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✍️✍️Late Effects Of Blood And Marrow Transplantation ___________________________________________ Abstract Hematopoietic cell transplantation is a curative treatment for a variety of hematologic diseases. Advances in transplantation technology have reduced early transplant-relatedmortality and expanded application of transplantation to older patients and to a wider variety of diseases. Management of late effects after transplantation is increasingly important for a growing number of long-term survivors that is estimated to be half a million worldwide. Many studies have shown that transplant survivors suffer from significant late effects that adversely affect morbidity, mortality, working status and quality of life. Late effects include diseases of the cardiovascular, pulmonary, and endocrine systems, dysfunction of the thyroid gland, gonads, liver and kidneys, infertility, iron overload, bone diseases, infection, solid cancer, and neuropsychological effects. The leading causes of late mortality include recurrent malignancy, lung diseases, infection, secondary cancers and chronic graft-versus-host disease. The aim of this review is to facilitate better care of adult transplant survivors by summarizing accumulated evidence, new insights, and practical information about individual late effects. Further research is needed to understand the biology of late effects allowing better prevention and treatment strategies to be developed. Introduction Hematopoietic cell transplantation (HCT) is a curative treatment for a variety of hematologic diseases.1 The safety of HCT has improved over the decades,2 indications for HCT have expanded to older patients,3 and almost all patients are able to find suitable allogeneic donors by the growing use of cord blood4 and haploidentical transplantation.5 These current conditions have contributed to a growing number of HCT survivors, estimated to be half a million worldwide.6 Patients who are disease-free at two or five years after HCT have a greater than 80% subsequent 10-year survival rate,7–10 but many studies show that HCT survivors suffer from significant late effects that adversely affect morbidity, mortality, working status and quality of life.7–13 A prospective observational study of 1022 survivors who underwent HCT between 1974 and 1998 showed that 66% of the survivors had at least one chronic condition and 18% had severe or life-threatening conditions.14 A retrospective study of 1087 contemporary survivors also showed that the cumulative incidence of any non-malignant late effect at five years after HCT was 45% among autologous and 79% among allogeneic recipients, and 2.5% of autologous and 26% of allogeneic recipients had three or more late effects.15 Life expectancy among 5-year survivors remained 30% lower compared with the general population, regardless of their current ages and years since HCT.9 The leading causes of excess deaths in 5-year survivors included secondary malignancies (27%) and recurrent disease (14%), followed by infections (12%), chronic graft-versus-host disease (GvHD) (11%), cardiovascular diseases (11%), and respiratory diseases (7%).9 The aim of this review is to facilitate better care of adult HCT survivors by summarizing accumulated evidence, new insights, and practical information about individual late effects (Figure 1). Recurrent disease and chronic GvHD are not discussed and readers are referred to other reviews.16–20 Figure 1. Download figure Open in new tab Download powerpoint Figure 1. Late effects of blood and marrow transplantation. Cardiovascular diseases Cardiovascular diseases (CVD) after HCT include cardiomyopathy, congestive heart failure, valvular dysfunction, arrhythmia, pericarditis, and coronary artery disease.21 Their cumulative incidences were 5%–10% at ten years after HCT,22–24 accounting for 2%–11% of mortality among long-term survivors.8,9,25 The incidence of CVD and its associated mortality were 1.4–3.5-fold higher compared with the general population.8,9,24,25 HCT survivors are more likely to have conventional risk factors such as dyslipidemia and diabetes than the general population.26 Early diagnosis and treatment of modifiable risk factors is important. We usually treat hypertension more than 140/90 mmHg on 2 separate visits or more than 130/80 mmHg for patients with diabetes or renal disease.27 The first step is lifestyle modification including weight reduction, dietary sodium reduction and regular physical activity, followed by initiating antihypertensive drugs such as angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs). Anthracycline exposure and chest radiation are the major risk factors for CVD after HCT.21 Several studies showed that dexrazoxane, ACE inhibitors, ARBs and beta-blockers can prevent anthracycline-related cardiomyopathy in the non-HCT setting.28–32 Once cardiomyopathy is established, it is important to initiate appropriate treatment. ACE inhibitors and beta-blockers have been effective in improving left ventricular function.33 Pulmonary diseases Non-infectious late complications of the lung include bronchiolitis obliterans syndrome (BOS), cryptogenic organizing pneumonia (COP) and pulmonary hypertension. BOS represents chronic GvHD of the lung, and is characterized by the new onset of fixed airflow obstruction after allogeneic HCT.34 According to the strict 2005 National Institutes of Health (NIH) diagnostic criteria for chronic GvHD, incidence of BOS was 5.5% and its prevalence was 15% among patients with chronic GvHD.35 Symptoms of BOS include dyspnea on exertion, cough and wheezing, but early BOS may be asymptomatic until significant lung function is lost.36 One study showed rapid decline in %FEV1 during the six months before BOS diagnosis, with a lower %FEV1 at diagnosis associated with worse survival.37 In our practice, we perform pulmonary function tests every three months including %FEV1 and FEV1/FVC among patients with active chronic GvHD. When testing shows significant new airflow obstruction, we repeat testing every month until stability is confirmed.38 Plasma matrix metalloproteinase 3 levels39 and parametric response mapping from CT scans40 might be useful diagnostic tests for BOS but these have not yet entered clinical practice. Standard treatment of BOS is prednisone at 1 mg/kg per day, followed by a taper to reach a lower, alternate-day regimen.38 A multicenter prospective study showed that addition of FAM (inhaled fluticasone propionate at 440 μg twice a day, azithromycin at 250 mg taken 3 days per week, and montelukast at 10 mg nightly) to prednisone treatment stabilized pulmonary function in 70% of patients with newly diagnosed BOS and permitted systemic steroid exposure to be reduced.41 Cryptogenic organizing pneumonia is a disorder involving bronchioles, alveolar ducts, and alveoli, the lumen of which become filled with buds of granulation tissue consisting of fibroblasts.42 Clinical symptoms include dry cough, shortness of breath, and fever. Bronchoalveolar lavage is performed to exclude infection. Lung biopsy is required for definitive diagnosis, but an empiric diagnosis is often based on radiographic findings of diffuse, peripheral, fluffy infiltrates consistent with airspace consolidation. Pulmonary function testing shows restrictive changes and low diffusing capacity of the lungs for carbon monoxide. The incidence of COP is 2%–10%,43,44 and it is strongly associated with acute and chronic GvHD.45 COP usually responds within 5–7 days to prednisone at 1 mg/kg per day, which is continued for one month followed by a slow taper over five months because COP can often recur. Small case series suggest potential benefits of macrolides for treatment of COP.46 Pulmonary hypertension is an uncommon but potentially fatal complication after HCT, with a reported prevalence of 2.4%.47 The most common symptoms are hypoxia, tachypnea, dyspnea, and acute respiratory failure,48 and if untreated, pulmonary hypertension can result in a progressive increase in pulmonary vascular resistance, right ventricular failure and death. Since initial symptoms are non-specific, it is likely to be underdiagnosed after HCT. Although cardiac catheterization is the gold standard for diagnosis of pulmonary hypertension, high-resolution chest computed tomography and echocardiography are non-invasive and useful diagnostic modalities. The most common types are pulmonary arterial hypertension and pulmonary veno-occlusive disease, sometimes associated with transplant-associated microangiopathy and inherited or acquired hemolytic anemia.48 First-line therapies are supplemental oxygen and phosphodiesterase-5 inhibitors, followed by inhaled nitric oxide, diuretics, bipyridine inotropes and after-load reducing agents.48 Endocrine diseases Major late effects in the endocrine system include thyroid dysfunction, diabetes, dyslipidemia, and adrenal insufficiency. Hypothyroidism occurs in 30% of patients by 25 years after HCT.49 Risk factors include age under ten years, conditioning containing radiation, busulfan or cyclophosphamide, and hematologic malignancies.49,50 The international guidelines recommend checking serum thyroid-stimulating hormone and free thyroxine levels every year.21 For patients who received radiolabeled iodine antibody therapy, thyroid function should be checked earlier starting at three and six months after HCT, and other times as clinically indicated. Standard criteria are used to initiate replacement therapy for hypothyroidism. Some patients develop hyperthyroidism after HCT as a rare complication.51 Diabetes occurs in 8%–41% of patients after allogeneic HCT and in 3% of patients after autologous HCT.15,52,53 Its incidence after allogeneic HCT is 3.65 times higher compared with their siblings.54 Initial treatment is therapeutic lifestyle counseling, but many patients require hypoglycemic agents or insulin. Dyslipidemia occurs in 9%–61% of HCT survivors.53,55 Despite no established consensus for management of dyslipidemia after HCT, our practice is to initiate therapeutic lifestyle counseling followed by statin therapy when LDL cholesterol exceeds 130–190 mg/dL according to the estimated risk of CVD, based on the National Cholesterol Education Program Adult Treatment Panel III guidelines56 and the recently suggested approach after allogeneic HCT.57 The 2013 ACC/AHA guidelines do not specify the targeted levels for LDL cholesterol, and addition of statin therapy is based on calculated risk for future cardiovascular events.58 Addition of omega-3-acid ethyl esters or fibrate is considered when fasting triglycerides exceed 200–499 mg/dL. Adrenal insufficiency occurs in 13% of patients after allogeneic HCT and 1% of patients after autologous HCT,15 and can be confirmed by a cortisol-stimulation test. Once adrenal insufficiency is diagnosed, physiological glucocorticoid replacement and a very slow terminal taper is needed. Patients should carry notification that they have adrenal insufficiency to alert emergency medical providers. For chronic GvHD therapy, the risk of adrenal insufficiency is lower with alternate-day administration of corticosteroids than with daily dosing,59 although patients with brittle diabetes need daily dosing to allow for optimal glucose control. Male gonadal dysfunction and infertility Hypogonadism is common after HCT. Impaired spermatogenesis, erectile dysfunction, low testosterone, and low libido occur in male patients. Erectile dysfunction and low libido have been associated