LPC HIV Awareness and Comfort Zone, Las Piñas (2025)

09/02/2022

AIDS, COLLAGEN, BONE MARROW

Part II.

Patients with AIDS showed significantly reduced trabecular bone thickness (Table 1). A significant positive correlation was observed between the trabecular bone thickness and age of patients with AIDS (rS = 0.0349; P = .006), and a significant negative correlation was observed between the trabecular thickness and BMI in the same patient group (rS = −0.156; P < .001).

The percentage of collagen fibers in the trabecular bone was significantly higher in patients with AIDS (Fig. 1, Table 1). A negative and statistically non-significant correlation was observed between the percentage of collagen fibers and the age of patients with AIDS (rS = −0.0107; P = .600), and a negative and statistically significant correlation was observed between collagen percentage and BMI in the same patient group (rS = −0.024; P < .001).

4. Study limitations
As this study was conducted using data collected from autopsy reports, many relevant information for the bone health it cannot be obtained, such as smoking, menopause, use of hormone therapy, use of antiretroviral therapy, CD4 count and viral load at the time of death, among other factors that possibly influence bone formation. A cross-sectional study conducted in São Paulo (Brazil), which included 4.332 women over 40 years who were treated in primary care service, observed the prevalence of osteoporosis (33%) and osteoporotic fractures (11.5%) in these patients [15]. Hypoestrogenism is considered an important risk factor for low bone mineral density and recent studies correlated the occurrence of osteoporosis with the time of menopause. The same reasoning applies to the use of hormone therapy for prevention of osteoporosis. The beneficial effects of estrogen therapy on the preservation of BMI and reduce the risk of fractures are well established in the literature [16]. A World Health Organization study indicated that smoking confers substantial risk for future fracture, regardless of a BMI [17]. Researchers have shown that individuals with low CD4 levels have low bone mineral density; antiretroviral therapy affects the bone structure as leads to a recovery of bone turnover [18].

5. Discussion

The changes of the bone marrow have been the subject of several studies in patients with HIV/AIDS. Its different constituents, such as trabecular bone, collagen fibers, and cellularity show up in the affected syndrome.

