Treatments for Hyper-IgM Syndrome
Treatments for Hyper-IgM Syndrome
The list of treatments mentioned in various sources
for Hyper-IgM Syndrome
includes the following list.
Always seek professional medical advice about any treatment
or change in treatment plans.
Hyper-IgM Syndrome: Is the Diagnosis Correct?
The first step in getting correct treatment is
to get a correct diagnosis.
Differential diagnosis list for Hyper-IgM Syndrome may include:
Discussion of treatments for Hyper-IgM Syndrome:
Genes and Disease by the National Center for Biotechnology (Excerpt)
Treatment of HIM mainly consists of regular IV replacement of the missing IgG antibodies and prompt treatment of infections. Long lasting immunity, however, cannot be maintained without a bone marrow transplant, which is done when a suitable donor is available.
(Source: Genes and Disease by the National Center for Biotechnology)
Primary Immune Deficiency, NIAID Fact Sheet: NIAID (Excerpt)
Patients receive injections of
intravenous immunogloblulin (IVIG) every three to four weeks. For
neutropenia, patients can take granulocyte colony-stimulating factor
(G-CSF). Their doctor may also prescribe antibiotics to prevent the
respiratory infection, pneumocystis carinii pneumonia. (Source: excerpt from Primary Immune Deficiency, NIAID Fact Sheet: NIAID)
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Acquired immunodeficiency syndrome:
Treatment
(Professional Guide to Diseases (Eighth Edition))
There is no cure for either HIV or AIDS. However, significant advances have been made to help patients control signs and symptoms and impair disease progression. Because HIV can become resistant to any drug, health care professionals use combination treatments and multiple drug regimens to suppress the virus. Patients on medication remain infectious.
An effective method of treatment is highly active antiretroviral therapy (HAART). HAART aims to reduce the number of HIV particles in the blood as measured by viral load, thus increasing T-cell counts and improving the immunologic system’s functioning. A regular and vigilant medication regimen is critical or resistance will develop because HIV strains mutate and can become resistant to HAART relatively easily.
The nucleoside analogues (sometimes called reverse transcriptase inhibitors) have been the mainstay of AIDS therapy in recent years. These drugs interfere with viral reverse transcriptase, which impairs HIV’s ability to turn its ribonucleic acid into deoxyribonucleic acid for insertion into the host cell.
Antiretroviral therapy typically begins when the patient’s CD4+ T-cell count drops to less than 500/µl or when the patient develops an opportunistic infection. Most clinicians recommend starting the patient on a combination of these drugs in an attempt to gain the maximum benefit and to inhibit the production of resistant mutant strains of HIV. The drug combinations and dosages are then altered, depending on the patient’s response.
Increasingly, physicians are basing changes in therapy on the patient’s viral load rather than on his CD4+ T-cell count. Because the CD4+ count is influenced by the total white blood cell count, changes in the CD4+ count may have nothing to do with changes in the patient’s HIV status. Many physicians suggest that patients on antiretroviral therapy have their viral load checked every 3 months.
The increasing use of protease inhibitors (PIs) has greatly increased the life expectancy of patients with AIDS. These drugs block the enzyme protease, which HIV needs to produce virions, the viral particles that spread the virus to other cells. The use of PIs dramatically reduces viral load — sometimes to undetectable levels — while producing a corresponding increase in the CD4+ T-cell count and, because they act at a different site than nucleoside analogues, the PIs don’t produce additional adverse effects when added to a patient’s regimen.
Antiviral therapy includes the use of multiple combined drug therapies that suppress the replication of the HIV virus in the body. After antiviral therapy is initiated, treatment should be aggressive. Initially, highly active antiviral therapy, consisting of a triple drug therapy regimen — a PI and two non-nucleoside reverse transcriptase inhibitors — is recommended. In addition to these primary treatments, anti-infectives are used to combat opportunistic infections (some are used prophylactically to help patients resist opportunistic infections), and antineoplastic drugs are used to fight associated neoplasms. Supportive treatments help maintain nutritional status and relieve pain and other distressing physical and psychological symptoms.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Common variable immunodeficiency:
Treatment
(Professional Guide to Diseases (Eighth Edition))
Treatment and care of patients with common variable immunodeficiency are essentially the same as for those with X-linked hypogammaglobulinemia.
Injection of immune globulin (usually weekly to monthly) helps maintain the immune response. Because these injections are painful, give them deep into a large muscle mass, such as the gluteal or thigh muscles, and massage well. If the dosage is more than 1.5 ml, divide the dose and inject it into more than one site; for frequent injections, rotate the injection sites. Because immune globulin is composed primarily of IgG, the patient may also need fresh frozen plasma infusions to provide IgA and IgM.
Antibiotics are the mainstay for combating infection. Regular X-rays and pulmonary function studies help monitor lung infection; chest physiotherapy may be ordered to forestall or help clear such infection.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Severe combined immunodeficiency disease:
Treatment
(Professional Guide to Diseases (Eighth Edition))
Treatment aims to restore the immune response and prevent infection. Histocompatible bone marrow transplantation is the only satisfactory treatment available to correct immunodeficiency. Because bone marrow cells must be human leukocyte antigen and mixed leukocyte culture matched, the most common donors are histocompatible siblings. However, because bone marrow transplant can produce a potentially fatal graft-versus-host (GVH) reaction, newer methods of bone marrow transplant that eliminate GVH reaction (such as lectin separation and the use of monoclonal antibodies) are being evaluated.