with both physical and psychosocial factors.60,61 Testosterone replacement may be considered for patients with low testosterone levels and has improved sexual function, libido and bone mass, although monitoring prostate-specific antigen and testosterone levels is necessary.62,63 Azoospermia occurred in 70% of male patients, and spermatogenesis recovered in 90% of patients conditioned with cyclophosphamide alone, in 50% of patients conditioned with cyclophosphamide plus busulfan or thiotepa, and in 17% of patients conditioned with total body irradiation (TBI).64 Semen banking or cryopreservation of testicular tissue should be discussed before HCT with patients desiring fertility. Female gonadal dysfunction, infertility and pregnancy Ovarian insufficiency, vaginal changes and low libido occur in female patients. A historical study showed that ovarian failure occurred in more than 90% of female patients after HCT and recovered in 92% of patients conditioned with cyclophosphamide alone, but only in 24% of patients conditioned with cyclophosphamide and TBI.65 A pilot study showed that only 10% of patients had ovarian failure after reduced-intensity allogeneic HCT.66 The use of hormone replacement therapy for premature ovarian failure should be individualized based on the patient age, severity of menopausal symptoms, low bone density, risk of breast cancer, clotting predisposition and liver abnormalities.67 Since efficacy of gonadotropin-releasing hormone agonists in preserving fertility in cancer patients is controversial,68,69 cryopreservation of oocytes, ovarian tissue, or embryos should be discussed with patients desiring fertility.70 The largest study of pregnancy after HCT showed that 0.87% of patients or their partners had pregnancies after allogeneic HCT, and 0.36% of those after autologous HCT.71 We generally recommend that women wait 2–5 years after HCT before attempting conception since rates of relapse are generally highest in the first two years after HCT. Another concern is the theoretical risk of recurrent malignancy because of disturbance of the graft-versus-leukemia effect, and some cases of recurrent chronic myeloid leukemia after conception have been reported.71 Pregnancy outcomes are generally good with no increase in the risk of fetal malformations, although these pregnancies are considered high risk because of higher maternal risks of pregnancy complications.71 Iron overload Iron overload is rare after autologous HCT72 but common after allogeneic HCT.73,74 Previous prospective studies showed that 30%–60% of long-term survivors of allogeneic HCT had elevated serum ferritin levels and 25%–50% had elevated liver iron concentration on T2* magnetic resonance imaging (MRI).73,74 Since serum ferritin does not specifically reflect iron overload and can be elevated in hepatic and systemic inflammation, additional testing is required if the ferritin is elevated. We favor transferrin saturation, which is widely available and defined as the ratio of serum iron concentration divided by total iron-binding capacity.75 Normal transferrin saturation is less than 50% in males and less than 45% in females. Patients with iron overload usually have saturation more than 60%. HFE genotyping is considered in patients with a family history of hemochromatosis and in patients of Northern or Western European ethnicity. When saturation is not elevated, other etiologies for an elevated ferritin including inflammation, metabolic syndrome, and alcoholism should be ruled out. The most accurate test of tissue iron concentration is liver biopsy, but the procedure is invasive and may cause serious complications. Thus, T2* MRI and other modalities (FerriScan and superconducting quantum interference device) have been increasingly used.76 Importantly, liver tests are often normal among long-term survivors with iron overload, so hepatitis and GvHD should also be considered when results of liver tests are elevated.77 Iron overload may cause cardiomyopathy. Studies of thalassemia patients showed that cardiomyopathy typically took more than ten years to be clinically evident,78 and that many patients improved with intensive chelation therapy.79 Although a prospective study and a meta-analysis showed no statistical association of liver iron concentration with mortality after allogeneic HCT,80,81 our practice is to start phlebotomy of 5 mL/kg or 250–300 mL every 3–4 weeks as long as hematocrit is more than 35% until serum ferritin falls below 1000 ng/mL. Deferasirox, an oral chelating agent, is considered for patients with anemia precluding phlebotomy. Liver diseases Late liver diseases include chronic hepatitis B, chronic hepatitis C, liver cirrhosis, nodular regenerative hyperplasia and focal nodular hyperplasia.77 Hepatitis B-infected patients have an increased risk of fulminant liver failure. One study reported a 35% risk of HBV reactivation after HCT even among patients with isolated anti-HBc antibodies, mostly during steroid treatment for GvHD.82 Patients treated with anti-CD20 antibodies have an increased risk of HBV reactivation. Antiviral prophylaxis using entecavir or lamivudine will prevent almost all fulminant cases if initiated before the start of conditioning regimens in patients with positive blood HBV DNA levels.83 Patients with latent HBV (i.e. anti-HBc+/HBV DNA−) should be monitored monthly with HBV DNA levels after HCT and antiviral treatment should be initiated when viremia is detected.83 Hepatitis C virus infection in HCT survivors almost always results in chronic hepatitis.84,85 Typically, asymptomatic elevation of alanine aminotransferase occurs 2–4 months after HCT, coinciding with tapering of immunosuppressive medications. There may be little liver-related mortality in the first ten years after HCT,84 but liver cirrhosis occurs later with a cumulative incidence of 4%–24% at 20 years.85,86 A large retrospective study showed that hepatitis C-infected patients had an increased risk of 2-year non-relapse mortality due to hepatic problems and bacterial infection.87 Antiviral therapy for HCV has not been given early after HCT, but may improve both oncological and hepatic outcomes after HCT.88 Ribavirin and interferon-based therapy have been used for patients who have discontinued all immunosuppressive medications without active GvHD, but it can cause pancytopenia and GvHD. Recently, highly effective and well tolerated direct acting antiviral agents with more than 90% rates of sustained virological response have been developed, and interferon-free regimens are now the treatments of choice.89,90 Nodular regenerative hyperplasia is a rare liver condition characterized by a widespread benign transformation of the hepatic parenchyma into small regenerative nodules.77 This process is usually asymptomatic unless portal hypertension develops. Focal nodular hyperplasia occurs in 12% of HCT survivors, and possibly reflects sinusoidal injury caused by myeloablative conditioning regimens.91 Kidney diseases Chronic kidney disease (CKD) is defined as an elevated serum creatinine level, or a decreased glomerular filtration rate (GFR) less than 60 mL/min/1.73 m2 for three months or longer.92 CKD occurs in approximately 20% of HCT recipients.93–95 There are three major etiologies of CKD after HCT: thrombotic microangiopathy (TMA), nephrotic syndrome and idiopathic CKD. Other etiologies include persistent acute kidney injury and BK virus nephropathy.96 Whenever possible, renal biopsy should be considered to accurately diagnose the etiology of CKD and to provide appropriate management.97 Thrombotic microangiopathy occurs in 2%–21% of patients after HCT, and is characterized by renal dysfunction, thrombocytopenia, neurological dysfunction, hemolytic anemia with schistocytes, elevated lactate dehydrogenase and decreased haptoglobin.98,99 Risk factors of TMA include TBI, calcineurin inhibitors, and acute and chronic GvHD.100–102 TMA-related kidney injury often improves with tapering or stopping calcineurin inhibitors, but full renal function is rarely restored.103 In some cases TMA did not improve until GvHD was treated.104 Efficacy of plasma exchange is limited.105 Nephrotic syndrome occurs in 6%–8% of patients after allogeneic HCT.106,107 Membranous nephropathy comprised 61% of cases, and minimal change disease comprised 22% of cases, with a median onset of 14 months and eight months after HCT, respectively.108 Mechanisms of membranous nephropathy are thought to be formation of immune complexes through allo- or auto-antibodies recognizing antigens expressed by the podocyte, while T cells are implicated with minimal change disease.109 Nephrotic syndrome after HCT is often associated with chronic GvHD and tapering of immunosuppressive medications. Initial treatment is prednisone 1 mg/kg/day in addition to calcineurin inhibitors. Complete response was observed in 90% of patients with minimal change in disease, but only in 27% of patients with membranous nephropathy.108 Refractory cases may be treated with rituximab or mycophenolate mofetil.110 Idiopathic CKD comprises most cases of CKD. Risk factors include acute GvHD, chronic GvHD, acute kidney injury, long-term use of calcineurin inhibitors and previous autologous HCT,94,111 suggesting that GvHD, accompanying treatment and inflammatory conditions may have pathogenic roles in this entity. Associations of TBI with risk of CKD have been controversial.94,112 ACE inhibitors and ARBs have been used to treat CKD and hypertension associated with CKD.113 Bone diseases Late complications of bone include osteopenia, osteoporosis and avascular necrosis (AVN).114 Osteoporosis has been reported in as many as 50% of HCT recipients.115,116 The diagnoses of osteopenia and osteoporosis are made by measuring T-scores with dual-energy X-ray absorptiometry. A T-score between −1.0 and −2.5 indicates osteopenia, and a T-score less than −2.5 or presence of a fragility fracture indicates osteoporosis.117 Multiple risk factors are implicated including chemotherapy, radiation, corticosteroids, calcineurin inhibitors, vitamin D deficiency, and gonadal failure.116,118 Bone loss occurs within 6–12 months after HCT, and recovery of bone mineral density (BMD) begins from the lumber spine, followed by a slower recovery in the femoral neck. The use of corticosteroids is the strongest risk factor for osteoporosis. General preventative recommendations include adequate intake of calcium of 1200 mg per day or over and vitamin D of 1000 IU (25 μg) per day or over, regular weight-bearing exercise, and avoidance of smoking and excessive alcohol. Bisphosphonates are the primary treatment for bone loss.119 Patients who are taking 5 mg or more daily prednisone-equivalent steroids for three months or more should have screening BMD tests for osteoporosis, and bisphosphonate treatment may be indicated until corticosteroid treatment is discontinued or for up to five years.120 Second-line treatment includes calcitonin, raloxifene, denusomab, romosozumab, and blosozumab, though their reported use in HCT recipients is limited and adverse effects may be more prominent than with the bisphosphonates. Avascular necrosis occurs in 4%–19% of HCT survivors with a cumulative incidence of 3%–10% at five years after HCT.121,122 AVN causes severe bone pain and bone destruction, causing significant impairment in quality of life. AVN typically affects the femoral heads, but sometimes affects other joints such as the knee and shoulders.21 Risk factors for AVN include corticosteroids, calcineurin inhibitors, older