In this study, patients with AIDS had significantly reduced trabecular bone thickness. Another study showed that the prevalence of osteopenia and osteoporosis is 3-fold higher in patients infected with HIV than in non-infected patients. The mechanisms responsible for these changes are still not completely understood. However, chronic inflammation caused by HIV infection was associated with bone resorption, and the virus itself may also directly affect osteoclast activity [19], [20]. HIV Tat, a regulatory protein of viral transcription, has been found to increase differentiation of precursor cells into osteoclast [21]. Tat viral protein was associated with increased osteoclast activity formation by 70%, HIV Tat being biologically active in driving a pro-osteoclastic phenotype [22]. The balance between bone formation and reabsorption becomes progressively negative with aging, and most of bone loss occurs after the age of 65 years, which is more intense in women due to the drop of estrogen levels [23]. However, a significant proportion of trabecular bone loss throughout life is age related and estrogen independent, since trabecular bone is not as sensitive to the estrogen effects in maintaining bone mass as the cortical bone [24], [25].
Some studies indicate that oxidative stress, which increases with aging and is accentuated by s*x steroid deficiency, may be an important factor leading to impaired bone formation with aging [24]. The balance between bone formation and resorption becomes increasingly negative with increasing age, and most of the bone loss occurs after 65 years of age and is actually more intense in women due to the sudden drop in estrogen levels [23]; however, a significant proportion of trabecular bone loss is directly related to age, regardless of estrogen levels; this is because the trabecular bone does not have the same sensitivity to estrogen in terms of bone mass maintenance purposes, as with the cortical bone [24], [25]. Some studies suggest that increased oxidative stress, which occurs with aging and is marked by a deficiency of s*x steroids, may be an important cause of poor bone formation [25].
Collagen deposition in trabecular bones was significantly higher in patients with AIDS and was more pronounced in younger patients and those with lower BMI. Mature osteoblasts synthesize molecules involved in bone formation or regulation of osteoclast activity, such as collagen type I. These osteoblasts may be infected with HIV and directly affected by viral replication [26]. Some studies have shown that low body weight contributes to low bone mineral density, besides increasing the risk of fracture, especially in older women. Increased peripheral conversion of gonadal hormones in obese patients improve the maintenance of bone mass, protecting against the adverse effects of estrogen deficiency on the skeleton [16]. BMI lower than 25 kg/m2 was associated with a 3-fold increase in the risk of developing osteoporosis and the protective effect of body weight or BMI on bone has previously been reported. The conversion of androgens to estrogens is an important source of circulating estrogens; it occurs in adipose tissue and bone cells, and the local concentration of estradiol seems to contribute significantly to skeletal homeostasis. Collagen loss plays a major role in the pathogenesis of osteoporosis. It has been postulated previously that hormone reposition therapy in menopause leads to an increase in bone mass by an increase in the collagen levels in bone, by elevating estrogen levels [27], [28].
Although this study did not observe a significant change in cellularity, a variety of nonspecific morphological abnormalities may be observed microscopically in the bone marrow of patients infected with HIV. Global hypercellularity may occur in the initial course of AIDS or during systemic infections because of cellular hyperplasia of granulocyte lineages and megakaryocytes. Increased hypocellularity and adipose tissue atrophy have been observed as consequences of the debilitation that occurs in later stages of AIDS [29], [30].
Anatomically, the spaces in the bone marrow are compartmentalized, allowing immune and bone cells to interact and influence each other. Therefore, bone homeostasis is often influenced by immune responses, particularly when the immune system is activated or compromised [1]. Increasing evidence indicates that bone marrow suppression is caused by viral infection of accessory cells, which results in impairment of stromal function and an altered hematopoietic growth factor network [31].
In this study, the bone marrow of patients with AIDS showed thinning and increased collagen deposition in trabecular bone. The bone marrow stroma consists of a mixture of cellular and extracellular components, namely fibroblasts, adipocytes, endothelial cells, macrophages, adhesion molecules, and growth factors and, when amended, contributes to the development of hematological abnormalities in patients with HIV/AIDS [32], [33]. Fibroblasts are an important source of trophic factors or inhibitory regulating the development of hematopoietic progenitor cells. Direct infection of stromal components such as macrophages, megakaryocytes, and fibroblasts convert these cells into HIV reservoirs and inhibit their ability to support growth of hematopoietic progenitor cells [32], [33], [34].
Infection of these cells can result in deregulated expression of adhesion molecules and regulatory cytokines and play an important role in the development of cytopenias and susceptibility to infections [35], [36]. Immune dysfunction in HIV-infected individuals are primarily due to high levels inflammatory cytokines such as TNF-α, IFN-α, IFN-γ, and TGF-β, which are present in bone marrow biopsies and serum of patients with the syndrome [37].
Previous experimental studies on HIV/AIDS have shown that collagen production and pathological deposition were associated with early induction of immunoregulatory response in secondary lymphoid tissues consisted of regulatory T cells as well as other types of cells expressing TGF-β [38], suggesting that this cytokine is an important pro-fibrotic signal from HIV/AIDS disease.
Some authors also show a statistical correlation between CD41 lymphocyte count and the degree of reticulin fibrosis, indicating that the mechanism of bone marrow fibrosis is independent of the disease state [39], [40].
In these patients, abnormalities are often observed in all bone marrow cells, including the matrix. It is hoped that this study contribute to further studies that could demonstrate the relationship of bone marrow changes with the immune and nutritional status of patients infected with HIV and the presence of opportunistic infections. The interpretation of the evaluated parameters in this study can be very helpful in the diagnosis of conditions associated with HIV infection, contributing to clinical improvement and life expectancy of the patient.

09/02/2022

AIDS, COLLAGEN, BONE MARROW

Part I.

1. Introduction
The AIDS is a systemic disease with multiple complications. Bone marrow abnormalities are observed in all stages of HIV infection, and their frequency increases with disease progression [1]. Low bone mineral density and a decreased bone mass have been reported in male and female HIV-infected patients of several ages [2], [3].

HIV infection may compromise hematopoiesis by directly infecting progenitor cells or by causing changes in the bone marrow microenvironment, which may affect its ability to support proliferation and differentiation of progenitor cells [4]. The investigation of the bone marrow healthy is important in patients with peripheral hematological abnormalities. Anemia is present in most of HIV infected symptomatic like normocytic normochromic anemia or anemia of chronic disease [5].

HIV is able to infect a variety of stromal elements of the bone marrow, including monocytes and macrophages, endothelial and myoepithelial cells, and fibroblasts [6], [7], [8]. Previous studies have shown that increased bone marrow fibrosis is commonly observed in patients with HIV/AIDS; however, the relationship between this deposition and CD4 T-lymphocyte counts remains controversial [9].