Fetal thymus and liver transplants have achieved limited success. Immune globulin administration may also play a role in treatment. Some SCID infants have received long-term protection by being isolated in a completely sterile environment. However, this approach isn’t effective if the infant already has had recurring infections.
Gene therapy is being used to treat ADA deficiency.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Tearing, increased [Epiphora]:
Patient counseling
(Professional Guide to Signs & Symptoms (Fifth Edition))
Instruct the patient not to touch the unaffected eye to avoid possible cross-contamination. Teach the patient not to share eye makeup or pillowcases and to practice good hand-washing techniques.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Common variable immunodeficiency:
Treatment
(Handbook of Diseases)
Patients with common variable immunodeficiency need essentially the same treatment as patients with X-linked hypogammaglobulinemia.
I.V. immune globulin (usually weekly to monthly) helps maintain immune response. Because immune globulin is made up primarily of IgG, the patient may also need fresh frozen plasma infusions to provide IgA and IgM.
Antibiotics are the mainstay for combating infection. Regular X-rays and pulmonary function studies help monitor infection in the lungs; chest physiotherapy may forestall or help clear such infection.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Human immunodeficiency virus infection:
Treatment
(Handbook of Diseases)
No cure has yet been found for the disorder; however, primary therapy for HIV infection includes three different types of antiretroviral agents:
❑ protease inhibitors (PIs), such as ritonavir, indinavir, nelfinavir, and saquinavir
❑ nucleoside reverse transcriptase inhibitors (NRTIs), such as zidovudine, didanosine, zalcitabine, lamivudine, and stavudine
❑ nonnucleoside reverse transcriptase inhibitors (NNRTIs), such as nevirapine and delavirdine.
These agents, used in various combinations, are designed to inhibit HIV viral replication. Other potential therapies include immunomodulatory agents designed to boost the weakened immune system and anti-infective and antineoplastic agents to combat opportunistic infections and associated cancers; some are used prophylactically to help patients resist opportunistic infections.
Current treatment protocols combine three agents in an effort to gain the maximum benefit with the fewest adverse reactions. Such regimens include one PI and are considered the most effective treatment. Many variations and drug interactions are under study. Combination therapy helps inhibit the production of resistant, mutant strains. Supportive treatments help maintain nutritional status and relieve pain and other distressing physical and psychological symptoms.
Many pathogens respond to anti-infective drugs but tend to recur after treatment ends. For this reason, most patients need continuous anti-infective treatment, presumably for life or until the drug is no longer tolerated or effective.
UNDER STUDY: Once-daily dosing with antiretroviral drugs, such as didanosine, efavirenz, lamivudine, and tenofovir, to increase treatment adherence to drug-resistant variants of HIV is under investigation. A combination of amprenavir, a protease inhibitor, boosted with ritonavir has been approved, and other new antiretroviral drugs are currently in development for new dosing schedules.
Zidovudine
Treatment with zidovudine has proven effective in slowing the progression of HIV infection, decreasing opportunistic infections, and prolonging survival. However, it commonly produces serious adverse reactions and toxicities. The drug is typically combined with other agents (such as lamivudine) but has also been used as a single agent for pregnant HIV-positive women.
The current recommendation is to take 100 mg every 4 hours for a total daily dose of 600 mg, or 500 mg if the patient doesn’t want to interrupt sleep. Other NRTIs, such as didanosine and zalcitabine, may also be used in combination regimens for patients who can’t tolerate or no longer respond to zidovudine.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Severe combined immunodeficiency disease:
Treatment
(Handbook of Diseases)
Restoring immune response and preventing infection are the first goals of treatment. Histocompatible bone marrow transplant is the only satisfactory treatment available to correct immunodeficiency.
Because bone marrow cells must be matched according to human leukocyte antigen and mixed leukocyte culture, the most common donors are histocompatible siblings. But bone marrow transplant can produce a potentially fatal graft-versus-host (GVH) reaction, so newer methods of bone marrow transplant that eliminate GVH reaction (such as lectin separation and the use of monoclonal antibodies) are being evaluated.
Fetal thymus and liver transplants have achieved limited success. Administration of immune globulin may also play a role in treatment. Some SCID infants have received long-term protection by being isolated in a completely sterile environment. However, this approach isn’t effective if the infant already has had recurring infections.
Gene therapy is being used for ADA deficiency.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Hyper-aldosteronism:
Treatment
(Handbook of Diseases)
The treatment for aldosterone-producing adenoma is unilateral adrenalectomy. Potassium-sparing diuretics (spironolactone and amiloride) are used to control hyperaldosteronism in patients with bilateral hyperplasia or those with unilateral adenoma who are unable to undergo surgery.
Treatment of secondary hyperaldosteronism must include correction of the underlying cause.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Hyper-parathyroidism:
Treatment
(Handbook of Diseases)
Effective treatment varies, depending on the cause of the disease.