age and TBI conditioning.114 When AVN is suspected, diagnostic MRI should be performed. Early involvement of an orthopedic specialist is important for management of AVN, including conservative treatment, joint-preserving surgery and joint replacement surgery.21,114 Infectious diseases All HCT survivors have some degree of immunodeficiency, particularly during the first year after HCT.123 If patients are able to stop immunosuppressive medications without GvHD or recurrent disease, many recover adequate immune function by one year after HCT. Patients with chronic GvHD, however, remain immunodeficient and have a high risk of infections. Common late infections are caused by Pneumocystis jirovecii, encapsulated bacteria, fungi, varicella-zoster virus (VZV), cytomegalovirus, and respiratory viruses. Patients may report more frequent episodes of upper respiratory infections and sinusitis. All patients should receive prophylaxis against Pneumocystis jirovecii for at least one year after HCT or until 3–6 months after all immunosuppressive medication is discontinued, whichever occurs later. The preferred drug is trimethoprim-sulfamethoxazole, but dapsone or atovaquone could be substituted for patients who are allergic to or intolerant of trimethoprim-sulfamethoxazole. In particular, patients with chronic GvHD are highly susceptible to encapsulated bacteria such as Streptococcus pneumoniae, Haemophilus influenzae and Neisseria meningitidis due to low levels of opsonizing antibodies, low CD4+ T-cell counts, poor reticuloendothelial function and suppressive effects of immunosuppressive medications on phagocytosis. Vaccination against these bacteria is recommended.124 Efficacy of vaccination in increasing antibody levels has been shown in several prospective studies.125,126 Chemoprophylaxis is always recommended due to the unpredictable protection provided by vaccination. The first-line drug is trimethoprim-sulfamethoxazole, but if it is not tolerated, penicillin or azithromycin is substituted until 3–6 months after discontinuation of all immunosuppressive medications. Invasive fungal infection occurs in 1% of patients after autologous HCT and in 6%–8% of patients after allogeneic HCT.127 GvHD and long-term use of corticosteroids have been a major risk factor associated with onset of invasive fungal infection.128 As recommended in the European guidelines, mold prophylaxis with posaconazole or voriconazole may be considered for patients with GvHD requiring high-dose corticosteroid treatment.129 Varicella-zoster virus-seropositive patients should receive prophylaxis with acyclovir or valacyclovir during the first year after HCT or until six months after discontinuation of immunosuppressive medications. A standard dose of acyclovir is 800 mg twice daily,130 but some studies showed that 200 mg once daily was effective in preventing VZV reactivation.131 Acyclovir should be started empirically if the patient presents with an acute abdomen or hepatitis typical of fulminant visceral VZV infection.132 CMV monitoring in blood is continued beyond 100 days after HCT until one year for patients at risk of late CMV disease, including CMV-seropositive patients receiving high-dose corticosteroids, those who have already experienced CMV reactivation, and cord blood transplantation.133 Pre-emptive therapy is usually considered for CMV levels of 250 IU/mL or more (equivalent to ≥1000 copies/mL) or a positive antigenemia test. Community-acquired respiratory virus infections are an important cause of morbidity and mortality after HCT. The most frequent viruses include rhinovirus, respiratory syncytial virus (RSV), parainfluenza viruses (PIV), human metapneumovirus, and influenza viruses as these frequently cause lower respiratory tract disease associated with 12%–100% mortality.134 An immunodeficiency scoring index can predict severity of RSV infection.135 Aerosolized ribavirin showed efficacy in treating lower tract RSV after HCT.136 Combination therapy with immunomodulators such as intravenous immunoglobulin or palivizumab has been seen to have variable success.137 Treatment for PIV infection has not been established. Efficacy of ribavirin has been limited for patients with lower respiratory tract infection of PIV.138 Novel drugs such as a recombinant sialidase fusion protein and a hemagglutinin-neuraminidase inhibitor are under investigation.138 Solid cancers There is an increased risk of solid cancers following both autologous and allogeneic HCT compared with the general population. The cumulative incidence is 1%–6% at ten years after HCT, and continues to rise over time without a plateau.139–142 The most common sites include oral cavity, skin, breast and thyroid, but rates are also elevated in esophagus, liver, nervous system, bone and connective tissues compared with the general population.143 Myeloablative TBI, young age at HCT, chronic GvHD and prolonged immunosuppressive medications beyond two years are well-documented risk factors for many types of cancers.143 All HCT recipients should be advised of the risk of second cancers and should be encouraged to undergo recommended screening tests based on their predisposition.143 The 5-year overall survival rates after diagnosis of solid cancers varied by cancer site, with 88%–100% for thyroid, testis and melanoma, approximately 50% for breast, mouth, soft tissue and female reproductive organs, and 20% or less for bone, lower gastrointestinal tract, and central nervous system.144 These rates were similar to those of de novo cancers, except that rates were lower for female reproductive organs, bone, colorectum, and central nervous system, although further studies are warranted to confirm this observation. There is emerging evidence that human papilloma virus (HPV) is involved in the pathogenesis of squamous cell cancer after HCT.145,146 The efficacy of HPV vaccination in preventing squamous cell cancer after HCT remains to be determined in prospective studies.147 Neuropsychological effects Neuropsychological effects after HCT are being increasingly recognized and include, among others, depression, post-traumatic stress disorder, and neurocognitive deficits. Depression occurs in 12%–30% of HCT survivors and is more frequent in female patients, younger patients and those with poor social support, history of recurrent disease, chronic pain, and chronic GvHD.148 Post-traumatic stress disorder occurs in 28% of patients at six months after HCT and may persist for 5%–13% of cases, although its risk factors are not yet clear.148–150 Neurocognitive deficits, so called “chemo brain”, have adverse functional impacts on HCT survivors who return to work and daily activities that require short-term memory, information-processing speed, multitasking and co-ordination.151 Neuropsychological tests can help identify neurocognitive deficits. Most evidence is derived from studies of breast cancer survivors, with estimated rates of deficits ranging from 16% to 50% up to ten years after treatment.152,153 Potential mechanisms for chemotherapy-induced neurocognitive changes include cytokine and immune dysregulation, damage to DNA and telomere length through cytotoxic agents, oxidative stress and hormonal changes.154 In cases of HCT survivors, there may be additional deficits derived from neurological complications including nervous system infection (HHV-6, fungi, etc.), immune-mediated damage, and toxicities of calcineurin inhibitors such as TMA and posterior reversible encephalopathy syndrome. A prospective observational study showed that neurocognitive function declined substantially at 80 days after HCT, returned to pre-transplantation levels at one year, and continued to improve between one and five years after HCT, except for motor dexterity and verbal learning and retention.155 Mostly mild, neurocognitive dysfunction according to the Global Deficit Score persisted at five years in 42% of long-term survivors.155 Rehabilitation programs have succeeded in improving neurocognitive functions,156 and methylphenidate and modafinil have demonstrated variable efficacies to improve neurocognitive function in non-HCT cancer patients.157,158 Efficacies of these interventions remaine to be determined among HCT survivors. Influence of newer practices on late effects An understanding of the influence of newer practices such as cord blood transplantation, non-TBI or reduced-intensity conditioning regimens and older patients on the incidence and severity of late effects awaits longer follow up. For example, TBI is associated with an increased risk of many late effects such as cardiovascular diseases, COP, hypothyroidism, diabetes, dyslipidemia, infertility, TMA-related kidney injury, bone density loss, avascular necrosis, and secondary solid cancer.49,54,100,102,114,118,143,159,160 The use of non-TBI conditioning regimens might reduce the burden of these late effects among HCT survivors. Some studies found that cumulative incidences of late effects did not differ much after reduced-intensity regimens compared with myeloablative regimens,15,161 and reduced-intensity conditioning was associated with a higher risk of recurrent malignancy among patients with myeloid malignancy.162 One study showed that the risk of AVN was elevated after cord blood transplantation, but graft source had a limited influence on other long-term health status and QOL.163 Consensus guidelines for late effects and prevention behaviors Incidence, mortality, morbidity and management of individual late effects are summarized in Tables 1 and 2. Recognizing the importance of managing late effects after HCT, the Center for International Blood and Marrow Transplant Research (CIBMTR), the European Group for Blood and Marrow Transplantation (EBMT), and the American Society for Bone Marrow Transplantation (ASBMT) developed recommendations in 2006 for screening and prevention practices for HCT survivors.164 Consensus recommendations were up-dated in 2011 including other international transplant communities.21 The NIH convened working groups to formulate late effects initiatives in 2015.148,165–169 View inlineDownload powerpoint Table 1. Late effects after blood and marrow transplantation View inlineDownload powerpoint Table 2. Tests, preventive approaches and treatment of late effects. Despite higher levels of engagement with health care providers, HCT survivors had similar health and prevention behaviors as matched untransplanted controls, suggesting the need for further education of both HCT survivors and health practitioners.170 Major modifiable predictors of lower adherence to preventive care practices were concerns about medical costs and lack of knowledge.171 Conclusion While the number of HCT survivors is growing, there is no evidence that the burden of late effects is lessening. HCT survivors face myriad late effects that can limit their functioning, require prolonged or life-long medical treatment, reduce their quality of life and also shorten their survival. To the extent that the HCT procedure itself causes these late effects, the transplant community has a responsibility to appropriately monitor, treat and ultimately try to prevent late effects. Given the dispersion of survivors and the varied structure of health care, hematologists, oncologists, primary care physicians and medical subspecialists are all involved in providing this care. Further research is needed to understand the biology of late effects to help identify better prevention and treatment strategiesDr. Ved Srivastava3 Likes4 Answers