Osteoporosis was three-fold more prevalent in individuals infected with HIV compared to non-infected individuals. The chronic inflammation caused by the virus has been associated with bone resorption and osteoclast activity [3]. Moreover, anti-retroviral therapy has been correlated with changes in bone metabolism, which render patients more susceptible to osteopenia and osteoporosis [10].

Because histopathological studies of bone marrow from autopsied patients with AIDS are rare, the aim of this study was to analyze the trabecular thickness, percentage of collagen in the trabeculae, and bone marrow cellularity in autopsied patients with AIDS. The results of this study provide a scientific basis for understanding this microenvironment better, which will support the development of therapies to reduce bone changes during HIV infection.

2. Materials and methods
This study was approved by the Triângulo Mineiro Federal University Research Ethics Committee, approval number 850.

Sixty bone marrow samples were collected from the middle third of the sternum during autopsies performed at the Clinical Hospital at the Triângulo Mineiro Federal University, Uberaba, Minas Gerais, Brazil, being a retrospective study that occurred between 1983 and 2007. These data were collected by 2 pathologists of the General Pathology division of Clinical Hospital at the Triângulo Mineiro Federal University which is responsible for autopsies. From those reports were obtained data such as age, gender, skin color, and body mass index (BMI). The patients were divided into 2 groups: with AIDS (n = 30) or without AIDS (n = 30). The control group was selected with the attempt to pair age, gender, and race with the group of patients with AIDS.

AIDS diagnosis was confirmed by evidence of at least one AIDS-defining disease presented by the patient and by CD4 T lymphocyte count below 200 cells/mm3 [11], [12]. Inclusion criteria for AIDS patients were defined as those who owned at least one of the following defining diseases: invasive cervical cancer, extrapulmonary cryptococcosis, Herpes simplex mucocutaneous, or non-Hodgkin lymphoma [13]. All the patients with AIDS observed in this study died of infection during the post- HAART era. However, not all of them had made use of the therapy, which may be explained by the fact that many of them looked for health services in an advanced stage of the disease. Opportunistic infections were not considered in the selection of patients. There were no exclusion criteria.

Bone marrow fragments were subjected to histological processing, and serial 4-μm thick sections were cut. Cellularity (hypercellularity, normality, or hypocellularity) was assessed by observing hematoxylin-eosin (HE) stained slides under an objective lens with a magnification power of 5× (final magnification ×200). To evaluate trabecular thickness, slides stained with HE were observed under an objective lens with a magnification power of 20× (final magnification ×800); the thickness was expressed in micrometers (μm). To obtain these measures, each histological section was divided into 4 fields, and 5 trabeculae were randomly selected in each field. In each trabecula, 5 minor axis measurements (100 measurements per slide) were performed, determined by the accumulated mean method [14].

Picrosirius stained slides were used to quantify collagen expression in the trabecular bones. Histological sections were analyzed under polarized light with an objective lens having a magnification power of 5× (final magnification ×200). Collagen deposition, quantified by the observer, presented as birefringence with orange to red shading. Ten trabeculae from each of the 4 fields per histological section were analyzed, with a total of 40 measurements per slide. Collagen percentage and trabecular thickness were quantified by using a video camera coupled to a common light microscope and an image analysis system (KS300 – Kontron Zeiss). Taking these criteria into account, these measurements were made by a researcher individually.

Statistical analyses were performed by using the SigmaStat software suite. After applying the Kolmogorov-Smirnov test, the Student t test was used in case of normal distribution and similar variances; the Mann-Whitney U test (T) was used to analyze non-parametric distributions. Correlations were analyzed by using the Pearson (r) and Spearman (rS) tests. Differences in probability (P) lower than 5% (P < .05) were considered statistically significant.

3. Results
Sixty bone marrow samples were collected from autopsied patients. The average age of patients with or without AIDS was 31.86 ± 7.59 years and 48.73 ± 16.44 years, respectively, and the BMI of patients with and without AIDS was 20.43 ± 4.14 kg/m2 and 25.21 ± 6.45 kg/m2, respectively (Table 1). At the AIDS group, 7 patients were female (23.33%) and 23 were male (76.66%); 25 were white (83.33%) and 5 were nonwhite (16.66%). At the without-AIDS group, 11 patients were female (36.66%) and 19 were male (63.33%); 24 were white (80%) and 6 nonwhite (20%).