Primary disease
Treatment for primary hyperparathyroidism may include surgery to remove the adenoma or, depending on the extent of hyperplasia, all but one-half of one gland (the remaining part of the gland is necessary to maintain normal PTH levels). Such surgery may relieve bone pain within 3 days. However, renal damage may be irreversible.
Clinical tip Patients with primary hyperparathyroidism should be considered for surgery when:
❑ calcium levels are greater than or equal to 1 mg/dl above normal
❑ osteoporosis is present
❑ recurrent peptic ulcer disease is present
❑ nephrolithiasis is present
❑ impaired kidney function is noted
❑ patient is young or consistent follow-up is unavailable.
Preoperatively — or if surgery isn’t feasible or necessary — other treatments can decrease calcium levels. They include forcing fluids, limiting dietary intake of calcium, and promoting sodium and calcium excretion through forced diuresis using normal saline solution (up to 6 L in life-threatening circumstances), furosemide, or ethacrynic acid.
Other treatments include administering oral sodium or potassium phosphate, subcutaneous calcitonin, I.V. plicamycin, or I.V. biphosphonates. In primary hyperparathyroidism, surgery is the only definitive therapy. There are no effective long-term medical therapies for hyperparathyroidism.
Therapy for potential postoperative magnesium and phosphate deficiencies includes I.V. administration of magnesium and phosphate or sodium phosphate solution given by mouth or retention enema. In addition, during the first 4 to 5 days after surgery, when serum calcium falls to low normal levels, supplemental calcium may be necessary; vitamin D or calcitriol may also be used to raise the serum calcium level.
Secondary disease
Treatment of secondary hyperparathyroidism must correct the underlying cause of parathyroid hyperplasia. It consists of vitamin D therapy or, in the patient with kidney disease, administration of an oral calcium preparation for hyperphosphatemia.
In the patient with renal failure, dialysis is necessary to lower phosphorus levels and may have to continue for the remainder of the patient’s life.
In the patient with chronic secondary hyperparathyroidism, the enlarged glands may not revert to normal size and function even after calcium levels have been controlled.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Hyper-lipoproteinemia:
Treatment
(Handbook of Diseases)
The first goal is to identify and treat any underlying problem such as diabetes. If no underlying problem exists, the primary treatment for types II, III, and IV is dietary management, especially restriction of cholesterol intake, simple sugars, and refined carbohydrates that will elevate triglyceride levels. Omega-3 essential fatty acids (fish oils) have proved useful in reducing serum triglycerides. Drug therapy (cholestyramine, clofibrate, or pharmaceutical non-flush niacin) may also be used to lower the plasma triglyceride or cholesterol level when diet alone is ineffective.
Type I
In type I hyperlipoproteinemia, treatment requires long-term weight reduction, with fat intake restricted to less than 20 g/day. A 20- to 40-g/day medium-chain triglyceride diet may be ordered to supplement caloric intake. The patient should also avoid alcoholic beverages to decrease plasma triglycerides. The prognosis is good with treatment; without treatment, death can result from pancreatitis.
Type II
For type II, dietary management to restore normal lipid levels and decrease the risk of atherosclerosis includes restriction of cholesterol intake to less than 300 mg/day for adults and less than 150 mg/day for children; triglyceride levels must be restricted to less than 100 mg/day for children and adults. The diet should also be high in polyunsaturated fats.
In familial hypercholesterolemia, nicotinic acid with a bile acid usually normalizes low-density lipoprotein levels. For severely affected children, portacaval shunt is a last resort to reduce plasma cholesterol levels.
The prognosis remains poor regardless of treatment; in homozygotes, myocardial infarction usually causes death before age 30.
Type III
For type III, dietary management includes restriction of cholesterol intake to less than 300 mg/day; carbohydrates must also be restricted, and polyunsaturated fats are increased. Clofibrate and niacin help lower blood lipid levels. Weight reduction is helpful. With strict adherence to the prescribed diet, the prognosis is good.
Type IV
For type IV, weight reduction may normalize blood lipid levels without additional treatment. Long-term dietary management includes restricted cholesterol intake, increased polyunsaturated fats, and avoidance of alcoholic beverages. Clofibrate and niacin may lower plasma lipid levels.
The prognosis remains uncertain because of predisposition to premature CAD.
Type V
The most effective treatment for type V is weight reduction and long-term maintenance of a low-fat diet. Alcoholic beverages must be avoided. Niacin, clofibrate, gemfibrozil, and a 20- to 40-g/day medium-chain triglyceride diet may prove helpful.
The prognosis is uncertain because of the risk of pancreatitis. Increased fat intake may cause recurrent bouts of illness, possibly leading to pseudocyst formation, hemorrhage, and death.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Salivation, increased:
Patient counseling
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Teach the patient the importance of proper oral hygiene to prevent odor and dental problems. Remind him to seek regular dental care.
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Tearing, increased:
Patient counseling
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Instruct the patient not to touch the unaffected eye to avoid possible cross-contamination. Teach the patient not to share eye makeup or pillowcases and to practice good hand-washing techniques.
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
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