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LEAD POISONING- A SERIOUS THREAT TO HEALTH Lead poisoning is a type of metal poisoning caused by lead in the body.The brain is the most sensitive.Symptoms may include abdominal pain, constipation, headaches, irritability, memory problems, inability to have children, and tingling in the hands and feet. It causes almost 10% of intellectual disability of otherwise unknown cause and can result in behavioral problems. Some of the effects are permanent. In severe cases anemia, seizures, coma, or deathmay occur. Lead poisoning Synonyms Plumbism, colica pictorum, saturnism, Devon colic, painter's colic An X ray demonstrating the characteristic finding of lead poisoning in humans—dense metaphyseal lines. Specialty Toxicology Symptoms Intellectual disability, abdominal pain, constipation, headaches, irritability, memory problems, inability to have children, tingling in the hands and feet Complications Anemia, seizures, coma Causes Exposure to lead via contaminated air, water, dust, food, consumer products Risk factors Being a child Diagnostic method Blood lead level Differential diagnosis Iron deficiency anemia, malabsorption, anxiety disorder, polyneuropathy Prevention Removing lead from the home, improved monitoring in the workplace, laws that ban lead in products Treatment Chelation therapy Medication Dimercaprol, edetate calcium disodium, succimer Deaths 853,000 (2013) Exposure to lead can occur by contaminated air, water, dust, food, or consumer products. Children are at greater risk as they are more likely to put objects in their mouth such as those that contain lead paint and absorb a greater proportion of the lead that they eat. Exposure at work is a common cause of lead poisoning in adults with certain occupations at particular risk.Diagnosis is typically by measurement of the blood lead level. The Centers for Disease Control (US) has set the upper limit for blood lead for adults at 10 µg/dl (10 µg/100 g) and for children at 5 µg/dl. Elevated lead may also be detected by changes in red blood cellsor dense lines in the bones of children as seen on X-ray. Lead poisoning is preventable. This includes by individual efforts such as removing lead-containing items from the home, workplace efforts such as improved ventilation and monitoring,and nationwide policies such as laws that ban lead in products such as paint and gasoline, reduce allowable levels in water or soil, and provide for cleanup of contaminated soil. The major treatments are removal of the source of lead and the use of medications that bind lead so it can be eliminated from the body, known as chelation therapy.Chelation therapy in children is recommended when blood levels are greater than 40–45 µg/dl.Medications used include dimercaprol, edetate calcium disodium, and succimer. In 2013 lead is believed to have resulted in 853,000 deaths. It occurs most commonly in the developing world.Those who are poor are at greater risk.Lead is believed to result in 0.6% of the world's disease burden. People have been mining and using lead for thousands of years. Descriptions of lead poisoning date to at least 2000 BC, while efforts to limit lead's use date back to at least the 16th century.Concerns for low levels of exposure begin in the 1970s with there being no safe threshold for lead exposure. Classification Classically, "lead poisoning" or "lead intoxication" has been defined as exposure to high levels of lead typically associated with severe health effects. Poisoning is a pattern of symptoms that occur with toxic effects from mid to high levels of exposure; toxicity is a wider spectrum of effects, including subclinical ones (those that do not cause symptoms). However, professionals often use "lead poisoning" and "lead toxicity" interchangeably, and official sources do not always restrict the use of "lead poisoning" to refer only to symptomatic effects of lead. The amount of lead in the blood and tissues, as well as the time course of exposure, determine toxicity. Lead poisoning may be acute (from intense exposure of short duration) or chronic (from repeat low-level exposure over a prolonged period), but the latter is much more common. Diagnosis and treatment of lead exposure are based on blood lead level (the amount of lead in the blood), measured in micrograms of lead per deciliter of blood (μg/dL). Urine lead levels may be used as well, though less commonly. In cases of chronic exposure lead often sequesters in the highest concentrations first in the bones, then in the kidneys. If a provider is performing a provocative excretion test, or "chelation challenge", a measurement obtained from urine rather than blood is likely to provide a more accurate representation of total lead burden to a skilled interpreter. The US Centers for Disease Control and Prevention and the World Health Organization state that a blood lead level of 10 μg/dL or above is a cause for concern; however, lead may impair development and have harmful health effects even at lower levels, and there is no known safe exposure level.Authorities such as the American Academy of Pediatrics define lead poisoning as blood lead levels higher than 10 μg/dL. Lead forms a variety of compounds and exists in the environment in various forms. Features of poisoning differ depending on whether the agent is an organic compound (one that contains carbon), or an inorganic one. Organic lead poisoning is now very rare, because countries across the world have phased out the use of organic lead compounds as gasoline additives, but such compounds are still used in industrial settings. Organic lead compounds, which cross the skin and respiratory tract easily, affect the central nervous system predominantly. Signs and symptoms Symptoms of lead poisoning. Lead poisoning can cause a variety of symptoms and signs which vary depending on the individual and the duration of lead exposure.Symptoms are nonspecific and may be subtle, and someone with elevated lead levels may have no symptoms.Symptoms usually develop over weeks to months as lead builds up in the body during a chronic exposure, but acute symptoms from brief, intense exposures also occur. Symptoms from exposure to organic lead, which is probably more toxic than inorganic lead due to its lipid solubility, occur rapidly. Poisoning by organic lead compounds has symptoms predominantly in the central nervous system, such as insomnia, delirium, cognitive deficits, tremor, hallucinations, and convulsions. Symptoms may be different in adults and children; the main symptoms in adults are headache, abdominal pain, memory loss, kidney failure, male reproductive problems, and weakness, pain, or tingling in the extremities. Early symptoms of lead poisoning in adults are commonly nonspecific and include depression, loss of appetite, intermittent abdominal pain, nausea, diarrhea, constipation, and muscle pain. Other early signs in adults include malaise, fatigue, decreased libido, and problems with sleep. An unusual taste in the mouth and personality changes are also early signs. In adults, symptoms can occur at levels above 40 μg/dL, but are more likely to occur only above 50–60 μg/dL.Symptoms begin to appear in children generally at around 60 μg/dL.However, the lead levels at which symptoms appear vary widely depending on unknown characteristics of each individual. At blood lead levels between 25 and 60 μg/dL, neuropsychiatric effects such as delayed reaction times, irritability, and difficulty concentrating, as well as slowed motor nerve conduction and headache can occur. Anemia may appear at blood lead levels higher than 50 μg/dL. In adults, abdominal colic, involving paroxysms of pain, may appear at blood lead levels greater than 80 μg/dL. Signs that occur in adults at blood lead levels exceeding 100 μg/dL include wrist drop and foot drop, and signs of encephalopathy (a condition characterized by brain swelling), such as those that accompany increased pressure within the skull, delirium, coma, seizures, and headache. In children, signs of encephalopathy such as bizarre behavior, discoordination, and apathy occur at lead levels exceeding 70 μg/dL. For both adults and children, it is rare to be asymptomatic if blood lead levels exceed 100 μg/dL. Acute poisoning In acute poisoning, typical neurological signs are pain, muscle weakness, numbness and tingling, and, rarely, symptoms associated with inflammation of the brain. Abdominal pain, nausea, vomiting, diarrhea, and constipation are other acute symptoms. Lead's effects on the mouth include astringency and a metallic taste.Gastrointestinal problems, such as constipation, diarrhea, poor appetite, or weight loss, are common in acute poisoning. Absorption of large amounts of lead over a short time can cause shock (insufficient fluid in the circulatory system) due to loss of water from the gastrointestinal tract. Hemolysis (the rupture of red blood cells) due to acute poisoning can cause anemia and hemoglobin in the urine. Damage to kidneys can cause changes in urination such as decreased urine output.People who survive acute poisoning often go on to display symptoms of chronic poisoning. Chronic poisoning Chronic poisoning usually presents with symptoms affecting multiple systems, but is associated with three main types of symptoms: gastrointestinal, neuromuscular, and neurological.Central nervous system and neuromuscular symptoms usually result from intense exposure, while gastrointestinal symptoms usually result from exposure over longer periods.Signs of chronic exposure include loss of short-term memory or concentration, depression, nausea, abdominal pain, loss of coordination, and numbness and tingling in the extremities.[unreliable medical source?] Fatigue, problems with sleep, headaches, stupor, slurred speech, and anemia are also found in chronic lead poisoning. A "lead hue" of the skin with pallor and/or lividity is another feature. A blue line along the gum with bluish black edging to the teeth, known as a Burton line, is another indication of chronic lead poisoning.Children with chronic poisoning may refuse to play or may have hyperkineticor aggressive behavior disorders.Visual disturbance may present with gradually progressing blurred vision as a result of central scotoma, caused by toxic optic neuritis. Effects on children As lead safety standards become more stringent, fewer children in the US are found to have elevated lead levels. A woman who has elevated blood lead levels during pregnancy is at greater risk of a prematurely birth or with a low birth weight. Children are more at risk for lead poisoning because their smaller bodies are in a continuous state of growth and development. Lead is absorbed at a faster rate compared to adults, which causes more physical harm than to older people. Furthermore, children, especially as they are learning to crawl and walk, are constantly on the floor and therefore more prone to ingesting and inhaling dust that is contaminated with lead. The classic signs and symptoms in children are loss of appetite, abdominal pain, vomiting, weight loss, constipation, anemia, kidney failure, irritability, lethargy, learning disabilities, and behavioral problems. Slow development of normal childhood behaviors, such as talking and use of words, and permanent intellectual disability are both commonly seen. Although less common, it is possible for fingernails to develop leukonychia striata if exposed to abnormally high lead concentrations. By organ system Lead affects every one of the body's organ systems, especially the nervous system, but also the bones and teeth, the kidneys, and the cardiovascular, immune, and reproductive systems.Hearing loss and tooth decay have been linked to lead exposure, as have cataracts. Intrauterine and neonatal lead exposure promote tooth decay. Aside from the developmental effects unique to young children, the health effects experienced by adults are similar to those in children, although the thresholds are generally higher. Kidneys Kidney damage occurs with exposure to high levels of lead, and evidence suggests that lower levels can damage kidneys as well. The toxic effect of lead causes nephropathy and may cause Fanconi syndrome, in which the proximal tubular function of the kidney is impaired. Long-term exposure at levels lower than those that cause lead nephropathy have also been reported as nephrotoxic in patients from developed countries that had chronic kidney disease or were at risk because of hypertension or diabetes mellitus.Lead poisoning inhibits excretion of the waste product urate and causes a predispositDr. Yogesh Deshpande2 Likes1 Answer