Table 1. Constitutional and morphometric data from bone marrow of autopsied patients with or without AIDS

02/02/2022

Kaposi's sarcoma

Kaposi's sarcoma is a type of cancer that forms in the lining of blood and lymph vessels. The tumors (lesions) of Kaposi's sarcoma typically appear as painless purplish spots on the legs, feet or face. Lesions can also appear in the ge***al area, mouth or lymph nodes. In severe Kaposi's sarcoma, lesions may develop in the digestive tract and lungs.

The underlying cause of Kaposi's sarcoma is infection with a virus called human herpesvirus 8 (HHV-8). In healthy people, HHV-8 infection usually causes no symptoms because the immune system keeps it under control. In people with weakened immune systems, however, HHV-8 has the potential to trigger Kaposi's sarcoma.
People infected with human immunodeficiency virus (HIV) — the virus that causes AIDS — have the highest risk of Kaposi's sarcoma. The immune system damage caused by HIV allows cells harboring HHV-8 to multiply. Through unknown mechanisms, the characteristic lesions form.
Recipients of organ transplants who take immune system-suppressing drugs to prevent transplant rejection also are at risk of Kaposi's sarcoma. In this population, though, the disease tends to be milder and easier to control than it is in people with AIDS.
Another type of Kaposi's sarcoma occurs in older men of Eastern European, Mediterranean and Middle Eastern descent. Known as classic Kaposi's sarcoma, this cancer progresses slowly and typically causes few serious problems.
A fourth type of Kaposi's sarcoma that affects people of all ages occurs in equatorial Africa.

Diagnosis

To determine if a suspicious-looking skin lesion is Kaposi's sarcoma, your doctor will need to perform a biopsy, which involves removing a small piece of tissue for examination in a laboratory.

Tests to diagnose internal Kaposi's sarcoma include:

F***l occult blood test. This test detects hidden blood in stool, which can be a sign of Kaposi's sarcoma in the digestive tract.Chest X-ray. A chest X-ray may reveal abnormalities suggesting Kaposi's sarcoma in the lung.Bronchoscopy. In this test, a thin tube (bronchoscope) is passed through your nose or mouth into your lungs to view their lining and take samples of abnormal areas.Upper endoscopy. This test uses a thin tube (endoscope) passed through your mouth to examine the esophagus, stomach and first part of your small intestine. If your doctor suspects Kaposi's sarcoma inside any of these organs, a biopsy of the affected tissue is taken to confirm the disease.Colonoscopy. In this test, a thin tube (colonoscope) is passed through your re**um and advanced into your colon to examine the walls of these organs. Abnormalities suggesting Kaposi's sarcoma in the re**um or colon can also be biopsied during colonoscopy.

Bronchoscopy is unnecessary for diagnosis of Kaposi's sarcoma unless you have unexplained breathing problems or an abnormal chest X-ray. Similarly, unless a f***l occult blood test finds blood in your stool, you may be able to avoid upper endoscopy or colonoscopy.

Treatment

The treatment for Kaposi's sarcoma varies, depending on these factors:

Type of disease. Historically, AIDS-related Kaposi's sarcoma has been more serious than classic or transplant-related disease. Thanks to increasingly effective antiviral drug combinations and improved prevention of other AIDS-related infections, Kaposi's sarcoma has become less common and less severe in people with AIDS.

Number and location of lesions. Widespread skin lesions and internal lesions require different treatment from isolated lesions.

Effects of the lesions. Lesions in the mouth and throat make eating difficult, while lesions in the lung can cause shortness of breath. Large lesions, particularly on the upper legs, can lead to painful swelling and difficulty moving around.

General health. The immune system impairment that makes you vulnerable to Kaposi's sarcoma also makes certain treatments, such as powerful chemotherapy drugs, too risky to try. The same is true if you also have another type of cancer, poorly controlled diabetes or any serious, chronic disease.

