joint is mentally divided into quadrants and patellar mobility is assessed in both directions. The second diagnostic step is a complete and (Reprinted from DeLee and Drez, eds. Thus, proximal lesions will (patellar and/or trochlear subchondral bone). On the contrary, distal lesions which when positive (appearance of pain) are tender in the early degrees of knee flexion. The knee is then flexed association between proximal patellar tendi- fully and kept firmly in a sustained flexion for nosis and abnormal patellar tracking. The test is positive if the in order to discard patellar tendinopathy, palpa- patient complains of increasing pain after a tion of the inferior pole of the patella ought to be pain-free interlude of 15 to 30 seconds. To perform Allen and colleagues1 have found, in patients this test we press downward on the proximal referred with anterior knee pain, a significant patella, with which the inferior pole of the Figure 6. Palpation on the distal pole of the patella and the proximal patellar tendon. Evaluation of the Patient with Anterior Knee Pain and Patellar Instability 97 patella tilts anteriorly. This maneuver lets us In order to evaluate instability we also per- palpate the proximal patellar tendon attach- form the patellar glide test. However, quite often there is a mild ten- displacement of the patella greater than or equal derness at the attachment of the patellar tendon to 3 quadrants, with the patellar glide test, is at the inferior pole of the patella in sportsplay- consistent with incompetent lateral or medial ing subjects.
Prognosis Collins MP buy 500 mg hydrea amex, Periquet MI hydrea 500mg with amex, Mendell JR purchase hydrea 500mg otc, et al (2003) Nonsystemic vasculitic neuropathy: Reference insights from a clinical cohort hydrea 500mg line. Neurology 61: 623–630 266 Neuropathies associated with paraproteinemias Genetic testing NCV/EMG Laboratory Imaging Biopsy + ++ Bone + Type of paraproteinemia Type of polyneuropathy Treatment Multiple Myeloma Different types of polyneuropathy Treatment of myeloma Amyloidosis may develop MGUS Sensorimotor or CIDP like Immunosuppression cheap hydrea 500mg otc, (monoclonal gammopathy of various therapies are described undetermined significance) MGUS – MAG Distal involvement generic hydrea 500 mg with amex, predominantly Little beneficial effect of therapy large fibers with ataxia and pseudoathetoid movements POEMS Syndrome CIDP like Treatment of the myeloma, plasma- pheresis Waldenstrom’s Distal sensorimotor neuropathy, Treatment of Waldenstrom’s macroglobulinemia predilection for large fibers Amyloidosis (AL type) Polyneuropathy: autonomic Colchicine, steroids involvement, involvement of skeletal muscle Neuropathy in conjunction with multiple myeloma Anatomy/distribution Axonal neuropathy occurs with amyloid deposits. Symptoms Patients experience distal symmetric motor and sensory dysfunction. Clinical syndrome/ Exam shows proximal and distal weakness and sensory loss, mononeuropathies signs and autonomic dysfunction. Serum electrophoresis can show IgA or IgG monoclonal gammopathy. Bone marrow studies reveal myeloma, and examination of the skeletal system can show osteolysis. The primary therapeutic goal is treatment of the myeloma and supportive care. Therapy Neuropathies associated with monoclonal gammopathies: monoclonal gammopathy of undetermined significance (MGUS) Symptoms may be motor, sensory, or sensorimotor depending on IgM antibody Symptoms specificity. Exam shows distal greater than proximal weakness and sensory loss. Clinical syndrome/signs Disease is primarily associated with IgM, IgA and IgG gammopathy. Pathogenesis NCV maybe slowed (see description for CIDP). Serum electrophoresis reveals a Diagnosis monoclonal gammopathy. Bone marrow studies and skeletal examination should be normal, confirming that the gammopathy is of “unknown signifi- cance. Immunosuppression (prednisone) plus plasma exchange is effective in patient’s Therapy with IgG and IgA gammopathies and a CIDP like picture. Patients who present with an axonal neuropathy are less responsive to treatment. IgM paraproteinemia with anti-MAG antibodies Half of patients with MGUS develop antibodies against MAG (myelin associat- ed glycoprotein). Patients have a moderate to severe sensory loss with distal weakness. Nerve conduction velocities are significantly slowed with temporal dispersion and conduction block. These patients do not respond to therapy, but the disorder itself is usually indolent. Large fiber sensory function is lost, and there may be tremor. Symptoms The disease presents as a sensorimotor neuropathy with predilection of large- Clinical syndrome/ fiber dysfunction. It is difficult to distinguish from MGUS, and MGUS may signs evolve into Waldenstrom’s over time. There is likely an auto-immune attack against peripheral nerves. Pathogenesis There is no evidence of osseous changes with imaging. Diagnosis 268 Laboratory studies can show IgM monoclonal gammopathy, IgM antibodies to MAG, GMI, sulfatide, GD1a or GD1b. Therapy Chemotherapy, intravenous gammaglobulin or plasmapheresis are usually not effective. Prognosis Neuropathy is usually not improved with treatment.