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Friends today I am discussing about a problem known as Thyroid Disease & Pregnancy. Thyroid disease is a group of disorders that affects the thyroid gland. The thyroid is a small, butterfly-shaped gland in the front of your neck that makes thyroid hormones. Thyroid hormones control how your body uses energy, so they affect the way nearly every organ in your body works—even the way your heart beats. The thyroid is a small gland in your neck that makes thyroid hormones. Sometimes the thyroid makes too much or too little of these hormones. Too much thyroid hormone is called hyperthyroidism and can cause many of your body’s functions to speed up. “Hyper” means the thyroid is overactive. Too little thyroid hormone is called hypothyroidism and can cause many of your body’s functions to slow down. “Hypo” means the thyroid is underactive. If you have thyroid problems, you can still have a healthy pregnancy and protect your baby’s health by having regular thyroid function tests and taking any medicines that your doctor prescribes. What role do thyroid hormones play in pregnancy? Thyroid hormones are crucial for normal development of your baby’s brain and nervous system. During the first trimester—the first 3 months of pregnancy—your baby depends on your supply of thyroid hormone, which comes through the placenta . At around 12 weeks, your baby’s thyroid starts to work on its own, but it doesn’t make enough thyroid hormone until 18 to 20 weeks of pregnancy. Two pregnancy-related hormones—human chorionic gonadotropin (hCG) and estrogen—cause higher measured thyroid hormone levels in your blood. The thyroid enlarges slightly in healthy women during pregnancy, but usually not enough for a health care professional to feel during a physical exam. Thyroid problems can be hard to diagnose in pregnancy due to higher levels of thyroid hormones and other symptoms that occur in both pregnancy and thyroid disorders. Some symptoms of hyperthyroidism or hypothyroidism are easier to spot and may prompt your doctor to test you for these thyroid diseases. Another type of thyroid disease, postpartum thyroiditis, can occur after your baby is born. Hyperthyroidism in Pregnancy Some signs and symptoms of hyperthyroidism often occur in normal pregnancies, including faster heart rate, trouble dealing with heat, and tiredness. Other signs and symptoms can suggest hyperthyroidism: fast and irregular heartbeat shaky hands unexplained weight loss or failure to have normal pregnancy weight gain Causes of hyperthyroidism in pregnancy Hyperthyroidism in pregnancy is usually caused by Graves’ disease and occurs in 1 to 4 of every 1,000 pregnancies in the United States.1 Graves’ disease is an autoimmune disorder. With this disease, your immune system makes antibodies that cause the thyroid to make too much thyroid hormone. This antibody is called thyroid stimulating immunoglobulin, or TSI. Graves’ disease may first appear during pregnancy. However, if you already have Graves’ disease, your symptoms could improve in your second and third trimesters. Some parts of your immune system are less active later in pregnancy so your immune system makes less TSI. This may be why symptoms improve. Graves’ disease often gets worse again in the first few months after your baby is born, when TSI levels go up again. If you have Graves’ disease, your doctor will most likely test your thyroid function monthly throughout your pregnancy and may need to treat your hyperthyroidism.1 Thyroid hormone levels that are too high can harm your health and your baby’s. Pregnant woman having her blood drawn If you have Graves’ disease, your doctor will most likely test your thyroid function monthly during your pregnancy. Rarely, hyperthyroidism in pregnancy is linked to hyperemesis gravidarum —severe nausea and vomiting that can lead to weight loss and dehydration. Experts believe this severe nausea and vomiting is caused by high levels of hCG early in pregnancy. High hCG levels can cause the thyroid to make too much thyroid hormone. This type of hyperthyroidism usually goes away during the second half of pregnancy. Less often, one or more nodules, or lumps in your thyroid, make too much thyroid hormone. Untreated hyperthyroidism during pregnancy can lead to miscarriage premature birth low birthweight preeclampsia—a dangerous rise in blood pressure in late pregnancy thyroid storm—a sudden, severe worsening of symptoms congestive heart failure Rarely, Graves’ disease may also affect a baby’s thyroid, causing it to make too much thyroid hormone. Even if your hyperthyroidism was cured by radioactive iodine treatment to destroy thyroid cells or surgery to remove your thyroid, your body still makes the TSI antibody. When levels of this antibody are high, TSI may travel to your baby’s bloodstream. Just as TSI caused your own thyroid to make too much thyroid hormone, it can also cause your baby’s thyroid to make too much. Tell your doctor if you’ve had surgery or radioactive iodine treatment for Graves’ disease so he or she can check your TSI levels. If they are very high, your doctor will monitor your baby for thyroid-related problems later in your pregnancy. An overactive thyroid in a newborn can lead to a fast heart rate, which can lead to heart failure early closing of the soft spot in the baby’s skull poor weight gain irritability Sometimes an enlarged thyroid can press against your baby’s windpipe and make it hard for your baby to breathe. If you have Graves’ disease, your health care team should closely monitor you and your newborn. How do doctors diagnose hyperthyroidism in pregnancy? Your doctor will review your symptoms and do some blood tests to measure your thyroid hormone levels. Your doctor may also look for antibodies in your blood to see if Graves’ disease is causing your hyperthyroidism. Learn more about thyroid tests and what the results mean. How do doctors treat hyperthyroidism during pregnancy? If you have mild hyperthyroidism during pregnancy, you probably won’t need treatment. If your hyperthyroidism is linked to hyperemesis gravidarum, you only need treatment for vomiting and dehydration. If your hyperthyroidism is more severe, your doctor may prescribe antithyroid medicines, which cause your thyroid to make less thyroid hormone. This treatment prevents too much of your thyroid hormone from getting into your baby’s bloodstream. You may want to see a specialist, such as an endocrinologist or expert in maternal-fetal medicine, who can carefully monitor your baby to make sure you’re getting the right dose. Doctors most often treat pregnant women with the antithyroid medicine propylthiouracil (PTU) during the first 3 months of pregnancy. Another type of antithyroid medicine, methimazole , is easier to take and has fewer side effects, but is slightly more likely to cause serious birth defects than PTU. Birth defects with either type of medicine are rare. Sometimes doctors switch to methimazole after the first trimester of pregnancy. Some women no longer need antithyroid medicine in the third trimester. Small amounts of antithyroid medicine move into the baby’s bloodstream and lower the amount of thyroid hormone the baby makes. If you take antithyroid medicine, your doctor will prescribe the lowest possible dose to avoid hypothyroidism in your baby but enough to treat the high thyroid hormone levels that can also affect your baby. Antithyroid medicines can cause side effects in some people, including allergic reactions such as rashes and itching rarely, a decrease in the number of white blood cells in the body, which can make it harder for your body to fight infection liver failure, in rare cases Stop your antithyroid medicine and call your doctor right away if you develop any of these symptoms while taking antithyroid medicines: yellowing of your skin or the whites of your eyes, called jaundice dull pain in your abdomen constant sore throat fever If you don’t hear back from your doctor the same day, you should go to the nearest emergency room. You should also contact your doctor if any of these symptoms develop for the first time while you’re taking antithyroid medicines: increased tiredness or weakness loss of appetite skin rash or itching easy bruising If you are allergic to or have severe side effects from antithyroid medicines, your doctor may consider surgery to remove part or most of your thyroid gland. The best time for thyroid surgery during pregnancy is in the second trimester. Radioactive iodine treatment is not an option for pregnant women because it can damage the baby’s thyroid gland. Hypothyroidism in Pregnancy Symptoms of an underactive thyroid are often the same for pregnant women as for other people with hypothyroidism. Symptoms include extreme tiredness trouble dealing with cold muscle cramps severe constipation problems with memory or concentration Woman with a coat shivering outdoors You may have symptoms of hypothyroidism, such as trouble dealing with cold. Most cases of hypothyroidism in pregnancy are mild and may not have symptoms. What causes hypothyroidism in pregnancy? Hypothyroidism in pregnancy is usually caused by Hashimoto’s disease and occurs in 2 to 3 out of every 100 pregnancies.1 Hashimoto’s disease is an autoimmune disorder. In Hashimoto’s disease, the immune system makes antibodies that attack the thyroid, causing inflammation and damage that make it less able to make thyroid hormones. How can hypothyroidism affect me and my baby? Untreated hypothyroidism during pregnancy can lead to preeclampsia—a dangerous rise in blood pressure in late pregnancy anemia miscarriage low birthweight stillbirth congestive heart failure, rarely These problems occur most often with severe hypothyroidism. Because thyroid hormones are so important to your baby’s brain and nervous system development, untreated hypothyroidism—especially during the first trimester—can cause low IQ and problems with normal development. How do doctors diagnose hypothyroidism in pregnancy? Your doctor will review your symptoms and do some blood tests to measure your thyroid hormone levels. Your doctor may also look for certain antibodies in your blood to see if Hashimoto’s disease is causing your hypothyroidism. Learn more about thyroid tests and what the results mean. How do doctors treat hypothyroidism during pregnancy? Treatment for hypothyroidism involves replacing the hormone that your