For AIDS-related Kaposi's sarcoma, the first step in treatment is to start or switch to an antiviral drug combination that will reduce the amount of the virus that causes HIV/AIDS and increase the number of certain immune cells in your body. Sometimes, this is the only treatment needed.
When possible, people with transplant-related Kaposi's sarcoma may be able to stop taking immune system-suppressing medication. This allows the immune system to eliminate the cancer in some cases. Switching to a different immunosuppressive medication can also bring improvement.
Treatments for small skin lesions include:

Minor surgery (excision)

Burning (electrodessication) or freezing (cryotherapy)

Low-dose radiation, which is also helpful for lesions in the mouth

Injection of the chemotherapy drug vinblastine directly into lesions

Application of a vitamin A-like drug (retinoid)

Lesions treated in any of these ways are likely to return within a couple of years. When this happens, treatment can often be repeated.
Radiation is the usual treatment for those with multiple skin lesions. The type of radiation used and the locations of lesions being treated vary from person to person. When more than 25 lesions are present, chemotherapy with standard anti-cancer drugs may be helpful. Chemotherapy is also used to treat Kaposi's sarcoma in the lymph nodes and digestive tract.

30/01/2022

What Happens to My HIV Test Results?

Your HIV test results become part of your medical record. Therefore, the results could be disclosed to third-party payers (such as medical insurance companies) and other authorized parties. A positive test result will also be reported to the appropriate health department.

How Can My HIV Test Results Be Kept Confidential?

Though HIV tests performed at most doctors offices become part of the patient's medical record, there are places you can go that provide confidential HIV testing. These places will perform HIV tests without even taking your name (anonymous testing). An anonymous HIV test does not become part of your medical record.

Should you discover that you have HIV, inform your medical providers so that you can receive proper care.

What to Do After Being Diagnosed as HIV-Positive

If you've just found out that you're HIV-positive, you may feel overwhelmed, fearful, and alone. But you’re far from alone. People and resources are available to help you and the more than 1 million HIV-positive people living in the U.S. today.
It may help to remember that being HIV-positive is not the virtual death sentence it once was. HIV (human immunodeficiency virus) can lead to AIDS (acquired immunodeficiency syndrome). But being HIV-positive does not necessarily mean that you have AIDS. New treatments have turned being HIV-positive into a chronic condition for many people. With a healthy lifestyle and the right medical care, many HIV-positive people are living long, productive lives.

Still, learning that you are HIV-positive may leave you reeling. Where should you turn for help? Who should you tell? What should you do first? Here are a few guideposts to help you through this difficult time.

26/01/2022

How CD4 Counts Help Treat HIV and AIDS

The CD4 count is a test that measures how many CD4 cells you have in your blood. These are a type of white blood cell, called T-cells, that move throughout your body to find and destroy bacteria, viruses, and other invading germs.
Your test results help your doctor know how much damage has been done to your immune system and what's likely to happen next if antiretroviral treatment (ART) is not initiated. All persons with HIV should be started on ART regardless of whether the CD4 count is high or low. The CD4 count should increase in response to effective ART.
Keeping your CD4 count up with an effective ART can hold off symptoms and complications of HIV and help you live longer. In fact, studies have found that patients who adhere to regular treatments can achieve a life span similar to persons who have not been infected with HIV.

Persons with very low CD4 counts may need to take drugs to prevent specific opportunistic infections (OIs) in addition to taking their ART. Once the CD4 count increases in response to ART, it may be possible to stop taking these OI medications.

What Does HIV Do to CD4 Cells?

HIV damages your immune system because it targets CD4 cells. The virus grabs on to the surface of a cell, gets inside, and becomes a part of it. When the infected CD4 cell dies, it releases more copies of HIV into the bloomstream.
Those new bits of virus find and take over more CD4 cells, and the cycle continues. This leads to fewer and fewer HIV-free, working CD4 cells.

HIV can destroy entire "families" of CD4 cells, and then the germs these cells fight have easy access to your body. The resulting illnesses are called opportunistic infections (OIs) because they take advantage of your body's lack of defense.

What the Results Mean

A normal CD4 count is from 500 to 1,400 cells per cubic millimeter of blood. CD4 counts decrease over time in persons who are not receiving ART. At levels below 200 cells per cubic millimeter, patients become susceptible to a wide variety of OIs, many of which can be fatal.

24/01/2022

What are the different tests that help monitor my HIV?

Your health care provider will use blood tests to monitor your HIV infection. These tests help your health care provider make decisions about changes to your treatment.

CD4 Count

▪︎Your CD4 count is the number of CD4 cells you have in your blood. CD4 cells help your body fight infections.
▪︎HIV attacks and lowers the number of CD4 cells in your blood. This makes it difficult for your body to fight infections.
▪︎Your health care provider will check your CD4 count every 3 to 6 months.

Viral Load Test

Viral load is the amount of HIV in your blood.

Your health care provider will use a viral load test to determine your viral load.