own thyroid can no longer make. Your doctor will most likely prescribe levothyroxine , a thyroid hormone medicine that is the same as T4, one of the hormones the thyroid normally makes. Levothyroxine is safe for your baby and especially important until your baby can make his or her own thyroid hormone. Your thyroid makes a second type of hormone, T3. Early in pregnancy, T3 can’t enter your baby’s brain like T4 can. Instead, any T3 that your baby’s brain needs is made from T4. T3 is included in a lot of thyroid medicines made with animal thyroid, such as Armour Thyroid, but is not useful for your baby’s brain development. These medicines contain too much T3 and not enough T4, and should not be used during pregnancy. Experts recommend only using levothyroxine (T4) while you’re pregnant. Some women with subclinical hypothyroidism—a mild form of the disease with no clear symptoms—may not need treatment. Pregnant woman with a pill in one hand and a glass of water in the other Your doctor may prescribe levothyroxine to treat your hypothyroidism. If you had hypothyroidism before you became pregnant and are taking levothyroxine, you will probably need to increase your dose. Most thyroid specialists recommend taking two extra doses of thyroid medicine per week, starting right away. Contact your doctor as soon as you know you’re pregnant. Your doctor will most likely test your thyroid hormone levels every 4 to 6 weeks for the first half of your pregnancy, and at least once after 30 weeks.1 You may need to adjust your dose a few times. Postpartum Thyroiditis What is postpartum thyroiditis? Postpartum thyroiditis is an inflammation of the thyroid that affects about 1 in 20 women during the first year after giving birth1 and is more common in women with type 1 diabetes. The inflammation causes stored thyroid hormone to leak out of your thyroid gland. At first, the leakage raises the hormone levels in your blood, leading to hyperthyroidism. The hyperthyroidism may last up to 3 months. After that, some damage to your thyroid may cause it to become underactive. Your hypothyroidism may last up to a year after your baby is born. However, in some women, hypothyroidism doesn’t go away. Not all women who have postpartum thyroiditis go through both phases. Some only go through the hyperthyroid phase, and some only the hypothyroid phase. What are the symptoms of postpartum thyroiditis? The hyperthyroid phase often has no symptoms—or only mild ones. Symptoms may include irritability, trouble dealing with heat, tiredness, trouble sleeping, and fast heartbeat. Symptoms of the hypothyroid phase may be mistaken for the “baby blues”—the tiredness and moodiness that sometimes occur after the baby is born. Symptoms of hypothyroidism may also include trouble dealing with cold; dry skin; trouble concentrating; and tingling in your hands, arms, feet, or legs. If these symptoms occur in the first few months after your baby is born or you develop postpartum depression , talk with your doctor as soon as possible. What causes postpartum thyroiditis? Postpartum thyroiditis is an autoimmune condition similar to Hashimoto’s disease. If you have postpartum thyroiditis, you may have already had a mild form of autoimmune thyroiditis that flares up after you give birth. Woman holding her baby. Postpartum thyroiditis may last up to a year after your baby is born. How do doctors diagnose postpartum thyroiditis? If you have symptoms of postpartum thyroiditis, your doctor will order blood tests to check your thyroid hormone levels. How do doctors treat postpartum thyroiditis? The hyperthyroid stage of postpartum thyroiditis rarely needs treatment. If your symptoms are bothering you, your doctor may prescribe a beta-blocker, a medicine that slows your heart rate. Antithyroid medicines are not useful in postpartum thyroiditis, but if you have Grave’s disease, it may worsen after your baby is born and you may need antithyroid medicines. You’re more likely to have symptoms during the hypothyroid stage. Your doctor may prescribe thyroid hormone medicine to help with your symptoms. If your hypothyroidism doesn’t go away, you will need to take thyroid hormone medicine for the rest of your life. Is it safe to breastfeed while I’m taking beta-blockers, thyroid hormone, or antithyroid medicines? Certain beta-blockers are safe to use while you’re breastfeeding because only a small amount shows up in breast milk. The lowest possible dose to relieve your symptoms is best. Only a small amount of thyroid hormone medicine reaches your baby through breast milk, so it’s safe to take while you’re breastfeeding. However, in the case of antithyroid drugs, your doctor will most likely limit your dose to no more than 20 milligrams (mg) of methimazole or, less commonly, 400 mg of PTU. Thyroid Disease and Eating During Pregnancy What should I eat during pregnancy to help keep my thyroid and my baby’s thyroid working well? Because the thyroid uses iodine to make thyroid hormone, iodine is an important mineral for you while you’re pregnant. During pregnancy, your baby gets iodine from your diet. You’ll need more iodine when you’re pregnant—about 250 micrograms a day.1 Good sources of iodine are dairy foods, seafood, eggs, meat, poultry, and iodized salt—salt with added iodine. Experts recommend taking a prenatal vitamin with 150 micrograms of iodine to make sure you’re getting enough, especially if you don’t use iodized salt.1 You also need more iodine while you’re breastfeeding since your baby gets iodine from breast milk. However, too much iodine from supplements such as seaweed can cause thyroid problems. Talk with your doctor about an eating plan that’s right for you and what supplements you should take. Learn more about a healthy diet and nutrition during pregnancy . Homeopathy provides remedies which treat not just the above symptoms but the person as a whole. Sepia Officinalis: Used when the patient presents with the following symptoms. Weak, slightly yellow appearance Tendency to faint, especially when in cold temperatures Extreme intolerance to cold, even in warm surroundings Increased irritability Hair loss Increased menstrual flow that occurs ahead of schedule Constipation Increased desire for pickles and acidic foodstuff Calcarea Carbonica: This popular medicine is useful when patients present with the following symptoms. Fat, flabby, fair person Increased intolerance to cold Excessive sweating, especially in the head Aversion to fatty foods Peculiar food habits including craving for eggs, chalk, pencils, lime, Increased menstruation that is also prolonged and is associated with feet turning cold Lycopodium Clavatum: Useful in patients who present with these symptoms: Physically weakened Increased irritability Excessive hair fall Face is pale yellow with blue circles around the eyes Craving for foods that are hot and sweet Acidity that is worse in the evenings Gastric issues including excessive flatulence Constipation with painful, hard, incomplete stooling Graphites: Presenting symptoms where Graphites are mainly used include: Obesity Intolerance to cold Depressed emotionally, timid, indecisive, weeping, listening to music Bloated, gassy abdomen Chronic constipation with hard, painful stooling process Lodium: Good appetite but lose weight quickly Tendency to eat at regular intervals Excessive warmth and need to stay in a cool environment Anxiety about present Excessive palpitations Lachesis Mutus: These patient present with the following symptoms: Feeling extremely hot, so inability to wear tight clothes Generally sad with no inclination to do any work Tendency to stay aloof and alone Excessive talkativeness Women around menopausal ageDr. Rajesh Gupta9 Likes22 Answers
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*Restless leg syndrome (RLS* ☝ *Today about*☝ Definition Restless leg syndrome (RLS) or Willis-Ekbom disease(WED) is a common cause of painful legs. The leg pain of restless leg syndrome typically eases with motion of the legs and becomes more noticeable at rest. Restless leg syndrome also features worsening of symptoms and leg pain during the early evening or later at night. Restless leg syndrome Restless leg syndrome is often abbreviated RLS; it has also been termed shaking leg syndrome. Night time involuntary jerking of the legs during sleep is also known as periodic leg/limb movement disorder. History The first known medical description of RLS was by Sir Thomas Willis in 1672. Willis emphasized the sleep disruption and limb movements experienced by people with RLS. Initially published in Latin (De Anima Brutorum, 1672) but later translated to English (The London Practice of Physick, 1685), The term “fidgets in the legs” has also been used as early as the early nineteenth century. Subsequently, other descriptions of RLS were published, including those by Francois Boissier de Sauvages (1763), Magnus Huss (1849), Theodur Wittmaack (1861), George Miller Beard (1880), Georges Gilles de la Tourette (1898), Hermann Oppenheim (1923) and Frederick Gerard Allison (1943). However, it was not until almost three centuries after Willis, in 1945, that Karl-Axel Ekbom (1907–1977) provided a detailed and comprehensive report of this condition in his doctoral thesis, Restless legs: clinical study of hitherto overlooked disease. Ekbom coined the term “restless legs” and continued work on this disorder throughout his career. He described the essential diagnostic symptoms, differential diagnosis from other conditions, prevalence, relation to anemia, and common occurrence during pregnancy. Epidemiology Except perhaps in Asian populations, RLS is a common disorder, occurring in about 10% of the population. The age-adjusted prevalence of RLS determined by telephone interviews in a random population of 1803 adults in Kentucky was 10%. A Canadian survey of 2019 adults estimated the prevalence of RLS symptoms at 17% for women and 13% for men. A population-based survey in West Pomerania, Germany, of 4107 subjects found an overall 10.6% prevalence. Using standardized questions in face-to-face interviews, Rothdach et al. reported an overall prevalence of 9.8% in 369 participants ages 65-83 years in Augsburg, Germany. In a study from Japan, 4612 participants living in urban residential areas were assessed for a single symptom of RLS by a self-administered questionnaire of the following two items: (1) Have you ever been told you jerk your legs or kick sometimes and (2) have you ever experienced sleep disturbance due to a creeping sensation or hot feeling in your legs? The prevalence of RLS ranged from 3% in women ages 20-29 years to 7% in women ages 50-59 years and correlated with age. In contrast to the first three studies, RLS had a higher prevalence in men than women, with the difference reaching significance in those 40-49 years old; in men there was no positive correlation with age. Face-to-face interviews of 157 consecutive individuals ages 55 years and older participating in a health screening program and 1000 consecutive individuals ages 21 years and older from a primary health care center in Singapore yielded much lower prevalence data. Using IRLSSG criteria, the prevalence of RLS in this predominantly Asian population was 0.6% in the older (1 male) and 0.1% (1 female) in the younger cohorts. In the Kentucky and Singapore studies, there was no gender difference; however, in the two German studies, the prevalence was higher in women and in the Japanese study it was higher in men. The Canadian study reported a significantly higher occurrence of bedtime leg restlessness in women. Types Restless legs syndrome (RLS) can be either primary or secondary, and the causes vary. Primary RLS is a neurological disorder. Although the majority of people with RLS begin to experience symptoms in their middle years, some may have signs of the problem in childhood. Their symptoms may slowly progress for years before becoming a regular occurrence. Secondary RLS tends to be more severe than the primary type and stems from another underlying condition, including the following: Anemia or low blood-iron levels Folate deficiency Nerve damage due to diabetes or other conditions Kidney disease or dialysis Attention deficit disorder (ADD) Attention deficit/hyperactivity disorder (ADHD) Pregnancy Rheumatoid arthritis Parkinson’s disease Risk factors RLS/WED can develop at any age, even during childhood. The disorder is more common with increasing age and more common in women than in men. Restless legs syndrome usually isn’t related to a serious underlying medical problem. However, RLS/WED sometimes accompanies other conditions, such as: Peripheral neuropathy: This damage to the nerves in your hands and feet is sometimes due to chronic diseases such as diabetes and alcoholism. Iron deficiency: Even without anemia, iron deficiency can cause or worsen RLS/WED. If you have a history of bleeding from your stomach or bowels, experience heavy menstrual periods or repeatedly donate blood, you may have iron deficiency. Kidney failure: If you have kidney failure, you may also have iron deficiency, often with anemia. When kidneys don’t function properly, iron stores in your blood can decrease. This, with other changes in body chemistry, may cause or worsen RLS/WED. Causes The cause of restless leg syndrome is unknown in most people. However, restless leg syndrome has been associated with Pregnancy, Obesity, Smoking, Iron deficiency and anemia, Nerve disease, Polyneuropathy (which can be associated with hypothyroidism, heavy metal toxicity, toxins, and many other conditions), Other hormone diseases such as diabetes, and Kidney failure (which can be associated with vitamin and mineral deficiency). Some drugs and medications have been associated with restless leg syndrome including: Caffeine, Alcohol, H2-histamine blockers (such as ranitidine [Zantac] and cimetidine [Tagamet]), and certain antidepressants (such as amitriptyline [Elavil, Endep]). Occasionally, restless leg syndrome run in families. Recent studies have shown that restless leg syndrome appears to become more common as a person ages. Also, poor venous circulation of the legs (such as with varicose veins) can cause restless leg syndrome. Symptoms The International Restless Legs Syndrome Study Group described the following symptoms of restless legs syndrome (RLS): Strange itching, tingling, or “crawling” sensations occurring deep within the legs; these sensations may also occur in the arms. A compelling urge to move the limbs to relieve these sensations Restlessness — floor pacing, tossing and turning in bed, rubbing the legs Symptoms may occur only with lying down or sitting. Sometimes, persistent symptoms worsen while lying down or sitting and improve with activity. In very severe cases, the symptoms may not improve with activity. Other symptoms of RLS include the following: Sleep disturbances and daytime sleepiness Involuntary, repetitive, periodic, jerking limb movements that occur either in sleep or while awake and at rest; these movements are called periodic leg movements of sleep or periodic limb movement disorder. Up to 90% of people with RLS also have this condition. In some people with RLS, the symptoms do not occur every night but come and go. These people may go weeks or months without symptoms (remission) before the symptoms return again. Complications Restless legs syndrome rarely results in any serious consequences. However, in some cases severe and persistent symptoms can cause considerable mental distress, chronic insomnia, and daytime sleepiness. In addition, since restless legs syndrome (RLS) is worse when resting, people with severe RLS may avoid daily activities that involve long periods of sitting, such as going to movies or traveling long distances. Diagnosis and test There’s no single test for diagnosing restless legs syndrome. A diagnosis will be based on your symptoms, your medical and family history, a physical examination, and your test results. Your GP should be able to diagnose restless legs syndrome, but they may refer you to a neurologist if there’s any uncertainty. There are four main criteria your GP or specialist will look for to confirm a diagnosis. These are: an overwhelming urge to move your legs, usually with an uncomfortable sensation such as itching or tingling your symptoms occur or get worse when you’re resting or inactive your symptoms are relieved by moving your legs or rubbing them your symptoms are worse during the evening or at night Blood tests Your GP may refer you for blood tests to confirm or rule out possible underlying causes of restless legs syndrome. For example, you may have blood tests to rule out conditions such as anaemia, diabetes and kidney function problems. It’s particularly important to find out the levels of iron in your blood because low iron levels can sometimes cause secondary restless legs syndrome. Low iron levels can be treated with iron tablets. Sleep tests If you have restless legs syndrome and your sleep is being severely disrupted, sleep tests such as a suggested immobilisation test may be recommended. The test involves lying on a bed for a set period of time without moving your legs while any involuntary leg movements are monitored. Occasionally, polysomnography may be recommended. This is a test that measures your breathing rate, brain waves and heartbeat throughout the course of a night. The results will confirm whether you have periodic limb movements in sleep (PLMS). Treatment and medications Treatment for RLS is targeted at easing symptoms. In people with mild to moderate restless legs syndrome, lifestyle changes, such as beginning a regular exercise program, establishing regular sleep patterns, and eliminating or decreasing the use of caffeine, alcohol, and tobacco, may be helpful. Treatment of an RLS-associated condition also may provide relief of symptoms. Other non-drug RLS treatments may include: Leg massages Hot baths or heating pads or ice packs applied to the legs Good sleep habits A vibrating pad called Relaxis Medications may be helpful as RLS treatments, but the same drugs are not helpful for everyone. In fact, a drug that relieves symptoms in one person may worsen them in another. In other cases, a drug that works for a while may lose its effectiveness over time. Drugs used to treat RLS include: Dopaminergic drugs, which act on the neurotransmitter dopamine in the brain. Mirapex, Neupro, and Requip are FDA-approved for treatment of moderate to severe RLS. Others, such as levodopa, may also be prescribed. Benzodiazepines, a class of sedative medications, may be used to help with sleep, but they can cause daytime drowsiness. Narcotic pain relievers may be used for severe pain. Anticonvulsants, or antiseizure drugs, such as Tegretol, Lyrica, Neurontin, and Horizant. Although there is no cure for restless legs syndrome, current treatments can help control the condition, decrease symptoms, and improve sleep. Lifestyle and home remedies Making simple lifestyle changes can help alleviate symptoms of RLS/WED. Try baths and massages: Soaking in a warm bath and massaging your legs can relax your muscles. Apply warm or cool packs: Use of heat or cold, or alternating use of the two, may lessen your limb sensations. Try relaxation techniques: such as meditation or yoga. Stress can aggravate RLS/WED. Learn to relax, especially before bedtime. Establish good sleep hygiene: Fatigue tends to worsen symptoms of RLS/WED, so it’s important that you practice good sleep hygiene. Ideally, have a cool, quiet, comfortable sleeping environment; go to bed and rise at the same time daily; and get adequate sleep. Some people with RLS/WED find that going to bed later and rising later in the day helps in getting enough sleep. Exercise: Getting moderate, regular exercise may relieve symptoms of RLS/WED, but overdoing it or working out too late in the day may intensify symptoms. Avoid caffeine: Sometimes cutting back on caffeine may help restless legs. Try to avoid caffeine-containing products, including chocolate and caffeinated beverages, such as coffee, tea and soft drinks, for a few weeks to see if this helps.Dr. Shailendra Kawtikwar9 Likes15 Answers
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Panchakarma- Five Teatments -1 Pancha Karma is the cornerstone to Ayurvedic management of disease. Pancha Karma is the process which gets to the root cause of the problem and corrects the essential balance of 'Tridosha' in body. Pancha Karma is not only good for alleviating disease but is also a useful tool in maintaining excellent health. Ayurveda advises undergoing Pancha Karma at the seasonal changes to clean the body, improve the digestion and to improve the metabolic processes. Panchakarma is a Sanskrit word that means "five actions" or "five treatments ". This age-old science of purifying the body is an ancient branch of Ayurveda, The Treatment in Ayurveda consists of two main types. One is Shaman Chikitsa, used to subdue the vitiated Doshas, due to which any ailments may be produced. It is administered by using various medicinal herbo-mineral preparations. However, if the Doshas are vitiated beyond a particular level, they give rise to various endotoxins, which have a tendency to be accumulated in the minute channels. These are beyond the level of pacification and hence need to be eliminated or removed from the body. In such cases, the second type of treatment, which is Shodhan Chikitsa or cleansing therapy, is indicated. Since it consists of the five types of main therapies, it is known as the Panchakarma Chikitsa. Panchakarma has been given a special place in all the ancient Ayurvedic texts. Aacharya Charak, the author of the most important ancient text on internal medicine, has described a wide use of Panchakarma therapy for almost all the major diseases. Two separate sections, Kalpa Sthanam, and Siddhi Sthanam in Charak Samhita describe the details of special decoctions and other preparations used for Panchakarma therapy. Panchakarma includes three parts namely: Poorva Karma (Preparatory Methods)which includes : Paachan (Digestion) Snehan (Internal and external oleation) Swedan (Fomentation) Pradhan Karma (Main methods)which includes : Vaman (Induced vomiting) Virechan (Induced purgation) Basti (Medicated enema) Nasya (Nasal medicine) Rakta Mokshan (Artificial bloodletting) Pashchat Karma (Post-Therapeutic Measures)which includes: Sansarjan Krama (Specific dietetics), DhumaPana (smoking of medicinal cigars) and some rules to follow specific activities. Purvakarma : Pre-purification Measures Before the actual operation of purification begins, there is a need to prepare the body in prescribed methods to encourage the body to let go of the toxins. The two procedures are 'snehan' and 'swedan'. Snehan is the oil massage. Oil is applied to the entire body with a particular type of massage which helps the toxins to move towards the gastro-intestinal tract. Oil massage also makes the superficial and deep tissues soft and supple. Snehan is given daily for three to seven days, as indicated. Swedan is