When your viral load is high, you have more HIV in your body. This means your immune system is not fighting HIV very well.

You should have a viral load test

every 4 to 6 months,

before you take a new HIV medicine, and

around 2 to 8 weeks after starting or changing medicine.

22/01/2022

What do I need to do as part of my HIV care?
Keep Your Medical Appointments

Use a calendar to mark your appointment days.

Set reminders on your phone.

Download an app on your phone that can help remind you of your medical appointments.

Keep your appointment card in a place where you will see it.

Ask a family member or friend to help you remember your appointment.

Talk Honestly with Your Health Care Provider

Your health care provider needs to have the most accurate information to manage your care and treatment.

Write down questions you want to discuss with your health care provider. Be ready to write down the answers.

Keep track of your lab results, medical visits, and care and treatment plans.

Make sure your health care providers have your correct contact information.

Take Your HIV Medicine as Prescribed

This will help keep your viral load low and your CD4 count high.

Take your HIV medicine exactly how your health care provider tells you to—at specific times of the day, with or without certain kinds of food.

Keep track of your medicine and schedule.

Talk to your health care provider or pharmacist if you have questions about when or how to take your medicine, or if you are experiencing any side effects.

20/01/2022

Who should be on my health care team?

Finding a health care teamexternal icon that is knowledgeable about HIV care is an important step. Your health care team will help you manage your care and treatment.

Primary HIV Health Care Provider

Your primary HIV health care provider should lead your health care team. Your primary HIV health care provider may be a

▪︎Medical Doctor (MD or DO),
▪︎Nurse Practitioner (NP), or
▪︎Physician Assistant (PA).

Your primary HIV health care provider will

▪︎determine which HIV medicine is best for you,
▪︎prescribe HIV medicine (called antiretroviral therapy or ART),
▪︎monitor your progress and help you manage your health, and
▪︎put you in touch with other HIV providers who can address your needs.Other HIV Providers

Your health care team may include other providers who are experts in taking care of people with HIV.

▪︎Allied health care professionals like nurses, mental health providers, pharmacists, nutritionists, and dentists.
▪︎Social service providers like social workers, case managers, substance use specialists, and patient navigators.

18/01/2022

Sticking to my treatment plan is hard. How can I deal with the challenges?

Tell your health care provider right away if you’re having trouble sticking to your plan. Together you can identify the reasons you’re skipping medications and make a plan to address those reasons.

Talk to your health care provider about problems taking your HIV medicine.

Problems taking pills. This can make staying on treatment challenging. Your health care provider can offer tips and ideas for addressing these problems.Side effects from medicine. Nausea or diarrhea can make a person not want to take their pills. There are medicines or other support, like nutritional counseling to make sure you’re getting important nutrients. This can help with the most common side effects.Treatment fatigue. Some people find that sticking to their treatment plan becomes harder over time. Make it a point to talk to your health care provider about staying on your treatment plan.

Plan ahead and keep extra medicine with you.

A busy schedule. Work or travel away from home can make it easy to forget to take pills. It may be possible to keep extra medicine at work or in your car. But talk to your health care provider first. Some medications are affected by extreme temperatures and it is not always possible to keep medications at work.

Find help for mental health or substance use disorders.

Being sick or depressed. How you feel mentally and physically can affect your willingness to stick to your treatment plan. Your health care provider, social worker, or case manager can refer you to a mental health provider or local support groups.Alcohol or drug use. If substance use is interfering with your ability to keep yourself healthy, it may be time to quit or better manage it.If you need help finding substance use disorder treatment or mental health services, use SAMHSA’s Treatment Locatorexternal icon.

Talk to your health care provider if you miss a lot of doses of your HIV medicine.

Missing a dose. In most cases, you can take your medicine as soon as you realize you missed a dose. Then take the next dose at your usual scheduled time (unless your pharmacist or health care provider has told you something different).

Missing a lot of doses. Talk to your health care provider or pharmacist about ways to help you remember your medicine. You and your health care provider may even decide to change your treatment routine to fit your health care needs and life situation.
Will HIV treatment interfere with my hormone therapy?

There are no known drug interactions between HIV medicine and hormone therapy.

Talk to your health care provider if you are worried about taking HIV medicine and hormone therapy at the same time. Your health care provider will help you stay healthy and ensure your hormone therapy stays on track.

What if my treatment is not working?

Your health care provider may change your prescription.

A change is not unusual because the same treatment does not affect everyone in the same way.

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