sudation or sweating and is given every day immediately following the snehan. An herbal concoction may be added to the steam to further loosen the toxins from the individual. Swedan liquefies the toxins and increases the movement of toxins into the gastro-intestinal tract. After three to seven days of snehan and swedan, the doshas become well "ripened". A particular panchakarma method is then given according to the individual's constitution and disorder, prakruti and vikruti, respectively. Panchakarma - Five Basic Shodhans: Cleansing Methods 1) Vaman : therapeutic vomiting or emesis 2) Virechan : purgation 3) Basti : enema 4) Nasya : elimination of toxins through the nose 5) Rakta moksha : detoxification of the blood Vaman: Emesis Therapy When there is congestion in the lungs causing repeated attacks of bronchitis, colds, cough or asthma, the Ayurvedic treatment is therapeutic vomiting, vaman, to eliminate the kapha causing the excess mucus. First, after the snehan and swedan, three to four glasses of licorice or salt water is administered, then vomiting is stimulated by rubbing the tongue which triggers the vomiting center through the gag reflex. One may alternatively take two to three glasses of salt water which will also aggravate kapha and then rub the tongue to induce vomiting. Once the mucus is released the patient will feel instantly relieved. It is likely that congestion, wheezing and breathlessness will disappear and that the sinuses will become clear. Therapeutic vomiting is also indicated in chronic asthma, diabetes, chronic cold, lymphatic congestion, chronic indigestion and edema. Emetic Substances: madan-emetic nut, madhuka-yastimadhu-licorice, neem-bitter leaf, bimbi, kutaj-kurchi- conessi bark, murva-clematis, triloba-devdaru-deodar, Cedrus deodara, Salt, NaCl, ela-cardamom, nux vomica. Indications for Vaman : used for all kapha type disorders good for pitta headache, dizziness, and nausea will help to release blocked emotions respiratory congestion bronchitis chronic cold sinus congestion kaphagenic asthma Contra-Indications for Vaman : below the age of 12 or over age 65 menstruation pre-menstrual period (one week prior) pregnancy emaciation delicate or sensitive person with too much fear, grief or anxiety hypoglycemia vata prakruti vata diseases heart diseases during vata season acute fever diarrhea obesity Virechan : Purgation Therapy When excess bile, pitta, is secreted and accumulated in the gall bladder, liver and small intestine, it tends to result in rashes, skin inflammation, acne, chronic attacks of fever, biliary vomiting, nausea and jaundice. Ayurvedic literature suggests in these conditions the administration of therapeutic purgation or a therapeutic laxative. Virechan is facilitated with senna leaves, flax seeds, psyllium husks or triphala in a combination that is appropriate for the individual person. Virechan Substances: Senna, prune, bran, flaxseed husk, dandelion root, psyllium seed, cow's milk, salt, castor oil, raisins, mango juice, triphala. Indications for Virechan: allergic rash skin inflammation acne, dermatitis, eczema chronic fever ascites biliary vomiting jaundice urinary disorder enlargement of the spleen internal worms burning sensation in the eyes inflammation of the eyes conjunctivitis gout Contra-Indications for Virechan: low agni acute fever diarrhea severe constipation bleeding from rectum or lung cavities foreign body in the stomach after enema emaciation or weakness prolapsed rectum alcoholism dehydration childhood old age ulcerative colitisAyurveda-Panchakarma Basti & Nasya -2 Basti: Enema Therapy Vata's predominant site is the colon. Ayurvedic basti involves the introduction into the rectum of herbal concoctions of sesame oil, and certain herbal preparations in a liquid medium. Basti, is the most effective treatment of vata disorders, although many enemas over a prescribed period of time are usually required. It relieves constipation, distention, chronic fever, cold, sexual disorders, kidney stones, heart pain, backache, sciatica and other pains in the joints. Many other vata disorders such as arthritis, rheumatism, gout, muscle spasms and headaches may also be treated with basti. Vata is a very active principle in pathogenesis. If we can control vata through the use of basti, we have gone a long way in going to the root cause of the vast majority of diseases. Vata is the main etiological factor in the manifestation of diseases. It is the motive force behind the elimination and retention of feces, urine, bile and other excreta. There are eight main types of basti, according to traditional texts, each with their own indications and contra-indications as listed below. 1. Anuvasana (oil enema) is used in pure vata disorders and when a person is having excess hunger or dryness related to vata imbalances. 2. Niruha-Asthapana (decoction enema) is used, among other conditions, for evacuation of vata, nervous diseases, gastro-intestinal vata conditions, gout, certain fever conditions, unconsciousness, certain urinary conditions, appetite, pain, hyperacidity and heart diseases. 3. Uttara Basti (through the urethra with men or vagina with women) is used for selected semen and ovulation disorders and for some problems involving painful urination or bladder infections. This is not to be used for someone with diabetes. 4. Matra Basti (daily oil enema) is used by someone emaciated by overwork or too much exercise, too much heavy lifting, walking too long of a distance, too much sexual activity or someone with chronic vata disorders. It does not need to be accompanied by any strict dietary restriction or daily routine and can be administered, in the appropriate cases, in all seasons. It gives strength, promotes weight and helps elimination of waste products. 5. Karma Basti (schedule of 30 bastis), 6. Kala Basti (schedule of 15 bastis; 10 oil + 5 decoction) 7. Yoga Basti (schedule of 8 bastis; 5 oil + 3 decoction). 8. Bruhana Basti (nutritional enema) is used for providing deep nutrition in select conditions. Traditionally, highly nutritive substances have been used, such as warm milk, meat broth, bone marrow soup and herbs like shatavari or ashwagandha. General Indications for Basti: constipation low back ache gout rheumatism sciatica arthritis nervous disorders vata headache emaciation muscular atrophy General Contra-Indications for Basti (include but are not limited to the following): Enema therapy should not be used if the patient is suffering from diarrhea, bleeding of the rectum, chronic indigestion, breathlessness, diabetes, fever, emaciation, severe anemia, pulmonary tuberculosis, old age or for children below the age of seven years. for oil enemas: diabetes, obesity, indigestion, low agni, enlarged liver or spleen, unconsciousness, tuberculosis and cough. for decoction enemas: debility, hiccough, hemorrhoids, inflammation of anus, piles, diarrhea, pregnancy, ascites, diabetes and some conditions involving painful or difficult breathing. for nutritional enemas: diabetes, obesity, lymphatic obstruction, ascites. for urethra or vaginal enemas: diabetes Nasya: Nasal Administration The nose is the doorway to the brain and it is also the doorway to consciousness. The nasal administration of medication is called nasya. An excess of bodily humors accumulated in the sinus, throat, nose or head areas is eliminated by means of the nearest possible opening, the nose. Prana, life force as nerve energy, enters the body through the breath taken in through the nose. Prana is in the brain and maintains sensory and motor functions. Prana also governs mental activities, memory, concentration and intellectual activities. Deranged prana creates defective functioning of all these activities and produces headaches, convulsions, loss of memory and reduced sensory perception. Thus nasal administration, nasya is indicated for prana disorders, sinus congestion, migraine headaches, convulsions and certain eye and ear problems. There are six main types of nasya, as listed below. 1. Pradhamana (virechan) Nasya (cleansing nasya) uses dry powders (rather than oils) that are blown into the nose with a tube. Pradhamana nasya is mainly used for kapha types of diseases involving headaches, heaviness in the head, cold, nasal congestion, sticky eyes, hoarseness of voice due to sticky kapha, sinusitis, cervical lymph adenitis, tumors, worms, some skin diseases, epilepsy, drowsiness, Parkinsonism, inflammation of the nasal mucosa, attachment, greed and lust. Traditionally, powders such as brahmi are used. 2. Bruhana Nasya (nutrition nasya) uses ghee, oils, salt, shatavari ghee, ashwagandha ghee and medicated milk and is used mainly for vata disorders. It is said to benefit conditions resulting from vata imbalances such as vata-type headaches, migraine headache, dryness of voice, dry nose, nervousness, anxiety, fear, dizziness, emptiness, negativity, heaviness of eyelids, bursitis, stiffness in the neck, dry sinuses and loss of sense of smell. 3. Shaman Nasya (sedative nasya) is used according to which dosha is aggravated but mainly for pitta-type disorders such as thinning of hair, conjunctivitis and ringing in the ears. Generally certain herbal medicated decoctions, teas and medicated oils are used. 4. Navana Nasya (decoction nasya) is used in vata-pitta or kapha-pitta disorders and is made from decoctions and oils together. 5. Marshya Nasya (ghee or oil nasya) 6. Prati Marshya (daily oil nasya) This helps to open deep tissues and can be done every day and at any time to release stress. Substances Used in Nasya: brahmi, ginger, ghee oils, decoctions, onion, garlic, Piper longum, black pepper, curry pepper, rose, jasmine, mogra flowers and henna. Indications for Nasya: stress emotional imbalances stiffness in the neck & shoulders dryness of the nose sinus congestion hoarseness migraine headache convulsions Contra-Indications for Nasya: sinus infections pregnancy menstruation after sex, bathing, eating or drinking of alcohol should not be used below 7 years or over 80 years of age Click here to read more about 'Nasyakarma' Raktamoksha : Traditional Ayurvedic Method for Purification and Cleansing of the Blood Toxins present in the gastro-intestinal tract are absorbed into the blood and circulated throughout the body. This condition is called toxemia, which is the basic cause of repeated infections, hypertension and certain other circulatory conditions. This includes repeated attacks of skin disorders such as urticaria, rashes, herpes, eczema, acne, leukoderma, chronic itching or hives. In such conditions, along with internal medication, elimination of the toxins and purification of the blood is necessary. Raktamoksha is also indicated for cases of enlarged liver, spleen and gout. Extracting a small amount of blood from a vein relieves the tension created by the pittagenic toxins in the blood. Bloodletting also stimulates the spleen to produce antitoxic substances which helps to stimulate the immune system. Toxins are neutralized enabling radical cures in many blood born disorders. Bloodletting is contraindicated in cases of anemia, edema, extreme weakness, diabetes and in children and elderly persons. Indications for Raktamoksha: urticaria rash acne eczema scabies leukoderma chronic itching hives enlarged liver or spleen gout Contra-Indications for Raktamoksha: anemia edema weakness young children old age during pregnancy during menstruation Read more about Various Diseases and Indicated Panchakarma procedures for them > @Dr. Tapan Kumar Sau11 Likes15 Answers